Eczema, Urticaria, and other Skin Conditions

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.

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:

1. Avena-Woods C. Overview of atopic dermatitis. Am J Manag Care. 2017;23(8 Suppl):S115-S123.

2. Berke R, Singh A, Guralnick M. Atopic dermatitis: an overview. Am Fam Physician. 2012;86(1):35-42.

3. Staff, Familydoctor.org Editorial. “Eczema vs Atopic Dermatitis - Types and Causes.” Familydoctor.org, 26 May 2020, https://familydoctor.org/condition/eczema-and-atopic-dermatitis/.

4. 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:

1. Badri T, Kumar P, Oakley AM. Plaque Psoriasis. [Updated 2021 Aug 11]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-.

2. 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:

1. Thomas DR. Psychosocial effects of acne. J Cutan Med Surg. 2004;8 Suppl 4:3-5. doi: 10.1007/s10227-004-0752-x.

2. 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.