One of the most common forms of dermatitis is eczema, which occurs more in children than adults. This skin condition presents as dry, itchy skin that leads to rashes due to itching, rubbing and irritation. When the person continues to itch and rub their skin, the skin will thicken causing lichenification. Genetic, environmental and lifestyle factors play a role in this condition. A common gene mutation observed in atopic dermatitis is Filaggrin, which is responsible for making the skin’s outer layer by forming corneocytes. People with eczema have a dysfunctional and unorganized skin barrier which causes dry skin since there is water and moisture loss. In addition, they have a decreased number of beta-defensins, which are host defense peptides so they are more prone to infections. The damaged skin provides less protections against irritants, allergens, viruses and bacterias. They are more prone to Staphylococcus aureus infections which can make eczema worse and need to be treated with antibiotics. Eczema herpeticum, a medical emergency, can also occur caused by the ****** simplex virus-1. Treatment and management of eczema are skin hydration and topical anti-inflammatory medications. Moisturizing products such as emollients and ointments are used to hydrate the skin and keep it from drying out. Steroid creams or topical pimecrolimus and tacrolimus can be used to treat flare-ups. Topical steroids shouldn’t be used daily because there are numerous long term side effects including atrophy, telangiectasia and rebound dermatitis. Oral antihistamines can be taken at bedtime to help with disturbed sleep caused by itching. It is essential to educate patients on eliminating and avoiding triggers and allergens that might cause flare-ups.
References
Nemeth V, Evans J. Eczema. [Updated 2020 Mar 24]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK538209/
InformedHealth.org [Internet]. Cologne, Germany: Institute for Quality and Efficiency in Health Care (IQWiG); 2006-. Eczema: Overview. 2013 Sep 26 [Updated 2017 Feb 23].Available from: https://www.ncbi.nlm.nih.gov/books/NBK279399/
Eczema, also known as atopic dermatitis, is a chronic skin condition that affects millions of people worldwide, causing dry, itchy, and inflamed patches of skin. It often begins in childhood but can occur at any age, with symptoms that last into adulthood. Eczema can be a result of genetic predisposition, environmental factors, and immune system dysregulation. Individuals with eczema often have a weakened skin barrier, making their skin more vulnerable to irritants, allergens, and infections. Common symptoms include dry, sensitive skin, redness, thickened or scaly patches, and intense itching, which can lead to scratching and further skin damage. Triggers such as harsh soaps, detergents, certain fabrics, allergens like dust mites and pollen, extreme weather conditions, and emotional stress can exacerbate symptoms. Treatment for eczema focuses on relieving symptoms, repairing the skin barrier, and preventing flare-ups. Moisturizers are a big part of disease management. Products containing petrolatum or lanolin such as, Eucerin,or Aquaphor can be particularly effective in maintaining hydration and protecting the skin. Topical corticosteroids are widely used during flare-ups to reduce inflammation and itching. For sensitive areas such as the face and neck, non-steroidal alternatives like topical calcineurin inhibitors, including tacrolimus and pimecrolimus, may be prescribed. Systemic treatments like oral corticosteroids, immunosuppressants such as methotrexate, and biologics like dupilumab are reserved for severe or refractory cases. With all topical products it is important to keep in mind to “Wash hands after application, apply a thin layer only to the affected are twice a day, and use the smallest amount needed to control symptoms.” (RxPrep UWorld) Lifestyle adjustments are also important in managing eczema. Patients are encouraged to use gentle, fragrance-free cleansers, take lukewarm baths, and avoid over-scrubbing or using harsh towels. Patients can “look for products with the National Eczema Association Seal of Acceptance™ to find moisturizers free of fragrances, dyes, and other common allergens." (National Eczema Association). Wearing soft, breathable fabrics like cotton instead of wool or synthetic materials can prevent irritation. Stress management techniques, such as meditation, yoga, or deep-breathing exercises, may help reduce flare-ups triggered by emotional stress. Additionally, some patients benefit from antihistamines may be used to alleviate nighttime itching and improve sleep, although they do not directly address the underlying inflammation.
Preventive measures are equally important in controlling eczema. Identifying and avoiding specific triggers, such as certain foods or environmental allergens, can significantly reduce the frequency of flare-ups. Maintaining a consistent skincare routine that includes moisturizing multiple times a day is crucial for keeping the skin barrier intact. In severe cases, regular follow-up with a dermatologist or allergist can help tailor treatments and monitor progress. While eczema cannot be cured, with proper management, many individuals can effectively control their symptoms and lead more comfortable lives.
UWorld RxPrep NAPLEX Review 2025 Chapter 39 Common Skin Conditions Page 521
https://nationaleczema.org/eczema-management/
Eczema, Urticaria, and other Skin Conditions
Eczema, often referred to as dermatitis, includes a variety of skin conditions, such as atopic eczema or atopic dermatitis (AD). It is characterized by a specific reaction pattern with variable clinical manifestations and a common histologic feature known as spongiosis (intercellular edema of the epidermis). Primary symptoms include red spots (erythematous macules), small raised bumps (papules), and fluid-filled blisters (vesicles), which can merge to form larger patches and plaques. In severe cases, secondary symptoms such as weeping and crusting from infection or scratching may become prominent. In chronic eczema, the skin may thicken and the normal skin lines become more pronounced (lichenification), altering the typical appearance of eczema. A characteristic defect in AD that contributes to the pathophysiology is an impaired epidermal barrier. In many patients, a mutation in the gene encoding filaggrin, a structural protein in the stratum corneum, is responsible. Patients with AD may display various immunoregulatory abnormalities, including IgE synthesis and impaired/delayed-type hypersensitivity reactions.
Treatment of Atopic Dermatitis:
Therapy for AD should include avoiding skin irritants, using moisturizers regularly, and applying topical anti-inflammatory agents carefully. Low- to-mid potency topical glucocorticoids are commonly used. For the face and skin folds, low-potency glucocorticoids or non-glucocorticoid anti-inflammatory agents should be used to minimize the risk of skin thinning. If infection is suspected, especially with crusted and weeping lesions, the affected area should be cultured and treated with appropriate antibiotics. Dicloxacillin or Cephalexin, typically for 7-10 days, are commonly used. For methicillin-resistant Staphylococcus aureus (MRSA) infections, antibiotics such as trimethoprim-sulfamethoxazole, minocycline, doxycycline, and clindamycin are recommended. Furthermore supportive care such as barrier-repair products aid in restoring the skin's protective layer. Itch control is essential in AD treatment; antihistamines such as diphenhydramine, hydroxyzine, and doxepin are most commonly used due to their sedative effects. In severe cases systemic glucocorticoids can be used for patients who do not respond to topical treatments. Long-term use is not recommended as symptoms usually return after stopping the medication. Furthermore, for chronic, severe AD other systemic treatments like cyclosporine and dupilumab can be considered.
Urticaria:
Urticaria also known as hives is a skin reaction that causes itchy welts. Chronic hives are welts that last for more than six weeks and return often over months or years. Urticaria can occur on any area of the body as well as circumscribed wheals with erythematous raised serpiginous borders and blanched centers which may develop into giant wheals. The mast cells play a crucial role in most forms of urticaria by releasing histamine, which subsequently acts on capillaries and cutaneous nerve endings to produce the itchy red wheals. Acute urticaria is most often due to exposure to a food, environmental, or drug allergen or viral infection, while chronic urticaria is often idiopathic.
Treatment Overview:
For most types of urticaria, H1 antihistamines effectively reduce both swelling as well as itching. Long-acting, non-sedating agents such as loratidine, desloratadine, and fexofenadine, or low-sedating agents such as cetirizine or levocetirizine, are typically used first and can be dosed up to four times daily. Additionally, older generation antihistamines, such as chlorpheniramine or diphenhydramine, cause sedation and psychomotor impairment. Their anticholinergic effects can include visual disturbances, urinary retention, and constipation. Clinical guidelines recommend adding an H2 antagonist such as ranitidine or famotidine at standard dosages, along with a CysLT1 receptor antagonist such as montelukast (10 mg daily) or zafirlukast (20 mg twice daily), may enhance efficacy when H1 antihistamines are insufficient. Furthermore, for patients with chronic urticaria that have failed to respond to above combinations now have an option for an alternative therapy; a monoclonal anti-IgE antibody such as Omalizumab. While preventing and dealing with urticaria may cause challenges, patients can proactively manage their condition by recognizing early signs and symptoms, avoiding known triggers, and taking necessary precautions such as bathing and changing clothes after exposure to potential allergens like pollen or animals.
https://accesspharmacy-mhmedical-com.jerome.stjohns.edu/content.aspx?sectionid=268014720&bookid=3097&Resultclick=2
https://accesspharmacy-mhmedical-com.jerome.stjohns.edu/content.aspx?sectionid=264533761&bookid=3095#275935692
Atopic dermatitis, commonly known as eczema, is a persistent inflammatory skin condition affecting approximately 17.8 million people in the United States. It presents with itchy, red, and scaly skin lesions, and is most prevalent in children, impacting around 15% to 20% of children and 1% to 3% of adults. Over recent decades, its incidence has risen substantially in industrialized nations, often manifesting before age 5. Early diagnosis and treatment are crucial to mitigate complications and enhance quality of life. Filaggrin protein abnormalities in the epidermis are believed to underlie its genetic basis, fostering immune cell interaction with external antigens, resulting in intense itching, scratching, and inflammation, perpetuating a cycle of discomfort.
Atopic dermatitis evolves through acute, subacute, and chronic phases, each displaying distinctive characteristics. Acute presentations feature vesicular, weeping, crusted eruptions, while subacute phases exhibit dry, scaly, erythematous papules and plaques. Chronic manifestations demonstrate lichenification from repetitive scratching. Pityriasis alba, common in children, displays hypopigmented, poorly defined plaques with fine scales. Typically, flexural skin surfaces, neck, eyelids, face, wrists, feet, and hands are involved. Symptoms often commence with dry, itchy skin, progressing to redness, swelling, and soreness, with potential crusting and scaling.
While atopic dermatitis has no cure, symptom management and prolonging remission intervals are achievable goals. Avoiding triggers such as viral infections, allergens, cosmetics, fragrances, and extreme weather is paramount. Hot water exacerbates irritation; hence, warm or cool water with mild, non-drying soaps is recommended. Loose, cotton clothing aids ventilation and reduces overheating. Regular moisturizing maintains skin softness and elasticity, preventing cracks. Topical corticosteroids, tailored to age, severity, and site involvement, alleviate itching and inflammation, although prolonged use may elicit adverse effects like skin thinning. Calcineurin inhibitors, like pimecrolimus and tacrolimus, serve as secondary options, especially for individuals prone to corticosteroid-induced atrophy.
Seborrheic dermatitis, commonly referred to as dandruff, primarily affects the scalp and is prevalent in infants under 3 months, pubescent children, and adults aged 40-60 years. It affects approximately 3% of the population, with males being more susceptible. Dandruff manifests as light, white to yellow flakes on the scalp and hair without accompanying redness, often accompanied by mild itching, extending to the hairline, behind the ears, and eyebrows. Histological examination reveals epidermal hyperplasia, parakeratosis, and the presence of malassezia yeasts. Neutrophil infiltration may also be observed.
Treatment for dandruff predominantly involves topical antifungal and anti-inflammatory agents. Commonly used topical antifungals include ketoconazole, ciclopirox olamine, selenium sulfide, and zinc pyrithione, administered via shampoo formulations typically applied twice weekly initially and less frequently for maintenance. Topical corticosteroids, like hydrocortisone and betamethasone dipropionate, serve as anti-inflammatory agents, with fluocinolone available in shampoo form. Coal tar, functioning as an antifungal, anti-inflammatory, and sebum production reducer, is another option, usually applied 1-2 times weekly as a shampoo. These treatments may elicit side effects such as itching or burning sensations, skin atrophy, or folliculitis, necessitating patient education and monitoring. Coal tar shampoos, available without prescription, offer a self-treatment option for motivated individuals.
Dall'Oglio, F., Nasca, M. R., Gerbino, C., & Micali, G. (2022). An Overview of the Diagnosis and Management of Seborrheic Dermatitis. Clinical, cosmetic and investigational dermatology, 15, 1537–1548. https://doi.org/10.2147/CCID.S284671
Nemeth V, Syed HA, Evans J. Eczema. [Updated 2024 Mar 1]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK538209/
Eczema, Urticaria, and Other Skin Conditions
Atopic Dermatitis
Atopic dermatitis (AD), or eczema, is the most commonly occurring chronic skin condition with a prevalence of up to to 13% in the United States. The signs and symptoms of AD include dry skin, lesions and lichenification. AD is often comorbid with other chronic ‘allergic disorders’, such as asthma and food allergies. AD can also increase the likelihood of other IgE mediated conditions, such as allergic rhinitis (Kim J).
The pathophysiology is defined by immune dysregulation that impairs the skin barrier. AD can also be genetic, due to a mutation in fillagrin transglutaminase (FLG), which can compromise epidermal permeability, causing increased penetration of allergens and microbes. Additionally, genetic polymorphic changes in Interleukins (IL) can cause abnormal, overreactive inflammatory responses, thus further compromising the epidermal barrier. IL-4 and IL-13 are key immunomodulators in potentiating skin barrier dysfunction, and IL-31 is responsible for itchiness, which patients can experience with AD (Kim J, Kolb L).
Treatment for AD is comprised of four components: trigger avoidance, daily skin care, anti- inflammatory therapy, and complementary medicine. Trigger avoidance consists of avoiding allergens, such as using fragrance- free products and removing environmental triggers. Skin care involves using emollients two times a day to prevent skin drying. Topical steroids are first- line agents for anti- inflammatory therapy. They are used for treating flare- ups and then tapered and used as maintenance therapy for prevention. Side effects of topical steroid use include telangiectasia and skin atrophy with chronic use. Second line agents include topical calcineurin inhibitors, pimecrolimus and tacrolimus, and topical PDE-4 inhibitors, crisaborole. Uncontrolled AD can be treated using UV light phototherapy in combination with oral immunosuppressants. Monoclonal antibodies can also be used for patients with AD, with dupilumab being clinically indicated and approved for use. Complementary therapies include bleach baths, low allergen diets, and probiotic supplementation (Kolb L).
Urticaria
Urticaria is an allergic reaction known commonly as hives. It can be characterized as acute and self- resolving in less than 6 weeks, or chronic- lasting more than 6 weeks. Chronic urticaria can further be categorized as inducible or idiopathic based on history and exposure to triggers. Signs and symptoms of hives include wheals and pruritis, with or without localized or systemic edema. Chronic urticaria affects up to 2% of the population. The etiology is not fully defined, but it is believed to be IgE- mediated, which causes mast cell activation and release of histamine (Dabija D).
Urticaria management consists of identifying and avoiding triggers, as well as pharmacological management if indicated. First line agents are second- generation antihistamines, such as loratadine, cetirizine and fexofenadine. These agents are to be taken regularly for them to exert their antihistaminic effects. Second generation H1 blockers have a more tolerable side effect profile, causing minimal drowsiness, as compared to first generation agents. If a patient has inducible chronic urticaria, patients may take their antihistamine 2 to 4 hours before exposure to prevent the reaction, as opposed to idiopathic chronic urticaria. Other agents for chronic urticaria include omalizumab, which binds free IgE to mediate and decrease the reaction that causes the urticaria. Omalizumab is indicated when patients are unresponsive to antihistamines. For short flares of hives, systemic corticosteroids can be used to reduce symptom severity and flare duration. Topical steroids are not indicated in urticaria. Cyclosporine is a last line agent, due to its systemic toxicities, and is only used in patients that have refractory chronic urticaria and have failed antihistamine therapy (Dabija D).
Psoriasis
Psoriasis is an inflammatory condition that causes the erythematous and scaly plaques on the arms, scalp and back regions of the body. Psoriasis is chronic and waxes and wanes, with periods of flares and then improvement. Occurrence in the general population is up to 5% (Kim WB).
True etiology is unknown, but the genetic disease is mediated by T- lymphocytes and there is a strong association with HLA antigens. Activated T- lymphocytes trigger abnormal keratinocyte turnover, thus forming the thick plaques. Environmental factors, such as allergens and weather, and certain drugs can trigger flares in patients. Among others, chloroquine, lithium, beta-blockers, steroids, and NSAIDs can worsen psoriasis (Nair PA, Kim WB).
Management of psoriasis includes emollients and moisturizers, topical and systemic therapies, and phototherapy. Topical therapies include topical steroids and calcipotriene as monotherapies or in combination. Ultraviolet B (UVB) phototherapy is used in combination with oral immunosuppressants or alone. If UVB therapy is not available or cannot be used, oral immunosuppressants or biologics can be used. Approved biologics include adalimumab, etanercept, infliximab, and ustekinumab. With any immunosuppressant, including biologics, there is a risk of secondary infections. Second line therapies include combinations of UVB light and a biologic or methotrexate with a biologic (Kim WB).
Citations:
Dabija D, Tadi P, Danosos GN. Chronic Urticaria. [Updated 2023 Apr 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK555910/
Kim J, Kim BE, Leung DYM. Pathophysiology of atopic dermatitis: Clinical implications. Allergy Asthma Proc. 2019;40(2):84-92. doi:10.2500/aap.2019.40.4202
Kim WB, Jerome D, Yeung J. Diagnosis and management of psoriasis. Can Fam Physician. 2017;63(4):278-285.
Kolb L, Ferrer-Bruker SJ. Atopic Dermatitis. [Updated 2023 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK448071/
Nair PA, Badri T. Psoriasis. [Updated 2023 Apr 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK448194/
Eczema is an umbrella term for a group of inflammatory skin conditions that mainly cause itchiness, dry skin, rashes, scaly patches, blisters and skin infections. There are many different types of eczema and these include atopic dermatitis, contact dermatitis, dyshidrotic eczema, nummular eczema, seborrheic dermatitis and stasis dermatitis. Eczema may manifest as red and inflamed skin in individuals with lighter skin tones, while those with darker skin tones may experience it as brown, purple, gray, or ashen. The predominant symptom of eczema is itching. In the United States, 31.6 million people have some form of eczema and it is estimated that 1 in 10 individuals will develop eczema during their lifetime, with prevalence peaking in early childhood. People of all skin colors, race, and ethnicities can be affected by eczema.
