HIV-Associated Pruritus MARY RUTH BUCHNESS, MD MIGUEL SANCHEZ, MD
ruritus is a common complaint in the HIV-infected patient.’ In this population, pruritus may be associated with primary skin disease, may be found with underlying systemic disease, or may be idiopathic in origin. It may be disabling enough to interfere with the quality of a person’s life, and it may be difficult and frustrating to treat. Therefore, it is important for the physician to understand the common causes of pruritus in the HIV-infected patient (Table 1) so that the underlying contributing factors can be eliminated and effective treatment instituted expeditiously. Prior to the era of HIV infection, the causes of pruritus could be classified into three groups-pruritus secondary to skin disease, usually with primary lesions present; pruritus secondary to skin disease, usually with secondary lesions only; and pruritus due to underlying systemic disease. Skin diseases with pruritic primary lesions include infestations and infections such as scabies, other insect bites (fleas, bedbugs), parasitic diseases (for example, onchocerciasis), folliculitis, varicella, dermatophytosis, noninfectious inflammatory conditions such as the papulosquamous diseases (psoriasis, atopic dermatitis, lichen planus, mycosis fungoides), lichen simplex chronicus, certain bullous diseases (dermatitis herpetiformis and bullous pemphigoid), allergic phenomena (drug eruptions, contact dermatitis, and urticaria), miliaria, sunburn, xerosis, and cutaneous mastocytosis. Pediculosis, fiberglass dermatitis, and pruritus vulvae and ani are pruritic skin diseases that may present with secondary lesions only. Generalized or localized pruritus without rash may be due to a number of systemic diseases. Chronic renal
P
From the Dermatology Service, Department of Veterans Affairs, New York, New York, and the Dermatology Department, New York University School of Medicine, New York, New York. Address correspondence to Mary Ruth Buchness, M.D., Assistant Chief of Dermatology Services, Department of Veterans Affairs, 423 E. 23rd Street, New York, NY 20010.
0 1991 by Elsevier Science Publishing
Co., Inc.
l
0738-081x/91/$3.50
failure, especially associated with hemodialysis, is the most prevalent nondermatologic cause of generalized pruriti~.~ Cholestatic liver disease, some endocrinopathies (thyroid disease, diabetes, carcinoid syndrome), internal malignancies (Hodgkin’s disease, other lymphomas, polycythemia Vera, multiple myeloma, and visceral malignancy), iron deficiency anemia, psychiatric disorders such as delusions of parasitosis, systemic parasitic infestations, and ingestion of certain drugs have all been associated with pruritu~.*~~ Pruritus associated with HIV infection may be due to any of the above diseases, some of which occur more frequently or with greater severity in the setting of HIV infection.15-” For example, “exaggerated scabies”’ has been described in four HIV-infected patients who had widespread, intensely pruritic lesions located outside of the distribution typical of scabies. We have also encountered HIV-infected patients with crusted scabies (Plates 38, 39). Xerosis is a common cutaneous finding in the HIV-infected patier@ and may be responsible for pruritus in some cases. A pruritic folliculitis due to Staphlococcus uweus has been described in patients with AIDS-related complex (ARC). l This infection responds to treatment with systemic and topical antibiotics. Lymphomas, hepatic disease, and drug eruptions are common in AIDS patients and should be considered as possible causes of pruritus in this patient population.
