Bernard A Cohen, MD, is the section editor for Dermcase and professor of pediatrics and dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.

Bernard A Cohen, MD

You are called to the emergency department to evaluate a healthy 9-day-old girl with erosions near her eyes, nose, and skin creases on the arm. She also has a positive Nikolsky sign (Figures A, B). The newborn is crying and uncomfortable, but is still feeding well. Upon examination, she is red from head to toe and has widespread erosions and crusting. The patient is afebrile with clear mucous membranes. 

Diagnosis: Staphylococcal scaled skin syndrome (SSSS)

Differential diagnosisfor diffuse erythema

Given these clinical skin findings, initial differential diagnoses include Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) and bullous impetigo. A history of drug intake or viral infection typically precedes SJS/TEN.

 Additionally, SJS/TEN involves the mucous membranes of the conjunctiva, mouth, trachea, esophagus, anus, and genitalia.

 Bullous impetigo is characterized by small superficial blistering lesions with expanding crusts that are localized to the areas of skin infection.

Pemphigus foliaceus (PF) is rare in children but presents with similar superficial blisters as seen in staphylococcal scalded skin syndrome (SSSS). The adhesion molecule desmoglein-1 in the superficial epidermis is the target of both the autoantibodies in PF and SSSS toxins.

 PF can be confirmed with an immunochemical study to detect the presence of skin autoantibodies.

A hot water burn is another differential to be considered given the reddening, blistering, and sloughing of the skin.

SSSS is a reportedly rare, but likely more common than described, exfoliative disease of the skin mediated by epidermolytic toxins A and B produced by 

 The disease predominantly occurs in neonates of 3 to 15 days of age, children aged younger than 5 years, and adults with various comorbidities.

 Children are at greater risk due to their immature renal system and lack of immunity.

 In young children, the lack of prior exposure to SSSS-produced toxins triggers the development of anti- bodies to the causative agents, which protects against recurrence of SSSS in healthy patients. However, on first exposure, the toxins bind to and disrupt the adhesion molecule desmoglein-1 that is present in keratinized skin, but not in the mucous membranes. Be- tween 2010 and 2014, SSSS incidence increased 81% among infants younger than 1 year.

Key clinical features of SSSS include a brief prodromal phase where there may be fever and/or irritability, followed by diffuse erythema with superficial blistering and crusting that tends to be most prominent in areas of skin rubbing, such as the mucocutaneous junction and skin creases. Skin appears reddish and scalded after blisters rupture, and the Nikolsky sign (the easy separation of skin layers upon horizontal pressure to the skin) is present.

 Diagnosis of SSSS can be reached clinically and confirmed with bacterial culture. If in doubt, SSSS can be confirmed via skin biopsy, which shows superficial subgranular intraepidermal cleavage without necrosis.

Treatment of SSSS consists of antistaphylococcal antibiotics, temperature regulation, maintaining fluid and electrolyte balance, and skin care. SSSS-associated strains of 

 are usually methicillin-sensitive, so penicillinase-resistant beta-lactams, or cephalosporins, are favored for empiric management of SSSS.

 Vancomycin can be considered if a patient fails to improve following several days of treatment and methicillin-resistant strains of 

Clindamycin, a ribosomal inhibitor, is often recommended as a first-line agent to decrease SSSS toxin production, but up to 50% or more of triggering organisms may be resistant to clindamycin, and toxin binding may already be maximized at the time of diagnosis.

Thick moisturizers are important to protect the skin and decrease pain.

 In particular, moisturizers for the lips, which usually become crusty and painful, are essential to help with continued feeding in infants as their oral cavity remains unaffected by SSSS.

There is not an identifiable primary infection in many children with SSSS, but colonization can be demonstrated by obtaining bacterial cultures from sites of colonization, such as the medial canthi, nasopharynx, moist umbilical cord, and diaper area.

The patient was diagnosed with SSSS and treated with parenteral ceftriaxone and clindamycin. Bacterial cultures from her nares grew MRSA and the clindamycin was discontinued. The rash improved dramatically over the subsequent 36 hours followed by diffuse desquamation. The patient was discharged from the ICU 2 days later, on oral cephalexin.