Atopic dermatitis is the most common form of eczema. This type of eczema is chronic and occurs when an overactive immune system leads to dry and itchy skin due to the compromised skin barrier. Eczema is not contagious and cannot be transmitted from one person to another. Although the precise cause of eczema remains unknown, research suggests that its development involves a complex relationship between genetic factors and environmental triggers. Many individuals with eczema frequently experience additional symptoms such as hay fever, allergic asthma, and food allergies. Ensuring proper and consistent skin care is crucial for both preventing and managing eczema. Common triggers may include extended exposure to dry air, extreme heat or cold, some types of soap, shampoos that cause dander, bubble bath products, body wash, and facial cleansers, laundry detergents and fabric softeners with chemical additives, certain fabrics like wool or polyester in clothing and sheets, surface cleaners and disinfectants, natural liquids like the juice from fruit, vegetables and meats, fragrances in candles, and some metals, especially nickel, in jewelry or utensils.
In the early stages and up to the age of 2 years, it is typical for infants to develop a red rash, possibly oozing when scratched, on the face, scalp, and/or the skin around joints that come into contact when bent. Concerns may arise among parents who suspect atopic dermatitis in the diaper area, but it is important to note that this condition rarely manifests in that specific area. During childhood, usually 2 years of age to puberty, it is most common for a red thickened rash, which may ooze or bleed when scratched, to appear on the elbows and knees, usually in the bend, neck, and/or ankles. During the teenage and adult years, it is most common for a red to dark brown scaly rash, which may bleed and crust when scratched, to appear on the hands, neck, elbows and knees, usually in the bend, skin around the eyes and ankles and feet. Other common skin features of atopic dermatitis include an extra fold of skin under the eye, which is known as a Dennie-Morgan fold, darkening of the skin beneath the eyes, and extra skin creases on the palms of the hands and soles of the feet. Furthermore, people with atopic dermatitis often have other conditions, such as sthma and allergies, including food allergies, other skin diseases, such as ichthyosis, which causes dry, thickened skin, depression or anxiety, and sleep loss.
References:
https://nationaleczema.org/research/eczema-facts/
https://nationaleczema.org/eczema/
https://www.niams.nih.gov/health-topics/atopic-dermatitis
Eczema, also referred to as atopic dermatitis, is a chronic skin condition that commonly begins in childhood and may persist into adulthood. The pathophysiology of eczema involves a complex interplay of genetic, environmental, and immunologic factors. Genetic predisposition plays a role, with involvement of mutations in genes affecting the skin barrier and immune response. Most notably, mutations in the filaggrin gene – a vital gene responsible for the tough corneocytes that form the protective outermost layer of the skin – lead to haphazard organization of skin cells that results in a dysfunctional skin barrier. Skin barrier dysfunction allows for water loss and decreased protection from harmful substances, leading to dry skin that is more susceptible to infections. Individuals with eczema are also more sensitive to environmental irritants such as allergens and fragrances, leading to inflammation and exacerbation/development of lesions. Eczema development is commonly associated with other “allergic diseases” (known as the “atopic march”) including asthma (50%), food allergies, and allergic rhinitis (75%). Eczema manifests as intensely pruritic, erythematous papules in flexural areas such as the elbows and knees. Chronic eczema, especially with excessive scratching, may be characterized by lichenification (thickening of the skin) and fibrous papules with dermal and epidermal infiltration by lymphocytes and macrophages. Treatment options for eczema involve emollients to maintain skin hydration and topical anti-inflammatory medications for flare-ups.
Psoriasis is a chronic, inflammatory skin condition; exact etiology is unknown, but it is considered to be an autoimmune disease mediated by T-cells. Activated T-cells stimulate proliferation of keratinocytes, resulting in rapid skin cell turnover and the formation of thick plaques characteristic of psoriasis. Genetic factors are significant, with familial occurrence and HLA antigens (specifically HLA-Cw6) commonly reported in psoriatic patients. Other factors such as medications (lithium, beta-blockers, etc.), infections, trauma, stress, obesity, and smoking may exacerbate/induce lesions. Psoriasis affects different parts of the body including the flexural areas, scalp, nails, eyes (in about 10% of patients), and joints (known as psoriatic arthritis). The condition manifests as well-defined, erythematous plaques covered with white/silvery scales that may appear flaky due to epidermal cells failing to secret lipids. In addition to joint damage (caused by psoriatic arthritis), psoriasis may be complicated by depression and an increased risk of cardiovascular disease. Diagnosis of psoriasis is based on clinical morphology and measurement tools are used to assess severity of the condition, which is essential for treatment. Treatment options for mild to moderate psoriasis include emollients and coal tar, corticosteroids, or vitamin D analogs. In more severe psoriasis, and in patients who fail topical therapy, methotrexate and/or biological agents may be effective.
Psoriasis and eczema are both common skin conditions with overlapping clinical manifestations, which makes distinguishing between the two difficult. Historically, psoriasis and eczema were considered mutually exclusive, with opposing inflammatory pathways required for their activation. However, recent evidence suggests the two conditions can indeed coexist. Patients with concomitant eczema and psoriasis often have greater hand involvement, poor response to topical therapy, and the need for multiple systemic agents. While further research is required to characterize this patient population, healthcare professionals can aid in accurate diagnosis and management of patients with these conditions.
References
Barry K, Zancanaro P, Casseres R, et al. Concomitant atopic dermatitis and psoriasis – a retrospective review. J Dermatolog Treat. 2021 Nov;32(7):716-20. https://web-s-ebscohost-com.jerome.stjohns.edu/ehost/detail/detail?vid=8&sid=b142a667-d34b-434d-9e5d-872509e4c12a%40redis&bdata=JnNpdGU9ZWhvc3QtbGl2ZQ%3d%3d#AN=153046006&db=aph
Griffiths CEM, van de Kerkhof P, Czarnecka-Operacz M. Psoriasis and atopic dermatitis. Dermatol Ther. 2017 Jan;7(Suppl 1):31-41. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5289118/
Nair PA, Badri T. Psoriasis [updated 2023 Apr 3]. In: StatPearls [internet]. Treasure Island (FL): StatPearls Publishing. 2023 Jan. https://www.ncbi.nlm.nih.gov/books/NBK448194/
Nemeth V, Evans J. Eczema [updated 2022 Aug 8]. In: StatPearls [internet]. Treasure Island (FL): StatPearls Publishing. 2023 Jan. https://www.ncbi.nlm.nih.gov/books/NBK538209/
Vitiligo is a chronic skin disorder characterized by a progressive loss of pigmentation, resulting in depigmented patches on the skin. Although it is uncommon, affecting approximately 1% of individuals worldwide, it is considered the most frequent cause of skin depigmentation. Vitiligo is unpredictable; the extent, distribution, and progression of depigmentation varies from person to person and with the type of vitiligo. The exact etiology of vitiligo remains unclear but is considered to be multifactorial, involving a complex interplay of genetic, environmental, and autoimmune factors.
Vitiligo occurs due to the destruction of melanocytes, an epidermal cell that produces the pigment responsible for skin tone and photoprotection from UV radiation. The immune-mediated destruction of these cells may be prompted by various factors such as genetic susceptibility and environmental triggers including stress, trauma or skin damage from severe sunburns/wounds, or exposure to certain chemicals. Genetic predisposition plays a significant role; about 20% of individuals with vitiligo have family history of the condition and research suggests more than 30 genes associated with immune and melanocyte function may increase susceptibility. Moreover, a family or personal history of other autoimmune conditions such as diabetes mellitus, thyroid disorders, or pernicious anemia, may elevate the risk of vitiligo development.
Vitiligo manifests as depigmented patches, or macules, on the skin, typically more pronounced on individuals with darker skin tones. The macules are often well-defined with irregular borders, occurring most commonly on the face (around the mouth and eyes), hands, underarms, and extremities. Hair follicles in affected areas may lose pigmentation, resulting in white or prematurely gray hair. The Koebner phenomenon, or development of macules at specific trauma-prone sites such as wounds, burns, or abrasions, is also common in vitiligo. Vitiligo is often classified as either nonsegmental or segmental based on the distribution and stability of the condition. The most common type is nonsegmental vitiligo, which tends to spread slowly with new patches developing periodically throughout an individual’s life. Nonsegmental vitiligo may be further categorized as (1) acral/acrofacial (only involves extremities and/or the face), (2) generalized (random distribution of macules across the body), or (3) universal (depigmentation affects about 80% of the body surface area). Conversely, segmental vitiligo is defined by rapid, unilateral depigmentation that stabilizes and rarely progresses after 6 to 12 months.
Complications of vitiligo primarily revolve around the psychosocial impact of visible skin changes including social stigmatization and lowered self-esteem. However, vitiligo may also lead to other problems specifically related to melanocyte destruction. Due to a lack of melanin, the depigmented skin areas are more susceptible to sunburn and prone to other skin conditions such as skin infections or skin cancer. Furthermore, vitiligo may be associated with inflammation of the iris (iritis) or middle layer of the eye (uveitis) and partial hearing loss due to loss of cochlear melanocytes.
The macules caused by vitiligo are usually permanent, although treatment options aim to address cosmetic concerns and potentially restore pigmentation. Opzelura (ruxolitinib) is a topical JAK inhibitor recently approved for the restoration of pigmentation in individuals with vitiligo. Other options include topical corticosteroids, calcineurin inhibitors, phototherapy (UVB radiation or combination of Psoralen and exposure to UVA radiation [PUVA]), and surgical interventions such as skin grafting. Tattooing and/or micropigmentation should be avoided due to the risk of koebnerization. The choice of treatment depends on the extent and location of depigmentation, disease stability, and patient preferences. However, all patients should be educated on the slow response of treatment, treatment failure, and likelihood of disease progression with treatment. Patient education and psychological support are integral components of vitiligo management, emphasizing the importance of a multidisciplinary approach to address both the physical and psychosocial aspects of the condition.
References
Ahmed jan N, Masood S. Vitiligo [updated 2023 Aug 7]. In: StatPearls [internet]. Treasure Island (FL): StatPearls Publishing. 2023 Jan. https://www.ncbi.nlm.nih.gov/books/NBK559149/
Grimes PE. Vitiligo: management and prognosis. Wolters-Kluwer: UpToDate. 2023 Aug. https://www-uptodate-com.jerome.stjohns.edu/contents/vitiligo-management-and-prognosis#H1950195090
Grimes PE. Vitiligo: pathogenesis, clinical features, and diagnosis. Wolters Kluwer: UpToDate. 2023 Jul. https://www-uptodate-com.jerome.stjohns.edu/contents/vitiligo-pathogenesis-clinical-features-and-diagnosis#H1838574464
Migayron L, Boniface K, Seneschal J. Vitiligo, from physiopathology to emerging treatments: a review. Dermatol Ther. 2020 Dec:10(6):1185-98. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7649199/
Speeckaert R, van Geel N. Vitiligo: an update on pathophysiology and treatment options. Am J Clin Dermatol. 2017 Dec;18(6):733-44. https://www.proquest.com/docview/1973330972/E1942BF38A7A456EPQ/10?accountid=14068
Vitiligo and Eczema
Vitiligo is defined as a “chronic stigmatizing disease, already known for millennia, which mainly affects melanocytes from the epidermis basal layer, leading to the development of hypochromic and achromic patches.” In other words, areas or patches of the skin tend to be noticeably lighter than the rest of the body, or have no color at all (appearing completely white). This disease has been studied and it is not contagious, but it is genetic and has to do with specific genes. These lesions can be all different sizes, shapes and shades of color. While there are complications that can stem from vitiligo, the most impactful affects are the psychological ones. According to the ABD, “one of the major consequences of the disease is its psychological impact, since vitiligo can have strong effects on patients' self-esteem, with a subsequent increase in severe depression cases and a sharp sense of social discrimination resulting in quality of life deterioration.” Along with the psychological burden of vitiligo, patients can also go into a depressive state knowing that there is no known cure for vitiligo. There is a new vitiligo treatment that has hit the markets, but it has not been proven 100% effective as yet. The cream is called Opzelura and the active ingredient is ruxolitinib, a JAK inhibitor. This drug works by binding “to the JAK1 and JAK2 enzymes and is thought to inhibit IFN-γ mediated JAK-STAT signaling.”
Eczema “is an inflammatory skin condition that causes itchiness, dry skin, rashes, scaly patches, blisters and skin infections.” The term “eczema” is very broad, but it encompasses the forms of eczema such as: atopic dermatitis, seborrheic dermatitis and contact dermatitis to name a few. Eczema is a very common condition and affects over 30 million people in America alone. Treatments for eczema typically consist of keeping the dry skin moisturized with ointments and creams. There are many home remedies that patients try as well, some have been effective in certain cases whereas some have not. Many find relief from oatmeal or baking soda bath soaks, whereas others need to take a dose of Benadryl (diphenhydramine) to get the itching to subside. Doctors can prescribe topical corticosteroids to help with the itchiness and dull the sensations that can come from prolonged itching and dryness, however it is important to note that like vitiligo, there is no cure for eczema. There is only supportive care and symptomatic treatment, which is what the topical corticosteroids and home remedies provide to the patients.
Resources:
Gomes Tarle, Roberto. “Vitiligo - Part 1.” Shibboleth Authentication Request, www-ncbi-nlm-nih-gov.jerome.stjohns.edu/pmc/articles/PMC4056705/. Accessed 24 Aug. 2023.
“What Is Eczema?” National Eczema Association, 2 Dec. 2022, nationaleczema.org/eczema/.
“OPZELURA Mechanism of Action.” OPZELURA, www.opzelurahcp.com/vitiligo/mechanism-of-action. Accessed 24 Aug. 2023.
Eczema, Urticaria, Psoriasis
Skin disorders affect millions of people worldwide, causing discomfort, distress, and challenges in daily life. Eczema, urticaria, and psoriasis are three prevalent skin conditions, each with its unique characteristics, triggers, and management approaches.
Eczema, also known as atopic dermatitis, is a chronic inflammatory skin condition that affects both children and adults. It is characterized by dry, itchy, red, and inflamed skin. The condition often starts in infancy, and though many children outgrow it, some may continue to experience symptoms into adulthood. Though the exact cause of eczema is not fully understood, it is believed to result from genetic and environmental factors. Additionally, triggers such as irritants, allergens, stress, temperature changes, and certain foods can exacerbate symptoms. Eczema typically presents as patches of dry, itchy skin that may become red, swollen, and cracked. In severe cases, the skin may bleed, crust, and ooze. The affected areas commonly include the face, neck, inner elbows, and behind the knees. Management of eczema involves a multi-faceted approach. Moisturizing the skin regularly helps maintain hydration and prevents flare-ups. Topical corticosteroids and immunomodulators are commonly prescribed to reduce inflammation and itchiness during active flare-ups. Antihistamines can help alleviate itching, and avoiding known triggers is essential in preventing recurrences.
Urticaria, commonly known as hives, is a skin condition characterized by the sudden appearance of itchy, raised welts or wheals on the skin. These welts may vary in size and shape and can appear anywhere on the body. Acute urticaria often lasts for a few hours to a few days, while chronic urticaria persists for more than six weeks. Urticaria occurs due to the release of histamine and other chemicals from specialized cells in the skin called mast cells. This release is triggered by various factors, including allergic reactions to food, medication, insect stings, or environmental allergens. Stress, infections, and autoimmune disorders can also lead to the development of hives. he primary symptom of urticaria is the appearance of raised, itchy welts on the skin, which can be pale or red. The welts may change shape, size, and location rapidly and can be accompanied by a burning or stinging sensation. In severe cases, the condition may lead to angioedema, which involves swelling in the deeper layers of the skin. The treatment of urticaria depends on its underlying cause and severity. For mild cases, over-the-counter antihistamines can provide relief. In more severe or chronic cases, prescription antihistamines, corticosteroids, or immunosuppressive drugs may be necessary. Identifying and avoiding triggers play a crucial role in preventing recurrent episodes.
Psoriasis is a chronic autoimmune skin condition that's caused by a buildup of skin cells. This excessive cell turnover leads to the formation of thick, silvery scales and red patches on the skin's surface. Psoriasis affects about 2% of the global population and can occur at any age. The exact cause of psoriasis is not fully understood, but it is believed to involve a malfunction of the immune system. Genetic factors play a significant role, as people with a family history of psoriasis are at a higher risk of developing the condition. Triggers such as stress, infections, certain medications, and injury to the skin can exacerbate symptoms. Psoriasis commonly appears as red, raised patches covered with silvery scales, which can be itchy and painful. These patches often occur on the scalp, elbows, knees, and lower back, but they can affect other areas as well. In addition to skin symptoms, psoriasis can lead to joint pain and inflammation in some cases, known as psoriatic arthritis. Psoriasis treatment aims to slow down cell turnover, reduce inflammation, and alleviate symptoms. Topical treatments like corticosteroids, vitamin D analogs, and retinoids are used for mild to moderate cases. For more severe or widespread psoriasis, phototherapy (light therapy) and systemic medications like immunosuppressants or biologics may be prescribed. Lifestyle changes, including stress management and regular moisturization, can also be helpful in managing the condition.
References:
Adams E. S. (2004). Identifying and controlling metabolic skin disorders: eczema, psoriasis, and exercise-induced urticaria. The Physician and sportsmedicine, 32(8), 29–40. https://doi.org/10.3810/psm.2004.08.507
Kayiran MA, Akdeniz N. Diagnosis and treatment of urticaria in primary care. North Clin Istanb. 2019 Feb 14;6(1):93-99. doi: 10.14744/nci.2018.75010.
Eczema
Atopic dermatitis is a chronic pruritic inflammatory skin condition that generally presents at an early age. It is the most common type of eczema, which is a general term for several types of skin inflammation. This inflammatory skin condition causes itchiness, dry skin, rashes, scaly patches, blisters, and skin infections. This condition can have periods of exacerbation, or flare-ups, followed by periods of remission. The onset of atopic dermatitis most commonly occurs between three and six months of age, with the majority of patients developing symptoms before reaching 5 years.