Pruritic Diseases Unique to HIV Infection There are some causes of pruritus that appear to be relatively specific for HIV infection. Idiopathic generalized pruritis has been described as a presenting sign of AIDS in at least one patient,’ with pruritus preceding the onset of opportunistic infections by 1 year. Multiple papular dermatoses have been described in HIV-infected patients. A characteristic eruption has been seen in 20% of 35 patients followed for HIV disease.a The
11
112
BUCHNESS
AND
SANCHEZ
Clinics in Dermatology 2991;9:221-124
Table 1. Pruritus in HIV Infection Uniquely HIV-Associated
Diseases
Eosinophilic pustular folliculitis Papular dermatosis of AIDS Ofher Causes Xerosis Atopic dermatitis Seborrheic dermatitis Psoriasis Scabies Bullous disease Drug reaction Lymphoma Liver disease Endocrinopathy
eruption consisted of hundreds of discrete skin papules measuring 2 - 5 mm, located on the head, neck, and upper trunk. The lesions were occasionally pruritic and had a waxing and waning course. Skin biopsies showed superficial perivascular infiltrates of mononuclear cells, with granulomas present in one case. A pruritic papular eruption was present in 18% of 284 hospitalized HIV-positive patients in Africa.9 The eruption was characterized by discrete, flesh-colored l2-mm papules located on the arms and legs, especially distally. Skin biopsy specimens showed epidermal spongiosis and a perivascular infiltrate consisting of mononuclear cells and occasional eosinophils. There was no response to treatment with antihistamines and topical steroid, antifungal, or antiparasitic creams. The authors note that the presence of an unexplained papular pruritic eruption is a predictor of HIV seropositivity, in that 87% of consecutive African patients referred for this type of eruption of greater than 1 month duration were HIV seropositive. The rate of seropositivity increased to 95% with the characteristic dermatitis and loss of more than 10% of normal body weight. A similar eruption consisting of pruritic papules on the lower extremities of seven AIDS patients in Florida was described.‘O The histology of the lesions was nonspecific, with a lymphohistiocytic infiltrate and occasional eosinophils. Of note is that five of the seven patients had increased circulating antibody titers to antigens in the salivary glands of a mosquito common to the area, leading to the hypothesis that these lesions represent a chronic “recall” reaction to mosquito salivary gland antigen retained in the skin. Soeprono and Schinella initially described AIDS-related eosinophilic pustular folliculitis in three patients with AIDS or ARC in 1986.” Although the morphology of the lesions was variable in the three patients, the histol-
ogy was uniform and diagnostic, with follicular spongiosis and infiltration by neutrophils and eosinophils (Plate 40). Ultraviolet B (UVB) phototherapy’* and psoralens plus ultraviolet A (PUVA)13 have been reported to be effective in the treatment of AIDS-related eosinophilic pustular folliculitis, which characteristically is extremely pruritic and may significantly interfere with the quality of an affected person’s life. This dermatitis does not respond to treatment with oral Hi receptor-blocking antihistamines, topical emollients, topical corticosteroids, topical antipruritic lotions, topical and oral antibiotics, or zidovudine. A decrease in pruritus and number and size of lesions is noted after six to nine phototherapy treatments in most cases (Plates 41 and 42), and the lesions recur on discontinuation of phototherapy.12J3 The effect of UVB phototherapy on the lesions seems to be local rather than systemic, as patients treated on one-half of the body cleared only on the treated side.14 Several therapies have been anectodally reported to help HIV-associated EPF. We have found dapsone, indomethocin, high-potency topical corticosteroids, and topical or systemic antibiotics to be generally ineffective. Antihistamines, even at high doses, frequently do not control the itching and topical lotions with menthol, camphor, or anesthetics provide minimal comfort. The etiology of AIDS-related eosinophilic pustular folliculitis is unknown. Bacteria, mycobacteria, and fungi have not been cultured from lesions or seen on histologic sections. Demodex mites have rarely been found within involved follicles. Histamine levels were normal in 12 patients tested, and direct and indirect immunofluorescence testing have not yielded consistent