1. Meshram GG, Kaur N, Hura KS. Staphylococcal scalded skin syndrome: A pediatric dermatology case report. 

. 2018;6:2050313X17750890. doi:10.1177/2050313X17750890

2. Lepe K, Yarrarapu SNS, Zito PM. Pemphigus foliaceus

 StatPearls; 2021. Accessed August 5, 2021. 

https://www.ncbi.nlm.nih.gov/books/NBK499829/

3. Ross A, Shoff HW. Staphylococcal scalded skin syndrome

 StatPearls; 2020. Accessed August 5, 2021. 

https://www.ncbi.nlm.nih.gov/books/NBK448135/

4. Wang Z, Feig JL, Mannschreck DB, Cohen BA. Antibiotic sensitivity and clinical outcomes in staphylococcal scalded skin syndrome. 

. 2020;37(1):222-223. doi:10.1111/pde.14014

Articles

A healthy 9-day-old girl presents with erosions near her eyes, nose, and skin creases on the arm as well as a positive Nikolsky sign. What's the diagnosis?

Diffuse erythematous rash in a healthy, afebrile infant

Approximately 85% of teenagers are affected by acne vulgaris at some point; up to 20% may develop facial scarring, which can be severe and permanent. Acne can also lead to psychological distress, lower self-esteem, anxiety, and even depression.

For these reasons, acne vulgaris should be treated promptly; in this article, we will discuss the condition in patients aged 13 to 19 years.

This inflammatory skin condition, which appears most commonly on the face (but can also affect the chest, shoulders, and upper back), often occurs because of a blockage of the pilosebaceous unit, increased sebum production, altered keratinization, and increased colonization of 

2. Are there common triggers and risk factors for acne?

Changes in hormones commonly trigger teenage acne. Testosterone usually increases during puberty and is one of the main causes of teenage acne. Many patients may believe that this hormone is only a trigger in boys, but testosterone levels also peak in girls around puberty. In most patients, the acne will resolve in adulthood.

Some common risk factors for acne include genetic predisposition, anxiety, stress, menstrual cycle, heat, and humidity. Use of cosmetic products, poor skin hygiene, and pregnancy may also trigger acne. Steroid use is another common trigger and may be seen in both male and female athletes who desire more muscle mass to improve their performance.

3. What are the different types of acne? How is it graded?

Acne can be comedonal, papulopustular, mixed, or nodular. In terms of severity, there are numerous different grading methods. It is crucial to recognize the type of acne because the clinical type and severity may affect treatment. The US Food and Drug Administration recommends grading acne via an Investigator’s Global Assessment scale (Table).

Common topical and oral treatments include salicylic acid, benzoyl peroxide, antibiotics, and retinoids. Oral isotretinoin (a retinoid) is by far the most effective, but this drug has the potential to cause numerous adverse events, including birth defects, liver abnormalities, and inflammatory bowel disease. Most clinicians will determine treatment based on both the clinical type and severity of acne.

What conditions contribute to severe acne in teenagers?

Polycystic ovarian syndrome, Cushing syndrome, and congenital adrenal hyperplasia can lead to the development of acne in teenagers and will be accompanied by other symptoms. For example, with polycystic ovarian syndrome, patients may have irregular menstrual periods, excessive body hair growth, and hair thinning.

It effects most teenagers and can lead to mental distress. Here are 5 important facts about acne vulgaris in adolescents.

Acne vulgaris in teenagers

An otherwise healthy 6-month-old boy has a 1-cm area of recurrent blistering with surrounding erythema on his right cheek that developed shortly after birth.

Diagnosis: Solitary mastocytoma with blistering

Solitary bullous eruption with surrounding erythema

Mastocytosis is a condition that involves an accumulation of mast cells in 1 or more organ systems such as the skin, liver, bone marrow, or small intestine.

 Cutaneous mastocytosis (CM) is usually found in very young children and predominantly involves dermal infiltrates of mast cells.

 The condition can be divided into maculopapular CM, diffuse CM, and solitary CM. The prognosis of solitary CM is excellent, with most patients experiencing spontaneous resolution before puberty. However, in patients with disease onset after age 2 years, solitary CM may continue into adulthood.

 Children with solitary lesions, multiple skin lesions, or diffuse mastocytosis confined to the skin (rare in infants) all have a good prognosis. Diffuse cutaneous disease with systemic involvement is much less common in infants and is often persistent. It is rarely associated with myeloproliferative disease.