Treatment of atopic dermatitis includes nonpharmacologic management strategies. The goals of treatment are to provide symptomatic relief, controlling the itching during periods of exacerbation. Control atopic dermatitis, identify and eliminate triggers, prevent future exacerbations, and minimize adverse events. Treatment should clear skin lesions, anywhere from days to weeks depending on the severity of the disease. There are both nonpharmacological and pharmacological approaches to treatment. Nonpharmacological approaches include applying moisturizers frequently throughout the day, taking lukewarm baths and applying moisturizer immediately after bathing, using non soap cleaners, wet therapy, wearing soft cotton fabrics, keeping cool, and identifying and removing irritants or allergens. Pharmacological therapy is chosen based on disease severity. Topical corticosteroids are the standards of care, and the drug treatment of choice for atopic dermatitis. The choice and strength of corticosteroids once again are dependent on the severity and site of the disease. A second line treatment includes phototherapy, which was found to be very effective as UV light sources on the skin have immunosuppressive, immunomodulating, anti-inflammatory, and antipruritic effects.
Urticaria
Hives, also known as urticaria, affect approximately 20 percents of people at some point during their lifetime. It is characterized by raised itchy bumps that can either be red or skin-colored, and blanching. Hives can be triggered by many things, certain foods, medications, insect stings or bites, physical stimuli, latex, blood transfusions pet dander and pollen, some plants, and so much more. Hives can appear on an area of the bod, change shape, appear, and disappear, and move around on the body, The red or skin-colored wheals are bumps with clear edges that appear suddenly. There are two types of hives, acute hives, which are short lived, and chronic hives which can occur almost daily for six weeks. The management and treatment of hives begins with avoiding known triggers. Therapy depends on the severity and can begin with cool compresses to relieve itching, prescription antihistamines, or anti-inflammatory medications.
Psoriasis
Psoriasis is a chronic disease that waxes and wanes and is never cured. It is an immune mediated disease characterized by inflammation. Patients present with visible signs of inflammation such as raised plaques and scales on the skin. This occurs because the overactive immune system speeds up cell growth from growing and shedding in one month, to a matter of three to four days. Most commonly these plaques appear on the elbows, knees, and scalp. Psoriasis appears as erythematous and pruritic lesions that can be single at predisposed areas or generalized over wide body surfaces. Similar to atopic dermatitis, the signs and symptoms have periods of exacerbation, and periods of remission. Triggers of psoriasis include stress, seasonal changes, and some drugs. This disease is lifelong, that may be very visible and emotionally distressing for patients. Therefore, management of this condition is multifaceted and can change according to the severity of the illness.
Treatment of psoriasis is usually done with agents that modulate the abnormal immune response, such as topical corticosteroids and biologic agents. Topical therapies that affect cell turnover, like retinoids, are also effective. The goals of psoriasis treatment focus on minimizing or eliminating the visible signs of psoriasis, alleviating pruritis, reducing the frequency of flare-ups, minimizing nonspecific triggers such as mild trauma, sunburn, chemical irritants, avoiding adverse effects of treatment, and improving or maintaining the patients quality of life.
References
Law R.M., & Law D.S., & Maibach H.I. (2020). Dermatologic drug reactions, contact dermatitis, and common skin conditions. DiPiro J.T., & Yee G.C., & Posey L, & Haines S.T., & Nolin T.D., & Ellingrod V(Eds.), Pharmacotherapy: A Pathophysiologic Approach, 11e. McGraw Hill. https://accesspharmacy-mhmedical-com.jerome.stjohns.edu/content.aspx?bookid=2577§ionid=239762003
Hives (Urticaria) | Causes, symptoms & treatment. (2022, April 13). ACAAI Public Website. https://acaai.org/allergies/allergic-conditions/skin-allergy/hives/
Psoriasis: causes, triggers and treatments. (n.d.). https://www.psoriasis.org/about-psoriasis/
National Eczema Association. (2022, December 2). Eczema (atopic dermatitis): Causes, symptoms, and treatment. https://nationaleczema.org/eczema/
Eczema, Urticaria, and Other Skin Conditions
Eczema, also known as, atopic dermatitis, is a chronic inflammatory skin condition commonly diagnosed in children. Eczema usually begins in childhood and can be followed with other conditions like asthma, rhino conjunctivitis, or eosinophilia (Napolitano et al.) It can also begin in adolescence or adulthood. Eczema impacts approximately 15 to 20% of children. The pathophysiology combines genetic factors, defects in skin barrier, alterations in immune function, and changes in microbiome. Alterations in the skin barrier may be due to loss of function mutations in filaggrin and other proteins leading to the dryness of skin. Altered immune responses are due to the imbalance between T helper cell type 1/17 and type 2/22. There is an intensified response from the Th2/22 cells. The clinical features of atopic dermatitis differ based on age. For infants less than 2 years of age, there are itchy, red, papules and vesicles with exudate and crust. They are located on the face, trunk, limbs and nappy area. For children older than 2, there is dry skin and lichenified papules and plaques. They are mainly located on the skin of the hands and feet. If there is facial involvement, it is mostly around the eyes. Adults present with papules and plaques with lichenification. They are commonly located on the face, neck, hands, or eyelids. Treatment mostly consists of topical emollients and corticosteroids. Topical calcineurin inhibitors like tacrolimus and pimecrolimus can also be used. For severe disease, systemic corticosteroids can be used.
Urticaria is the sudden presence of wheals or hives, sometimes with edema of the tissue. It is caused by food allergens, pseudo allergens, medications, infections, or insects. Urticaria is caused by the release of histamine mediated by IgE or non-IgE and other inflammatory mediators released from mast cells or basophils. Wheals can appear anywhere on the skin and can appear rapidly within minutes. It can be classified as acute if it recurs within 6 weeks and chronic if it lasts longer than 6 weeks. Angioedema is similar to urticaria, but histamine and inflammatory mediators are released in the deeper dermis and subcutaneous tissues, whereas urticaria is associated with release in the dermis. In 80 to 90% of cases of chronic urticaria, it is idiopathic and avoidance of triggers is most important. Second generation antihistamines are the main treatments for acute and chronic urticaria since they can be dosed less frequently and avoid side effects. First generation antihistamines are more sedating and should be used with caution in older adults. It is recommended that the patients avoid alcohol, aspirin, and NSAIDs because they can worsen the condition.
Psoriasis is a chronic skin condition classified by inflammation, genetic predispositions, and autoimmune implications. There are many types of psoriasis, but about 90% of cases are psoriasis vulgaris classified by scaly plaques on the skin. The plaques are red and itchy and can appear on the trunk, limbs, and scalp. The inflammation is uncontrolled leading to uncontrolled keratinocyte proliferation with abnormal differentiation. Innate and adaptive immune systems are responsible for psoriatic inflammation making it autoimmune and autoinflammatory. The inflammation associated with psoriasis can affect different organ systems, demonstrating that it is likely a systemic disease. Patients with psoriasis have increased risk of comorbidities like hypertension, hyperlipidemia, type 2 diabetes, coronary artery disease, and increased body mass index. Inflammation can also be present in the joints which is considered psoriatic arthritis. It can also be present in the nails, affecting more than half of patients with psoriasis. Mild to moderate psoriasis can be treated with topical glucocorticoids, vitamin D analogues, and phototherapy. Other treatments include methotrexate, retinoids, cyclosporin, monoclonal antibodies, and a PDE4 inhibitor apremilast. Many drugs are being further researched for the treatment of this disease.
Resources
Napolitano, M., Fabbrocini, G., Martora, F., Genco, L., Noto, M., & Patruno, C. (2022). Children atopic dermatitis: Diagnosis, mimics, overlaps, and therapeutic implication. Dermatologic therapy, 35(12), e15901. https://doi.org/10.1111/dth.15901
Rendon, A., & Schäkel, K. (2019). Psoriasis Pathogenesis and Treatment. International journal of molecular sciences, 20(6), 1475. https://doi.org/10.3390/ijms20061475
Schaefer P. (2017). Acute and Chronic Urticaria: Evaluation and Treatment. American family physician, 95(11), 717–724.
Written by Aleksandra Agranovich
Eczema
Eczema is a chronic, inflammatory skin disease that affects many people within the United Stated. Also known as atopic dermatitis, this condition manifests through dryness itchiness, and inflammation. Although it commonly occurs in children, adolescents and adults may experience it throughout their lifetime. This common disease is characterized by pruritis, disrupted epidermal barrier function, and immunoglobulin E-mediated sensitization (Sohn, 2011). Risk factors may include genetics, contact allergens, environmental factors, sensitivity to heat, food allergy/ intolerance, infection, and chemicals. Although there is no cure for eczema, there are multiple treatments available (including moisturizers, steroids, and topical agents).
Dermatitis
Dermatitis is a common skin condition that may be due to an underlying inflammatory response. Dermatitis is usually characterized by itchiness, blistering, and dryness of the skin. Although dermatitis is not life threatening, it can negatively affect a person’s quality of life.
Some things to keep in mind for patients experiencing symptoms of dermatitis:
· Moisturize your skin daily
· Avoid allergens
· Avoid scratching
· Avoid products that contain alcohols and detergents
· Do not take extremely hot showers
Urticaria
Urticaria, or hives commonly occur when an individual is exposed to certain types of allergens. Whether these allergens are food or drug related, symptoms usually present with redness, welts, itchiness, and possibly angioedema of the lips, mouth, or tongue. Common treatments for urticaria include antihistamines like (loratadine, diphenhydramine, cetirizine, and fexofenadine). The most important way to prevent a possible hive outbreak is to stay away from the allergens that cause it.
Vitiligo
Vitiligo is a common skin disorder that results in skin depigmentation. This condition is characterized by loss of melanocytes which results in non-scaley, chalky-white macules (Karger, 2020). A few factor that may contribute to vitiligo include genetics and oxidative stress. Although treatment is not necessary for vitiligo, phototherapy, topical/ systemic immunosuppressants, and surgery is available. This condition is merely cosmetic and does not have any unique symptoms.
Dandruff
Dandruff, also known as seborrheic dermatitis, is a condition that causes dry, flaky skin (usually on the scalp). According to a study, the pathogenesis of seborrheic dermatitis usually contributes to internal factors (such as oil secretions), environmental factors, and skin surface fungal colonization. Common treatments for dandruff include topical anti-fungal and anti-inflammatory agents, lithium gluconate, phototherapy, immune modulators such as topical calcineurin inhibitors, and metronidazole (Borda, 2016). Non-pharmacological agents for the treatments of this condition may include tea tree oil and coal tar.
Resources
Leins, Liz, and David Orchard. “Eczema management in school-aged children.” Australian family physician vol. 46,12 (2017): 896-899.
Sohn, Andrew et al. “Eczema.” The Mount Sinai journal of medicine, New York vol. 78,5 (2011): 730-9. doi:10.1002/msj.20289
Bergqvist, Christina, and Khaled Ezzedine. “Vitiligo: A Review.” Dermatology (Basel, Switzerland) vol. 236,6 (2020): 571-592. doi:10.1159/000506103
Borda, Luis J, and Tongyu C Wikramanayake. “Seborrheic Dermatitis and Dandruff: A Comprehensive Review.” Journal of clinical and investigative dermatology vol. 3,2 (2015): 10.13188/2373-1044.1000019. doi:10.13188/2373-1044.1000019
There can be many types of skin inflammation, one of the most common types is Eczema which is also known as atopic dermatitis. It is the most common type of skin condition in infants and young children. It causes dry, itchy skin usually around the elbows, behind the knees, and hands and feet. It is important to not irritate the skin by scratching. Eczema is not a contagious condition and the cause of it is unknown, but theories support it is from genetic and environmental conditions. Treatments include skin ointments, creams, lotions, medications, and general good skin hygiene. Patients should avoid known triggers that cause drug skin such as seasonal change, perfumes, and soap. Some known over-the-counter moistures are aqua-hot and eucerin. If prescription medication is needed, treat first with topical steroids. If steroids fail, topical calcineurin inhibitors such as tacrolimus and topical PDE-4 inhibitors, and Dupilumab.
Another condition which affects the skin is dandruff, it occurs when the scalp is itchy with white oily flakes which is dead skin in the hair and is located on the shoulder, back or clothing. It can be due to either eczema or fungal disease. For mild dandruff, regular cleansing with gentle shampoo to reduce oil and skin cell buildup. If regular shampoo does not work, try medicated shampoo two to three times a week. Ketoconazole 1%/2% shampoo (Nizoral A-D0, selenium sulfide (Selsun), Pyrithione zinc (head and shoulders), and coal tar shampoo.
Hives (urticaria) are red, itchy welts that result from a skin reaction. The welts vary in size and appear and fade repeatedly as the reaction runs its course. The condition is considered chronic hives if the welts appear for more than six weeks and recur frequently over months or years. Often, the cause of chronic hives is not clear. Chronic hives can be very uncomfortable and interfere with sleep and daily activities. For many people, antihistamines and anti-itch medications provide relief.
Symptoms include batches of red skin which can appear anywhere not the body, welts can vary in size, change shape, itching (can be severe). Common medications used to treat hives are antihistamines such as loratadine (Claritin), fexofenadine (Allegra), Cetirizine (Zyrtec), and desloratadine (Clarinex). Lifestyle changes such as light clothing, avoiding scratching, hydration, and avoiding known triggers should also be applied.
References:
2021 RxPrep: Chapter 39: Common Skin Conditions. Pages 566-568.
Eczema | dermatitis | atopic dermatitis. MedlinePlus. https://medlineplus.gov/eczema.html#:~:text=Eczema%20is%20a%20term%20for,swell%20and%20itch%20even%20more. Published October 27, 2021. Accessed April 13, 2022.
Urticaria or hives hives (urticaria) are red, itchy welts that result from a skin reaction. the welts vary in size and appear and fade repeatedl. Akshay Arogyam Ayurvedic Clinic and Panchakarma Centre. https://www.akshayarogyam.com/latest-update/urticaria-or-hives-/11. Accessed April 13, 2022.
Vitiligo
Vitiligo is a skin disorder which affects approximately 0.5-2% of the population worldwide. Vitiligo is characterized by the loss of functional melanocytes. Melanocytes are the melanin-producing cells in the stratum basale of the skin and gives rise to the pigmented skin color. Patients with vitiligo present with loss of skin pigmentation in certain areas. The areas are chalky-white in appearance with distinct margins. There are three types of vitiligo, segmented vitiligo, non-segmented vitiligo and mixed vitiligo. Segmented vitiligo begins at an early age and affects only one area on one side of the body. Non-segmented vitiligo usually appears on smaller areas of the body like the hands, around the eyes and mouth, or on the feet and then spreads to the neck, chest, knees, and legs. Mix vitiligo is when the segmented and non-segmented types occur in the same person but may occur at different points in their life.
There are several proposed mechanisms for the melanocyte destruction in vitiligo such as genetic, autoimmune responses, oxidative stress, and melanocyte detachment mechanisms. The genetic component of vitiligo is not completely understood but it is known that around 20% of patients with the condition have at least one first-degree relative with vitiligo. Tyrosinase is an important enzyme in the biosynthesis of melanin and is a major autoantigen in vitiligo which may be responsible for the genetic component of the condition. Oxidative stress is another possible cause of the development of vitiligo. Oxidative stress can initiate the destruction of melanocytes in patients with melanocytes that are more susceptible to oxidative stress. This increased susceptibility may be due to an imbalance of elevated oxidative stress markers and a depletion of antioxidative mechanisms in the skin and in the blood.
The treatment of vitiligo is dependent upon the patient’s motivation for treatment. Many patients opt to use therapy on areas that are exposed such as the face, neck, or hands. The most common treatments are phototherapy or topical and systemic immunosuppressant agents. The face, neck and trunk respond best to therapy while the lips and extremities are more resistant to therapy. Patients may also choose to use cosmetics like foundation or self-tanner to even out their skin color on areas that are exposed. Treatment is not medically necessary and is really based on the patient’s desire.
Resources:
Bergqvist C, Ezzedine K: Vitiligo: A Review. Dermatology 2020;236:571-592. doi: 10.1159/000506103
Types of vitiligo. Global Vitiligo Foundation. https://globalvitiligofoundation.org/faqs/types-of-vitiligo/#non-segmental-vitiligo-nsv. Published March 29, 2022. Accessed April 1, 2022.
Dandruff
Seborrheic dermatitis, or dandruff, is a common skin condition which affects the scalp. The incidence of dandruff is highest in infants up to 3 months of age, children during puberty and adults age 40-60 years. It affects approximately 3% of the population with males affected more than females. Dandruff presents as light, white to yellow and dispersed flaking on the scalp and hair without erythema. Mild pruritus is also associated with dandruff and it can spread to hairline, retro-auricular area, and eyebrows. Histology shows epidermal hyperplasia, parakeratosis and malassezia yeasts surrounding the parakeratotic cells. Neutrophil infiltration can also be seen.
The most common treatment of dandruff includes topical antifungal and anti-inflammatory products. The popular topical antifungals used are ketoconazole, ciclopirox olamine, selenium sulfide, and zinc pyrithione. These antifungals come in shampoo formulations which are applied to the scalp generally twice weekly for initial treatment and then less frequently for maintenance therapy. Side effects of the antifungals are similar with the most common being itching or burning sensation when applied to the scalp. Topical corticosteroids are used as anti-inflammatory treatment. Hydrocortisone, betamethasone dipropionate and desonide are available as cream or lotion formulations and are applied twice daily. Fluocinolone is another corticosteroid option which comes in a shampoo formulation also applied once or twice daily. Patients may be less adherent to treatment with corticosteroids due to the frequency of application. These come with side effects like skin atrophy, folliculitis and telangiectasias. Coal tar is another option for treatment. It comes as a shampoo which is applied to the scalp 1-2 times per week. It works as an antifungal, anti-inflammatory and it reduces sebum production. Coal tar shampoo can be purchased without a prescription so it may be a good option for patients who would like to self-treat the condition.
Resources:
Dermatitis and Dandruff: A Comprehensive Review. J Clin Investig Dermatol. 2015;3(2):10.13188/2373-1044.1000019. doi:10.13188/2373-1044.1000019
Schwartz RA, Janusz CA, Janniger CK. Seborrheic dermatitis: An overview. American Family Physician. https://www.aafp.org/afp/2006/0701/p125.html. Published July 1, 2006. Accessed March 31, 2022.
