Pruritic patches and plaques - Clinical Advisor

Pruritic patches and plaques

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Case #1

A 32-year-old woman presents with what a primary care physician believed was a “fungal infection” on both knees. The infection had been present there for 3 months. She denies any other affected areas; however, she admits to having had a similar rash in the past, behind her knees and on her arms. She has been treating the area with over-the-counter antifungal creams twice daily with little improvement. Her past medical history is significant for insulin-dependent diabetes and possible eczema as a child, for which she was treated with topical steroids. She denies any new medications or product changes in her skin care routine. She admits to having overly dry skin in the past few months and significant pruritus with the lesions.

Case #2

A 63-year-old man presents with an itchy intermittent rash on his chest and back for several months. Of note, he has a history of eczema in the past that was treated with topical steroids. He admits to recent increased sun exposure and several changes in medications, including the initiation of metformin for newly diagnosed type 2 diabetes. In addition to the diabetes, his medical history is significant for hypertension, hyperlipidemia, and hypothyroidism. The patient says that the current rash has worsened. He has been self-treating with diphenhydramine and over-the-counter calamine lotion. On examination, the patient is found to have scaly, thin, erythematous patches and plaques.

 

Case #1Atopic dermatitis (eczema) is a chronic, pruritic condition primarily affecting infants and children. The hallmark manifestation of atopic dermatitis is dry skin and pruritus, but it can present in many ways depending on the patient's age and the duration...

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Case #1

Atopic dermatitis (eczema) is a chronic, pruritic condition primarily affecting infants and children. The hallmark manifestation of atopic dermatitis is dry skin and pruritus, but it can present in many ways depending on the patient’s age and the duration of the disease. 

In acute atopic dermatitis, erythematous vesicles and papules with exudates and crusting are present. Patients with subacute and chronic eczema present with dry and scaly papules with overlying excoriations. Skin thickening with hyperlinearity (lichenification) due to scratching is commonly seen in chronic cases. Postinflammatory hyperpigmentation or hypopigmentation can also be seen. 

Lesions at different stages of healing and acuity are often seen at the same time. The distribution of lesions is commonly seen in the flexural surfaces of the extremities. In infants, the rash typically occurs on the face, scalp, and torso. 

The cause of atopic dermatitis is still not fully understood, although a number of genetic and environmental factors have been identified. Loss of function mutations in the filaggrin gene (FLG) causes a defect in the skin barrier and is associated with a high risk of atopic dermatitis.1,2 Serine protease inhibitor Kazal-type 5 (SPINK5), a gene that encodes for a protease responsible for proper filaggrin formation, has also been associated with increased risk of eczema.3 Other loci, including 5q31 (KIF3A), 11q13 (OVOL1), and 19p13 (ADAMTS10/ACTL9), have also been associated with increased risk of atopic dermatitis.4 

Family history of atopic diseases (eczema, asthma, and allergic rhinitis) is a major risk factor of atopic dermatitis. Family history of atopy is positive in approximately 70% of patients who develop atopic dermatitis. This risk increases if one or both parents have a history of atopy.5 

Increased immunoglobulin E (IgE) levels are found in about 80% of patients with atopic dermatitis. Levels tend to increase with increased disease severity, but some patients with severe eczema can have normal serum levels of IgE.6 

Atopic dermatitis affects approximately 11% of children in the United States.7 However, the incidence of atopic dermatitis has increased over the past 20 years internationally.8 In adults, data on prevalence are limited, but it affects less than 1% of adults.5 Most cases of atopic dermatitis start before age 5 years, and 85% of cases begin before age 1 year. Data also suggest a slightly higher prevalence in girls and women (1.3:1 ratio).9 

Common complications are secondary infections due to bacteria or viruses. Patients with atopic dermatitis are more susceptible to infections due to a defective skin barrier. Impetigo, or superinfections of lesions by Staphylococcus aureus, is common, as most patients are colonized. Secondary infection by herpes simplex virus, also called eczema herpeticum, is a rarer complication, occurring in less than 3% of patients with atopic dermatitis.10 

Differential diagnosis for atopic dermatitis includes contact dermatitis, seborrheic dermatitis, and psoriasis. Distribution and shape of lesions, along with a careful patient history, can help differentiate atopic dermatitis from contact dermatitis. Clinicians should ask patients about any new products they may be using, or exposure to other common irritants such as poison ivy. Seborrheic dermatitis is differentiated from eczema by its characteristic greasy scale, as well as its distribution, which is commonly on the scalp, nose, chin, and forehead. Psoriasis can resemble atopic dermatitis but is commonly found on extensor surfaces, such as elbows and knees, compared with atopic dermatitis, which appears on the flexural surfaces. Silvery scale is also characteristic of psoriasis. Mycosis fungoides can also be considered in cases in which atopic dermatitis does not respond to treatment. 

