Dermatology in HIV — Viva

Q1: Overview and presentation (2 min)

A patient with untreated HIV develops a rash. How do you approach the cutaneous manifestations of HIV, and what proportion of patients are affected?

Over 90 percent of untreated HIV patients develop cutaneous disease, and the skin is often the first organ to declare the diagnosis. The key organising principle is the CD4-stratified model: early disease (CD4 above 500) brings severe common dermatoses — seborrhoeic dermatitis, oral candidiasis, recurrent HSV, multidermatomal zoster; moderate immunosuppression (CD4 200 to 500) adds oral hairy leukoplakia, Kaposi sarcoma, eosinophilic folliculitis and molluscum; severe immunosuppression (below 200) adds chronic ulcerative herpes (over 1 month is AIDS-defining), disseminated fungi, crusted scabies and bacillary angiomatosis; very severe (below 50) adds disseminated MAC and CMV. ART transforms the prognosis — most conditions resolve with immune restoration.

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Q2: The oral distinction (2 min)

Your patient has white lesions on the tongue. How do you distinguish oral candidiasis from oral hairy leukoplakia, and why does it matter?

This is the classic exam distinction. Candidiasis is white, curd-like, scrapable (wipes off with gauze leaving an erythematous base), KOH-positive (pseudohyphae), and occurs at CD4 below 500. Oral hairy leukoplakia is a white, corrugated, non-scrapable plaque on the lateral border of the tongue, caused by EBV, and is pathognomonic for HIV (CD4 below 200 to 300). The bedside gauze-wipe test settles it. Both improve with ART. OHL is benign but is a powerful marker of HIV.

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Q3: Purple papules (3 min)

The patient has purple-brown nodules on the hard palate and lower legs. What is your differential, and how do you confirm the diagnosis?

The two principal entities are Kaposi sarcoma and bacillary angiomatosis. KS (HHV-8, AIDS-defining) shows purple-brown papules/nodules/plaques, classically on the lower extremities and hard palate (highly suggestive in HIV); histology shows spindle cells forming slit-like vascular spaces with extravasated RBCs, and HHV-8 immunohistochemistry is positive. Bacillary angiomatosis (Bartonella henselae/quintana) produces friable red-purple vascular papules that mimic KS, but histology shows a lobular capillary proliferation with neutrophils and a positive Warthin-Starry stain (black bacilli). Treatment differs fundamentally: KS gets ART ± chemo/radiotherapy; bacillary angiomatosis gets erythromycin or doxycycline for at least 3 months. A third mimic — disseminated cryptococcosis — produces umbilicated translucent papules on the face; if suspected, do a serum cryptococcal antigen and lumbar puncture, because cutaneous cryptococcosis means disseminated disease.

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Q4: Drug eruptions and IRIS (3 min)

The patient starts ART and cotrimoxazole prophylaxis. What cutaneous drug reactions do you anticipate, and what is IRIS?

HIV patients have a 10 to 100-fold increased risk of drug eruptions. The high-yield culprits: cotrimoxazole (morbilliform, the commonest; can desensitise for mild reactions), abacavir (systemic hypersensitivity, HLA-B*5701-restricted — screen every patient before starting; never rechallenge), nevirapine (SJS/TEN), and efavirenz (rash plus vivid dreams/neuropsychiatric symptoms).^[2][5]

^[1][2]IRIS — immune reconstitution inflammatory syndrome — is paradoxical worsening or unmasking of disease within weeks of starting ART, as recovering immunity reacts to antigens that were previously "quiet". Risk factors: low baseline CD4, high CD4 rise, untreated opportunistic infection at ART start. Cutaneous IRIS flares KS, psoriasis, acne, molluscum, or unmasks cryptococcosis, MAC and HSV. Management: do NOT stop ART; treat the condition; systemic corticosteroids for severe (for example KS-IRIS) cases. The critical distinction is IRIS (falling viral load, rising CD4) versus treatment failure (rising viral load) — always check a viral load.

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Q5: Management principles and prognosis (2 min)

Summarise your management and the prognosis of HIV skin disease.

Five pillars: (1) ART — the cornerstone, effective for essentially all HIV skin disease; (2) condition-specific dermatological therapy (antifungals, antivirals, phototherapy); (3) drug-eruption management (STOP the drug; HLA-B*5701 screen for abacavir; nevirapine caution); (4) IRIS management (continue ART ± steroids); (5) cancer screening (KS, SCC, BCC, melanoma, AIN). Prognosis is transformed by ART — the majority of dermatoses resolve with immune restoration, and epidemic KS frequently regresses. The worst prognosis is in late presenters, untreated virus, disseminated fungal disease, and SJS/TEN.^[2][5][3]

References5ShowHide

1. [1]Müller M, Wandel S, Colebunders R, et al. Immune reconstitution inflammatory syndrome in patients starting antiretroviral therapy for HIV infection: a systematic review and meta-analysis Lancet Infect Dis, 2010.PMID 20334848
2. [2]Karadag AS, Elmas OF, Altunay IK, et al. Cutaneous manifestations associated with HIV infections: A great imitator Clin Dermatol, 2020.PMID 32513397
3. [3]Patel R, Lurain K, Yarchoan R, et al. Clinical management of Kaposi sarcoma herpesvirus-associated diseases: an update on disease manifestations and treatment strategies Expert Rev Anti Infect Ther, 2023.PMID 37578202
4. [4]Rathee M, Jain P. Hairy Leukoplakia 2026.PMID 32119478
5. [5]Mohseni Afshar Z, Goodarzi A, Emadi SN, et al. A Comprehensive Review on HIV-Associated Dermatologic Manifestations: From Epidemiology to Clinical Management Int J Microbiol, 2023.PMID 37496761