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phototherapy, emollients, and retinoids. Methotrexate therapy may exacerbate immune
dysregulation.[972,983]
Reiter’s syndrome is increased in frequency and severity in association with HIV
infection; it has been reported in 4 to 10% of HIV infected persons. Persons with HLA-B27 are
more likely to develop this disease. It includes the findings of arthritis, uveitis, and
conjunctivitis, though only two of the three may be present in HIV-infected persons. The most
characteristic appearance is a palmoplantar pustular dermatosis that may be associated with nail
dystrophy, periungual erythema, and hyperkeratosis. The lesions initially present as
erythematous macules, and over the course of several days, these become hyperkeratotic, waxy
papules associated with an erythematous halo. Multiple papules coalesce and eventually form
thickened horny plaques. The distribution of these hyperkeratotic lesions is on the palms and
soles and less commonly involving the trunk and proximal extremities. Microscopically, lesions
resembling those of pustular psoriasis may be present, and treatment modalities are similar to
psoriasis. A relapsing course is common.[985,983]
Eosinophilic folliculitis seen in patients with HIV infection typically occurs in the
advanced stage or with immune restoration. It presents as a chronic eruption of 2 to 3 millimeter
intensely pruritic follicular papules in the head, neck, trunk, and upper arm regions. On biopsy,
there is a folliculocentric predominance of eosinophils and lymphocytes, with frequently
associated lysis of the sebaceous gland. Secondary changes include excoriation, prurigo
nodularis, and lichen simplex chronicus. Histologically, this eruption is distinguished from
suppurative folliculitis caused by bacteria such as Staphylococcus aureus by the lack of
neutrophilic infiltrates and the predominance of lymphocytes and/or eosinophils at the follicular
isthmus and sebaceous gland duct. Though infectious organisms may be identified in
conjunction with eosinophilic folliculitis, they are considered non-pathogenic, However,
treatment that give more than transient relief, such as corticosteroids, have included permethrin
and itraconazole.[983]
Xerosis generalisata, or dry skin syndrome, may be present in up to 30% of HIV infected
patients and is characterized by fine diffuse hyperpigmented scaling and crusting with severe
pruritus unresponsive to antihistaminic therapy. Histologically xerosis resembles irritant contact
dermatitis. Other findings have included palmoplantar keratoderma, ichthyosis, and eczematous
dermatitis. Emollients have been employed as therapy.[981,983]
Atopic dermatitis manifests as erythematous scaling plaques with associated papules or
vesicles. Affected persons may also have asthma, allergic rhinitis, and allergic conjunctivitis.
The intense pruritus can lead to secondary changes from excoriation of infection, as well as
lichenification with lichen simplex chronicus. On biopsy, there is a superficial perivascular
infiltrate of lymphocytes and eosinophils together with epidermal hyperplasia and foci of
spongiosis. Laboratory findings often include an elevated IgE and peripheral eosinophilia.
Emollients, topical corticosteroids, oral antihistamines, and phototherapy have been used to treat
atopic dermatitis.[983]

ONYCHOMYCOSIS.-- The superficial mycoses are common, and the term
onychomycosis refers to infection of nails. Risk factors include male sex, active sports
participation, commercial swimming pools, occlusive footwear, trauma, smoking, and psoriasis.
Toenails are more frequently affected than fingernails because they grow three times slower. The
five major clinical presentations of onychomycosis include:[986]