The incidence of CM is estimated to be around 5 to 10 new cases in 1 million individuals, or 1 in every 1000 to 8000 dermatology outpatients, but it may be as often as 1 in 200 first-time patients at pediatric dermatology clinics.5 It is estimated that 10% to 15% of all pediatric cases of CM are solitary CM. Although the condition typically affects infants, particularly in the first 3 months of life, there have been reported cases of adult onset.

Most cases of mastocytosis are due to a gain-of-function mutation in the 

 gene, which encodes a receptor tyrosine kinase that regulates cell growth and division in addition to regulating the production of mast cells. Most of these somatic mutations occur spontaneously and are therefore not heritable.

 However, there have been some case reports of familial cases.

When the patient’s skin lesion is stroked or rubbed, mast cell degranulation occurs and forms a wheal known as Darier sign. Blisters result from buildup of tryptase between the epidermis and dermis.3 Although not usually necessary, diagnosis can be confirmed by a skin biopsy, which would show a dense infiltrate of mast cells.

 Additionally, during an attack, tryptase and histamine levels may be increased. An absence of systemic systems should be noted to rule out systemic mastocytosis, which could show more extensive blistering in a larger surface area, a high serum total tryptase level, gastrointestinal disturbances, osteolysis, organomegaly, ascites, or cytopenias.

Patients should avoid triggers of mast cell degranulation. Common triggers include heat, friction, alcohol, narcotics, sunlight, nonsteroidal anti-inflammatory drugs, anesthetics, bee stings, and more. When symptoms are triggered, they can be managed with antihistamines, sodium cromoglycate, acetylsalicylic acid, or ketotifen. Topical steroids may be used to manage lesion progression, and topical antibiotics can be used to prevent infection in blisters.

When the area with recurrent blistering was rubbed, the infant developed a blister with surrounding urticarial erythema, typical of a positive Darier sign. The patient was given an oral antihistamine for symptomatic treatment, and a discussion was had with his parents about ways to avoid rubbing the area. Over the next 3 to 4 months, the blistering stopped and the redness with rubbing improved dramatically. The patient’s parents were counseled that continued regression of the lesion and improvement in symptoms should be expected.

Cleveland Clinic. Mastocytosis. Updated November 18, 2015. Accessed July 28, 2020. 

https://my.clevelandclinic.org/health/articles/5908-mastocytosis#:~:text=Mastocytosis%20is%20a%20condition%20that,of%20the%20body%20are%20affected

Koga H, Kokubo T, Akaishi M, Iida K, Korematsu S. Neonatal onset diffuse cutaneous mastocytosis: a case report and review of the literature. 

. 2011;28(5):542-546. doi:10.1111/j.1525-1470.2010.01212.x

Leung AKC, Lam JM, Leong KF. Childhood solitary cutaneous mastocytoma: clinical manifestations, diagnosis, evaluation, and management. 

. 2019;15(1):42-46. doi:10.2174/1573396315666181120163952

Azaña JM, Torrelo A, Matito A. Update on mastocytosis (part 2): categories, prognosis, and treatment. 

2016;107:15-22. doi: 10.1016/j.adengl.2015.11.002

Horny H-P, Sotlar K, Valent P, Hartmann K. Mastocytosis: a disease of the hematopoietic stem cell. 

. 2008;105(40):686-692. doi:10.3238/arztebl.2008.0686

Azaña JM, Torrelo A, Matito A. Update on mastocytosis (part 1): pathophysiology, clinical features, and diagnosis. 

. 2016;107(1):5-14. doi:10.1016/j.ad.2015.09.007

A 6-month-old male with solitary mastocytoma

In 2015, the annual estimated cost of atopic dermatitis in the United States was 5 billion dollars.

 The onset of atopic dermatitis usually occurs in childhood. The majority of patients present with this disease prior to 12 months of age and 85% of patients develop this disease before age 5 years.

 Typically, atopic dermatitis has a chronic, relapsing course that may persist from childhood well into adulthood. In this article, we address frequently asked questions from patients.

1. If eczema is adequately controlled, is the risk of developing other disorders in the atopic march reduced?

The atopic march refers to the progression of diseases in certain patients. These patients usually start with atopic dermatitis and subsequently develop asthma, allergic rhinitis, food allergies, or other atopic diseases throughout their life.

 For example, approximately 30% to 50% of patients with atopic dermatitis also have allergic rhinitis and the prevalence of asthma among patients with atopic dermatitis is about 26%.