results.14 Onemicrometer plastic-embedded section of skin biopsy specimens from 15 patients with AIDS-related eosinophilic pustular folliculitis were studied to characterize the cellular infiltrate.14 Of note was the presence of degranulating eosinophils and degranulating mast cells in the skin of most patients studied (Plates 43 and 44), suggesting a role for these cell types in the pathogenesis of this disease. Some authors believe eosinophilic pustular folliculitis and the other papular dermatoses of HIV infection to be reaction patterns due to abnormal host responses to infectious agents, 8~11to saprophytes,” or to antigens related to insect bites.9J0 The evaluation and management of pruritus other than EPF in the HIV-infected patient is a challenge to the physician. In selected patients the history may be important, especially if the patient is on medications that could cause pruritus, has affected household members, which should lead to a search for scabies infestation or arthropods in the dwelling, or if the patient has a history of underlying systemic disease such as diabetes mellitus or
BUCHNESS AND SANCHEZ
Clinics in Dermatology 2992;9:122-114 chronic renal failure. The history may, however, be unrevealing or irrelevant, as in the case reported by Shapiro et al’ of a patient with a history of insulin-dependent diabetes mellitus for 15 years and generalized pruritus for 1 year in association with HIV infection, suggesting that HIV infection rather than diabetes was responsible for the patient’s pruritus. The physical examination may reveal primary lesions such as scabetic burrows, xerosis, or papules, but in some patients only secondary lesions will be evident. Skin biopsy may be useful even in the case of excoriated lesions because the pathologic changes in the papular dermatoses are often deep to the epidermis. In the papular dermatoses, it is important to rule out easily treatable etiologies such as pityrosporum folliculitis because in the less well understood papular dermatoses, such as eosinophilic pustular folliculitis, the patient may require more prolonged and involved treatment. Likewise, some of the more serious and life-threatening diseases, such as disseminated tuberculosis, mycobacterium avium-intercellulare or deep fungal infection can present with papular lesions.
Treatment Treatment is straightforward if there is an obvious underlying etiology in pruritic lesions in the HIV-infected patient. More commonly, the patient presents with generalized pruritus without skin lesions or with one of the papular dermatoses of unknown etiology. In these cases, an attempt should be made to treat the pruritus conservatively with emollients, topical antipruritics, and antihistamines. Conventional antihistamine dosages are usually used initially, but often must be increased to higher levels. Some patients find that they obtain sufficient relief with these measures, and occasionally a patient with eosinophilic pustular folliculitis has a spontaneous remission.14 Cases of severe pruritus, which are perceived by the patient as interfering with sleep and the activities of daily living, require treatment with phototherapy. Theoretically, the use of this modality could lead to an increase in immunosuppression, but more rapid progression of HIV infection to ARC or AIDS, or an increase in the number of opportunistic infections, has not been reportedin the literature, nor has it been the case in our experience with several dozen HIV-positive patients treated with phototherapy.
Conclusions There are many causes of pruritus in patients with HIV infection, ranging from those that have afflicted patients
113
HIV-ASSOCIATED PRURITUS
prior to the HIV era to some pruritic processes relatively specific to the HIV-infected population. With a careful history, search for lesions, and skin biopsy, the etiology of pruritus can often be determined and treated appropriately, with resultant improvement in the patient’s quality of life.
