AIDS-Associated Psoriasiform Dermatitis - An Uncommonly Reported Entity Occurring Along with Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)

Sir,

Psoriasiform dermatitis comprises a group of disorders, which clinically and/or histologically simulates psoriasis and is common in HIV (human immunodeficiency virus)-infected individuals. These include a group of disorders that either in the beginning or during progression resemble psoriasis or seborrhoeic dermatitis. The histologic features of HIV-associated psoriasiform dermatitis are uniform regardless of varying clinical presentations.

A 36-year-old man, known case of HIV infection on HAART (tenofovir, lamivudine, efavirenz) and cotrimoxazole (Cotrimoxazole), presented with fever and pain in the abdomen along with yellowish discoloration of eyes and urine 4 weeks after starting therapy. After 10 days he developed swelling, predominantly around eyes, and face followed by intense itching and eruption of multiple pinhead-sized reddish lesions all over body.

Initial examination revealed fever of 101.2°F with multiple bilateral axillary and inguinal lymphadenopathy, erythematous coalescing maculopapular rash symmetrically involving the whole body, periorbital edema, and icterus. Blood tests showed raised total leucocyte count (TLC 18,000/cmm), AEC 7300 eosinophils/mm³, and few atypical lymphocytes. Liver function tests showed aspartate and alanine aminotransferases values of 1182 and 1396 IU/l, total bilirubin 18.0 mg/dL, normal prothrombin time, serum creatinine 2.2 mg/dL, and blood urea 84 mg/dL. Regiscar scoring of the patient was 6 and he was diagnosed as a case of drug reaction with eosinophilia and systemic symptoms (DRESS) most likely due to septran. All medications were discontinued and the patient was started on oral prednisolone (1 mg/kg body weight) and monitored for signs of clinical recovery. Within a week the erythema started to decrease and exfoliation with fine scales started. His TLC, liver enzymes, and renal parameters started normalizing within a week of therapy and the individual showed symptomatic improvement with a decrease in erythema and scaling and absence of fever.

However, after 10 days of improvement, the patient started developing whitish-yellow thick scales over the scalp, neck, trunk, and all four extremities including palms and soles [Figures 1–3]. Palms also showed a few pustules. Oral mucosa revealed angular cheilitis and candidiasis. His condition worsened and he developed fever along with tachycardia, hypotension, and decreased urinary output (features suggestive of septic shock). Cultures were sent and a skin biopsy was done. His CD4 count was 219 cells/μL with an HIV viral load of 10,000,000 copies/mL. He was started on inotropes, fluids, and antibiotics. HAART was restarted (tenofovir, lamivudine, efavirenz).

Figure 1.

Diffuse scaling is seen involving the face, neck, and trunk

Figure 3.

(a) Thick hyperkeratotic greasy plaques over the sole with exfoliation b) thick greasy scales over hand c) swelling and greasy scales present around nail-folds of the hand

Figure 2.

Thick adherent yellowish-white crusted plaques seen involving the entire scalp and neck

Skin biopsy revealed confluent parakeratosis with a predilection for the hair follicle, acanthosis, and irregular elongation of rete ridges, and focal supra papillary thinning. A moderate degree of spongiosis with exocytosis of neutrophils and lymphocytes into the epidermis. Few apoptotic keratinocytes were noted. The upper dermis shows a moderate perivascular inflammatory infiltrate of lymphocytes and neutrophils [Figure 4].

Figure 4.

(a) H and E (40×) shows epidermis with irregular acanthosis with parakeratosis and moderate upper dermal perivascular lymphocytic infiltrate. (b) H and E (100×) shows parakeratosis and extensive exocytosis with foci of supra-papillary thinning. (c) H and E stained section (400× magnification) shows epidermis with exocytosis and few necrotic keratinocytes (arrows)

Based on the above clinical and histopathological picture a presumptive diagnosis of HIV-induced psoriasiform dermatitis was given and the patient was started on oral Acitretin (50 mg). The individual showed considerable improvement with complete resolution of all skin lesions in the next 8 weeks [Figure 5]. Acitretin and prednisolone were gradually tapered off over the next 2 months.

Figure 5.

Complete resolution of skin lesions after eight weeks of therapy

HIV associated psoriasiform dermatitis is a papulosquamous dermatosis with an estimated prevalence of about 2%–5% with the spectrum including (i) seborrhoeic dermatitis, (ii) psoriasis, (iii) Reiter's syndrome, (iv) pityriasis rubra pilaris, and (v) xerosis and ichthyosis.[1]

In HIV infection misleading and unusual clinical presentations of these disorders with severe disease and frequent exacerbations are characteristic and several morphological types can co-exist in the same patient.[2,3]

In a study by Romani et al.[4] HIV associated psoriasiform dermatitis was characterized by constant involvement of the face and seborrhoeic areas, extensive pustulosis of the palms and soles, with hyperkeratotic areas resembling keratoderma blenorrhagica and there was also severe and universal nail involvement, with hyperkeratosis, yellow discoloration and marked onycholysis. Acral predominance of psoriasiform lesions and inverse or flexural distribution of psoriasis were common features. Nearly 50% of the patients eventually developed psoriatic erythroderma. According to Sehgal, et al.[5] HIV-associated psoriasiform lesions are more “angry looking” with a prominent component of seborrhoeic dermatitis.

This was similar to our case which after adequate treatment showed persistent thick greasy scales involving the seborrhoeic areas of body, extensive involvement of axillae, inguinal and perianal area with slow healing moist erythematous erosive plaques and thick hyperkeratotic plaques involving palms and soles pointing toward acral predominance of psoriasiform lesions.

The histologic features of HIV-associated psoriasiform dermatitis are same across the spectrum of varying clinical presentations which include psoriasiform hyperplasia of the epidermis with no thinning of the suprapapillary plate, with keratinocyte necrosis and lymphocyte karyorrhexis. A relative decrease of the number of CD45RO T -lymphocytes with an increase in the number of plasma cells has also been reported in this disorder. These features allow differentiation of HIV-associated psoriasiform dermatitis from psoriasis and seborrheic dermatitis in patients without AIDS.[6]

Heat shock proteins (HSPs), such as HSP65 andHSP72, in keratinocytes, are the main mediators responsible for HIV-associated psoriasiform dermatitis. HSP-activated T cells secrete interferon-gamma (IFN-γ) and tumor necrosis factor which has been implicated in the pathogenesis of psoriasiform hyperplasias. There is also evidence supporting the role of heat shock proteins as inducers of cross-immunity reactions that could be involved in the pathogenesis of psoriasis.[6]

Treatment in patients with HIV associated psoriasiform dermatitis poses special difficulties, but marked clinical improvement is often obtained with Acitretin, RePUVA (retinoid with photochemotherapy), or cyclosporine A in the absence of any adverse effects. Acitretin in a mean daily dose of 1 mg per kg, is an effective and safe therapy for severe psoriasiform dermatitis in HIV-infected patients. In our patient, clinical remission was achieved with acitretin within six weeks of its use.

In conclusion, severe psoriasiform dermatitis in HlV-infected patients often assumes a severe and atypical clinical pattern with overlapping features of varied papulosquamous diseases and can lead to confusion. Good clinico-histopathological correlation can help in clinching the diagnosis and treatment of this not so commonly reported but very debilitating condition.

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