 A dysfunctional skin barrier can cause sensitization to antigens leading to other atopic diseases and a number of studies show that early treatment of eczema can reduce the risk of developing other atopic disorders.

2. What factors cause exacerbation of atopic dermatitis?

Some of the most common triggers include anxiety, dry skin, high temperatures, ichthyosis, irritants, itching, stress, and sweat.

Maintaining skin hydration is crucial in atopic dermatitis and emollients are one of the mainstay treatments for this condition. Regular emollient use can decrease the need for topical corticosteroids. Most providers recommend a water-based, fragrance-free moisturizer. Patients should apply emollients at least daily, particularly after swimming and bathing, and avoid taking long, hot showers. They should also avoid or limit their use of nonsoap cleansers. Irritants include detergents, perspiration, solvents, wool, and other rough materials.

Scratching can exacerbate and maintain the inflammation and drive the itch-scratch cycle, so any measures that decrease inflammation and scratching may decrease symptoms and skin findings. Patients should also avoid high humidity, temperature extremes, and attempt to decrease their stress as much as possible.

3. How does atopic dermatitis affect quality of life (QOL)?

It significantly decreases [a patient’s] QOL. In one study, among all chronic conditions in children, atopic dermatitis had the second highest impact on QOL.

 In adults, QOL is also severely impacted by the symptoms and emotional impact of this disease.

 In some cases, patients with atopic dermatitis may even change their occupation because of the skin condition.

 Atopic dermatitis can cause constant itching or scratching, difficulty sleeping, and embarrassment.

This skin condition is also associated with cardiovascular, inflammatory, and psychiatric conditions.

 Many of the symptoms of atopic dermatitis, such as sleep disturbance and decreased self-esteem, are risk factors for the development of psychiatric disorders. Atopic dermatitis is also associated with increased risk of anxiety and depression.

4. How does atopic dermatitis evolve over time?

In infants, atopic dermatitis primarily affects the face, scalp, and extensor surfaces of the extremities. In children, atopic dermatitis primarily affects the flexural folds of the extremities and neck. In adults, atopic dermatitis primarily affects the hands and inner creases of the elbows and knees. Older kids and adults with severe itching and behavioral issues may be at risk for prurigo nodularis, which presents as dramatically thickened plaques and nodules in these areas or at times disseminated.

Standard of care can vary depending on the severity of the disease. In general, topical emollients and corticosteroids are the mainstay therapies.

Topical corticosteroids decrease inflammation, colonization of 

, and pruritus. The potency should be based on the severity and location of the atopic dermatitis. For patients with atopic dermatitis in regions where corticosteroid use is not recommended, such as the face or skin folds, topical calcineurin inhibitors can be used. These include the tacrolimus ointment and pimecrolimus cream, which were approved nearly a decade ago, and these medications should be considered as an alternative treatment for atopic dermatitis.

 Although a black box warning was implemented in 2005 for the topical calcineurin inhibitors because of limited safety data and concern of risk of malignancies (despite protests by the American Academy of Dermatology and American Academy of Allergy, Asthma, and Immunology), long-term studies showed no evidence for these claims.

Emollients are also crucial in atopic dermatitis because they improve the barrier function and prevent dryness.

 Along with medications, skin protective measures should be emphasized to avoid exacerbations of the disease. In addition, many patients have trouble sleeping and melatonin can be helpful.

For many of the topical medications and emollients, providers often underestimate the quantity needed. The quantity should depend on the severity and surface area of the skin that is involved. For reference, approximately 2 g are required for a single application to the face, 3 g are required for a single application to 1 arm, and 4 g are required for a single application to 1 leg. Approximately 30 to 60 g are needed to cover the entire body for a single application. For 3 daily applications to the entire body for 2 weeks, approximately 42 to 84 oz are needed.

6. Is topical steroid use safe and effective for treating atopic dermatitis?

Studies have consistently demonstrated that topical steroids are effective in treating atopic dermatitis and topical steroids are currently one of the mainstay therapies for the treatment of this disease.

 They are safe in adults and children when used appropriately with careful discussion of frequency and length of application with guidelines for specific body sites. All patients should be counseled on the possible adverse effects of corticosteroids, including atrophy and striae.