Keratosis pilaris is a very common skin condition which most commonly affects the upper arms or front of the thighs with inflammatory papules, or tiny bumps. It usually first presents in early childhood and becomes more extensive as the child ages. Keratosis pilaris is thought to be caused by an abnormal follicular epithelial keratinization which causes an infundibular plug to form. The plugs lead to erythema and scaling around the follicle opening. The condition is diagnosed by evaluating the skin with a dermatoscope. During the evaluation, the provider will see hair shafts which are thin and short, coiled, or stuck in the stratum corneum.
Treatment of keratosis pilaris is not necessary since the condition is asymptomatic and non-threatening. Generally, it will improve over time. Many patients find that the bumps resolve in the summer time when the weather is more humid and then return again in the winter when the weather is dry. Patients should also maintain adequate skin hygiene by using hypoallergenic soaps in order to help the condition. If patients do not want to wait for the bumps to resolve on their own there are topical treatments that may be used such as salicylic acid lotion 6% or urea cream 20%. Salicylic acid works by producing desquamation of hyperkeratotic epithelium via dissolution of the intercellular cement. Urea cream works by softening the hyperkeratotic areas and dissolving the intracellular matrix. Chemical peels with gycolic acid have also been used to improve the appearance of keratosis pilaris. Although these treatment options may help, they will not cure the condition and even when resolution of the bumps occurs, they may still reappear at a later time.
Resources:
Pennycook KB, McCready TA. Keratosis pilaris. StatPearls [Internet]. https://www.ncbi.nlm.nih.gov/books/NBK546708/. Published July 26, 2021. Accessed March 30, 2022.
Keratosis pilaris: Overview. American Academy of Dermatology. https://www.aad.org/public/diseases/a-z/keratosis-pilaris-overview. Accessed March 30, 2022.
Rosacea
Rosacea is a chronic inflammatory skin disease primarily affecting the central face which includes the cheeks, chin, nose, and forehead. It presents as facial erythema, telangiectasias, and inflammatory papules or pustules. Many patients with rosacea also have ocular involvement with symptoms like dryness, photophobia, conjunctivitis, and blepharitis. Rosacea is more frequently diagnosed in patients with fair skin of northern European descent. Rosacea can lead to patients experiencing mental comorbidities like depression, anxiety, and low self-esteem due to their physical appearance.
Dysregulation of immune and neurocutaneous mechanisms are the main pathways related to the development of rosacea. In rosacea, innate immune activation can be triggered by microbes like demodex species and bacillus oleronius and staphylococcus epidermidis bacteria. This innate immune activation leads to upregulation of keratinocyte-derived toll-like receptor 2 (TLR2) and proteinase-activated receptor 2 (PAR2). The upregulation of these receptors leads to erythema and angiogenesis. In addition, TLR2 can elicit erythema, telangiectasia, and inflammation via expression of cytokines, chemokines, proteases, and angiogenic factors. The neurocutaneous mechanisms may be mediated through transient receptor potential (TRP) ankyrin and vanilloid subfamilies. These subfamilies respond to different external triggers like temperature change, exercise, UV, spicy foods, and alcohol, leading to a release of substance P and pituitary adenylate cyclase-activating peptide which lead to activation of inflammatory mechanisms.
The treatment of rosacea includes non-pharmacologic and pharmacologic therapies. Patients with rosacea often complain about easy facial flushing. This can be minimized by avoiding triggers such as extreme temperatures, sunlight, spicy foods, alcohol, and acute psychologic stressors. General skin care is also an important topic for patients with rosacea to learn about. The three main foundations of skin care for rosacea are frequent skin moisturization, gentle skin cleansing, and avoidance of irritating topical products. Toners, astringents, and chemical exfoliating products are types products that may irritate the skin and cause worsening of symptoms. Skin should be moisturized twice daily to reduce discomfort and gentle cleansing should be done once daily.
Laser and light-based therapies may also be utilized for treatment of rosacea. These therapies are most effective for the vascular features of the condition. Light energy is absorbed through the skin by hemoglobin in skin vessels leading to vessel heating and coagulation. Most often green or yellow light is used because they are absorbed better by hemoglobin. Improvement in facial erythema and telangiectasias are observed.
There are currently five topical agents approved by the FDA for the treatment of rosacea. Metronidazole is the first-line option. Metronidazole is a topical antibiotic which reduces oxidative stress thereby reducing erythema and inflammation. It comes in gel, cream, or lotion formulas with 0.75% or 1% strengths. The adverse effects associated with it are pruritus, irritation, and dryness. Azelaic acid is another topical agent used to reduce erythema and inflammation by reducing reactive oxygen species in neutrophils. Azelaic acid is similar in effectiveness to metronidazole, however it comes with higher frequency of adverse effects like dryness, stinging, and burning. Sulfacetamide is a second-line agent with not as much efficacy data as the first-line options. It should be avoided in patients with sulfur allergy. Brimonidine is a topical alpha-adrenergic receptor agonist agent with a different mechanism of action; it promotes vasoconstriction in order to reduce erythema. Ivermectin is the last topical agent approved for rosacea with an unknown mechanism. It is specifically indicated for papulopustular rosacea with a study showing that ivermectin was slightly more effective than topical metronidazole.
Resources:
Oge' LK, Herbert L. Muncie J, Phillips-Savoy AR. Rosacea: Diagnosis and treatment. American Family Physician. https://www.aafp.org/afp/2015/0801/p187.html. Published August 1, 2015. Accessed March 23, 2022.
van Zuuren EJ, Arents BWM, van der Linden MMD, Vermeulen S, Fedorowicz Z, Tan J. Rosacea: New Concepts in Classification and Treatment. Am J Clin Dermatol. 2021;22(4):457-465. doi:10.1007/s40257-021-00595-7
Shingles (Herpes Zoster)
Shingles, or herpes zoster, is a virus which occurs due to the reactivation of varicella zoster virus, or chicken pox. Primary infection with varicella zoster is most common in children, causing a rash to spread on the body. It is a highly contagious DNA virus and can be spread by airborne contact or direct contact with the rash. After this primary infection or vaccination for the virus, the varicella zoster virus remains dormant in the body. The memory T-cell immunity of varicella zoster decreases over time, usually after about 20 years, with the greater the decline, the greater the risk of herpes zoster infection. Certain risk factors such as age, stress, immunocompromised status and immunosuppressive drugs also play a role in virus reactivation. Adults above the age of 50 years have an increased risk for developing herpes zoster.
The symptoms of shingles start with the prodromal phase which presents as pain, fever, malaise, headache, itch, and paresthesia. A few hours to several days after the prodromal phase, unilateral, painful erythematous papules or macules will appear on the skin. These will progress to vesicles in 12-24 hours and then pustules in 1-7 days and finally crust over in 14-21 days.
As soon as a diagnosis can be made, antiviral therapy should be initiated for the best patient outcomes. Benefits from antiviral therapy and generally only seen in patients who receive therapy within 72 hours of rash onset. Acyclovir, valacyclovir, and famciclovir are the antiviral drugs of choice. These drugs help to prevent complications from herpes zoster like post-herpetic neuralgia. Acyclovir is a DNA polymerase inhibitor with lower bioavailability compared to the other agents and a higher dosing frequency of 5 times daily. Valacyclovir is a prodrug of acyclovir which has a dosing frequency of 3 times daily which may be more feasible for patients. Lastly, famciclovir is also a DNA polymerase inhibitor dose 3 times daily with a longer intracellular half-life and better bioavailability. These treatment options are well tolerated with some common side effects being nausea, headache, vomiting, dizziness, and abdominal pain. Corticosteroids such as prednisone may also be prescribed in conjunction with an antiviral to help control the pain. Pain can also be managed with over-the-counter analgesics but for more severe pain, narcotic medication may be needed.
One of the main complications of herpes zoster is post-herpetic neuralgia. Around 22% of patients with herpes zoster suffer from post-herpetic neuralgia. Post-herpetic neuralgia is defined as a herpes zoster pain persisting for more than 3-6 months after the onset of rash, or pain lasting even after complete healing of the rash. severe post-herpetic neuralgia can lead to sleep disturbance, depression, weight loss, chronic fatigue, and inability to perform daily activities. Treatment of post-herpetic neuralgia is targeted at pain control. Topical agents like capsaicin cream or lidocaine transdermal patches can be used for relief of pain. Tricyclic antidepressants such as amitriptyline or nortriptyline and gabapentin may be used as systemic treatment of the pain.
Prevention of herpes zoster can be achieved by vaccination with the Shingrix vaccine. The CDC recommends all adults age 50 years and older receive 2 doses of Shingrix, separated by 2-6 months. Adults 19 years and older with weakened immune systems should also receive 2 doses of the vaccine. The vaccine has been shown to be 97% effective in preventing shingles in people ages 50-69 years old and 91% effective in preventing shingles in people over the age of 70 years.
Resources:
Jianbo W, Koshy E, Mengting L, Kumar H. Epidemiology, treatment and prevention of herpes zoster: A comprehensive review. Indian Journal of Dermatology, Venereology and Leprology. 2018;84(3):251. doi:10.4103/ijdvl.ijdvl_1021_16
Shingrix shingles vaccination: What everyone should know. Centers for Disease Control and Prevention. https://www.cdc.gov/vaccines/vpd/shingles/public/shingrix/index.html. Published January 24, 2022. Accessed March 21, 2022.
Stankus SJ, Dlugopolski M, Packer D. Management of herpes zoster (shingles) and postherpetic neuralgia. Am Fam Physician. 2000;61(8):2437-2448.
Eczema is an inflammatory skin condition that causes dry skin, itchy skin, rashes, scaly patches, blisters, and skin infections. There are seven different types of eczema, atopic dermatitis, contact dermatitis, dyshidrotic eczema, nummular eczema, hand dermatitis, neurodermatitis, and stasis dermatitis. This skin condition is very common in children, but adults can get it too. Eczema is sometimes called atopic dermatitis, which is the most common. People with eczema often have allergies or asthma along with itchy, red skin.
Atopic dermatitis is the most common form of eczema, usually starting in childhood and often gets milder or goes away by childhood. Symptoms of atopic dermatitis usually include a rash that often forms in the creases of elbows or knees. The skin areas where the rash appears may turn lighter or darker, or get thicker, and small bumps may appear and leak fluid if scratched. Babies often get a rash on their scalp and cheeks. The skin can get infected if scratched. Atopic dermatitis happens when the skin’s natural barrier against the elements is weakened, making the skin less able to protect the person against irritants and allergens. It’s typically caused by a combination of factors such as genes, dry skin, an immune system problem, or triggers in the environment.
Contact dermatitis is caused by a reaction to substances a person touches. There are two types of contact dermatitis, allergic contact dermatitis, an immune system reaction to an irritant, and irritant contact dermatitis, that is from a chemical or other substance that irritates the skin. In contact dermatitis, the skin tends to itch, turn red, burns, and stings. Hives tend to form and fluid-filled blisters can form that may ooze and crust over. Over time, the skin may thicken and feel scaly or leathery. Dyshidrotic eczema causes small, fluid-filled blisters to form on the hands and feet. The blisters may itch or hurt and the skin can scale, crack, and flake. Dyshidrotic eczema can also be caused by allergies, but also damp hands and feet, exposure to substances such as nickel, cobalt, or chromium salt, or stress. Hand eczema typically is from exposure to chemicals that irritate the skin, from jobs like hairdressing or cleaning. In hand eczema, a person’s hand can get red, itchy, and dry, and also form cracks or blisters.
Neurodermatitis is similar to atopic dermatitis and causes thick, scaly patches to pop up on the skin. These patches can be all over the body and be very itchy, especially when a person is relaxed or asleep. Scratching the patches can cause bleeding and possible infection. Neurodermatitis usually starts in people who have other types of eczema or psoriasis. Nummular eczema causes itchy or scaly round coin-shaped spots to form on the skin from insect bites or allergic reactions to metals or chemicals. Stasis dermatitis happens when fluid leaks out of weakened veins into the skin and causes swelling, redness, itching, and pain.This usually happens in people with blood flow problems in their lower legs because of blood pooling due to heart malfunction. The legs can swell up and varicose veins can form.
There is no cure for eczema, but there are treatments like medical grade moisturizing creams, corticosteroid creams, antihistamines, light therapy, immunosuppressants, injectable biologics, bleach baths, cryotherapy, medical-grade honey, and acupuncture. For most types of eczemas, they come and go over time and managing flares is the best option. A few ways to prevent eczema flare-ups and manage symptoms would be to moisturize daily, apply cool compresses, blot skin with soft towel after bathing, avoid scratching, use fragrance-free detergents, cleansers, makeup, and other skincare products, wear gloves and protective clothing when handling chemicals, and wear loose-fitting clothes made from soft fibers like cotton. It’s also best to avoid any known triggers.
References:
Watson, S. (2020, August 25). 7 types of eczema: Symptoms, causes, and pictures. Healthline. Retrieved March 17, 2022, from https://www.healthline.com/health/types-of-eczema#eczema-expo
What is eczema? National Eczema Association. (2022, January 14). Retrieved March 17, 2022, from https://nationaleczema.org/eczema/
Eczema
Eczema, also known as atopic dermatitis, is a chronic pruritic inflammatory skin disease that affects around 5-20% of children. The condition also affects adults but data on its prevalence in adults is limited. Risk factors can be genetic or environmental. Multiple proposed mechanisms are involved in the development of atopic dermatitis. The main mechanism would be epidermal barrier dysfunction. The epidermal barrier function primarily resides in the stratum corneum. An altered stratum corneum results in increased transepidermal water loss, increased permeability and altered lipid composition. This dysfunction is usually caused by a genetic mutation of filaggrin. These multiple mutations of filaggrin also lead to loss of natural moisturizing factors. Another cause for barrier dysfunction comes from abnormal protein and enzyme processing. Changes in skin pH and calcium gradient can alter the expression of proteins and enzymes needed for barrier function. Environmental factors may also play a role in the development of atopic dermatitis. Prolonged exposure to reduced environmental humidity accelerates transepidermal water loss and aggravates the barrier defects allowing more inflammation to occur. Another environmental factor affecting atopic dermatitis would be stress. Stress causes changes in glucocorticoids which may inhibit the synthesis of ceramides, cholesterols, and free fatty acids normally found in healthy skin. Inhibition of ceramides, cholesterols and free fatty acids disrupts the hydrophobic barrier. The amount of calcium carbonate dissolved in the water and chlorine concentration in water, or water hardness, may also be correlated to atopic dermatitis. People exposed to hard water are more likely to have visible atopic dermatitis (Boothe 2017).
Atopic dermatitis is characterized by changes in the epidermis including epidermal edema, acanthosis (dark discoloration in body folds and creases), and hyperkeratosis (thickening of the skin’s outer layer). These histological changes clinically present as skin dryness, erythema, and oozing and crusting. The treatment of atopic dermatitis starts with eliminating exacerbating factors. These include excessive bathing without moisturization, low-humidity environments, emotional stress, dry skin, overheating of skin, and exposure to detergents. Emollients and moisturizers can be used to prevent dry skin. These products should be applied at least twice a day and always applied after bathing or hand washing. Along with moisturizers, topical corticosteroids are also an initial treatment option for atopic dermatitis. Patients with a mild condition would be prescribed a low-potency corticosteroid to be used for two to four weeks. Patients with a moderate condition should be prescribed medium- to high-potency corticosteroids to be used only for two weeks and then replaced with a lower-potency option. Topical calcineurin inhibitors can be used as an alternative to corticosteroids especially on areas such as the face, neck, and skin folds. For patients who do not respond to therapy with first line options, dupilumab is a newer agent that may be considered (American Academy of Dermatology, 2021). It was approved in 2017 for the treatment of atopic dermatitis, moderate to severe asthma, and chronic rhinosinusitis. It is a monoclonal antibody that binds to the interleukin-4 receptor and inhibits inflammatory processes related to atopic dermatitis. Dupilumab along with the other topical therapies as well as minimizing environmental factors are effective ways to manage atopic dermatitis.
References:
Atopic dermatitis clinical guideline. American Academy of Dermatology. https://www.aad.org/member/clinical-quality/guidelines/atopic-dermatitis. Accessed March 11, 2022.
David Boothe W, Tarbox JA, Tarbox MB. Atopic dermatitis: Pathophysiology. Advances in Experimental Medicine and Biology. October 2017:21-37. doi:10.1007/978-3-319-64804-0_3
Acne Vulgaris
Acne vulgaris is the most prevalent chronic skin disease in the United States. It affects almost 50 million people a year, usually adolescents and young adults, but may also persist into adults in their 30s and 40s. Acne is due to sebum overproduction, abnormal shedding of follicular epithelium, follicular colonization by Cutibacterium acnes (previously Propionibacterium acnes) and inflammation. Genetics and diet may also contribute to acne. Other factors such as psychological stress, tobacco smoke, and damaged or unhealthy skin may also be involved.
Acne lesions are usually seen on the face, chest or upper back, where there are more sebaceous glands. They may be noninflammatory closed comedones, opened comedones, inflammatory papules, nodules, pustules, or cysts. Opened comedones are whiteheads or papules formed by the accumulation of sebum/keratin within the hair follicle. Opened comedones are blackheads or distension of the hair follicle with keratin that leads to opening of the follicle, oxidation of lipids and deposition of melanin. Papules are small, red, inflamed blemishes that are clustered together and may be sore to the touch. Pustules are inflamed blemishes filled with pus. Pus is a mixture of oil, bacteria and dead skin cells that gets trapped under the skin. Nodules are bigger, swollen bumps that forms when hair follicles break down. This goes deeper into the skin and may affect multiple pores. Cysts are very large blemishes caused by a severe inflammatory reaction deep in the pore. It forms when there is a rupture of bacteria and oil to spread into the surrounding skin. Based on the severity and types of lesions, acne can be classified as mild, moderate or severe.
