A laboratory based epidemiologic study was done to determine the possible relationship of herpesvirus type 2 to carcinoma of the prostate. A total of 305 patients (224 with benign prostatic hypertrophy and 81 with prostatic carcinoma) who underwent transurethral resection of the prostate was studied. Viral cultures were obtained from urethral swabs and urine preoperatively. Prostatic tissue removed at operation was grown as tissue explants, using a monolayer cell culture technique, and examined by specific immunofluorescence and electron microscopy for evidence of herpesvirus type 2. The sera of the patients also were tested for specific antibody to herpesvirus type 2 by the indirect hemagglutination inhibition test. Although herpesvirus was not isolated 5 per cent of the patients had evidence of herpesvirus type 2 antigen in prostatic tissues by specific immunofluorescence. Electron microscopy failed to reveal the presence of viral particles. There was an increased prevalence of herpesvirus type 2 antibody in patients with carcinoma of the prostate compared to the controls with benign prostatic hypertrophy (p less than 0.05). Although marital status was similar the patients with prostatic cancer tended to marry at an earlier age, have more children, more sexual partners and more exposure to prostitutes than their counterparts with benign prostatic hypertrophy. The demonstration of specific herpesvirus type 2 antibody in patients with prostatic cancer supports an etiologic role for herpesvirus type 2 but further studies are needed to describe more definitively the relationship since the indexes of sexual activity are remarkably high in both groups.
Seventy-three immunocompromised patients with disseminated herpes zoster were evaluated in a double-blind controlled trial of acyclovir (n = 37) versus vidarabine (n = 36) therapy. Acyclovir was administered at 30 mg/kg/day at 8-h intervals and vidarabine was given as a continuous 12-h infusion at 10 mg/kg/day for 7 days (longer if resolution of cutaneous or visceral disease was incomplete). No demographic differences existed between treatment groups. No deaths attributable to varicella-zoster virus infection occurred within 1 month of treatment. Neither rates of cutaneous healing, resolution of acute neuritis, and frequency of postherpetic neuralgia nor adverse clinical and laboratory events differed between treatment groups. Acyclovir recipients were discharged from the hospital more promptly than vidarabine recipients (P = .04, log rank test). These data indicate that disseminated herpes zoster is amenable to therapy with either acyclovir or vidarabine; resultant mortality is low.
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