7. How can bleach baths help patients with atopic dermatitis? How does the formation of biofilms complicate treatment?

Patients with atopic dermatitis have more flares and greater eczema severity with higher levels of 

 Liquid chlorine beach, which is sodium hypochlorite 6% solution, is active against 

 and therefore diluted bleach baths with mildly warm water may improve symptoms in many patients.

 species can form biofilms in these patients, which makes the bacteria resistant to many antibiotics and the immune response.

8. What are some of the new and evolving therapies for atopic dermatitis?

Crisaborole is a topical phosphodiesterase inhibitor that was approved by the US Food and Drug Administration (FDA) in 2016 for adults and children aged as young as 2 years and in 2020, it was approved for infants as young as 3 months.

 Studies have shown that crisaborole is safe for long-term use.

Dupilumab, an interleukin (IL)-4 and IL-13 receptor-alpha antagonist, was also recently approved by the FDA for children aged 6 years or older with severe atopic dermatitis.

9. Are low vitamin D levels an issue and does supplementation help?

Vitamin D plays a role in the barrier function of the skin and immune regulation. Serum vitamin D levels are lower in patients that have atopic dermatitis and vitamin D supplementation may be beneficial for some patients.

10. If topical medications do not adequately treat the atopic dermatitis, what are the next steps?

Patients with moderate to severe disease despite adequate topical treatments may be treated with phototherapy. Patients with severe unresponsive disease may also respond to off-label systemic agents including methotrexate, cyclosporine, mycophenolate, and azathioprine. The newer systemic agents include dupilumab, as mentioned above, and other biologics. Dupilumab requires no routine laboratory monitoring and is much safer for long-term use compared with off-label systemic agents.

11. What to expect in the next few years?

There are many medications that may be used for atopic dermatitis in the future. As discussed above, crisaborole and dupilumab were recently approved by the FDA.

Future medications that show promise include the JAK-STAT inhibitors, baricitinib, upadacitinib, PF-04965842, ASN002, tofacitinib, ruxolit inib, and delgocit inib.22 Other medications that show promise include tapinarof (aryl hydrocarbon receptor modulating agent), lebrikizumab and tralokinumab (IL-4/IL-13 antagonists), and nemolizumab (IL-31Rα antagonist).

Because of the high prevalence among children, it is crucial for pediatricians to be familiar with atopic dermatitis. As summer approaches, it is important to recognize that heat can lead to dryness of the skin and histamine release in the skin. Furthermore, the warm weather leads to sweat production, which irritates the skin. Thus, summertime is associated with increased atopic dermatitis flare-ups.

Atopic dermatitis has a significant effect on a patient’s QOL. The mainstay therapy for atopic dermatitis includes topical corticosteroids and emollients. Early treatment of atopic dermatitis can prevent the development of subsequent atopic disorders. Alternative treatments include diluted liquid chlorine bleach baths and phototherapy. Several off-label systemic agents, such as methotrexate and cyclosporine, can also be used. However, dupilumab, a new biologic drug that was recently approved for atopic dermatitis, is much safer than systemic agents.

Nutten S. Atopic dermatitis: global epidemiology and risk factors. 

Drucker AM, Wang AR, Li W-Q, Sevetson E, Block JK, Qureshi AA. The burden of atopic dermatitis: summary of a report for the National Eczema Association. 

 2017;137(1):26-30. doi:10.1016/j.jid.2016.07.012

Oliveira C, Torres T. More than skin deep: the systemic nature of atopic dermatitis. 

. 2019;29(3):250-258. doi:10.1684/ejd.2019.3557

Weller K, Soost S, Worm M, Maurer M, Zuberbier T. Atopic dermatitis and allergic rhinitis--do co-effects in therapy exist? 

. 2012;10(4):221-239. doi:10.1111/j.1610-0387.2011.07885.x

Ravnborg N, Ambikaibalan D, Agnihotri G, et al. Prevalence of asthma in patients with atopic dermatitis: a systematic review and meta-analysis. 

. 2021;84(2):471-478. doi:10.1016/j.jaad.2020.02.055

Bantz SK, Zhu Z, Zheng T. The atopic march: progression from atopic dermatitis to allergic rhinitis and asthma. 

 2014;5(2):202. doi:10.4172/2155-9899.1000202

Beattie PE, Lewis-Jones MS. A comparative study of impairment of quality of life in children with skin disease and children with other chronic childhood diseases. 