Major outcomes of inflammatory acne lesions are post-inflammatory hyperpigmentation and acne scars. Post-inflammatory hyperpigmentation is discoloration left on the skin after a lesion. It is due to excess melanin that is produced as the skin heals. Acne scars are classified into atrophic and hypertrophic or keloid scars. Atrophic scars are three times more common than hypertrophic scars. Atrophic scars are due to the destruction of collagen in the dermis. They are classified into ice pick, boxcar, and rolling scars. Ice pick represents 60-70% of scars, boxcar 20-30% and rolling scars 15-25%. Ice pick scars are narrow (less than 2mm), punctiform and is in a V shaped that extends vertically to the deep dermis or subcutaneous tissue. Boxcar scars are wider, 1.5-4mm, and round to oval depressions with sharply demarcated vertical edges (U shaped). Boxcar scars can be shallow or deep, shallow being less than 0.5mm deep and deep being more than 0.5mm. Rolling scars are the widest, up to 5 mm, and abnormal fibrous anchoring of the dermis to the subcutis that leads to superficial shadowing and a rolling appearance (M shaped). These three different types of atrophic scars can be present on the same patient. Then, there are hypertrophic and keloid scars, which are associated with excess collagen deposition and decreased collagenase activity. They are typically more common in darker-skinned individuals. Hypertrophic scars are typically pink, raised, and firm with thick hyalinized collagen bundles that remain within the border of the acne lesion. On the other hand, keloid scars are reddish-purple papules and nodules that go beyond the borders of the acne lesion.
References
1. Fabbrocini G, Annunziata MC, D'Arco V, et al. Acne scars: pathogenesis, classification and treatment. Dermatol Res Pract. 2010;2010:893080. doi:10.1155/2010/893080
2. Oge' LK, Broussard A, Marshall MD. Acne Vulgaris: Diagnosis and Treatment. Am Fam Physician. 2019;100(8):475-484.
3. Palmer, Angela. “The Best Ways to Treat Acne Hyperpigmentation.” Verywell Health, Verywell Health, 27 Jan. 2021, https://www.verywellhealth.com/post-inflammatory-hyperpigmentation-15606.
4. Titus S, Hodge J. Diagnosis and treatment of acne. Am Fam Physician. 2012;86(8):734-740.
5. “Types of Acne Blemishes.” Patient Care at NYU Langone Health, https://nyulangone.org/conditions/acne/types.
Atopic Dermatitis
Atopic dermatitis, also known as eczema, is a chronic relapsing inflammatory skin condition affecting about 17.8 million people in the United States. It is a condition characterized by pruritic, erythematous and scaly skin lesions. It is the most common skin disease in children, affecting approximately 15% to 20% of children and 1% to 3% of adults. The incidence has increased by 2 to 3 fold during the past decades in industrialized countries. Onset is usually by age 5, and early diagnosis and treatment are essential to avoid complications and improve quality of life. Atopic dermatitis is thought to be caused by a genetic defect in the filaggrin protein disrupting the epidermis. This disruption leads to contact between immune cells in the dermis and antigens from the external environment, causing intense itching, scratching and inflammation. However, scratching leads to further disruption and inflammation; this is known as the itch-scratch cycle.
Atopic dermatitis presents in three phases: acute, subacute, and chronic. Acute atopic dermatitis is a vesicular, weeping, crusting eruption. Subacute atopic dermatitis is dry, scaly, erythematous papules and plaques. Chronic atopic dermatitis demonstrates lichenification from repeated scratching. Pityriasis alba is another presentation of atopic dermatitis that is common in children and characterized by hypopigmented, poorly demarcated plaques with fine scales. Usually, atopic dermatitis involves the flexural surfaces of the body, anterior and lateral neck, eyelids, forehead, face, wrists, dorsa of the feet, and hands. It may start out as dry, itchy skin and then become red, swollen and sore. The rash can crust over and start to scale.
Atopic dermatitis cannot be cured, but can be managed. Management consists of relieving symptoms and increasing the time between flare-ups. First, it is important to avoid the triggers of atopic dermatitis such as viral infections, food allergens, cosmetics, fragrances, and weather. Extremes of hot and cold weather can lead to sweating and dry skin. This causes skin irritation and makes eczema worse. Therefore, do not use hot water to take showers, instead use warm or cool water with mild, non drying soaps. Also, instead of tight clothes, wear loose, cotton clothing and avoid overheating.
It is important to use a moisturizer as it helps keep the skin soft and flexible and prevent skin cracks. As a first line treatment, a topical corticosteroid can be applied to the rash to reduce itching and calm inflammation. Topical corticosteroids come in different potencies, and it is important to be treated with the right strength, amount and formulation as determined by age, severity and sites involved. They should be used until the skin is smooth, feels like normal skin, and the inflammation and itch have settled, otherwise, the skin can flare up. Some side effects of topical corticosteroids include stretch marks, telangiectasia and thinning of the skin. Then, there are calcineurin inhibitors, such as pimecrolimus and tacrolimus, that are used as second line treatment for moderate to severe eczema and who are at risk of atrophy from topical corticosteroids. They do not share the side effect profile of corticosteroids, but there is a risk of immunosuppression.
References:
Avena-Woods C. Overview of atopic dermatitis. Am J Manag Care. 2017;23(8 Suppl):S115-S123.
Berke R, Singh A, Guralnick M. Atopic dermatitis: an overview. Am Fam Physician. 2012;86(1):35-42.
Staff, Familydoctor.org Editorial. “Eczema vs Atopic Dermatitis - Types and Causes.” Familydoctor.org, 26 May 2020, https://familydoctor.org/condition/eczema-and-atopic-dermatitis/.
Strathie Page S, Weston S, Loh R. Atopic dermatitis in children. Aust Fam Physician. 2016;45(5):293-296.
Tinea Versicolor
Tinea versicolor, or pityriasis versicolor, is a common fungal infection of the skin. The condition is characterized by hyper, or hypo, pigmented scaly skin. Typically, it effects the trunk, back, and proximal extremities, but can be found on any area of the body. Tinea versicolor is caused by a type of fungus called Malassezia, which is a part of the normal skin flora. The overgrowth of the fungus on the skin produces fine, scaly patches. Though tinea versicolor occurs worldwide, it is more common in areas with warm and humid conditions. The warm, humid weather is preferable for the growth of fungus. Because Malassezia yeasts grow in the more seborrheic areas of human skin, tines versicolor can be seen more commonly in young adults due to the increase of sebum produced by sebaceous glands during puberty. The lipid-rich environment created by the sebum production promotes the growth of the fungus.
Though the Malassezia fungus is part of the normal human skin flora, when an overgrowth occurs and the fungus converts to a pathogenic filamentous form, it is considered to be pathologic. Genetic disposition, environmental conditions, pregnancy, oily skin, and even topical applications of skin products can all play a role in the growth of the patches. Skin biopsies can be used to confirm a diagnosis, but it is not common. A skin biopsy would show hyper keratosis, acanthosis, and perivascular infiltrates in the dermis. Upon visual evaluation, the scaly lesions may not be clear but once stretched or scraped the effected skin can be easily seen. An ultraviolet black light may help reveal a coppery-orange fluorescence indicative of tinea versicolor on the skin. The areas effected may be itchy and even more so in humid and warm conditions, but otherwise no painful sensations occur. The condition is not contagious and does not lead to permanent scarring or pigmentation.
First-line treatment of tinea versicolor includes non-specific topical antifungal agents that remove dead tissue and prevent further growth of the fungus. These agents include selenium sulfide, zinc-pyrithione, and sulfur plus salicylic acid creams or shampoos. These treatments can be found over the counter included as the active ingredients in brands such as Selsun Blue and Head and Shoulders. Other antifungal treatment agetns include clotrimazole, ketoconazole, econazole, isoconazole, and miconazole. Ketoconazole is the most common topical treatment, and it is applied as a cream twice daily for 15 days or as a foaming solution. Oral medications can be used for treatment as second-line agents. They are used in severe, recurrent cases. Itraconazole and fluconazole are the most used oral antifungals for treatment. Prophylactic therapy may be recommended even when patches are not present to keep the fungal growths at bay. With treatment the patches will eventually retreat, but it is important to note that it may take weeks or months to disappear, even when the fungal growth has subsided.
References:
1. Karray M, McKinney WP. Tinea Versicolor. [Updated 2021 Aug 11]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482500/
2. Hudson A, Carroll B, Kim SJ. Folliculocentric tinea versicolor. Dermatol Online J. 2017;23(2):13030/qt5kj574bd. Published 2017 Feb 15.
There are many diseases caused by an inflammatory process. This inflammatory process that occurs in the body can affect a plethora of systems throughout the human body. Inflammatory diseases cause processes involved in asthma, Crohn’s disease, rheumatoid arthritis, and many other diseases. Having a constant battle with your own immune system can be exhausting for patients and their caregivers. Understanding the disease burden of inflammatory diseases is critical in being able to adequately treat these patients. Plaque psoriasis, which is a condition of the skin, is the most common immune-mediated disease. Plaque psoriasis, in severe cases, can affect a patients’ joints if not properly treated. Plaque psoriasis is not a life-threatening condition, but it is one that is difficult to treat. Patients with plaque psoriasis have different response rates to these treatments when compared to, for example, ACE inhibitors for hypertension. This is what makes this difficult to treat and frustrating for patients. Plaque psoriasis can be caused by many immune processes in the body, such as the keratinocyte hyperplasia, altered t-cell function, increased epidermal growth factor (EGF), interleukin 17 increased activation, and CD8 activation. Plaques are well-defined, red plaques of the skin. They can be covered with white-scaley plaques that are uncomfortable for patients. Inflammatory dermatologic conditions are some of the most highly-desired markets for pharmaceutical companies.
Tapinarof is a topical cream being investigated for the treatment of plaque psoriasis. It is An aryl-hydrocarbon receptor-modulating agent. It modulates the expression of interleukin-17, and this is how it regulates the immune system to treat plaque psoriasis. There were two identical trials evaluating the efficacy of tapinarof. There were two trials evaluating patients with mild-to-severe plaque psoriasis. Patients were assessed based on improvement in the Physician’s Global Assessment (PGA), with higher scores indicating more severe disease. Secondary endpoints at week 12 included reduction of at least 75% in the Psoriasis Area and Severity Index (PASI) score, a PGA score of 0 or 1, , and change from baseline in the body surface area affected by plaque psoriasis. There were over 1,000 patients enrolled in these two identical trials. There was a change in the PGA score in 35.4% of patients in the tapinarof treatment arm as compared to the vehicle control group. In the second trial, 40.2% of patients in the treatment arm achieved the primary outcome as compared to 6.3% in the vehicle control group. Tapinarof cream showed to be superior to the vehicle control group in reducing the intensity of plaque psoriasis over the 12 week trial period. Adverse events in the tapinarof group were folliculitis, contact dermatitis, headache, pruritus, nasopharyngitis, and upper respiratory tract infection. Many patients would consider those adverse effects tolerable for the relief of the inflammatory disease.
Although tapinarof is superior to the vehicle control for the treatment of plaque psoriasis, the number of responding participants was still not at the high levels we see with other drug classes. This is due to the multifactorial nature of the disease, and the difference in patient response rates. This is an emerging disease state that will see a lot of pharmaceutical action over the next few years.
Resources:
Badri T, Kumar P, Oakley AM. Plaque Psoriasis. [Updated 2021 Aug 11]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-.
Lebwohl MG, Stein Gold L, Strober B et al. Phase 3 Trials of Tapinarof Cream for Plaque Psoriasis. N Engl J Med. 2021 Dec 9;385(24):2219-2229.
Acne vulgaris is one of the most common skin conditions affecting children, young adults, and even adults. Acne can have a significant effect on patients in many more ways than one. Patients with acne vulgaris often suffer from psychosocial effects associated with their blemishes. These psychosocial effects can include depression, anxiety, altered perception of physical appearance and reduced social abilities. These effects can impact quality of life, and can lead to more severe mental health issues down the line for these patients.1 It is especially important to properly treat acne in patients due to the sensitive and critical age when acne often presents. Acne commonly begins during puberty, which can occur between the ages of 10 and 13. These are critical points in the development of proper self-esteem and self-worth. Acne, and subsequently anxiety and depression, are detrimental to these delicate patient populations. Although one of the most common conditions, affecting more than 50 million people in the United States of America, the exact cause is not precisely pinpointed. Acne is considered to be a multifactorial disease. The triggers of this inflammatory reaction can include diet, stress, neuroendocrine dysregulation, genetic and environmental factors. There is no secret formula for treating acne, but there are medications to help treat or alleviate acne.
Acne treatment is characterized based on the type of acne that a patient presents with. If a patient presents with only mild acne, the first line treatment will always be a topical regimen. There are several topical regimens that are recommended first line for mild acne, and the choice between the recommended treatments is, oftentimes, based on physician preference and personal experience. Patients can either be started on benzoyl peroxide or a topical retinoid, such as tretinoin. These are first line for many dermatologists due to the efficacy and tolerance. Other options for mild acne include combination therapy. This can include a combination of benzoyl peroxide plus an antibiotic like clindamycin. Patients can also be started on benzoyl peroxide plus a retinoid or a combination of all three kinds of drugs. Regimens can look something like this: clindamycin + benzoyl peroxide in the morning followed by tretinoin in the evening. Moderate acne is treated similarly to mild acne, but it always is a combination of multiple medications. Patients can start with benzoyl peroxide and a retinoid or an antibiotic. There can be any mix of the three core classes of medications. There is also add on oral antibiotic therapy added in the moderate category. This is often combined with a topical retinoid plus benzoyl peroxide. Patients can also be prescribed a topical antibiotic in addition to the oral antibiotic. In severe cases of acne, patients are often immediately started on an oral antibiotic plus a combination of the three core topical agents. In very severe cases, isotretinoin can be used as a “cure” for acne.2
Although acne is such a common disease, there is not yet a “secret formula” for its cure. There are many contributing factors, and each patient must be counseled using a multicenter approach to reducing or curing a patient’s acne. Other helpful tactics can include diet control, stress relief, and regular exercise.
References:
Thomas DR. Psychosocial effects of acne. J Cutan Med Surg. 2004;8 Suppl 4:3-5. doi: 10.1007/s10227-004-0752-x.
Andrea L. Zaenglein, Arun L. Pathy, Bethanee J. Schlosser et al. Guidelines of care for the management of acne vulgaris, Journal of the American Academy of Dermatology, Volume 74, Issue 5, 2016, Pages 945-973.
Tacrolimus (topical)
Written by: Hillary Pham and Jae Chang
The medication, Tacrolimus, is most known for its immunosuppressant activity for transplant patients. However, Tacrolimus is a calcineurin inhibitor that may also be used as a topical skin product.
The mechanism action as it inhibits calcineurin is that it is involved in making of the interleukin 2, which aids and produces the T cells. As we know, T cells are a part of the body’s immune response and helps to regulate it. It is passively absorbed into the affected skin and reduces skin inflammation by inhibiting the T-cell activation by binding to an immunophilin receptor, thereby inhibiting the activity of calcineurin. In regard to skin conditions, Tacrolimus is used for atopic dermatitis, psoriasis, and even vitiligo.
Tacrolimus ointment is a TCI (topical calcineurin inhibitor) and is the first of its class to be developed for the purpose of specifically treating atomic dermatitis. In short term studies, both 0.03% and 0.1% ointments were significantly effective for mild eczema, with no particular difference in efficacy between the two doses. However, tacrolimus ointment of 0.1% showed more rapid improvement in efficacy parameters than 0.03% for moderate to severe atopic dermatitis. Ultimately, when tacrolimus is used for atopic dermatitis, or eczema, it is to be applied in a thin layer of 0.03% or 0.1% ointment to the affected area twice daily. It is important the medication must be stopped when there are no more symptoms left. If there is no improvement seen within 6 weeks, patients should be re-examined to confirm the diagnosis. This dosage is typical for patients who are classified as to having moderate to severe eczema. As for its safety, tacrolimus is commonly seen to cause pruritus and burning sensation, erythema, soreness, stinging, and flushes especially after alcohol ingestion. These side effects are more commonly observed in adults than children and usually occurs during the first few days of treatment, then resolves spontaneously. It is important to avoid sunlight during tacrolimus ointment treatment due to its black box warning of increased cancer risk. Furthermore, mild to moderate infections are reported commonly with the use of topical tacrolimus.
In Psoriasis, Tacrolimus is only used as an off-label use. This means that Tacrolimus when used topically is not approved by FDA for safety and efficacy. However, numerous health care professionals do believe this medication can still benefit the patient. For psoriasis, it is to be applied topically in a thin layer of 0.03% or 0.1% ointment to the affected area twice daily. With regard to the efficacy of tacrolimus, many studies have shown mixed reports, most likely as a consequence of inadequate skin penetration through the plaques when used to treat plaque psoriasis; fortunately, other studies that involves the use of topical tacrolimus in combination with skin penetration enhancers have demonstrated enhanced efficacy. The most common adverse effects of tacrolimus include mild, self-limiting pruritus and warm sensation at the application site, which subsides quickly with continuation of the treatment.
For Vitiligo, it is also considered to be used as an off-label medication. It is to be applied topically of a 0.1% ointment to affected areas twice daily. However, unlike the other two conditions mentioned above, this may require several months for any beneficial response to show. Studies have demonstrated that tacrolimus as a monotherapy or adjuvant therapy for vitiligo is highly recommended as the use of tacrolimus has shown positive results. Further, combining tacrolimus to other treatments such as steroids or phototherapy may give superior results than tacrolimus monotherapy. Adverse effects associated with the use of tacrolimus were mild to moderate burning sensation, erythema and pruritus.
It is important to note that when Tacrolimus 0.03% is used as a topical agent as compared to an oral agent, it is only approved in people older than age 2 to help control the skin reaction. However, the Tacrolimus 0.1% dose is only approved for ages 16 years and older. Also patients must remember to apply it as directed, after the patient has moisturized first. Furthermore, patients must avoid strong sunlight when using these products. However, sunscreen or clothing may also be useful for patients taking topical Tacrolimus. As healthcare providers, we must be aware that there is a black box warning since the long-term safety of this drug is still unknown. Although it is rare for this medication, there is a potential risk of cancer development while on this medication. It is vital to not use this drug without a break for a long time unless directed by a doctor.
Reference:
Tacrolimus, Lexicomp (10/01/2021)
Baldo, A., Cafiero, M., Di Caterino, P., & Di Costanzo, L. (2009). Tacrolimus ointment in the management of atopic dermatitis. Clinical, cosmetic and investigational dermatology, 2, 1–7. https://doi.org/10.2147/ccid.s3378
Malecic, N., & Young, H. (2016). Tacrolimus for the management of psoriasis: clinical utility and place in therapy. Psoriasis (Auckland, N.Z.), 6, 153–163. https://doi.org/10.2147/PTT.S101233
Arora CJ, Rafiq M, Shumack S, Gupta M. The efficacy and safety of tacrolimus as mono- and adjunctive therapy for vitiligo: A systematic review of randomised clinical trials. Australas J Dermatol. 2020 Feb;61(1):e1-e9. doi: 10.1111/ajd.13096. Epub 2019 Jul 2. PMID: 31267534.
