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Skin Manifestations of Human Immunodeficiency Virus (HIV): Part 2

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Skin Manifestations of Human Immunodeficiency Virus (HIV): Part 2 • • Skin manifestations of human immunodeficiency virus (HIV): Part 2. Noninfectious skin manifestations BRADLEY S. KURGIS, DO The incidence of the acquired cies, and nonclassified skin changes found in immunodeficiency syndrome (AIDS) is ris­ IllV-infected patients, as well as the recom­ ing at an alarming rate. Usually, the first mended modes of therapy. clue that a patient has human immunode­ ficiency (HIV) infection is the emergence Noninfectious inflammatory diseases of a skin disease. Early diagnosis and ag­ Seborrheic dermatitis gressive therapy are vital in the manage­ Possibly the most common and earliest cuta­ ment of these conditions. In Part 1 of this neous manifestation of HIV infection is sebor­ article, the author discussed AIDS-related rheic dermatitis. This inflammatory condition infectious diseases of the skin. In Part 2, has an incidence of 3% in the general popula­ he discusses noninfectious inflammatory tion and has been found to be as high as 85% diseases, malignant cutaneous neoplasms, in patients seropositive for HIVI Seborrheic and nonclassified skin changes found in dermatitis in patients with AIDS differs from mv -infected individuals, as well as their that in a healthy individual in that it is explo­ optimal management. sive in onset, more extensive, and difficult to (Key words: Skin disease, human im­ treat. munodeficiency disease, acquired immu­ Involvement is seen primarily on the face nodeficiency syndrome) and scalp, but axillary and groin areas can be affected. Pityrosporum orbiculare organisms Noninfectious skin manifestations in pa­ have been found to be increased in seborrheic tients with the acquired immunodeficiency syn­ dermatitis as compared with normal skin, and drome (AIDS) include both dermatoses and ma­ respond to topical 2% ketoconazole combined lignant neoplasms. The first manifestations of with 2.5% hydrocortisone. If the condition is human immunodeficiency virus (IllV) disease severe, oral ketoconazole can be used at 200 usually are cutaneous. The appearance of cu­ mg to 400 mg daily for 2 weeks. Because of taneous disease is inversely proportional to the frequent recurrences, therapy must be applied CD4 T-cell count. As the count drops below to the skin long term. 250 cells/mm3, common skin malignancies and rashes begin to appear. Psoriasis Every patient seen with a new dermatosis Psoriasis can be altered in patients with AIDS. or malignancy commonly found in the IllV Most studies do not correlate an increase in population should be offered an IllV test. This the incidence of psoriasis with HIV infection2•3 offer can open a dialogue affording the oppor­ but, with the development of AIDS, existing tunity for the physician to learn if the patient psoriasis can become more severe and ex­ has any reason to suspect exposure to the IllV tremely difficult to treat. The rapid onset of Early identification and early treatment will acute eruptive psoriasis, or sudden exacerba­ delay the progression of IllV-associated skin tion, should suggest the possibility of IllV in­ disease. fection if the patient has risk factors for AIDS. Following is a description of various nonin­ In such cases, serologic testing for evidence of fectious inflammatory diseases, skin malign an- IllV is recommended. Reprint requests to Bradley S. Kurgis, DO , 1111 Las Therapy for AIDS-related psoriasis is chal­ Tablas Rd, Suite M, Templeton, CA 93465. lenging because most treatment modalities in- Clinical practice ' Kurgis JAOA • Vol 93 • No 2 • February 1993 • 223 volve a degree of immunosup­ pression. Methotrexate, corti­ costeroids, cyclosporin, and psoralen plus ultraviolet A pho­ totherapy should be avoided in HIV-infected patients because of the patients' already exist­ ing immunosuppression. Zido­ vudine (AZT) has shown a marked antipsoriatic effect without exhibiting a clear re­ lationship to the helper T-cell count.3 Thus, in the AIDS pa­ tient with psoriasis, treatment with AZT and topical modali­ ties is recommended. Ichthyosis Figure 1. Eosinophilic pustular folliculitis on back of patient with AIDS. Acquired ichthyosis on the Generalized papules and pustules are associated with severe itching. Histolo­ lower extremities is a common gic examination of these lesions reveals follicular inflammatory process con­ finding in AIDS patients.4,5 It taining many eosinophils. is characterized by dry, thick plaques with scales. Therapy is directed to­ phous dermatitis with numerous eosinophils. ward control of the scaling with topical urea The pustular folliculitis composed predomi­ and lactic acid compounds. It is not clear nantly of eosinophils is not a pattern seen in whether the acquired ichthyosis is caused by any other entity. Cultures and sensiti vi ty tests malnutrition and wasting immunosuppression, give negative results. Eosinophilic pustular fo1- or by an under lying malignancy. 