References 1. Duvik M. Staphlococcal infections and the pruritus of AIDS-related complex. Arch Dermatol 1989;123:1599. 2. Denman ST. A review of pruritus. J Am Acad Dermatol 1986;14:375-92. 3. Bernhard JD. Clinical aspects of pruritus. In Fitzpatrick TB et al (eds): Dermatology in general medicine, 3rd ed. New York, McGraw-Hill, 1987, pp 78-90. 4. Sadick N, Kaplan MH, Pahwa SG, Samgadharan MG. Unusual features of scabies complicating human T-lymphotropic virus type III infection. J Am Acad Dermatol 1986;15:482-86. 5. Farthing CF, Staughton RCD, Rowland Payne CME. Skin disease in homosexual patients with acquired immune deficiency syndrome (AIDS) and lesser forms of human T cell leukaemia virus (HTLV III) disease. Clin Exp Dermatol 1985;10:3-12. 6. Muhlemann MF, Anderson MG, Paradinas FJ, et al. Early warning skin signs in AIDS and persistent generalized lymphadenopathy. Br J Dermatol 1986;114:419 -24. 7. Shapiro RS, Samorodin C, Hood AF. Pruritus as a presenting sign of acquired immunodeficiency syndrome. J Am Acad Dermatol 1987;16:1115-17. 8. James WD, Redfield RR, Lupton GP, et al. A papular eruption associated with human T cell lymphotropic virus type III disease. J Am Acad Dermatol 1985;13:563-66. 9. Colebunders R, Mann JM, Francis H, et al. Generalized papular pruritic eruption in African patients with human immunodeficiency virus infection. AIDS 1987;1:117-21. 10. Penneys NS, Nayar JK, Bernstein H, Knight JW. Chronic pruritic eruption in patients with acquired immunodeficiency syndrome associated with increased antibody titers to mosquito salivary gland antigens. J Am Acad Dermatol 1989;21:421-25. 11. Soeprono FF, Schinella RA. Eosinophilic pustular folliculitis in patients with acquired immunodeticiency syndrome. J Am Acad Dermatol 1986;14:1020-22. 12. Buchness MR, Lim HW, Hatcher VA, et al. Eosinophiiic pustular folliculitis in the acquired immunodeficiency syndrome: Treatment with ultraviolet B phototherapy. N Engl J Med 1988;318:1183-86. 13. Gorin I, Lessana-Leibowitz M, Fortier P, et al. Successful treatment of the pruritus of human immunodeficiency virus infection and acquired immunodeficiency syndrome with psoralens plus ultraviolet A therapy. J Am Acad Dermatol 1989;20:511-13.
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14. Buchness MR, Gregory N, Lim HW, Soter NA. The role of mast cells and eosinophils in eosinophilic pustular folliculitis of the acquired immunodeficiency syndrome. Clin Res 1989;37:665A. 15. Pastore G, Santantonio T, Monno L, et al. Effects of HIV superinfection on HBV replication in a chronic HBsag carrier with liver disease. J Hepatol 1988;7:164-68.
Clinics in Dermatology 1991;9:211-114 16. Glassock RJ, Cohen AH, Danovitch G, Parsa KP; Human immunodeficiency virus and the kidney (review). Ann Intern Med 1990;112:35-49. 17. Shorrock K, Ellis IO, Finch RG. T-cell lymphoma associated with humanimmunodeficiencyvirus (HIV)infection. Histopathology 1990;16:189-91.
ruritus is a common complaint in the HIV-infected patient.’ In this population, pruritus may be associated with primary skin disease, may be found with underlying systemic disease, or may be idiopathic in origin. It may be disabling enough to interfere with the quality of a person’s life, and it may be difficult and frustrating to treat. Therefore, it is important for the physician to understand the common causes of pruritus in the HIV-infected patient (Table 1) so that the underlying contributing factors can be eliminated and effective treatment instituted expeditiously. Prior to the era of HIV infection, the causes of pruritus could be classified into three groups-pruritus secondary to skin disease, usually with primary lesions present; pruritus secondary to skin disease, usually with secondary lesions only; and pruritus due to underlying systemic disease. Skin diseases with pruritic primary lesions include infestations and infections such as scabies, other insect bites (fleas, bedbugs), parasitic diseases (for example, onchocerciasis), folliculitis, varicella, dermatophytosis, noninfectious inflammatory conditions such as the papulosquamous diseases (psoriasis, atopic dermatitis, lichen planus, mycosis fungoides), lichen simplex chronicus, certain bullous diseases (dermatitis herpetiformis and bullous pemphigoid), allergic phenomena (drug eruptions, contact dermatitis, and urticaria), miliaria, sunburn, xerosis, and cutaneous mastocytosis. Pediculosis, fiberglass dermatitis, and pruritus vulvae and ani are pruritic skin diseases that may present with secondary lesions only. Generalized or localized pruritus without rash may be due to a number of systemic diseases. Chronic renal
P
From the Dermatology Service, Department of Veterans Affairs, New York, New York, and the Dermatology Department, New York University School of Medicine, New York, New York. Address correspondence to Mary Ruth Buchness, M.D., Assistant Chief of Dermatology Services, Department of Veterans Affairs, 423 E. 23rd Street, New York, NY 20010.