Vitiligo
Vitiligo is a depigmenting skin disease where there is a loss of melanocytes, resulting white, smooth patches on the skin. There are several mechanisms that can be attributed to the loss of melanocytes such as genetics, autoimmune responses, oxidative stress and the production of inflammatory mediators. Vitiligo affects people of all ethnicities with no increased risk population and also equally affects both males and females. However, females tend to seek medical treatment more due to societal stigma. It can develop at any age but commonly occurs between the ages of 10 to 30 years. Around 20% of vitiligo patients have at least 1 first-degree relative with vitiligo, increasing the risk for disease by 10 fold. Genes relevant to the disease are involved in immune regulation, melanogenesis and apoptosis. For example, the TYR gene which codes for the enzyme tyrosinase involved in melanin synthesis has been found to been linked to a variant evident in vitiligo patients.
Patients presenting with vitiligo should have a comprehensive medical history and examination performed. Key things to be noted include age of onset, family history, rate of spread, current medications and profession. Body examination assesses type of vitiligo, physical extent of the disease, mucosal involvement and Koebner phenomenon (formation of skin lesions on parts of the body where one doesn’t typically experience lesions). There are two types of vitiligo: nonsegmental and segmental. Nonsegmental vitiligo is the more commonly occurring, challenging type. Its response is generally slow and its highly variable. Whereas, segmental vitiligo is rarer, onset is during childhood and has a more predictable course. One to two years after onset, there is little progression of the disease.
Topical, systemic, and light-based therapies are available for the treatment of vitiligo. Oral glucocorticoids are recommended for the cessation rapidly progressing and spreading vitiligo. 10 to 20 mg of oral prednisone per day is administered to adults for a maximum of two weeks. Simultaneous initiation of ultraviolet B (NBUVB) phototherapy may be more effective than oral corticosteroids alone. For localized nonsegmental stable vitiligo, topical corticosteroids can be applied once to twice daily. Topical calcineurin inhibitors tacrolimus and pimecrolimus are preferred to topical corticosteroids for patients with limited vitiligo due to risk of skin atrophy. Topical treatment for patients with disseminated vitiligo can be unpractical, so phototherapy can be administered two to three times weekly. Additionally, transplantation procedures using skin grafts can also be performed which transfers healthy melanocytes to the skin for the migration into areas of depigmentation.
References:
Bergqvist, C, and Ezzedin, K. “Vitiligo: A Review.” Karger, Karger, Nov. 2020.
Grimes, Pearl. “Vitiligo: Management and Prognosis.” UpToDate, UpToDate, Apr.
2021.
Melasma
Melasma is a skin disorder characterized by brown hyperpigmentation, symmetrically distributed mainly on the face. It can appear around the cheeks, bridge of nose, forehead, chin, and above the upper lip. There is a myriad of factors that could trigger melasma such as sun exposure, pregnancy, use of oral contraceptives, etc. People of color like those of Latin/Hispanic, African-American and Asian descent are more likely to get melasma as they have more active melanocytes. Additionally, people who have a blood relative with melasma also are much more likely to get melasma. It does often get worse during the summer season when exposure to the sun is increased. This is because UV radiation increases the activity of melanocytes. Melasma is also called “the mask of pregnancy” as it is super common during pregnancy which may be attributed to the hormone stimulation in females. Melasma does not cause other somatic symptoms but it does affect one’s quality of life as it is easily visible on the face and can lead to low self-esteem. Melasma can resolve on its own in some cases when the trigger is removed like when a woman gives birth or stops taking birth control. It can last a long time for some people but there are some treatment options available. First and foremost, photoprotection is essential, this includes sun-protective clothing and broad-spectrum sunscreens. Topical first-line treatment options are hydroquinone or for more severe melasma a fluocinolone, hydroquinone and tretinoin triple combination cream. An alternative topical therapy, azelaic acid is recommended if hydroquinone is not tolerated. Second-line treatments include chemical peels consisting of glycolic acid, salicylic acid, etc. However, their effects are only temporary as chemical peels temporarily only remove epidermal melanin and do not interfere with the activity of melanocytes.
References:
Grimes, Pearl, and Valerie Callender. “Melasma: Management.” UpToDate, Apr.
2021.
Handel, Ana Carolina et al. “Melasma: a clinical and epidemiological review.” Anais
brasileiros de dermatologia vol. 89,5 (2014): 771-82.
Passeron, Thierry, and Mauro Picardo. “Melasma, a Photoaging Disorder.” Wiley
Online Journal, Dec. 2017.
Dupixent
Atopic dermatitis, eczema, is an immune disorder that develops by 5 years of age. It causes extremely itchy rashes that come and go. Patients with atopic dermatitis have “super” sensitive skin and a decreased threshold foe irritation. The condition comes with oozing plaques of itchy skin and in chronic cases, thick elevated skin is present. Treatments for atopic dermatitis is centered around rehydration using emollients such as petroleum jelly and the cautious use of topical steroids to reduce inflammation and itching.
Dupixent (dupilumab) is new treatment for Atopic dermatitis developed by Sanofi Genzyme. Dupixent is a biologic that targets the underlying source of inflammation, healing the skin from within; a human monoclonal IgG4 antibody that inhibits interleukin-4 (IL-4) and interleukin-13 (IL-13) signaling by specifically binding to the IL-4Rα subunit shared by the IL-4 and IL-13 receptor complexes. Dupilumab inhibits IL-4 signaling via the Type I receptor and both IL-4 and IL-13 signaling through the Type II receptor. Within the immune system, IL-4 perpetuates the type 2 inflammatory cascade and its effects through a positive feedback loop, this drives Th2 differentiation. IL 3 and Il-4 play roles in IgE production and B cell class switching. They both increase vascular adhesion and permeability. Dupixent helps to repair the skin by targeting a key source of type 2 inflammation specifically targeting IL-4 and Il-3 signaling to reduce epidermal hyperplasia, modify lesion skin appearance, and modulate genes related to the epidermal pathology in atopic dermatitis. Dupixent is not an immunosuppressant or a steroid and requires no initial lab testing or ongoing lab monitoring.
Dupixent comes in 200mg and 300mg injections using weight-based dosing. Your initial dose of Dupixent is 2 injections under the skin at different injection sites. After, it is taken as 1 injection site every 2 weeks or every 4 weeks depending on your age and weight. If your dose schedule is every other week and you miss a dose of DUPIXENT: Give the DUPIXENT injection within 7 days from the missed dose, then continue with your original schedule. If the missed dose is not given within 7 days, wait until the next scheduled dose to give your DUPIXENT injection. If your dose schedule is every 4 weeks and you miss a dose of DUPIXENT: Give the DUPIXENT injection within 7 days from the missed dose, then continue with your original schedule. If the missed dose is not given within 7 days, start a new every 4-week dose schedule from the time you remember to take your DUPIXENT injection.
As of right now, Dupixent is not recommended in pregnant women, or those who are breast feeding as no studies have been conducted to know whether Dupixent is harmful to the unborn baby. The most common side effect is allergic site reaction/ hypersensitivity.
References:
MOA: Mechanism of Action. DUPIXENT® (dupilumab) Mechanism of Action. https://www.dupixenthcp.com/atopicdermatitis/about/mechanism-of-action. Accessed June 3, 2021.
Dupixent.Package insert. Sanofi Genzyme. 2021.
Seborrheic dermatitis is a skin disorder most common in male patients ages 20 to 50 years old, but also affects women, elderly and infants. Seborrheic dermatitis is also known as seborrhea, seborrheic eczema, dandruff or cradle cap. Seborrhea affects those with underlying neurologic diseases such as parkinsons and immunocompromised patients, specifically those who are HIV+ or have AIDs. While the actual cause of seborrhea is unclear it is linked to local immune response to antigens, environmental factors especially cold/dry weather and local expression of hormones.
Certain drugs are also known to cause seborrhea flare-ups such as isotretinoin, captopril, cimetidine, and interleukin-2. Patients treated with Parkinson's drugs such as lithium, buspirone, haloperidol decanoate and chlorpromazine are known to develop seborrhea. Patients with seborrhea may be affected by yeast of the genus Malassezia which is normally found in patients without seborrhea. Excessive growth of Malassezia produces fungal metabolites in sebum rich areas that’ll interact with triglycerides released from sebaceous glands serving as a cause for inflammation. Malassezia may also produce proinflammatory cytokines causing skin eruption and disrupting the skin barrier.
Seborrhea typically presents as greasy and scaly erythematous plaques often poorly demarcated (poorly marked lesions) and yellowish in color. In darker skinned patients with seborrhea their skin can also develop hyperpigmentation. Seborrhea usually appears in locations of the body known to have sebaceous glands; such as the face specifically the eyelids, eyebrows, nasolabial folds, glabella, and under facial hair for men. Seborrhea will also appear on the scalp, ear canal, back, armpit, gluteal cleft, groin, central and upper chest. Seborrhea on the scalp is a milder common form known as dandruff, often appearing as small dry flaky scales. Infants who develop seborrhea may involve neck creases, diaper area and on the scalp known as cradle cap. HIV+ patients with seborrhea may experience a sudden onset of lesions that'll appear more widespread and involve discharge.
Therapy goals include stopping further colonization of yeast on the skin, treating scales/crusts, decrease in sebum production and inflammation. It is shown that antifungal therapy to reduce the amount of Malassezia on the skin has proven to effectively treat seborrhea. First line treatment includes topical antifungals (shampoos, creams, liquids, sprays), and topical steroids for anti-inflammatory benefits.
For patients suffering from dandruff they must wash their scalp with antifungal shampoos containing ketoconazole, selenium sulfide, zinc pyrithione (ZPT) or ciclopirox daily/up to several times a week as a part of maintenance therapy. Ketoconazole 2% shampoo when used twice weekly is shown to have 73% improvement in dandruff, whereas ketoconazole 2% cream/gel/emulsion has been effective for facial seborrhea. For moderate to severe scalp seborrhea fluocinonide 0.05% solution and clobetasol 0.05% topical preparations have shown improvements. While topical corticosteroids such as hydrocortisone 1% are beneficial for symptoms of erythema associated with seborrhea, long term use will lead to skin atrophy. In terms of second line therapy, a regimen of terbinafine 250 mg pills once daily for 4 weeks has shown benefits for moderate to severe seborrhea. Pimecrolimus 1% cream, tacrolimus 0.1% ointment and metronidazole gel are appropriate options as well.
Bae E, Hancock MM, Cindy Bae Y, Usatine RP. Seborrheic Dermatitis. In: Usatine RP, Smith MA, Mayeaux, Jr. EJ, Chumley HS. eds. The Color Atlas and Synopsis of Family Medicine, 3e. McGraw-Hill; Accessed May 21, 2021. https://accessmedicine-mhmedical-com.jerome.stjohns.edu/content.aspx?bookid=2547§ionid=206797219
Lawley LP, McCall CO, Lawley TJ. Eczema, Psoriasis, Cutaneous Infections, Acne, and Other Common Skin Disorders. In: Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. eds. Harrison's Principles of Internal Medicine, 20e. McGraw-Hill; Accessed May 21, 2021. https://accessmedicine-mhmedical-com.jerome.stjohns.edu/content.aspx?bookid=2129§ionid=192013524
Berk T, Scheinfeld N. Seborrheic dermatitis. P T. 2010;35(6):348-352.
Eczema is defined as inflammatory skin disorders with unknown etiology or cause. Atopic dermatitis (AD) is a common form of eczema and is diagnosed within 6 months old to 1 years old. AD will display differently in adults and children, symptoms in children may eventually subside as they grow older or persist into adulthood. AD is a chronic/severe inflammatory condition concerning the epidermis, dermis, and immune system. Even though the cause of AD is not entirely clear, it can be linked to impaired skin barrier functions, dysfunctional immune system, infectious and environmental factors.
Over expression of pro-inflammatory cytokines (IL-4 & IL-5, TNF) and chemokine produced by TH2 cells/TH1 cells promote IgE production and lead to pruritic inflammation. Filaggrin gene (FLG) normally encodes a structural protein needed to maintain a strong and protective skin barrier particularly the epidermis. Mutations in FLG will contribute to a damaged skin barrier due to a decrease in skin barrier proteins/decreased protease inhibition and increased peptidase activity. Increased transepidermal water loss (TEWL) and decreased moisture retention seen in AD is due to decreased ceramides and cathelicidins; which impair the skin’s first-line of defense against pathogens leading to infiltration of allergens, bacteria and viruses. Atopic march is a process which begins with atopic dermatitis in infants who are sensitized, who later on develop IgE-mediated food allergies, asthma or allergic rhinitis. Triggers of AD include environmental factors such as pollution, climate, chemicals, microbial exposure and diet.
Infantile/childhood AD presents as scales and erythema on the cheeks, neck, forehead, and extremities. Pruritus or itching is a common symptom of AD, rubbing and scratching will lead to crust formation, pustule formation, and lichenification (thick plaques of skin often scaly, crusty and erythematous). Adult AD will present in the eyes, forehead, neck, hands, antecubital and popliteal fossae. Rashes can appear as purple, grey, brown or red in color. AD has three categories: acute, subacute and chronic AD. Acute AD appears as pruritic erythematous skin with papules (firm, raised lesion), vesicles (air/fluid-filled sacs) and serous exudates (secretions). Subacute AD appears as erythematous papules and scaly plaques. Chronic AD appears as lichenification and prominent skin marks.
The main focus for the treatment of AD is repairing the skin barrier through hydrating/maintaining barrier functionality, reducing itching and inflammation and preventing infections. No current cure for AD, so the goal is symptom management through appropriate non pharmacological and pharmacological treatment, adequate patient/caregiver education, and minimization of skin irritants. As pharmacists we must educate patients on lifestyle changes. Recommend use of emollient rich moisturizers such as petroleum, plant/mineral oils, ceramides and fatty acids. Advise patients to opt for cotton sheets/clothing, unscented/chemical-free laundry detergents and soaps when doing laundry. When bathing use lukewarm water, avoid highly fragranced soaps, and use hypoallergenic washes. Keep fingernails short and clean and wear gloves on the hands to prevent scratching.
Topical corticosteroids are first line treatment for AD because of their anti-inflammatory and immunosuppressive effects, short term use recommended to avoid long term effects including skin thinning, petechiae, striae and atrophy. Hydrocortisone available by prescription strengths 1% to 2.5% and nonprescription strengths 0.5% to 1%, ointments preferred over creams. Timecrolius and pimecrolimus are TCIs that are second line treatment for moderate to severe AD flare-ups but should also be limited to short term use to avoid skin irritation. Topical antihistamines can offer short term itch relief but use is not recommended. However, oral antihistamines may improve sleep for patients with AD who suffer from insomnia due to excessive itching/scratching. As for severe, refractory AD short term use of immunosuppressive agents such as cyclosporine can be used for patients who failed topical treatments.
Kim W. Benner, (2020), "Chapter 33: Atopic Dermatitis and Dry Skin," Handbook of Nonprescription Drugs: An Interactive Approach to Self-Care, 20th Edition. https://doi-org.jerome.stjohns.edu/10.21019/9781582123172.ch33
National Eczema Association. Atopic Dermatitis. https://nationaleczema.org/eczema/types-of-eczema/atopic-dermatitis/ (accessed 2021 May 19).
Kapur S, Watson W, Carr S. Atopic dermatitis. Allergy Asthma Clin Immunol. 2018;14(Suppl 2):52. Published 2018 Sep 12.
Hill DA, Spergel JM. The atopic march: Critical evidence and clinical relevance [published correction appears in Ann Allergy Asthma Immunol. 2018 Mar 9;:]. Ann Allergy Asthma Immunol. 2018;120(2):131-137.
Evaluating the therapeutic potential of VB-3222
A 2020 Indian Study in the Clinical, Cosmetic, and Investigational Dermatology Dove Press Journal was recently published to evaluate the therapeutic efficacy of a newly developed anti-dandruff regimen, VB-3222 compared to that of traditional therapies. VB-3222 is a shampoo that was developed to address the shortcomings of therapy that currently exist for dandruff sufferers. The researchers focused on the cause of seborrheic dermatitis: overgrowth and proliferation of the commensal scalp yeast known as Malassezia, combined with enhanced sebaceous gland activity and individual skin sensitivity. Whereas we have known for years that Malassezia overgrowth causes dandruff, it is recently coming to light that the severity of dandruff depends on the inherent immunological response of the individual and the integrity of the stratum corneum.
There are multiple products available for the treatment of dandruff, most containing one or more of the following active ingredients: ketoconazole, zinc pyrithione, selenium sulfide, and climbazole. While these products provide relief for some, there are many shortcomings associated with these conventional treatments. For example, the antifungal agents may alleviate the initial symptoms of dandruff by removing Malassezia from the scalp, but the inherent lipid imbalance in the microbial niche (one of the sources of dandruff) is not addressed. The stronger the anti-dandruff agent, the harsher the impact on the integrity of the stratum corneum. When the scalp is depleted of its commensal flora, it can provoke an inflammatory response on the scalp, which can in turn worsen dandruff. Lastly, the sensorial properties of these agents (brittle hair, dry hair, etc.) are less than desirable, and often discourage patients from use. This study was designed to determine the effect of a select medium chain fatty acid derivative (MCFA derivative) which could eventually take care of some of the limitations of the existing dandruff treatments. VB-3222 anti-dandruff shampoo was developed at Vyome Therapeutics Limited by adding a synthetic derivative of MCFA (named as “MRT”) to a mixture of zinc pyrithione dissolved in a well-accepted topical formulation base to obtain a smooth, rich, homogeneous solid material shampoo. The investigational product is referred to as “MRT” or VB-3222 for reporting of the study results.