4-8 liculitis(Figure 1) is refractory to topical and systemic corticosteroids, but treatment with Papular eruption of AIDS ultraviolet B phototherapy may lead to remis­ This eruption is a clinically distinct but his­ sion.9 tologically nonspecific condition. It has been reported in AIDS patients as discrete, red, pru­ Pruritus ritic papules appearing over the head, neck, Pruritus is a frequent complaint of AIDS and upper trunk.6 The eruption is chronic, dif­ patients and is often difficult to control. Pa­ ficult to treat, and very itchy. There is no cor­ tients scratch uncontrollably and create sec­ relation between the severity of the papular ondary infections. The itching may be in ar­ eruption and the progression of AIDS. eas of folliculitis or ichthyosis or in normal­ appearing skin. Mild topical hydrocortisone Eosinophilic pustular folliculitis and mentholated emollients may afford relief. Eosinophilic pustular folliculitis (EPF) is a A thorough skin examination for burrows and rare skin condition that, in the past, occurred a scabies smear should be performed to rule primarily in the Japanese.7 Patients with si­ out scabies. multaneous AIDS and EPF have been re­ ported.8 The folliculitis characteristically ap­ Morbilliform drug eruption due to tri­ pears as a pruritic, papulopustular dermatitis methoprim-sulfamethoxazole that affects the hair follicles on the face, scalp, Drug dermatitis reactions occur in more than and trunk. The papulopustules coalesce to half of AIDS patients who receive tri­ form chronic plaques. methoprim-sulfamethoxazole for Pneumocys­ A skin biopsy specimen reveals a polymor- tis carinii pneumonia.10 The rash appears as 224 • JAOA • Vol 93 • No 2 • February 1993 Clinical practice· Kurgis with therapy. The progression of disease often follows the relative collapse of the im­ mune system. Malignant neoplasms of the skin Kaposi's sarcoma Kaposi's sarcoma (KS) is the most common neoplasm in pa­ tients with AIDS. Before the advent of the AIDS epidemic of the 1980s, KS was a rare, slow-growing neoplasm seen only in elderly men of East­ ern European origin, black Af­ ricans, and patients with leu­ kemia. In the immunosup­ Figure 2. Multiple tumors of Kaposi's sarcoma in HIV -infected homosexual pressed AIDS patient, KS is man. These lesions are more advanced nodular tumors in patient with deterio­ rating T-cell count. an opportunistic neoplasm with a more rapid develop­ ment than its classic counter­ fine macules and papules that coalesce to form part. The patient may be seen with single or erythematous plaques. that may be general­ multiple skin lesions that can behave aggres­ ized. Urticarial eruptions with dermographism sively. Visceral, mucosal, and lymphatic in­ can occur. The rash may remain for a pro­ volvement can occur. longed period after discontinuation of tri­ Early skin lesions, often difficult to detect, methoprim-sulfamethoxazole. range from macules to indurated plaques; ad­ vanced lesions are large tumorous nodules .15 Other inflammatory dermatoses reported The lesions may appear anywhere on the skin in AIDS patients and range from pink to red to purple or dusky A long list of other inflammatory dermatoses brown. It is most common to see KS lesions have been reported in HIV infection: scabies, 11 arranged along skin tension lines and on mu­ porphyria cutanea tarda,12 atopic dermatitis, cous membranes (Figures 2 and 3). pellagra,13 and granuloma annulare-like erup­ Kaposi's sarcoma in AIDS patients appears tions.14 Most of these dermatoses are only spo­ to be largely restricted to homosexual and bi­ radically seen, and the association with HIV sexual men. However, the percentage of ho­ infection is not well established. These derma­ mosexual AIDS patients with KS has declined toses should be included in the differential di­ during the past 10 years. In 1980, 45% of ho­ agnosis of AIDS-related skin findings. mosexual men with AIDS had KS; today, only A definitive relationship exists between the 20% have the disease.15 Theories regarding level of immunocompetence and the develop­ this decline include changes in homosexual be­ ment ofthese entities. The majority of inflam­ havior, safer sexual practices, and a decrease matory dermatoses and proliferative disorders in recreational drug use. The fact that the rate occur as T-helper cell counts fall below 250/ of KS among homosexual men is decreasing mm3. It is important to recognize these prolif­ indicates that there may be some cofactor as­ erative skin disorders because, in addition to sociated with the homosexual lifestyle that in­ being associated with morbidity, these diseases fluences the development of KS. Cytomega­ reflect the level
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