Page 240 - AIDSBK23C

Page 240

IRIS may include traumatic injuries, tattoos, injection drug use sites, autoimmune diseases, and
vasculitis. Infectious agents produce granulomatous inflammation, and they must be diagnosed
by histologic stains or by culture methods. Antiretroviral therapy with on-nucleoside reverse
transcriptase inhibitor agents and/or protease inhibitors may induce a cutaneous rash about 10%
of the time, ranging from morbilliform exanthems to toxic epidermal necrolysis (TEN) and
Stevens-Johnson syndrome (STS).[982]

PAPULOSQUAMOUS DERMATOSES.-- A variety of papulosquamous dermatoses
may occur in persons with HIV infection, particularly with CD4 lymphocyte counts less than
150/µL. The most common condition seen in HIV-infected persons is seborrheic dermatitis,
which can occur at some point in up to 80 to 85% of this population, but only 4% of the general
population. The lesions appear as yellow to white scaly, greasy scales on erythematous patches
or plaques on scalp, eyebrows, nasolabial folds, and posterior auricular regions where sebaceous
gland activity can be increased. Microscopically, atypical features not seen in seborrheic
dermatitis of immunocompetent persons include pronounced hyperkeratosis with parakeratosis,
follicular plugging, acanthosis, spongiosis, lymphocyte and neutrophil exocytosis along with
dyskeratosis and keratinocyte necrosis. In patients with HIV infection, seborrheic dermatitis
tends to have a more rapid onset and be more extensive and severe than in immunocompromised
patients. Though it can occur at any stage of HIV infection, it is more likely to appear with
declining CD4 cell counts. Previously limited lesions may acutely become more severe and
extensive. Topical corticosteroid therapy can be effective therapy.[972,983]
Pruritus alone is a frequent accompaniment of advancing HIV infection, particularly
when CD4 counts drop below 50/microliter. This can be idiopathic, or part of a condition with
more specific findings.[983] An intensely pruritic papular eruption has been observed in HIV
infected persons, termed pruritic papular eruption (PPE). It is characterized by symmetrically
distributed papules with pruritus in the skin. This eruption consists of 2 to 8 mm erythematous
papules that become excoriated, leading to larger papules and nodules up to 1 cm, with marked
lichenification and hyperpigmentation. PPE-HIV occurs mainly in persons with HIV who have
mean CD4 lymphocyte counts of less than 200/µL. Eosinophil counts are significantly increased.
The density of CD8+ lymphocytes is increased while the density of CD4+ cells is decreased in
dermal infiltrates. Interleukin 5 is the predominant cytokine identified in the lesions. The CD8
lymphocytes and Langerhans cells appear to play a role in the pathogenesis of PPE-HIV. The
increased frequency of IL5 associated with abundant eosinophils in the lesions suggests a Th2
immune response in this form of dermatitis.[984] PPE skin lesions microscopically resemble an
insect bite, with superficial and deep perivascular interstitial lymphohistiocytic and eosinophilic
inflammatory infiltrates, with Langerhans cells normally distributed in the epidermis and seen
among the cellular components of dermal infiltrates.[982]
Psoriasis affects 2% to 5% of patients with HIV infection but only 1% of the general
population. Up to 10% of affected HIV infected persons may also develop arthritis. It can be
more severe, particularly with decreasing CD4 counts. A sudden onset, or an acute exacerbation
of stable disease, is more likely in the setting of HIV infection. There may be more than one
clinical pattern simultaneously, or the course may be complicated by exfoliative erythroderma.
Microscopic findings are similar to psoriasis in immunocompetent persons, but atypical features
with HIV can include fewer Munro microabscesses, irregular acanthosis, and less pronounced
thinning of the suprabasal plate. Therapies are similar to non-HIV-infected cases and include