 2006;155(1):145-151. doi:10.1111/j.1365-2133.2006.07185.x

Paller A, Jaworski JC, Simpson EL, et al. Major comorbidities of atopic dermatitis: beyond allergic disorders. 

 2018;19(6):821-838. doi:10.1007/s40257-018-0383-4

Silverberg JI. Comorbidities and the impact of atopic dermatitis. 

 2019;123(2):144-151. doi:10.1016/j.anai.2019.04.020

Thyssen JP, Hamann CR, Linneberg A, et al. Atopic dermatitis is associated with anxiety, depression, and suicidal ideation, but not with psychiatric hospitalization or suicide. 

 2018;73(1):214-220. doi:10.1111/all.13231

Eichenfield LF, Tom WL, Berger TG, et al. Guidelines of care for the management of atopic dermatitis: section 2. Management and treatment of atopic dermatitis with topical therapies. 

 2014;71(1):116-132. doi:10.1016/j.jaad.2014.03.023

Ashcroft DM, Dimmock P, Garside R, Stein K, Williams HC. Efficacy and tolerability of topical pimecrolimus and tacrolimus in the treatment of atopic dermatitis: meta-analysis of randomised controlled trials. 

 2005;330(7490):516. doi:10.1136/bmj.38376.439653.D3

Alsterholm M, Strömbeck L, Ljung A, et al. Variation in Staphylococcus aureus colonization in relation to disease severity in adults with atopic dermatitis during a five-month follow-up. 

 2017;97(7):802-807. doi:10.2340/00015555-2667

Tauber M, Balica S, Hsu C-Y, et al. Staphylococcus aureus density on lesional and nonlesional skin is strongly associated with disease severity in atopic dermatitis. 

 2016;137(4):1272-1274.e3. doi:10.1016/j.jaci.2015.07.052

Mohan GC, Lio PA. Comparison of dermatology and allergy guidelines for atopic dermatitis management. 

 2015;151(9):1009-1013. doi:10.1001/jamadermatol.2015.0250

Gonzalez T, Biagini Myers JM, Herr AB, Khurana Hershey GK. Staphylococcal biofilms in atopic dermatitis. 

 2017;17(12):81. doi:10.1007/s11882-017-0750-x

Paller AS, Tom WL, Lebwohl MG, et al. Efficacy and safety of crisaborole ointment, a novel, nonsteroidal phosphodiesterase 4 (PDE4) inhibitor for the topical treatment of atopic dermatitis (AD) in children and adults. 

 2016;75(3):494-503.e6. Published correction appears in 

Simpson EL, Akinlade B, Ardeleanu M. Two phase 3 trials of dupilumab versus placebo in atopic dermatitis. 

2017;376(11):1090-1091. doi:10.1056/NEJMc1700366

Kim MJ, Kim S-N, Lee YW, Choe YB, Ahn KJ. Vitamin D status and efficacy of vitamin D supplementation in atopic dermatitis: a systematic review and meta-analysis. 

Deleuran M, Thaçi D, Beck LA, et al. Dupilumab shows long-term safety and efficacy in patients with moderate to severe atopic dermatitis enrolled in a phase 3 open-label extension study. 

 2020;82(2):377-388. doi:10.1016/j.jaad.2019.07.074

Blauvelt A, de Bruin-Weller M, Gooderham M, et al. Long-term management of moderate-to-severe atopic dermatitis with dupilumab and concomitant topical corticosteroids (LIBERTY AD CHRONOS): a 1-year, randomised, double-blinded, placebo-controlled, phase 3 trial. 

 2017;389(10086):2287-2303. doi:10.1016/S0140-6736(17)31191-1

Nguyen HL, Anderson KR, Tollefson MM. New and emerging therapies for pediatric atopic dermatitis. 

 2019;21(4):239-260. doi:10.1007/s40272-019-00342-w

Atopic dermatitis is a chronic, inflammatory skin condition that affects 15% to 20% of children and 1% to 3% of adults in the United States. The prevalence of atopic dermatitis, which is also known as eczema, is increasing in developing and industrialized countries.

Bernard A Cohen, MD

Articles

Diffuse erythematous rash in a healthy, afebrile infant

Acne vulgaris in teenagers

A 6-month-old male with solitary mastocytoma

What you need to know about atopic dermatitis