0 1991 by Elsevier Science Publishing
Co., Inc.
l
0738-081x/91/$3.50
failure, especially associated with hemodialysis, is the most prevalent nondermatologic cause of generalized pruriti~.~ Cholestatic liver disease, some endocrinopathies (thyroid disease, diabetes, carcinoid syndrome), internal malignancies (Hodgkin’s disease, other lymphomas, polycythemia Vera, multiple myeloma, and visceral malignancy), iron deficiency anemia, psychiatric disorders such as delusions of parasitosis, systemic parasitic infestations, and ingestion of certain drugs have all been associated with pruritu~.*~~ Pruritus associated with HIV infection may be due to any of the above diseases, some of which occur more frequently or with greater severity in the setting of HIV infection.15-” For example, “exaggerated scabies”’ has been described in four HIV-infected patients who had widespread, intensely pruritic lesions located outside of the distribution typical of scabies. We have also encountered HIV-infected patients with crusted scabies (Plates 38, 39). Xerosis is a common cutaneous finding in the HIV-infected patier@ and may be responsible for pruritus in some cases. A pruritic folliculitis due to Staphlococcus uweus has been described in patients with AIDS-related complex (ARC). l This infection responds to treatment with systemic and topical antibiotics. Lymphomas, hepatic disease, and drug eruptions are common in AIDS patients and should be considered as possible causes of pruritus in this patient population.
Pruritic Diseases Unique to HIV Infection There are some causes of pruritus that appear to be relatively specific for HIV infection. Idiopathic generalized pruritis has been described as a presenting sign of AIDS in at least one patient,’ with pruritus preceding the onset of opportunistic infections by 1 year. Multiple papular dermatoses have been described in HIV-infected patients. A characteristic eruption has been seen in 20% of 35 patients followed for HIV disease.a The
11
112
BUCHNESS
AND
SANCHEZ
Clinics in Dermatology 2991;9:221-124
Table 1. Pruritus in HIV Infection Uniquely HIV-Associated
Diseases
Eosinophilic pustular folliculitis Papular dermatosis of AIDS Ofher Causes Xerosis Atopic dermatitis Seborrheic dermatitis Psoriasis Scabies Bullous disease Drug reaction Lymphoma Liver disease Endocrinopathy
eruption consisted of hundreds of discrete skin papules measuring 2 - 5 mm, located on the head, neck, and upper trunk. The lesions were occasionally pruritic and had a waxing and waning course. Skin biopsies showed superficial perivascular infiltrates of mononuclear cells, with granulomas present in one case. A pruritic papular eruption was present in 18% of 284 hospitalized HIV-positive patients in Africa.9 The eruption was characterized by discrete, flesh-colored l2-mm papules located on the arms and legs, especially distally. Skin biopsy specimens showed epidermal spongiosis and a perivascular infiltrate consisting of mononuclear cells and occasional eosinophils. There was no response to treatment with antihistamines and topical steroid, antifungal, or antiparasitic creams. The authors note that the presence of an unexplained papular pruritic eruption is a predictor of HIV seropositivity, in that 87% of consecutive African patients referred for this type of eruption of greater than 1 month duration were HIV seropositive. The rate of seropositivity increased to 95% with the characteristic dermatitis and loss of more than 10% of normal body weight. A similar eruption consisting of pruritic papules on the lower extremities of seven AIDS patients in Florida was described.‘O The histology of the lesions was nonspecific, with a lymphohistiocytic infiltrate and occasional eosinophils. Of note is that five of the seven patients had increased circulating antibody titers to antigens in the salivary glands of a mosquito common to the area, leading to the hypothesis that these lesions represent a chronic “recall” reaction to mosquito salivary gland antigen retained in the skin. Soeprono and Schinella initially described AIDS-related eosinophilic pustular folliculitis in three patients with AIDS or ARC in 1986.” Although the morphology of the lesions was variable in the three patients, the histol-
