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Following a 4-year controlled trial comparing early and later zidovudine treatment, we conducted an additional 3-year follow-up. Of the original 338 patients, 275 participated. Clinical outcome measures were AIDS and death. In the early therapy group (n = 170), 67 patients progressed to AIDS compared with 85 in the later therapy group (n = 168); the relative risk (RR) comparing early with later therapy was 0.72% (95% confidence interval [CI] 0.52-0.99; p = 0.044). The early therapy group had 74 deaths compared with 73 in the later therapy (RR = 0.98; 95% CI, 0.71-1.36; p = 0.91). The early group had a peak CD4+ count increase at 1-2 months and a delay of 1 year before CD4+ counts fell below baseline. For patients who received zidovudine for more than the median duration (20.3 months) before their first AIDS diagnosis, the RR for death was 2.08 (95% CI, 1.36-3.19, p = 0.001). Additional factors independently associated with poor prognosis following AIDS were a CD4+ count of < 100 cells/mm3 and increased severity of the first AIDS diagnosis, whereas use of another antiretroviral agent was associated with improved survival. We conclude that early zidovudine therapy delays progression to AIDS but does not affect survival. Patients who progress to AIDS while on prolonged zidovudine monotherapy many benefit from a change to other antiretroviral therapy(ies).

Background. Zidovudine is recommended for asymptomatic and early symptomatic human immunodeficiency virus (HIV) infection. The best time to initiate zidovudine treatment remains uncertain, however, and whether early treatment improves survival has not been established. Methods. We conducted a multicenter, randomized, double-blind trial that compared early zidovudine therapy (beginning at 1500 mg per day) with late therapy in HIV-infected patients who were symptomatic and had CD4+ counts between 0.2×109 and 0.5×109 cells per liter (200 to 500 per cubic millimeter) at entry. Those assigned to late therapy initially received placebo and began zidovudine when their CD4+ counts fell below 0.2×109 per liter (200 per cubic millimeter) or when the acquired immunodeficiency syndrome (AIDS) developed. Results. During a mean follow-up period of more than two years, there were 23 deaths in the early-therapy group (n = 170) and 20 deaths in the late-therapy group (n = 168) (P = 0.48; relative risk [late vs. e...

Three patients with severe Pneumocystis carinii pneumonia and acquired immunodeficiency syndrome, not responding to specific therapy with trimethoprim/sulfamethoxazole, were treated with a 24-hour course of high-dose methylprednisolone. Rapid improvements in the clinical status and the chest X-rays were detected. In two of the patients, in whom lung biopsy was performed before initiation of corticosteroids, an intense interstitial mononuclear cell infiltrate was seen. In the one patient who had lung biopsy after corticosteroid therapy, a scanty amount of mononuclear cells was demonstrated in the interstitium. Our experience suggests that corticosteroids may be useful as adjunctive agents in the treatment of severe P. carinii pneumonia not responding to specific anti-Pneumocystis therapy. This may be a result of inhibition of mononuclear cell accumulation within the lung by the steroid therapy.

To the Editor.— A major complication of hemodialysis is infection of the access site. Organisms implicated in accesssite infections have included Staphylococcus aureus, Staphylococcus epidermidis, Pseudomonas aeruginosa, Streptococcus faecalis, Streptococcus viridans , a variety of gram-negative bacilli, Listeria monocytogenes , 1 and Legionella pneumophila . 2 We report a case of a hemodialysis patient with an arteriovenous-graft infection caused by Candida albicans and emphasize the importance of Gram's stain in early evaluation of access-site infections. Report of a Case.— A 67-year-old man was healthy until 1984, when bilateral ureteral obstruction with renal failure developed; maintenance hemodialysis was started. In 1986, an arteriovenous shunt using a Gortex prosthesis was created in his left arm. Two weeks after surgery the patient became confused and serous yellow material was found oozing from the surgical wound. He remained afebrile, but his white blood cell count was 17·1×10 9 /L (17 100/mm 3 ), with 0·65 (65%) neutrophils (10%