Eczema, Urticaria, and other Skin Conditions

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.

1. https://accesspharmacy-mhmedical-com.jerome.stjohns.edu/content.aspx?sectionid=268014720&bookid=3097&Resultclick=2

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: 

1. 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

2. 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&sectionid=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.