ogy was uniform and diagnostic, with follicular spongiosis and infiltration by neutrophils and eosinophils (Plate 40). Ultraviolet B (UVB) phototherapy’* and psoralens plus ultraviolet A (PUVA)13 have been reported to be effective in the treatment of AIDS-related eosinophilic pustular folliculitis, which characteristically is extremely pruritic and may significantly interfere with the quality of an affected person’s life. This dermatitis does not respond to treatment with oral Hi receptor-blocking antihistamines, topical emollients, topical corticosteroids, topical antipruritic lotions, topical and oral antibiotics, or zidovudine. A decrease in pruritus and number and size of lesions is noted after six to nine phototherapy treatments in most cases (Plates 41 and 42), and the lesions recur on discontinuation of phototherapy.12J3 The effect of UVB phototherapy on the lesions seems to be local rather than systemic, as patients treated on one-half of the body cleared only on the treated side.14 Several therapies have been anectodally reported to help HIV-associated EPF. We have found dapsone, indomethocin, high-potency topical corticosteroids, and topical or systemic antibiotics to be generally ineffective. Antihistamines, even at high doses, frequently do not control the itching and topical lotions with menthol, camphor, or anesthetics provide minimal comfort. The etiology of AIDS-related eosinophilic pustular folliculitis is unknown. Bacteria, mycobacteria, and fungi have not been cultured from lesions or seen on histologic sections. Demodex mites have rarely been found within involved follicles. Histamine levels were normal in 12 patients tested, and direct and indirect immunofluorescence testing have not yielded consistent results.14 Onemicrometer plastic-embedded section of skin biopsy specimens from 15 patients with AIDS-related eosinophilic pustular folliculitis were studied to characterize the cellular infiltrate.14 Of note was the presence of degranulating eosinophils and degranulating mast cells in the skin of most patients studied (Plates 43 and 44), suggesting a role for these cell types in the pathogenesis of this disease. Some authors believe eosinophilic pustular folliculitis and the other papular dermatoses of HIV infection to be reaction patterns due to abnormal host responses to infectious agents, 8~11to saprophytes,” or to antigens related to insect bites.9J0 The evaluation and management of pruritus other than EPF in the HIV-infected patient is a challenge to the physician. In selected patients the history may be important, especially if the patient is on medications that could cause pruritus, has affected household members, which should lead to a search for scabies infestation or arthropods in the dwelling, or if the patient has a history of underlying systemic disease such as diabetes mellitus or
BUCHNESS AND SANCHEZ
Clinics in Dermatology 2992;9:122-114 chronic renal failure. The history may, however, be unrevealing or irrelevant, as in the case reported by Shapiro et al’ of a patient with a history of insulin-dependent diabetes mellitus for 15 years and generalized pruritus for 1 year in association with HIV infection, suggesting that HIV infection rather than diabetes was responsible for the patient’s pruritus. The physical examination may reveal primary lesions such as scabetic burrows, xerosis, or papules, but in some patients only secondary lesions will be evident. Skin biopsy may be useful even in the case of excoriated lesions because the pathologic changes in the papular dermatoses are often deep to the epidermis. In the papular dermatoses, it is important to rule out easily treatable etiologies such as pityrosporum folliculitis because in the less well understood papular dermatoses, such as eosinophilic pustular folliculitis, the patient may require more prolonged and involved treatment. Likewise, some of the more serious and life-threatening diseases, such as disseminated tuberculosis, mycobacterium avium-intercellulare or deep fungal infection can present with papular lesions.
Treatment Treatment is straightforward if there is an obvious underlying etiology in pruritic lesions in the HIV-infected patient. More commonly, the patient presents with generalized pruritus without skin lesions or with one of the papular dermatoses of unknown etiology. In these cases, an attempt should be made to treat the pruritus conservatively with emollients, topical antipruritics, and antihistamines. Conventional antihistamine dosages are usually used initially, but often must be increased to higher levels. Some patients find that they obtain sufficient relief with these measures, and occasionally a patient with eosinophilic pustular folliculitis has a spontaneous remission.14 Cases of severe pruritus, which are perceived by the patient as interfering with sleep and the activities of daily living, require treatment with phototherapy. Theoretically, the use of this modality could lead to an increase in immunosuppression, but more rapid progression of HIV infection to ARC or AIDS, or an increase in the number of opportunistic infections, has not been reportedin the literature, nor has it been the case in our experience with several dozen HIV-positive patients treated with phototherapy.
