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The acquired immunodeficiency syndrome (AIDS) is characterized by frequent infections, and the most common of which is pneumonia caused by Pneumocystis carinii. Some patients with P. carinii pneumonia develop a complication known as pneumothorax, in which air collects within the chest cavity, causing at least partial collapse of the lung. A study of AIDS patients with P. carinii pneumonia was performed to assess the frequency of pneumothorax and the predisposing factors to this condition. Of 1,030 AIDS patients with probable P. carinii pneumonia, 20 (2 percent) developed pneumothorax spontaneously. Patients who had experienced previous episodes of P. carinii pneumonia had a significantly increased risk of developing pneumothorax compared with patients experiencing their first bout of pneumonia. Additionally, those patients who were receiving an aerosolized form of pentamidine, an anti-Pneumocystis drug, were also found to have a greater risk for pneumothorax. Pneumothorax carries greater morbidity for AIDS patients than for others. Typically, the AIDS patients required chest tubes to correct the pneumothorax for 20 days, rather than the average three to four days. Chest tube therapy was adequate for only 4 of the 20; 5 needed surgical correction, and 11 underwent sclerotherapy, in which drugs are injected into the chest cavity to form scar tissue and seal the air leaks that caused the pneumothorax. Of the 20 patients who developed spontaneous pneumothorax, 19 had clear evidence of ongoing P. carinii pneumonia, despite the use of pentamidine by 18 of these patients. Interestingly, patients who developed pneumothorax tended to survive AIDS approximately 150 days longer than average AIDS patients, suggesting that their extended survival permitted them the opportunity to develop this complication. Based on these data, treating any AIDS patient who develops a spontaneous pneumothorax as if he had P. carinii pneumonia is prudent. (Consumer Summary produced by Reliance Medical Information, Inc.)

The effectiveness, safety, and patient tolerance of interferon-alpha and zidovudine in combination were assessed among 43 patients with Kaposi sarcoma and acquired immunodeficiency syndrome (AIDS). Kaposi sarcoma consists of malignant lesions affecting the skin and other body sites, most likely resulting from the decreased immune function of the patient. In this study, the toxic effects of the combined interferon-alpha and zidovudine regimen included: neutropenia, a decrease in neutrophils, a type of white blood cell; fatigue; elevated liver enzyme levels; anemia; and thrombocytopenia, a reduction in platelets, which are blood cells involved in clotting. The development of these toxic effects was related to the dose of the drugs. The largest doses of the medications that could be tolerated were determined. Among 37 patients who could be evaluated, 17 showed complete or partial regression of the Kaposi tumor. The levels of CD4 cells, a type of immune cell that is particularly vulnerable to the AIDS virus, serve as an indicator of disease activity. The medications were more effective among patients with baseline (before treatment) CD4 counts above 200 million cells per liter than patients with lower counts. The effects of the antiviral agents on CD4 cells were related to the initial CD4 count and the dose of interferon. The combined drug regimen decreased the levels of p24 antigen, the portion of the AIDS virus that causes an immune response, and the amounts of virus isolated from the blood. The results show that interferon-alpha combined with zidovudine can be safely used to treat patients with Kaposi sarcoma and AIDS. The effects of the drug combination on Kaposi tumor growth, replication of HIV, and immune function indicate that further investigation of this regimen is warranted; patients at various stages of HIV infection should be studied. (Consumer Summary produced by Reliance Medical Information, Inc.)

Infection by the protozoan Trypanosoma cruzi is common in Latin America but not in the United States. Immunocompromised individuals are especially vulnerable to this infection. A case is described of severe Chagas disease, or Trypanosomiasis, in an 11-year-old child with Hodgkin disease. The child had never travelled to an endemic area and the infection was eventually traced to a transfusion of platelets the patient had received. The blood donor was an asymptomatic Bolivian immigrant with chronic T. cruzi infection. The patient, who had been in remission from Hodgkin for almost one year after a splenectomy, radiotherapy and chemotherapy treatments, experienced fever and abnormal blood counts. Chemotherapy was resumed and a bone marrow biopsy was performed. The patient's condition continued to deteriorate and he developed fever, a drop in blood pressure, mild cardiac failure and tremors. A peripheral blood smear was taken which revealed T. cruzi and therapy with nifurtimox at a dose of 25 mg per kg body weight was begun. The child continued to worsen and he was given interferon-gamma. A positive reaction was observed on day seven, and after 20 days of interferon-gamma, along with 120 days of nifurtimox therapy, the patient had improved and all blood smears for the parasite were negative. The blood products the patient had previously received were traced to the donors, and one of the five that were located tested positive for T. cruzi. This case illustrates the importance of careful blood donor screening and it is suggested that better policies for identifying infected blood may be necessary. (Consumer Summary produced by Reliance Medical Information, Inc.)