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The possible etiologic agents that may cause gastrointestinal complaints in homosexually active men are multiple, and their diagnosis is complex. This article presents a logical approach to the work-up and diagnosis of gastrointestinal complaints in homosexually active men and to discuss their treatment and disease intervention.
This article describes some of the social and behavioral aspects of homosexual life styles, with particular reference to their implications for diagnosis, treatment, and continuing medical management. The cultural, psychologic, and sexual variables that may necessitate varying the management of homosexual or bisexual men compared with heterosexual men are emphasized. Areas of psychosomatic involvement, and the influence of social support and stigmatization on presentation and response, are also discussed.
Homosexual men are at risk for problems unique to their sexual orientation, and the management of even standard problems must often be altered. The recognition and management of problems related to the anorectum, breasts, and external genitalia in homosexual men are discussed.
The list of infectious agents that cause intestinal disorders in homosexual men is polymicrobial. Classic enteric pathogens, anorectal venereal pathogens, and more recently, opportunistic pathogens have been reported to occur in high prevalences in both symptomatic and asymptomatic homosexual men. This article reviews the epidemiology, clinical presentation, diagnosis, and treatment of these infections.
The case of a 44-year-old homosexual man with cryptosporidial enteritis associated with multiple opportunistic infections and increased T-suppressor cells is reported. This case calls attention to cryptosporidia as the cause of unremitting diarrhea in homosexual men with the syndrome of opportunistic infectious disease associated with acquired immunodeficiency.
Homosexual patients with persistent generalized lymphadenopathy usually show an abnormal expansion of paracortical T8+ lymphocytes relative to T4+ cells in lymph nodes with reactive follicular hyperplasia (RFH). This study was designed to characterize further the paracortical lymphocyte population in homosexual men with reactive follicular hyperplasia, because T8+ lymphocytes are antigenically and functionally heterogeneous. Frozen lymph node tissue from 10 patients was evaluated. Monoclonal antibodies to T8, Leu-15, NKH-1, Leu-7, and HLA-DR antigens were employed in the avidin-biotin complex immunoperoxidase technique. With digitized morphometry, positively stained cells for each marker were counted in five 0.145-mm2 microscopic fields. Four tonsils with RFH were used as controls. Most paracortical cells were T8+ (median, 4182 T8+ cells/five fields), and values were significantly higher than those for controls (median, 1518 T8+ cells p less than 0.006). In every case there were markedly fewer Leu 15-, NKH-1, Leu 7-, and HLA-DR-positive cells than T8+ cells (median values per five fields: Leu-15, 144; NKH-1, 12; Leu-7, 3; HLA-DR, 195). Moreover, these values were not significantly different from control values. Our findings suggest that the expanded paracortical T8+ population comprises cells with the immunophenotype of cytotoxic Leu-15-, T8+ lymphocytes, rather than natural killer or Leu-15+, T8+ suppressor cells.
Forty-five homosexual male subjects with human immunodeficiency virus (HIV) infection, who received care during a 4-month period in an ambulatory center for acquired immunodeficiency syndrome (AIDS), were classified according to their principal presentation with characteristic secondary infections (CDC group IV C, N = 28), cancers (IV D, N = 10), or limited or no symptoms (groups II, III, IV A, or IV B, N = 7). The incidence of allergic rhinitis and conjunctivitis increased after HIV seroconversion by approximately twofold in patients of groups IV C and IV D. The mean serum concentration of IgE was significantly higher for group IV C than for the other HIV-seropositive groups and for a control group of 45 HIV-seronegative homosexual male subjects from the same community who were studied concurrently. More patients in groups IV C and IV D had positive RASTs for a panel of environmental antigens than patients in the other HIV-seropositive groups and the HIV-seronegative control group. Patients with AIDS presenting with typical secondary infections thus have a high frequency of some clinical and laboratory manifestations of allergic diseases.
Four cases of Burkitt's-like lymphoma (undifferentiated, monoclonal, B-cell tumours) in homosexual men were seen in a 9-month period in San Francisco. One tumour contained both Epstein-Barr-virus nuclear antigen (EBNA) and cytomegalovirus (CMV) antigen. Another tumour contained EBNA, and a third contained no viral antigen, but EBNA and CMV antigens were detected in the overlying epithelium. This outbreak widens the array of neoplasms affecting immunosuppressed homosexual men and provides further evidence of an oncogenic role for EBV and CMV.
