Dermatologic problems occur in
90% of patients with HIV infection. From themacular, roseola-like rash seen with the acute seroconversion syndrome toextensive end-stageKS, cutaneous manifestations of HIV disease can be seenthroughout the course of HIV infection. Among the more common nonneoplasticproblems are seborrheic dermatitis, eosinophilic pustular folliculitus, andopportunistic infections. Extrapulmonary pneumocystosis may cause anecrotizing vasculitis. Neoplastic conditions are covered below in the section onmalignant diseases.
occurs in 3% of the general population and in up to 50%of patients with HIV infection. Seborrheic dermatitis increases in prevalenceand severity as the CD4+ T cell count declines. In HIV-infected patients,seborrheic dermatitis may be aggravated by concomitant infection with
, a yeastlike fungus; use of topical antifungal agents has beenrecommended in cases refractory to standard topical treatment.
Eosinophilic pustular folliculitis
is a rare dermatologic condition that is seenwith increased frequency in patients with HIV infection. It presents asmultiple, urticarial perifollicular papules that may coalesce into plaquelikelesions. Skin biopsy reveals an eosinophilic infiltrate of the hair follicle, which incertain cases has been associated with the presence of a mite. Patientstypically have an elevated serum IgE level and may respond to treatment withtopical anthelminthics. Patients with HIV infection have also been reported todevelop a severe form of
with hyperkeratotic psoriasiformlesions.Both
, although they are not reported to be increased infrequency, may be particularly severe when they occur in patients with HIVinfection. Preexisting psoriasis may become guttate in appearance and morerefractory to treatment in the setting of HIV infection.
Reactivation herpes zoster
) is seen in 10 to 20% of patients with HIVinfection. This reactivation syndrome of varicella-zoster virus indicates amodest decline in immune function and may be the first indication of clinicalimmunodeficiency. In one series, patients who developed shingles did so anaverage of 5 years after HIV infection. In a cohort of patients with HIVinfection and localized zoster, the subsequent rate of the development ofAIDS was 1% per month. In that study, AIDS was more likely to develop if theoutbreak of zoster was associated with severe pain, extensive skin involvement,or involvement of cranial or cervical dermatomes. The clinical manifestations ofreactivation zoster in HIV-infected patients, although indicative of immunologiccompromise, are not as severe as those seen in other immunodeficientconditions. Thus, while lesions may extend over several dermatomes (seePlateIID-37) and frank cutaneous dissemination may be seen, visceral involvementhas not been reported. In contrast to patients without a known underlying