686

We had planned a case-control study and we interviewed 13 men, from the same clinical practice as the men with KS, who were known to have had sex with other men but had no evidence of KS or HIV infection. It became clear, however, that appropriate controls would not be obtained. The men with KS were identified as being homosexual or bisexual after they were found to have KS. Because KS is linked with AIDS and homosexuality, these men may not have been openly homosexual and may not have even regarded themselves as such. If controls were selected from men who were known to be homosexual or bisexual, they may well have been more openly homosexual and more sexually active than the population from which the men with KS were drawn. Our hypothesis was that cases would report frequent sexual contacts involving exposure to faeces, but 3 men reported no history of insertive analingus, fisting, or insertive anal intercourse. Only 5 reported insertive analingus, but 9 reported receptive analingus. If KS is caused by a sexually transmitted agent, its transmission may not be limited to the faecal-oral route. These men constitute an important population for epidemiological and laboratory studies of the aetiology of this neoplasm. Division of STD/HIV Prevention, National Center for Prevention Services, Centers for Disease Control, Atlanta, Georgia 30333, USA

THOMAS A. PETERMAN

Department of Dermatology and Microbiology, New York University Medical Center

ALVIN E. FRIEDMAN-KIEN

Division of HIV/AIDS, National Center for Infectious Diseases, CDC, Atlanta

HAROLD W.

ICRF Cancer Epidemiology Unit, University of Oxford, Oxford, UK

VALERIE BERAL

JAFFE

TA, Berkelman RL, Jaffe HW. Kaposi’s sarcoma among persons with AIDS: a sexually transmitted infection? Lancet 1990; 335: 123-28. 2. Jacobson LP, Munoz A, Fox R, et al. Incidence of Kaposi’s sarcoma in a cohort of homosexual men infected with the human immunodeficiency virus type 1. J Acquir Immune Defic Syndr 1990; 3 (suppl 1): 524-31. 3. Friedman-Kien AE, Saltzman BR, Cao Y, et al. Kaposi’s sarcoma in HIV-negative homosexual men. Lancet 1990; 335: 168-69. 1. Beral V, Peterman

Use of cyclosporin for psoriasis in

HIV-positive patient SiR,-HIV selectively attacks CD4-positive T helper lymphocytes, and their numbers gradually decrease, resulting in the clinical features of AIDS. The administration of cyclosporin to such patients might therefore be contraindicated since the drug is believed to exert its immunosuppressant effect mainly by inhibiting activation of these same CD4 lymphocytes. However, a report of a transplant patient who was HIV positive and received cyclosporin for 8 years without detriment indicated that this is not necessarily so.t In HIV-positive patients who also have psoriasis the skin disease is often severe and intractable, which is paradoxical since there is evidence of an increase in activated CD4 lymphocytes in the lesions2 and the response to treatment with cyclosporin is often very good.3 Cyclosporin has generally been avoided in HIV-positive psoriatic patients and its use has not been evaluated. We report findings showing that it may be beneficial rather than harmful. A 48-year-old homosexual man had had his first attack of psoriasis in 1977 and had one hospital visit for this in 1982. Otherwise the condition had caused little inconvenience. He was known to have acquired HIV infection in 1986 during a visit to Boston. In 1988 his psoriatic lesions recurred and although at first minor were nevertheless resistant to standard topical therapy. During the next year the problem steadily worsened and he had to give up work. Several hospital admissions for intensive therapy, which included zidovudine, methotrexate, and etretinate combined with topical corticosteroids, were of marginal benefit. Such was his distress that in August, 1990, when his CD4-positive lymphocyte count was as low as 0 04 x 10/1 he was given cyclosporin in a dose of 5 mg/kg, on the basis that the effects of cyclosporin would be rapidly reversible if his skin was not improved or his general condition worsened. There was immediate benefit with rapid clearing of the