Conclusions There are many causes of pruritus in patients with HIV infection, ranging from those that have afflicted patients
113
HIV-ASSOCIATED PRURITUS
prior to the HIV era to some pruritic processes relatively specific to the HIV-infected population. With a careful history, search for lesions, and skin biopsy, the etiology of pruritus can often be determined and treated appropriately, with resultant improvement in the patient’s quality of life.
References 1. Duvik M. Staphlococcal infections and the pruritus of AIDS-related complex. Arch Dermatol 1989;123:1599. 2. Denman ST. A review of pruritus. J Am Acad Dermatol 1986;14:375-92. 3. Bernhard JD. Clinical aspects of pruritus. In Fitzpatrick TB et al (eds): Dermatology in general medicine, 3rd ed. New York, McGraw-Hill, 1987, pp 78-90. 4. Sadick N, Kaplan MH, Pahwa SG, Samgadharan MG. Unusual features of scabies complicating human T-lymphotropic virus type III infection. J Am Acad Dermatol 1986;15:482-86. 5. Farthing CF, Staughton RCD, Rowland Payne CME. Skin disease in homosexual patients with acquired immune deficiency syndrome (AIDS) and lesser forms of human T cell leukaemia virus (HTLV III) disease. Clin Exp Dermatol 1985;10:3-12. 6. Muhlemann MF, Anderson MG, Paradinas FJ, et al. Early warning skin signs in AIDS and persistent generalized lymphadenopathy. Br J Dermatol 1986;114:419 -24. 7. Shapiro RS, Samorodin C, Hood AF. Pruritus as a presenting sign of acquired immunodeficiency syndrome. J Am Acad Dermatol 1987;16:1115-17. 8. James WD, Redfield RR, Lupton GP, et al. A papular eruption associated with human T cell lymphotropic virus type III disease. J Am Acad Dermatol 1985;13:563-66. 9. Colebunders R, Mann JM, Francis H, et al. Generalized papular pruritic eruption in African patients with human immunodeficiency virus infection. AIDS 1987;1:117-21. 10. Penneys NS, Nayar JK, Bernstein H, Knight JW. Chronic pruritic eruption in patients with acquired immunodeficiency syndrome associated with increased antibody titers to mosquito salivary gland antigens. J Am Acad Dermatol 1989;21:421-25. 11. Soeprono FF, Schinella RA. Eosinophilic pustular folliculitis in patients with acquired immunodeticiency syndrome. J Am Acad Dermatol 1986;14:1020-22. 12. Buchness MR, Lim HW, Hatcher VA, et al. Eosinophiiic pustular folliculitis in the acquired immunodeficiency syndrome: Treatment with ultraviolet B phototherapy. N Engl J Med 1988;318:1183-86. 13. Gorin I, Lessana-Leibowitz M, Fortier P, et al. Successful treatment of the pruritus of human immunodeficiency virus infection and acquired immunodeficiency syndrome with psoralens plus ultraviolet A therapy. J Am Acad Dermatol 1989;20:511-13.
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14. Buchness MR, Gregory N, Lim HW, Soter NA. The role of mast cells and eosinophils in eosinophilic pustular folliculitis of the acquired immunodeficiency syndrome. Clin Res 1989;37:665A. 15. Pastore G, Santantonio T, Monno L, et al. Effects of HIV superinfection on HBV replication in a chronic HBsag carrier with liver disease. J Hepatol 1988;7:164-68.
Clinics in Dermatology 1991;9:211-114 16. Glassock RJ, Cohen AH, Danovitch G, Parsa KP; Human immunodeficiency virus and the kidney (review). Ann Intern Med 1990;112:35-49. 17. Shorrock K, Ellis IO, Finch RG. T-cell lymphoma associated with humanimmunodeficiencyvirus (HIV)infection. Histopathology 1990;16:189-91.