Results of the study showed that VB-3222 was very effective in exhibiting fungicidal activity within a few hours of treatment. At the end of 6 hours, anti-dandruff shampoo containing 1% zinc pyrithione with 3% of MRT has shown more than 3 log reductions in fungal presence, as compared to approximately a 2 log reduction for the comparator products. The difference in killing potential for VB-322 vs. other products was shown to be statistically significant. VB-3222 also proved efficacious in reducing pruritus and flaking. VB-3222 also demonstrated improvement in several scalp and hair-related sensorial parameters. Scalp dryness ws reduced consistently throughout the study and by day 16, 100% of patients reported no scalp dryness. At the end of the study, 70% of the population showed a reduction in itching and flaking dandruff compared to baseline. Side effects of the medication were mild, sporadic reporting of oiliness or dry scalp, and one report of stinging in the eye after accidental exposure to the shampoo.
Overall, VB-3222 has proved to be an effective investigative alternative in the treatment of moderate seborrheic dermatitis, or dandruff. VB-3222 was well tolerated in studies and was shown to be not only effective in reducing dandruff and fungal presence, but also to improve the sensorial qualities of the hair. These factors in combination make VB-3222 an exciting upcomer in the treatment of chronic seborrheic dermatitis.
Resources:
Sadhasivam S, Garkhal K, Singh H, et al. Newly Developed Anti-Dandruff Regimen, VB-3222, Delivers Enhanced Sensorial and Effective Therapeutic Benefits Against Moderate Adherent Dandruff. Clin Cosmet Investig Dermatol. 2020;13:187-195. Published 2020 Feb 21. doi:10.2147/CCID.S219109
Eczema is an umbrella term for a group of skin conditions characterized by inflamed, irritated, and itchy skin. According to the American Academy of Dermatology Association, eczema can refer to atopic dermatitis, contact dermatitis, dyshidrotic eczema, hand eczema, neurodermatitis, nummular eczema, or stasis dermatitis. Atopic dermatitis (AD) is one of the most common forms of eczema and it is defined as a chronic, pruritic inflammatory skin disease that can affect all ages. Symptoms may include erythema, edema, oozing, and pruritus, but it is important to note that symptoms can vary by age. AD is typically treated with topical agents but severe cases may also require systemic or phototherapy. Consistent use of moisturizers is a simple way to reduce disease severity and the need for pharmacologic intervention. Many drugstore moisturizers contain emollients, occlusives, and humectants that combat the xerostosis and transepidermal water loss caused by a dysfunctional epidermal barrier. A moisturizer works best on damp skin after showering/bathing because it can improve the skin’s hydration with additional application throughout the day when possible. Topical corticosteroids are another important part of managing AD since they act on a variety of immune cells to reduce inflammation and prevent relapses. Topical corticosteroid use is dependent on the patient’s age, affected area, severity, patient preference, and cost. Topical calcineurin inhibitors such as tacrolimus and pimecrolimus are also used to suppress inflammation and reduce relapses in mild to severe AD. Topical calcineurin inhibitors may be used together with topical corticosteroids to treat AD. There is not enough data to support the use of topical antimicrobials, topical antiseptics, or topical antihistamines to treat AD.
Urticaria is a skin condition characterized by wheals (hives) and/or angioedema. Wheals associated with urticaria appear as “a central swelling of variable size, almost invariably surrounded by reflex erythema, an itching or sometimes burning sensation, a fleeting nature, with the skin returning to its normal appearance, usually within 30 minutes to 24 hours” (2). Angioedema associated with urticaria appears as “a sudden, pronounced erythematous or skin coloured swelling of the lower dermis and subcutis or mucous membranes, sometimes pain, rather than itch, a resolution slower than that of wheals (can take up to 72 hours)” (2). Urticaria can be acute (lasting 6 weeks or less) or chronic (lasting over 6 weeks), and can be spontaneous (no specific inciting factor) or inducible (specific inciting factor identified). Urticaria involves the activation of mast cells that results in sensory nerve activation, vasodilation, plasma extravasation, and cell recruitment to urticarial lesions. Management of urticaria involves identifying, eliminating, and avoiding the underlying causes, and pharmacologic treatment to prevent mast cell activation and its effects. Causes of urticaria may include drugs, physical stimuli, infections, physical or emotional stress, and food. Pharmacotherapy involves H1-antihistamines (second generation is preferred), omalizumab (anti-IgE), and ciclosporin (off-label use for urticaria). Topical and oral corticosteroids are generally not recommended to treat urticaria, but a short course of oral systemic corticosteroids may be used in an acute exacerbation of urticaria.
Works Cited:
1. Eichenfield LF, Tom WL, Berger TG, et al. Guidelines of care for the management of atopic dermatitis: section 2. Management and treatment of atopic dermatitis with topical therapies. J Am Acad Dermatol. 2014;71(1):116-132. doi:10.1016/j.jaad.2014.03.023
2. Zuberbier T, Aberer W, Asero R, et al. The EAACI/GA²LEN/EDF/WAO guideline for the definition, classification, diagnosis and management of urticaria. Allergy. 2018;73(7):1393-1414. doi:10.1111/all.13397
Atopic eczema is a chronic, inflammatory skin disorder often affecting children. Although not life-threatening, its impact on patient quality of life is significant. Patients may experience eczema throughout their lives. Environmental factors and genetics may both play a role in the persistence of atopic eczema. The most basic treatment is avoiding aggravating factors along with cutaneous hydration to improve barrier function and relieve itchiness. When itchiness is relieved, there is a reduced need for topical steroid use, which may be resorted to in the presence of a flare up.
As learned previously in the anatomy of skin presentation, the skin’s natural response to aggravating stimuli, whether it be temperature, lack of moisturization, scents from laundry detergent, or physical irritants from harsh skin care products or scratching, is lichenification. This is the state in which your skin becomes thick and leathery over a prolonged period of irritation. Lichenification is not contagious nor harmful as much as it is inconvenient and not aesthetically pleasing to the eye. Patients may feel self-conscious about the patches of thickened skin but treatment is accessible and generally affordable as they are available over the counter. Moisturizers and topical steroids may be used to treat lichenification in addition to oral antihistamines to reduce the itching which caused it. However, the underlying cause for the itching must be addressed to effectively eradicate the condition.
Since atopic eczema is often a longstanding condition, patients may prefer over the counter, nonpharmacological treatment options as prolonged use of topical steroids is not ideal. Colloidal oatmeal is made from finely-ground oats and is available in cream or powder for reconstitution to relieve the burning sensation and soften inflamed skin. Bathe in the oatmeal bath for 15 minutes daily and moisturize with a high oil content product such as Eucerin afterwards to keep the skin from drying out. Some patients find that application of such a thick, oily moisturizer is unappealing, but they can cover the area with bandaging or clothing such as socks and long sleeve shirts before bedtime.
Each patient’s skin will react differently to over the counter products but most labeled for treatment of eczema are hypoallergenic. Treatment is considered effective when there are fewer flare ups as there is no definitive treatment. As a pharmacist, we should be able to advise patients on lifestyle modifications and journaling to document the frequency of flareups and varying methods used to reduce the symptoms. A change as simple as wearing loose-fitting clothing and using scentless soaps may be helpful. Temperature and humidity both play a role as well. It is recommended for patients to invest in a humidifier to assist with moisturization especially during drastic temperature hikes and drops during season changes. Patients who are unaware of their triggers should visit an allergist to identify common household items and environmental factors. It’s important for patients to understand what might work for someone else, might not work for them. Everyone’s skin reacts differently and although it may be inconvenient, atopic eczema is not contagious or harmful if properly managed.
1. A Comprehensive Review of the Treatment of Atopic Eczema, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4773205/
Psoriasis is a chronic, inflammatory skin condition that presents in many different ways. There are various types of psoriasis like chronic plaque psoriasis (being the most common subtype of psoriasis), guttate psoriasis, pustular psoriasis, and erythrodermic psoriasis. Psoriasis can also develop because of, or with other comorbidities like arthritis, obesity, metabolic syndrome, hypertension, diabetes, and atherosclerotic disease. Genetic predisposition is a major key risk factor for developing psoriasis, and some other environmental and behavioral factors been studied like elevated rates of smoking, obesity, and alcohol use. Medications and infections have also been identified as potential triggering or exacerbating factors for psoriasis. In terms of pathophysiology, it is a complex immune-mediated disease in which T lymphocytes, dendritic cells, and cytokines play a central role. The skin is then in a hyperproliferative state which presents as increased numbers of epidermal stem cells, increased numbers of cells undergoing DNA synthesis, a shortened cell cycle time for keratinocytes and a decreased turnover time of the epidermis. Chronic plaque psoriasis looks like symmetrically distributed, cutaneous plaques with common location sites being the scalp, extensor elbows, knees, and gluteal cleft. The plaques that form on the skin are erythematous with sharp margins ranging from 1 to 10 cm in diameter, that sometimes form a silver, thick scale on top. Bathing and topical emollients may remove the scale part of the lesion. These plaques look painful but are usually asymptomatic, possibly accompanied by pruritus.
A general treatment approach can involve both topical and systemic therapies with the goal of improving physical and psychosocial symptoms. The agent of choice is based on disease severity, relevant comorbidities, patient preference (including cost and convenience), efficacy, and evaluation of individual patient response. Patients who have more mild disease will usually start with a topical agent while those with more severe cases may require systemic therapy or phototherapy. Topical corticosteroids and emollients are common first line therapies, other options being vitamin D analogs (eg, calcipotriene and calcitriol), tar, and topical retinoids (tazarotene). Combination products are often prescribed, for example-betamethasone and halobetasol-tazarotene. More severe disease requires different therapy including either phototherapy or systemic therapies such as retinoids, methotrexate, cyclosporine, apremilast, or biologic immune modifying agents.
While phototherapy is effective, it can be costly and time consuming to go to a medical office each time. There are risks that come along with using UV light like damage to the skin and malignancy. Home – kits are an expensive option and can save time in the case of more severe disease considering biologic agents can be just as costly. Although expensive, in the long run these will end up saving money for the patient. UV radiation is proposed to act via antiproliferative effects (slowing keratinization) and anti-inflammatory effects (inducing apoptosis of pathogenic T cells in psoriatic plaques). A therapeutic dose of UV light can be given as narrowband ultraviolet B (UVB) phototherapy, broadband UVB phototherapy, or oral or bath psoralen plus ultraviolet A (PUVA) photochemotherapy.
1. Steven R Feldman, MD, PhD. Treatment of psoriasis in adults. UpToDate. Feb 2021.
2. Steven R Feldman, MD, PhD. Psoriasis: Epidemiology, clinical manifestations, and diagnosis. UpToDate. Dec 2019.
Urticaria is a skin condition known more commonly as hives. Hives are a type of skin rash that commonly occurs after allergic reaction or with the use of medications, foods, stress, etc. Chronic spontaneous urticaria is often defined as having hives for greater than 6 weeks. This condition is often associated with angioedema, which will affect a patient’s lips, cheeks, periorbital areas of the face, extremities, and genitals. There are different terms for this form of hives and angioedema, but chronic spontaneous urticaria is the preferred term per guidelines. This is a condition that typically only affects someone 2-5 years, but significantly impacts quality of life. The pathology of why this happens is not well understood, but the clinical manifestations are usually involving the skin and rarely become systemic.
It presents as hives, which are lesions that have an area of central swelling of various size, usually with surrounding erythema, and an itching sensation. These lesions can happen anywhere on the body or cover the entire body, with itching that can disrupt life greatly. Accompanying angioedema looks like episodic submucosal or subcutaneous swelling that is usually asymmetric in distribution and affects nondependent parts of the body. Any possible systemic side effects presenting in a patient with urticaria can be headache, fatigue, pain or swelling of joints, wheezing, flushing, gastrointestinal symptoms, or palpitations. This condition is often associated with various atopic and autoimmune disorders but no pathology theories have been conclusive.
In terms of treating this condition, it is looked at as a stepwise approach. Step one is usually a second generation antihistamine at a standard therapeutic dose, for example Cetirizine or Loratadine. If after two weeks, the patient’s hives are not improving, the dosage should be increased and an H2 antihistamine like Cimetidine can be added. Other options include a Leukotriene-receptor antagonist like Montelukast, or a first generation H1 antihistamine like Hydroxyzine. Further steps would include increasing dosing, and if nothing is working after weeks, a patient is considered to have refractory chronic spontaneous urticaria and may have to go on systemic glucocorticoids.
Goals of therapy are intended to reduce or eliminate symptoms for as long as the condition lasts. As pharmacists we always have a responsibility to help patients manage their disease, including counseling on nonpharmacologic methods. We should help ensure patients that chronic spontaneous urticaria is rarely permanent, rarely a sign of something else, and not an allergic reaction, and it’s managed well with medications. We can give patients information on exacerbating factors and what to avoid.
1. David A Khan, MD. Chronic spontaneous urticaria: Standard management and patient education. Uptodate. Aug 2020.
2. Sarbjit Saini, MD. Chronic spontaneous urticaria: Clinical manifestations, diagnosis, pathogenesis, and natural history. Uptodate. Jan 2021.
Atopic dermatitis, known as eczema, is a chronic skin condition in children and adults that most commonly appears as dry, patchy, inflamed, and itchy skin. Treatment of eczema focuses on reducing the pruritus and dermatitis, and preventing an exacerbation. As pharmacists, one of our focuses should always be minimizing therapeutic risks or adverse events in our patients. We should also always be educators, as we are often the first provider a patient will go to with a mild rash or dry skin. We can educate patients on what to avoid to either prevent atopic dermatitis or prevent worsening of their current atopic dermatitis, for example, heat and humidity, showering without moisturizing after, irritants like detergents and solvents, and emotional stress. For extreme itchiness, we can offer a patient an over the counter antihistamine.
When deciding on treatment, this condition is often separated into mild, moderate, severe or refractory. Drug choice can also be based on the most prominent symptom, like itchiness. Standard pharmacologic treatment for pruritus associated with eczema is based around topical anti-inflammatory therapy with topical corticosteroids or topical calcineurin inhibitors. Medications like Tacrolimus or Pimecrolimus have shown good efficacy in reducing the itching of the skin. Generally, the choice of the corticosteroid potency should be based upon the patient's age, body area involved, and degree of skin inflammation. Mainstay treatment for mild disease is a topical corticosteroid, like desonide or hydrocortisone, and emollients. For more moderate disease, some higher potency corticosteroids like fluocinolone, betamethasone or triamcinolone would be ideal choices for topical therapy. The issue with corticosteroid therapy is that long term use can lead to adrenal suppression, or side effects like skin atrophy/thinning and folliculitis. To avoid side effects or switch to due adverse effects from corticosteroids, topical calcineurin inhibitors are the next agent of choice.
For patients with more severe forms of eczema, systemic immunosuppressive therapy may be warranted as well as a treatment called phototherapy. Phototherapy is only for adults and it’s reserved for those who have failed any and all possible topical medication treatments. It is also extremely costly and requires multiple doctor’s office visits per week, and could increase risk of skin cancer with prolonged therapy. This is a last line option for people suffering with severe eczema.
As pharmacists, we are also responsible for nonpharmacologic advice and counseling for our patients or the parents of our patients. For a condition like eczema, it’s notable that it is much more common in children. And as important as medications are, taking measures to prevent the need for medications is just as important. For patients dealing with atopic dermatitis, there are a few ways they can prevent future flares. Daily application of moisturizer and emollient is key to protecting the skin barrier and preventing dry or flaky skin. There is some evidence that probiotics and supplements in children call help prevent this skin condition when they’re at a greater risk. Nutritional interventions have also been studied to prevent allergic or immune diseases in infants.
1. William L Weston, MD, William Howe, MD. Treatment of atopic dermatitis (eczema). Uptodate. Jan 2021.
Atopic eczema is a form of dermatitis that is developed in early childhood but can also affect patients of all ages at random; atopic dermatitis is characterized by redness and itchiness of the skin, occasionally accompanied by other comorbidities such as asthma or hay-fever. While the condition itself seems benign upon first impression, atopic dermatitis may have profound effects on a patient’s quality of life due to the visibility of the condition itself. In addition, the deep itchiness that comes as a result of atopic dermatitis may ultimately lead to sleep disturbances and integumentary trauma due to consistent itching. Atopic dermatitis is also considered the preliminary condition that can lead to the development of the “atopic march,” or development of further allergic skin disorders as time progresses. Some studies have shown that environmental factors may impact the development of atopid eczema, including family size, income status, and education level. Those who suffer from atopic dermatitis have most commonly been shown to be deficient in ceramides as well as peptides such as cathelicidins.
The primary treatment goal for patients who suffer from atopic dermatitis is to ensure that the hydration of the skin barrier is restored. Doing so will help reduce itching, limit inflammation and redness, and ultimately allow for the repair of the skin itself. Emollient moisturizers, topical corticosteroids, and immunosuppressant therapies may be utilized to assist in managing atopic dermatitis symptoms.
Another skin condition that has contributed to the deterioration of patient quality of life is urticaria. Also known as hives, this condition is characterized by an outbreak of swollen, pale red bumps or plaques known as wheals on the skin that appear suddenly. Hives are often the result of exposure to a trigger that causes an allergic reaction. Many factors such as infections, medicines, food, psychogenic factors, and respiratory allergens are accused of etiology, but sometimes, it is idiopathic. The symptoms of hives tend to resolve on their own, often disappearing within three hours of their first appearance with no trace. However, there are cases of urticaria that are chronic and recur at least twice over the course of 6 weeks. Some chronic cases of hives may even be triggered by external factors such as temperature.
In order to treat flare-ups of hives, the first step that must be taken is the elimination of triggers. As triggers are the number one cause behind hives, removing them from the patient is what needs to be done in order to prevent worsening of symptoms. In addition, drug therapy may include the use of an antihistamine such as diphenhydramine to block the inflammatory cascade that leads to the clinical manifestation of hives. Other measures that patients may take may include loose clothing and cooler showers as hot water may prove to be a trigger.
Overall, eczema and urticaria are two skin conditions that involve inflammation, redness, and itchiness of the skin. However, both disorders show slightly different clinical manifestations and their etiology are unique from one another. These differences are important to keep in mind, especially when trying to make clinical decisions to ensure proper treatment.
Resources:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6526977/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6157251/
Hyperpigmentation is a common skin condition that presents itself as darker patches on the skin. In many cases it can affect how people feel about themselves. Many people feel self-conscious about their hyperpigmentation which is a result of excessive melon in production. In certain areas of the skin. The causes for hyperpigmentation are many and can include acne scarring and sun damage. In parts of the body that aren’t exposed to sun or don’t have acne, such as the bikini line or the armpits, the hyperpigmentation can be due to hair removal, such as waxing and shaving, as well as hormone fluctuations. In a professional setting, procedures such as microdermabrasion can be done by licensed estheticians to slowly remove the outer layer of dead skin. For at home treatments there are a few possible strategies.