97 symptom-free homosexuals were studied clinically, serologically, and with in-vivo and in-vitro tests of cellular immune function in the context of the acquired immunodeficiency syndrome (AIDS). A high proportion of these men showed abnormalities: lymphopenia (33%), decreased T-helper/T-suppressor (Th/Ts) cell ratios (43%), both these abnormalities (12%), decreased total T-helper cells (15%), monocyte chemotactic (10%) and phagocytic (27%) defects, anergy to three recall antigens (32%), and anergy to purified protein derivative despite BCG inoculation (55%). The lymphocyte abnormalities and anergy characteristic of AIDS were seen in 5%. No clear clinical or serological associations were seen for the AIDS-like defects. Trends of association were seen between higher lymphocyte counts, lower Th/Ts ratios, more T-suppressor cells and serological evidence of previous virus infection. The combination of lymphocyte abnormalities and anergy observed in these symptom-free homosexuals may represent a latent phase of AIDS.
27% of 89 young, non-ill, homosexually active men in Los Angeles had a Leu-3(OKT4)/Leu-2(OKT8) ratio less than or equal to 0 . 8. The low ratio was due to a significantly raised mean number of Leu-2 cells, whereas individuals with acquired immune deficiency syndrome had a decrease in both Leu-3 and Leu-2 cells. The term "acquired immune augmentation" may be appropriate for those with a low ratio due to raised numbers of Leu-2 cells. Those practising passive (receptive) anal intercourse had a significantly higher mean number of Leu-2 cells than did those practising only active (insertive) anal intercourse or no anal intercourse. The results of this study suggest that two distinct conditions occur in homosexually active men. Whether acquired immune augmentation is a precursor of the rarer acquired immune deficiency syndrome or is an unrelated disorder needs to be determined. In this study passive anal intercourse was associated with acquired immune augmentation.
Between 1980 and 1984 28 homosexual men who had had ano-genital intercourse with patients with either acquired immunodeficiency syndrome (AIDS) or persistent generalised lymphadenopathy (PGL) were followed up. The pattern of the sexual links indicated that within this group there were two clusters, one consisting of 7 men and the other of 13.17 of the 28 contacts became ill with either AIDS or PGL; among those in the clusters, 4 died of AIDS and 11 had PGL, and of the rest 2 had PGL. 16 of the 19 men in the clusters who were tested for HTLV-III antibodies were seropositive, as were 7 of those not in the clusters. 111 men attending a genitourinary medicine clinic who had not had known contact with either AIDS or PGL patients and who were being screened for syphilis served as controls. Of these, 19/86 who were homosexual and 0/25 who were heterosexual were positive for HTLV-III antibodies. None of the 4 who died of AIDS had had contact with each other. The 2 in the first cluster seemed to have been linked by a symptomless HTLV-III-negative man, who was also probably the link between the two clusters, while in the second cluster the chief "carrier" seemed to be a seropositive man in whom PGL developed. These findings are consistent with the hypothesis that HTLV-III is the sexually transmitted causative agent of AIDS and PGL.
The prevalence of antibody to HTLV-III has increased from 3.7% (4/107) amongst unselected British homosexual men attending a London sexually transmitted disease (STD) clinic during one week in March, 1982, to 21% (26/124) in those attending during one week in July, 1984. Seropositive men had a significantly higher prevalence of infection with hepatitis B virus than did seronegative men. 82% (27/33) of the seropositive men in 1984 were symptomless or had only local genito-urinary symptoms referable to the STD for which they were attending. The evidence suggests that HTLV-III was initially an imported but is now an endemic sexually transmitted agent. As of July, 1984, at least 2600 homosexual men in London would probably have been infected.
Cells from the anorectal mucosa of 61 homosexual men were examined microscopically for evidence of papillomavirus infection and dysplastic changes. There was cytological evidence of dysplasia with concomitant features of human papillomavirus (HPV) infection on at least one occasion in 24 men and of papillomavirus infection without dysplasia on at least one occasion in a further 26: dysplasia was present for over one year in 9 of 14 men who were re-examined. Dysplasia was associated with a history of anal warts, frequent receptive anal intercourse, presence of serum antibody to human immunodeficiency virus (HIV), and immune dysfunction as judged by a low CD4/CD8 ratio, but not with the lifetime number of sexual partners. The association of longlasting dysplasia with anti-HIV was independent of the association with immune dysfunction. Thus infection of anorectal mucosal cells with papillomavirus seems to be frequent among homosexual men and may predispose to dysplasia.
14 of 280 young, sexually active men with acute urinary symptoms had pronounced bacteriuria--13 with Escherichia coli and 1 with Staphylococcus saprophyticus. 12 of the 14 bacteriuric men were homosexual or bisexual, compared with 3 of 22 non-bacteriuric control patients. Pyuria and symptoms of cystitis were more common in the bacteriuric men, and these men frequently had a urethral discharge on examination, and non-gonococcal urethritis on gram stain of the discharge. The E coli strains causing cystourethritis in these men showed properties previously associated with acute-urinary-tract infection in women, including O serotype, haemolysin production, mannose-resistant haemagglutination of human erythrocytes, and P-fimbriation. Sexually active homosexual men are a newly identified group at increased risk of acute urinary-tract infection, and E coli may contribute to non-gonococcal urethritis in this population.
