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Objective: To determine risk factors for the development of pneumothorax in patients with the acquired immunodeficiency syndrome (AIDS)., Design: Prospective cohort study., Setting: Tertiary care center., Patients: Of 1030 patients with AIDS who were followed at Memorial Sloan-Kettering Cancer Center between 1 January 1980 and 30 September 1989, 20 (2%) developed pneumothorax that was unrelated to trauma or a pulmonary procedure., Results: Of 20 patients with AIDS who presented with pneumothorax, 19 had compelling evidence of concurrent Pneumocystis carinii pneumonia. Using bivariate analysis, patients receiving aerosol pentamidine prophylaxis (relative risk, 17.6) and those with a history of P. carinii pneumonia (relative risk, 14.5) were more likely to develop pneumothorax. By Mantel-Haenszel stratified analysis, aerosol pentamidine use was a statistically significant risk factor independent of a history of P. carinii pneumonia. The pneumothorax-related mortality rate was 10% and there was considerable morbidity., Conclusions: Patients with AIDS at the highest risk for developing pneumothorax are those with a history of P. carinii pneumonia who are receiving aerosol pentamidine prophylaxis but who nevertheless develop P. carinii pneumonia. The benefits of aerosol pentamidine prophylaxis in these patients far outweigh this risk. Pneumocystis carinii pneumonia should be considered as the most likely diagnosis in any patient with AIDS who develops a pneumothorax.

Objective: To evaluate safety, tolerance, and potential efficacy of interferon-alpha and zidovudine combination therapy in patients with Kaposi sarcoma and the acquired immunodeficiency syndrome (AIDS)., Design: Open, phase-I study with randomization between two preparations of interferon-alpha., Setting: Outpatient clinic of a cancer research center., Patients: Forty-three patients with Kaposi sarcoma associated with AIDS., Interventions: Patients were treated with interferon-alpha, 4.5, 9, or 18 million U/d, and zidovudine, 100 or 200 mg orally every 4 hours., Measurements and Main Results: Neutropenia was the major dose-limiting toxicity. Fatigue, liver enzyme elevation, anemia, and thrombocytopenia were dose-limiting in some patients. Maximum tolerated dosages for interferon-alpha 2a with zidovudine, respectively, were 4.5 million U/d with 200 mg every 4 hours or 18 million U/d with 100 mg every 4 hours. An interferon-alpha n1 [corrected] dosage of 9 million U/d with zidovudine dosages of either 100 or 200 mg every 4 hours induced dose-limiting toxicity in most patients. Of 37 evaluable patients, 17 (46%; 95% CI, 30% to 62%) showed complete or partial tumor regression. Antitumor effects occurred more frequently in patients with baseline CD4 counts above 200 x 10(6) cells/L (65%) than in patients with lower baseline counts (30%, P = 0.05). Effects on CD4 cells were related to both initial CD4 count and interferon dose. Increased skin test reactivity and decreased serum human immunodeficiency virus (HIV) p24 antigen and virus recovery from blood cells were seen., Conclusions: Combined therapy with interferon-alpha and zidovudine can be safely administered to patients with AIDS and Kaposi sarcoma. The observed effects on tumor growth, HIV replication, and immune function support further studies of the combination in patients at various stages of HIV infection.

Central-nervous-system toxoplasmosis developed in 7 of 269 patients with the acquired immunodeficiency syndrome reported to the New York City Health Department through July 1982. Focal neurologic abnormalities, mass lesions on computed-tomographic brain scans, lymphocytic cerebrospinal fluid pleocytosis, and detectable IgG antibody to Toxoplasma gondii were common; but IgG titers of 1:1024 or more, IgM antibody to T. gondii, and positive open brain biopsies were uncommon. Serologic findings suggested that the disease resulted from recrudescent rather than primary infection. Four of five patients improved when treated with sulfonamides and pyrimethamine, but 2 had relapses. An aggressive diagnostic approach and sometimes even empiric therapy are warranted when central-nervous-system toxoplasmosis is suspected in a seropositive patient with the acquired immunodeficiency syndrome.