psoriatic lesions and a pronounced improvement in his wellbeing, although his CD4 count remained low. Almost complete control of his skin problem was achieved and maintained for 12 months with 200 mg cyclosporin daily, before he eventually died from neurological complications in August, 1991. No opportunistic infections occurred apart from one brief episode of oral thrush that responded to nystatin. He showed no signs of the rapid deterioration in his general condition that was initially feared would result from additional immunosuppression by cyclosporin. In this patient, in addition to unequivocal clearing of the psoriasis, there was a distinct impression of general benefit from treatment with cyclosporin. This is not the first time such an observation has been made. Striking improvement was recorded with cyclosporin in a 38-year-old patient with end-stage AIDS but later the conclusion that cyclosporin could "cure" was thought to be premature after a report of one week’s trial in six patients without controls.4 Nevertheless there is evidence that cyclosporin could be of benefit in HIV infection. Duesberg5 pointed out that less than 1 % of T lymphocytes are infected with the virus and claimed that there must be an explanation, other than straight cytotoxicity by the retrovirus, for the steady drop in CD4 lymphocytes. An autoimmune reaction against T lymphocytes triggered by the virus is one possibility. This suggestion has been lent support by the fmding that macaque monkeys inoculated with human T lymphocytes are protected from infection with SIV, a disease widely used as an animal model for HIV.6 Additionally, the HIV glycoproteins gp 120 and gp 41 may closely resemble class II MHC proteins.7 This implies that an immune reaction against HIV might crossreact with antigens expressed on activated lymphocytes, the result of which would be a steady destruction of CD4 cellsIf this proposal is correct cyclosporin could, by inhibiting activation of

lymphocytes and the beneficial in AIDS.

expression

of class II MHC

antigens,

be

Department of Dermatology, University Hospital, Queen’s Medical Centre, Nottingham NG7 2UH, UK

B. R. ALLEN

Jacobson SK, Calne RY, Wreghitt TG. Outcome of HIV infection in transplant patients on cyclosporin. Lancet 1991; 337: 794. 2. Borel JF. Mechanism of action and rationale for cyclosporin A therapy for psoriasis. Br J Dermatol 1990; 122 (suppl 36): 5-12. 3. A consensus report: cyclosporin A therapy for psoriasis. Br J Dermatol 1990; 122 (suppl 36): 1-3. 4. Walgate R. Politics of premature French claim of cure. Nature 1985; 318: 3. 5. Duesberg P. AIDS epidemiology: inconsistencies with human immunodeficiency 1.

virus and infectious disease. Proc Natl Acad Sci USA 1991; 88: 1575-79. 6. Stott EJ. Anti-cell antibody in macaques. Nature 1991; 353: 393. 7. Fleury S, Lamarre D, Meloche S, et al. Mutational analysis of the interaction between CD4 and Class II MHC: Class II antigens contact CD4 on a surface opposite the gp120-binding site. Cell 1991; 66: 1037-49. 8. Maddox J. AIDS research turned upside down. Nature 1991; 353: 297.

In-vitro activity of zidovudine against

mycoplasma SiR,—Dr Lafeuillade and colleagues (Jan 11, p 131) report that growth of mycoplasmas is inhibited by zidovudine in vitro, and the topic of mycoplasmas in AIDS has generated much debate.’ We have investigated the mycoplasmastatic or mycoplasmacidal activity of zidovudine. One of us first used the metabolism-inhibition technique 25 years ago to determine the antibiotic sensitivity of mycoplasmas2 and we have since had considerable experience of the procedureWe have therefore used this method to test the activity of zidovudine in doubling concentrations ranging from 0.01 J1g/ml to 20 j.lg/ml against Mycopbs7m fermentans (incognitus and PG18 strains), M pneumoniae, M horrrinis, and Ureaplasma urealytictan. The question of cidal or static activity did not arise for the latter three microorganisms because none of these was inhibited by the concentrations of zidovudine tested. The growth of both strains of Mfermentans was inhibited only by 20 J1.g/ml of zidovudine, but successful subculture showed that the organisms had not been killed. Why our findings do not accord with those of the French group is uncertain but we are confident of our results. We think that the failure of zidovudine to affect mycoplasma growth means that inhibition by this drug is not a factor that needs to be considered in

Use of cyclosporin for psoriasis in HIV-positive patient.

686 We had planned a case-control study and we interviewed 13 men, from the same clinical practice as the men with KS, who were known to have had sex...
180KB Sizes 0 Downloads 0 Views