The prevalence of antibody against human immunodeficiency virus (anti-HIV), which rose among British homosexual/bisexual men attending a London sexually-transmitted-disease clinic from 3.7% (4/107) in March, 1982, to 21% (26/124) in July, 1984, was 18.1% (17/94) in April/May 1985, 24.5% (61/249) in January, 1986, and 25.3% (25/99) in November/December, 1986. This slower rise in anti-HIV prevalence coincided with a fall in the annual gonorrhoea rate from 15.3% in 1982 to 5.1% in the first half of 1986 in the same male homosexual clinic population. Over the same period a reduction in the number of sexual partners and a change to safer sexual practices has been documented among homosexual and bisexual men taking part in a prospective study of the natural history of HIV infection. These data support the value of continuing preventive efforts to control viral spread in the absence of an effective vaccine or therapy.
BACKGROUND: In the Netherlands a nationwide study has shown that, in 38% of deaths, there have been medical decisions concerning the end of life (MDEL); 2.1% of all deaths were brought about by euthanasia or physician- assisted suicide (PAS). We investigated the incidence of MDEL in homosexual men with AIDS, suspecting that it might be higher, and studied the effect of euthanasia/PAS on survival time. METHODS: The patients were 131 male homosexual participants in a cohort study in Amsterdam, diagnosed between 1985 and 1992 as having AIDS; all had died before Jan 1, 1995. Clinical and laboratory data and information on mode of death were obtained from their physicians and by review of hospital records. Those who died by euthanasia/PAS or in whom there had been other MDEL were then compared with those who died naturally. FINDINGS: 29 men (22%) had died by euthanasia/PAS and in 17 (13%) another MDEL had been made; thus, more than one-third of these men had made medical decisions concerning the end of life. The greatest difference between the groups was in age at time of diagnosis-72% aged 40 or more in the euthanasia/PAS group compared with 38% in the natural death group. The likelihood (relative risk) of euthanasia/PAS increased with duration of survival after AIDS diagnosis. Comparison of the groups in terms of three laboratory markers (CD4+ and CD8+ cells and phytohaemagglutinin responses) in the two years before death, and estimates of these markers at the time of death, did not indicate any substantial shortening of life by euthanasia/PAS; in the judgment of the physicians, most of these patients would have died naturally within one month. INTERPRETATION: A possible reason for the high incidence of MDEL in this cohort was a good knowledge of the characteristics of AIDS acquired through long-term awareness of HIV infection. The higher rate of euthanasia in those with long survival from AIDS diagnosis could reflect either additional suffering or the greater opportunity to discuss this option with friends and physicians. Our findings indicate that euthanasia and other MDEL did little to shorten life; rather, they were an extreme form of palliation, applied in the terminal phase of a lethal disease.
The future design of controlled trials of antiviral therapy which might include homosexual hepatitis B virus (HBV) carriers requires base-line data on the spontaneous rate of loss of HBeAg and the prevalence of human T-lymphotropic virus III (HTLV-III/LAV) infection. Fifty-one untreated HBsAg and HBeAg-positive homosexual HBV carriers were followed for a median HBeAg-positive time of 23.5 months (range 6-85.5). Ten lost HBeAg, giving an annual rate of spontaneous loss of HBeAg of 10%. This rate is considerably higher than the apparent rate in a previous report and has considerable implications for the interpretation of previous, and the design of future, controlled trials in this population. A rapid rise in the prevalence of anti-HTLV-III/LAV amongst HBV carriers was demonstrated from 1981 such that by 1984 over 60% of HBV carriers were anti-HTLV-III-positive. HBV-DNA polymerase levels were not significantly different in asymptomatic anti-HTLV-III/LAV-positive compared to anti-HTLV-III/LAV-negative HBV carriers. Nevertheless, since chronic HTLV-III/LAV infection in its later stages may potentiate HBV replication, it is a factor that will need to be considered together with many others in any trial stratification procedure.
A recent outbreak of disseminated Kaposi's sarcoma has been recognized in homosexual men in New York, San Francisco, and Los Angeles. Biopsy specimens of skin lesions were obtained from nine of these homosexual men in Los Angeles and San Francisco. T lymphocyte subset antigens, factor VIII-related antigen, and HLA-Dr antigen were evaluated in situ in frozen sections using immunoperoxidase technics. Factor VIII-related antigen and HLA-Dr antigen were present on tumor cells, supporting a vascular endothelial origin of this neoplasm. Langerhans cells and T lymphocytes were present in numbers similar to that of normal skin in skin specimens from seven patients with Kaposi's sarcoma with visceral dissemination, but were increased in specimens from two patients with only cutaneous involvement.