Treatment of atopic dermatitis depends on the severity and chronicity of the disease. Goals primarily aim to manage symptoms of pruritus, prevent outbreaks and exacerbations, and reduce therapeutic side effects. All patients should avoid triggers and factors that worsen or exacerbate the disease. Some exacerbating factors include xerosis (dry skin), long, hot baths, high stress, and low humidity.11 

In patients with mild to moderate disease, emollients and low- to mid-potency topical steroids are the cornerstones of treatment. The strength of steroid should be chosen based on severity, age of the patient, and body surface area involvement. Mid- to high-potency corticosteroids should be avoided on the face, axilla, and groin due to lower skin thickness in those regions. Emollients should be used liberally to retain moisture.12

Topical calcineurin inhibitors, such as tacrolimus ointment, are a good option to consider when there is concern about skin atrophy or other side effects of corticosteroids. In acute exacerbations, short-term use of oral prednisone can sometimes reduce the duration of or abort these exacerbations. Topical antibiotics are used for patients with impetiginization. 

In cases of severe atopic dermatitis refractory to topical treatment, ultraviolet (UV) light therapy is helpful in adults. Psoralen plus UVA (PUVA) radiation, broadband UVA, broadband UVB, combined UVA and UVB, narrow-band UVB, and UVA1 have all been used with varying levels of success.13-16 

In our case, treatment with triamcinolone 0.1% ointment, applied twice daily to the affected areas, was initiated for atopic dermatitis. In 2 weeks, the lesions resolved with subsequent mild postinflammatory hyperpigmentation.

Case #2

Dermal hypersensitivity, also known as urticarial dermatitis, hypersensitivity dermatitis, or hypersensitivity urticarial reaction, is an extremely pruritic, chronic rash that resembles urticaria but lasts longer than 24 hours. It is characterized by erythematous papules that coalesce into plaques. Areas can appear urticarial or eczematous. 
The epidemiology of dermal hypersensitivity is not fully known. It appears to be more prevalent in patients aged 50 years or older. There have been more reported cases in girls and women than in boys and men.17 

The differential diagnosis includes scabies, allergic contact dermatitis, drug hypersensitivity reaction, and prodromal bullous pemphigoid. The diagnosis is often of exclusion because the rash is usually nonspecific. A careful medical history and list of medications from the patient is important to rule out contact dermatitis and drug reactions. 

In the early stages of bullous pemphigoid, lesions can appear urticarial, resembling dermal hypersensitivity. These lesions last several weeks or even months. Distinguishing features of prodromal bullous pemphigoid from urticarial dermatitis are the presence of vesicles and eosinophilic spongiosis on histology. Histologically, bullous pemphigoid typically has eosinophilic spongiosis with a deeper dermal perivascular lymphocytic and eosinophilic infiltrate in comparison with dermal hypersensitivity. Direct immunofluorescence and serologic testing for basement membrane antigens BP180 and BP230 can confirm the diagnosis of bullous pemphigoid.18 

Scabies can be confused with dermal hypersensitivity due to similar clinical and histologic presentations. Both are intensely pruritic, with scattered erythematous papules and plaques. Scabies is characterized more by significant scaling, as well as involvement of the hands, feet, and genitalia (in boys and men). 

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Histologically, dermal hypersensitivity is a commonly used dermatopathology term. It is characterized pathologically by perivascular lymphocytic infiltrates with eosinophils in papillary and upper reticular dermis. There is usually no to minimal epidermal involvement, with occasional spongiosis. 

First-line treatment for dermal hypersensitivity includes topical corticosteroids and antihistamines. Ultraviolet (UV) B phototherapy is another option for more severe or refractory cases. However, many cases are refractory to these initial treatment modalities. Systemic corticosteroids or other immunosuppressive agents, such as mycophenolate, have been beneficial in these cases.19 

In our patient, we performed a 4-mm punch biopsy, which was consistent with a dermal hypersensitivity reaction. The patient was instructed to take hydroxyzine, 25 mg at bedtime, and to apply clobetasol 0.05% ointment twice daily to affected areas. After 2 weeks of this treatment, the lesions had improved significantly.

Aaron Fong, BA, is a medical student and Rana Mays, MD, is a dermatology resident at Baylor College of Medicine in Houston.