Defects in T-cell function have been seen in patients with the acquired immunodeficiency syndrome. Although the cellular immune system plays a key role in host defense against Salmonella, there have been no detailed reports of salmonellosis in patients with this syndrome. We report our experience with salmonella infections in six patients. Salmonellosis in these patients was unusually severe, characterized by widespread infection, bacteremia, and relapse, despite standard antibiotic treatment. Because of the difficulty in eradicating salmonella infection in patients with the acquired immunodeficiency syndrome, long-term suppressive treatment with antibiotics seems warranted.

Forty-nine episodes of bacteremia and fungemia occurred in 38 of 336 patients with the acquired immunodeficiency syndrome seen at our institution since 1980. There were five types of infections. Infections commonly associated with a T-cell immunodeficiency disorder comprised 16 episodes and included those with Salmonella species, Listeria monocytogenes, Cryptococcus neoformans, and Histoplasma capsulatum. Infections commonly associated with a B-cell immunodeficiency disorder included those with Streptococcus pneumoniae and Haemophilus influenzae. Infections occurring with neutropenia were caused by Pseudomonas aeruginosa, Staphylococcus epidermidis, and Streptococcus faecalis. Other infections occurring in the hospital were caused by Candida albicans, Staphylococcus epidermidis, enteric gram-negative rods, Staphylococcus aureus, and mixed S. aureus and group G streptococcus. Other infections occurring out of the hospital included those with S. aureus, Clostridium perfringens, Shigella sonnei, Pseudomonas aeruginosa, and group B streptococcus. Because two thirds of the septicemias were caused by organisms other than T-cell opportunists, these pathogens should be anticipated during diagnostic evaluation and when formulating empiric therapy.

Eighteen episodes of community-acquired bacterial pneumonia were diagnosed in 13 patients among 336 with the acquired immunodeficiency syndrome (AIDS) cared for at Memorial Sloan-Kettering Cancer Center since 1979. Bacterial pathogens isolated in 16 of 18 episodes were Haemophilus influenzae in 8, Streptococcus pneumoniae in 6, group B streptococcus in 1, and Branhamella catarrhalis in 1. Eight episodes were presumed Pneumocystis carinii pneumonia until cultures obtained at bronchoscopy confirmed a bacterial cause. Specific antibacterial therapy was curative in 16 of 18 episodes; 2 patients died. Given an estimated yearly incidence of pneumococcal pneumonia in the general population of 2.6/1000, 1.09 cases were expected in our patients with AIDS; we saw 6 (p = 0.001), for an attack rate of 17.9/1000. Bacteria associated with B-cell defects should be anticipated when formulating empiric antibiotic therapy, pending a definitive diagnosis, for pulmonary infiltrates in patients with AIDS.

The microorganisms that regularly infect patients with the acquired immunodeficiency syndrome (AIDS) have become well recognized. Most take advantage of defects in T-lymphocyte function, but others, such as Streptococcus pneumoniae and Haemophilus influenzae, take advantage of B-cell defects. Still others, such as Staphylococcus aureus and Shigella species, occur or persist for reasons that are unclear. Infections with organisms associated with hospitalization and medical procedures are also seen and should be anticipated. Among the infections taking advantage of T-cell defects, Pneumocystis carinii pneumonia is the most commonly diagnosed, but cytomegalovirus infection may be equally common. Disseminated Mycobacterium avium-intracellulare infection has been found in one half of our patients at postmortem examination. The retrovirus responsible for AIDS commonly infects the central nervous system, as does Toxoplasma gondii. Although candida infections are common, dissemination is uncommon. Many of the infections respond to appropriate therapy but tend to recur when treatment is stopped. Often treatment courses must be prolonged even beyond those used in other immunocompromised hosts.

Disseminated infection with Mycobacterium avium complex developed in 67 patients with the acquired immunodeficiency syndrome (AIDS) who were followed at Memorial Sloan-Kettering Cancer Center. Twenty-nine patients were treated with two or more antimycobacterial drugs for a mean of 6 weeks, and 7 patients received therapy for less than 1 month. Most patients received ansamycin, clofazimine, and ethionamide or ethambutol. Clinical improvement did not occur in treated patients, and microbiologic cure was never obtained. Mycobacterial bacteremia persisted in 24 of 26 treated patients. Colony counts of M. avium complex in sequential blood cultures decreased in 3 patients. Every autopsied patient with M. avium complex infection diagnosed before death, whether treated or not, had disseminated M. avium complex infection at autopsy.