Lightning creams are available over the counter to help decrease pigmentation and are generally considered as safe. There are also stronger prescription forms that can be prescribed by a dermatologist.
Acids such as salicylic acid, vitamin C, and alpha hydroxy acids can exfoliate the top layer of your skin and even out your skin tone. Acids should be used only on people with fair skin tones as they can cause scarring on people who have darker skin.
Retinoids are also an option for the treatment of hyperpigmentation. Unlike acids, they work deep in the skin and treat the layers below our epidermis. This is usually not a first line treatment recommendation for hyperpigmentation, but it is safe for all skin tones.
A more aggressive form of hyperpigmentation treatment includes chemical peels, which reduce hyperpigmentation by removing the upper dermis. There are stronger chemical peels that can penetrate lower layers of the skin as well, but are also slightly more risky for having side effects such as skin irritation, redness, and blistering.
There are also laser peel treatments, which are also referred to as skin resurfacing. This strategy can be done by estheticians using targeted beams of light on the skin. There are two types of lasers that can be used. Ablative lasers remove layers of your skin and are a bit harsher than non-ablative lasers. Non-ablative lasers target only the dermis to promote collagen growth and tightening of the skin.
Intense pulse light therapy is another kind of laser treatment, which is also known as a photo facial. This kind of treatment usually requires multiple sessions and stimulants collagen growth.
When it comes to the skin the most important thing to note is that everyone’s treatment should be individualized. Patients will have different skin conditions and skin tones and should have customized plans made for them after a thorough examination of their skin to prevent any unwanted side effects or scarring. For example, it is very important to know that with darker skin laser therapy might not be the best choice as it can do more harm than good, and certain acids or lower strength chemical peels maybe more appropriate for people with darker skin tones to have the best results.
· Alpha hydroxy acids. (2017). https://www.fda.gov/Cosmetics/ProductsIngredients/Ingredients/ucm107940.htm
· Hyperpigmentation. (n.d.). http://www.aocd.org/?page=Hyperpigmentation
· Mayo Clinic Staff. (2017). Laser resurfacing. https://www.mayoclinic.org/tests-procedures/laser-resurfacing/about/pac-20385114
· Photofacial IPL. (n.d.). https://www.emoryhealthcare.org/centers-programs/aesthetic-center/non-surgical-services/photofacial-ipl.html
· Understanding the ingredients in skin care products. (2015). https://my.clevelandclinic.org/health/articles/10980-understanding-the-ingredients-in-skin-care-products
Rosacea is a chronic skin disease with an unknown cause and currently no cure. Treatment for rosacea has focused around minimizing the symptoms. They are four types of rosacea that present themselves differently and people can have more than one type at a time. Rosacea mainly presents itself on the face and looks like little pus filled red bumps. Rosacea flareups happen mostly in cycles, meaning that symptoms go away for some time before returning again.
Erythematotelangiectatic rosacea presents itself by symptoms of flushing and redness, visible blood vessels, as well as swollen and sensitive skin.
Papulopustular rosacea is often seen in middle-aged women and presents itself like acne breakouts. Skin can be sensitive and oily and it is also possible to see broken blood vessels.
Rhinophyma rosacea Is often seen in men and presents itself as thickening of the nose skin. The texture of the skin becomes bumpy with large pores and thick skin. In more widespread and rare cases, it can present on the chin, forehead, cheeks, and ears.
Ocular rosacea presents itself mainly in the eye area. It can affect the eye itself making it bloodshot and watery. It can also make eyes dry, itchy, and sensitive to light. Broken blood vessels may be observed on the eyelids and eyes can feel gritty. In this kind of rosacea, the most important treatment goal is taking care of the eye to prevent damage or infection.
There are certain things that should be noted in order to avoid having rosacea flareups or making current flareups worse. Diet is very important to avoid aggravating symptoms. Spicy foods, hot drinks, and foods that contain cinnamaldehyde (cinnamon, chocolate, tomatoes, and citrus) should be avoided. There are certain risk factors for rosacea including family history, being middle aged, and having fair skin with blonde hair and blue eyes. Being a woman is also a risk factor for rosacea, but men who have rosacea often experience more severe symptoms than women do. People who have Celtic or Scandinavian ancestors are more likely to develop the condition. In regard to skin care, it is better to choose water-based products and avoid products that contain alcohol, menthol, and witch hazel, which may dry out your skin. It is important to avoid sunlight and drinking alcohol to avoid aggravating or causing flareups. Laser and light treatments can help with some cases of rosacea and micro dermabrasion can be especially helpful for those who have experienced thickening skin. Individualized treatment is important and a thorough examination of the skin should be done before proceeding with any treatments.
· All about rosacea. (n.d.). rosacea.org/patients/allaboutrosacea.php
· Mayo Clinic Staff. (2018). Rosacea. mayoclinic.org/diseases-conditions/rosacea/symptoms-causes/syc-20353815
· Rosacea. (n.d.). aad.org/public/diseases/acne-and-rosacea/rosacea
· Rosacea: Overview. (2014). ncbi.nlm.nih.gov/pubmedhealth/PMH0072660
· Weiss E, et al. (2017). Diet and rosacea: The role of dietary change in the management of rosacea. DOI: 10.5826/dpc.0704a08
Atopic dermatitis, more commonly referred to as Eczema, is a condition of the skin characterized my itchy, inflamed, and very sensitive patches of skin. It is most commonly seen on the backs of knees, inner elbows, and arms. Eczema can come and go, and prevention of flare ups is key for treatment.
There are some key prevention strategies that can be done to avoid eczema flare ups. It is important to be mindful of avoiding hidden triggers. Eczema prone skin is very hypersensitive and many everyday items, such as perfumes and laundry detergent, can be irritants. Dust, cigarette smoke, chlorine from pool water, and even sand on the beach can be triggers. Make sure to wipe these irritants off the skin as soon as possible. It can also be helpful to avoid bathing and stick to warm showers. Taking long, hot baths and showers can remove the natural oils from the skin making it extremely dry and more at risk. Mild soap should be used on the skin and skin should be patted dry and coated with moisturizer after finishing. It is extremely important to stay hydrated and keep the skin moisturized. Applying thick layers of moisturizer will prevent the skin from drying out and therefore prevent any eczema flare ups. Steroid creams are a commonly prescribed a remedy for eczema flare up, but there are side effects. Long-term use of steroid creams can lead to stretch marks and thinned out skin. Staying properly hydrated and moisturized will prevent excessive need of steroid creams and protect your skin in the long term. A good choice for all eczema patients is to get tested for allergies to see if any common airborne particles, such as pet dander, pollen, or dust mites, may be triggering eczema flare ups. Food allergies, most commonly milk and wheat, could also trigger eczema flare ups.
Severe eczema that it doesn’t respond to creams or even systemic steroids may respond to ultraviolet light. They should be referred to see a dermatologist in order to make sure that UV light treatment is appropriate for their skin before proceeding with any treatments.
People with eczema also can benefit from lowering their stress levels through therapy, exercise, meditation, or any way that works best for them. Stress and anxiety have been found to trigger eczema outbreaks. Wearing clothes with soft and breathable fabrics is also important to avoid irritating the skin. In the winter months when the air is dryer and most homes have the heat on, it may be a good recommendation to get a humidifier so that the air inside the home doesn’t dry out the skin excessively.
The most important thing to note in regards to eczema is that consistency with prevention strategies is key. Everyone is triggered by different irritants and must customize their prevention strategies to work best for them. Staying consistent with hydration, moisturizing, and avoiding irritants can aid patients so that they rarely see flareups.
· Complementary and alternative treatments. (n.d.) nationaleczema.org/eczema/treatment/complementary-and-alternative/
· Contact. (n.d.). eczema.org/contact
· Oakley A, et al. (2016). Allergic contact dermatitis. (n.d.). dermnetnz.org/topics/allergic-contact-dermatitis/
Keratosis Pilaris is a skin condition that is also referred to as chicken skin. The reason it is referred to as chicken skin is because patches of small bumps on the skin are observed. These small bumps on the skin are actually dead skin cells that are plugging a hair follicle. It is more common to see keratosis pilaris on the upper arms and thighs, but it can also be observed on other parts of the body such as the face or buttocks. Unlike other skin conditions, such as eczema and psoriasis, chicken skin doesn’t cause any extreme discomfort or itching. It is important to take extra care during the winter as the cold weather can worsen keratosis pilaris by drying out the skin. Usually keratosis pilaris is observed between teenage years and 30 years old but can sometimes be seen in adults over 30.
The reason for the name keratosis pilaris is because of that buildup of keratin in the pores. This results in clogging a growing hair follicle and, therefore, a small bump forming where a hair should be protruding from the skin. Risk factors for keratosis pilaris include dry skin, eczema, hay fever, obesity, women, teenagers, and Celtic ancestry. Pregnancy can cause flareups of chicken skin because of the fluctuation in your hormones. Usually chicken skin goes away with time but there are a few dermatological and at home treatments that can help relieve symptoms.
A dermatologist may recommend or prescribe moisturizing treatments that include urea and lactic acid, as they soften dry skin as well as remove dead skin cells. Some more abrasive treatments include microdermabrasion and chemical peels which intensely exfoliate your skin. With treatment such as these it is very important to keep in mind that people with certain skin tones will not be able to use these treatments because it can result in scarring and damaging of their skin. For people who are trying to avoid pharmacologic treatment or abrasive dermatologic treatment, some recommendations can be made. Taking warm baths can help on open up pores and soften the skin and using a stiff brush can potentially remove the bumps. No one should take extremely long warm baths as that can dry out the skin by removing the body’s natural oils and be counterproductive. At home exfoliation can be done as well with a loofah or pumice stone and this would help by gently removing the dry dead skin. Hydrating lotions such as lotions that include lactic acid are also very helpful by not only hydrating the dead skin, but also encouraging cell turnover. Avoiding tight clothes on the affected areas can be helpful to prevent further irritation of the bumps, which could lead to them becoming larger and more inflamed. Using a humidifier in the bedroom or a small humidifier at the work office if you have a desk job can help to add moisture to the air around you preventing your skin from drying out. It is important to note that there is currently no cure for this and therefore it is very important to be consistent with prevention strategies.
· Ciliberto H, et al. (2013). Photopneumatic therapy for the treatment of keratosis pilaris. jddonline.com/articles/dermatology/S1545961613P0804X
· Ibrahim O, et al. (2015). Treatment of keratosis pilaris with 810-nm diode laser: A randomized clinical trial. DOI: 10.1001/jamadermatol.2014.2211
· Keratosis pilaris. (n.d.). aocd.org/page/KeratosisPilaris
· Keratosis pilaris: Overview. (n.d.). aad.org/public/diseases/a-z/keratosis-pilaris-treatment
· Mayo Clinic Staff. (2019). Keratosis pilaris. mayoclinic.org/diseases-conditions/keratosis-pilaris/symptoms-causes/syc-20351149
Eczema also known as atopic dermatitis is a condition that causes that skin to become red and itchy. It can occur at any age, but presents more commonly in children. There is no cure for eczema as of now, but there have been several methods used to help flare ups, especially in the pediatric population.
Symptoms can vary from person to present, but the most common presentations are dry, itchy skin; red patches all over body. Severe eczema can also lead to raised bumps, crusted/scaly skin. Scratching and breaking the skin can lead to infections and further complications. There are many “treatments” for eczema, but ultimately the goal is to reduce flare ups.
Coconut oil has a high saturated fat content and can have many benefits in skin care, hair care, and many other medical remedies. Coconut oil contains lauric acid, myristic acid, caprylic acid, palmitic acid, capric acid, oleic acid, linoleic acid, stearic acid; most of which individually is used to treat various skin conditions and used in many popular skin care products. It is said to have antimicrobial and anti-inflammatory properties. Acids, such as lauric acid can help fight harmful microorganisms. This is why it can provide relief in patients experiencing flare ups from atopic dermatitis.
There was a study done in 2013 (posted below), in which virgin coconut oil (VOD) was studied in a randomized, double blind trial in pediatric patients diagnosed with atopic dermatitis. Patients experiencing atopic dermatitis experience more transepidermal water loss and therefore experience severely dry skin, which can end up causing scaly, crusty skin. The index value calculated was based on the Scoring of Atopic dermatitis also known as SCORAD. Overall in the study it was shown that the patients using coconut oil had reduced flare ups and their skins retained more hydration.
https://onlinelibrary.wiley.com/doi/full/10.1111/ijd.12339
Seborrheic dermatitis, or dandruff, is part of a spectrum that affects the seborrheic areas of the body. Seborrheic dermatitis can affect other seborrheic areas as well, however, dandruff is restricted only to the scalp and the symptoms include itchy, flaking skin. Seborrheic dermatitis often presents as plaques with greasy-looking scales in regions rich in sebaceous glands, such as the scalp. In addition, it also usually involves itchy, flaking, scaling skin, inflammation and pruritus. Various intrinsic and environmental factors, such as sebaceous secretions, fungal colonization, and individual susceptibility all contribute to the seborrheic dermatitis. The aim of the study in the second article was to evaluate the safety and efficacy of an herbal and zinc pyrithione shampoo and a scalp lotion for the treatment of scalp seborrheic dermatitis and dandruff. Forty-nine subjects completed the study. At all time points, erythema and loose flaking showed significant clinical improvement in all participants compared with baseline. Symptoms measured include improvement on erythema, loose flaking, and dermatitis. All symptoms showed significant improvement after two weeks of treatment, and then showed further improvement until the end of the study period. This six-week, open-label safety and efficacy study demonstrated that using an herbal and zinc pyrithione-based shampoo and scalp lotion improved the symptoms and severity of scalp seborrheic dermatitis and dandruff symptoms. All factors demonstrated clinically meaningful reductions during the study, especially from baseline to the first visit. Subjects were extremely satisfied with the speed of improvement, the ease of use of the products, and the cosmetic characteristics of the shampoo and lotion.
References
Barak-shinar D, Green LJ. Scalp Seborrheic Dermatitis and Dandruff Therapy Using a Herbal and Zinc Pyrithione-based Therapy of Shampoo and Scalp Lotion. J Clin Aesthet Dermatol. 2018;11(1):26-31.
Borda LJ, Wikramanayake TC. Seborrheic Dermatitis and Dandruff: A Comprehensive Review. J Clin Investig Dermatol. 2015;3(2)
Seborrheic dermatitis is a common skin condition in which dandruff affects mainly the scalp whereas seborrheic dermatitis can occur on other oily parts of the body including face, eyebrow, and chest. There may be inflammation, redness, and pruritus scales. Dandruff affects about 50% of the adult world population and can negatively affect a person’s self esteem. It presents as white to yellow flakes on the scalp and hair. Seborrheic dermatitis is less common affecting 40% of infants up to 3 months and 1-3% of adults. Risks of development of seborrheic dermatitis are age, male sex, immunodeficiency such as HIV-AIDS, and neurologic diseases such as Parkinson and Alzheimer. The exact cause of these dermatological conditions are not well known but there are several theories including fungal colonization of Malassezia with disruption of the lipid balance on the skin surface, increased sebum secretion, genetic factors, nutrition, emotional stress and host epidermal conditions. Treatments of seborrheic dermatitis include symptom management with topical antifungal and anti-inflammatory medications. Typical products used include topical 1%-2% ketoconazole, 1% hydrocortisone,1% zinc pyrithione and 1% ciclopirox.Topical antifungals should be first line treatment and they have an anti-inflammatory effect. Potent corticosteroids should only be used for significant symptoms on a short term basis because of their side effects. Shampoo ingredients usually contain a combination of coal tar, sulfur, salicylic acid or sulfacetamide. It is important for the dermatologist or pharmacist to help educate and counsel patients on the appropriate use of the different products to manage their condition. Patients should have good skin care practices including an appropriate moisturizer.
References
Borda LJ, Wikramanayake TC. Seborrheic Dermatitis and Dandruff: A Comprehensive Review. J Clin Investig Dermatol. 2015;3(2):10.13188/2373-1044.1000019. doi:10.13188/2373-1044.1000019
Tucker D, Masood S. Seborrheic Dermatitis. [Updated 2020 Jun 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK551707/
Urticaria, or hives, is a common disease characterized by erythematous, edematous, and itchy plaques covering the skin. There are a variety of factors as to why someone may develop urticaria. First on the list are medications. Any drug may cause urticaria, however, the most common ones are penicillin, aspirin, NSAIDS, oral contraceptives, ACE inhibitors, and some opioids. Urticaria will begin to develop around 1–2 hours after administration of an oral drug. Any urticaria causing drug that is given systemically will cause hives to develop immediately. Foods that often cause hives are nuts, eggs, seafood, chocolate, meat, and alcohol. Preservatives such as dyes, benzoic acid derivatives, and salicylates can also cause hives to develop as well. In addition, respiratory allergens such as pollen, mold, mites, and animal hair, may cause urticaria when breathed in. Certain materials that make contact with the skin such as latex and cosmetics may cause urticaria by contact. Lastly, psychological factors such as stress, sadness, and depression may aggravate preexisting urticaria but can also induce urticaria. The initial treatment for urticaria is a standard dose of a second generation antihistamine. Second generation antihistamines penetrate the blood brain barrier less compared to first generation antihistamines, and as a result causes fewer central nervous system side effects. An alternative second-line treatment to second generation antihistamines in patients who still have severe urticaria despite high-dose antihistamine treatment, is a leukotriene receptor antagonist (LTRA) such as montelukast. In patients with severe acute urticaria, a brief treatment of oral corticosteroids can be given once antihistamines and LTRAs have been tried. Dose and duration is determined by the patient's weight and clinical response. Prolonged courses of oral steroids for chronic urticaria should be avoided because of the massive side effect profile regarding the long term administration of oral steroids.
References
Deacock SJ. An approach to the patient with urticaria. Clin Exp Immunol. 2008;153(2):151-61.
Kayiran MA, Akdeniz N. Diagnosis and treatment of urticaria in primary care. North Clin Istanb. 2019;6(1):93-99.