References

  1. Sandilands A, Sutherland C, Irvine AD, McLean WH. Filaggrin in the frontline: role in skin barrier function and disease. J Cell Sci. 2009;122(Pt 9):1285-1294.
  2. Kypriotou M, Huber M, Hohl D. The human epidermal differentiation complex: cornified envelope precursors, S100 proteins and the ‘fused genes’ family. Exp Dermatol. 2012;21:643-649.
  3. Zhao LP, Di Z, Zhang L, et al. Association of SPINK5 gene polymorphisms with atopic dermatitis in northeast china. J Eur Acad Dermatol Venereol. 2012;26:572-577.
  4. Paternoster L, Standl M, Chen CM, et al. Meta-analysis of genome-wide association studies identifies three new risk loci for atopic dermatitis. Nat Genet. 2011;44:187-192.
  5. Eichenfield LF, Tom WL, Chamlin SL, et al. Guidelines of care for the management of atopic dermatitis: section 1. Diagnosis and assessment of atopic dermatitis. J Am Acad Dermatol. 2014;70:338-351.
  6. Dhar S, Malakar R, Chattopadhyay S, Dhar S, Banerjee R, Ghosh A. Correlation of the severity of atopic dermatitis with absolute eosinophil counts in peripheral blood and serum IgE levels. Indian J Dermatol Venereol Leprol. 2005;71:246-249.
  7. Shaw TE, Currie GP, Koudelka CW, Simpson EL. Eczema prevalence in the united states: data from the 2003 National Survey of Children’s Health. J Invest Dermatol. 2011;131:67-73.
  8. Deckers IA, McLean S, Linssen S, Mommers M, van Schayck CP, Sheikh A. Investigating international time trends in the incidence and prevalence of atopic eczema 1990-2010: a systematic review of epidemiological studies. PLoS One. 2012;7:e39803.
  9. Mortz CG, Andersen KE, Dellgren C, Barington T, Bindslev-Jensen C. Atopic dermatitis from adolescence to adulthood in the TOACS cohort: prevalence, persistence, and comorbidities. Allergy. 2015;70:836-845.
  10. Leung DY. Why is eczema herpeticum unexpectedly rare? Antiviral Res. 2013;98:153-157.
  11. Ellis C, Luger T, Abeck D, et al; ICCAD II Faculty. International Consensus Conference on Atopic Dermatitis II (ICCAD II): clinical update and current treatment strategies. Br J Dermatol. 2003;148(suppl 63):3-10.
  12. Sidbury R, Davis DM, Cohen DE, et al; American Academy of Dermatology. Guidelines of care for the management of atopic dermatitis: section 3. Management and treatment with phototherapy and systemic agents. J Am Acad Dermatol. 2014;71:327-349.
  13. Jekler J, Larkö O. Combined UVA-UVB versus UVB phototherapy for atopic dermatitis: a paired-comparison study. J Am Acad Dermatol. 1990;22:49-53.
  14. Reynolds NJ, Franklin V, Gray JC, Diffey BL, Farr PM. Narrow-band ultraviolet B and broad-band ultraviolet A phototherapy in adult atopic eczema: a randomised controlled trial. Lancet. 2001;357:2012-2016.
  15. Taylor K, Swan DJ, Affleck A, Flohr C, Reynolds NJ; UK TREND and UK DCTN. Treatment of moderate-to-severe atopic eczema in adults within the UK: results of a national survey of dermatologists. Br J Dermatol. 2016 Dec 11. doi: 10.1111/bjd.15235 [Epub ahead of print]
  16. Fernández-Guarino M, Aboin-Gonzalez S, Barchino L, Velazquez D, Arsuaga C, Lázaro P. Treatment of moderate and severe adult chronic atopic dermatitis with narrow-band UVB and the combination of narrow-band UVB/UVA phototherapy. Dermatol Ther. 2016;29:19-23.
  17. Banan P, Butler G, Wu J. Retrospective chart review in a cohort of patients with urticarial dermatitis. Australas J Dermatol. 2014;55:137-139.
  18. Fung MA. The clinical and histopathologic spectrum of “dermal hypersensitivity reactions,” a nonspecific histologic diagnosis that is not very useful in clinical practice, and the concept of a “dermal hypersensitivity reaction pattern”. J Am Acad Dermatol. 2002;47:898-907.
  19. Kossard S, Hamann I, Wilkinson B. Defining urticarial dermatitis: a subset of dermal hypersensitivity reaction pattern. Arch Dermatol. 2006;142:29-34.
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