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Massive steatosis has recently been described among a few human immunodeficiency virus-seropositive patients who were receiving antiretroviral therapy. Although clinical and light-microscopic pathological findings were carefully described, no ultrastructural studies of the liver were performed in these cases. We report the light-microscopic and ultrastructural findings at autopsy of a 35-year-old woman with AIDS who developed severe lactic acidosis and hepatic failure. The patient had been receiving standard doses of zidovudine for 5 months when she was hospitalized because of the rapid onset of abdominal pain, nausea, and vomiting. The most significant findings at autopsy were massive hepatomegaly and steatosis. Ultrastructural examination of the liver and skeletal muscle showed slightly enlarged mitochondria in the liver but no mitochondrial changes in the skeletal muscle. The pathogenesis of mitochondrial toxicity associated with antiviral therapies is briefly discussed.

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Bafilomycin A(1), a selective inhibitor of V-type H(+)-translocating ATPase (V-ATPase), may be a useful adjunct in cancer chemotherapy (Altan et al. [1998] J Exp Med 187:1583-1598). Therapeutic uses of the enzyme inhibitor need to consider the agent's potential effects on normal (nontumor) cells. This study determined the effects of bafilomycin A(1) on resident alveolar macrophages (mphi). Treatment of alveolar mphi with bafilomycin A(1) (10 microM, 1 h) caused a significant decrement in cytosolic pH. This was accompanied by marked alteration of mphi bactericidal capabilities. The enzyme inhibitor caused a marginal reduction in the phagocytosis of opsonized Staphylococcus aureus and significantly suppressed intracellular killing of the phagocytosed bacteria. In keeping with the effects on intracellular killing, bafilomycin A(1) significantly reduced the production of reactive oxygen species (ROS). On the other hand, cell spreading was enhanced significantly by bafilomycin A(1). Comparable changes in ROS generation and mphi spreading were produced by altering cytosolic pH through changes in extracellular pH (pH(o)) in the absence of bafilomycin A(1). These findings suggest that the agent's effects on ROS production and mphi spreading were related to the accompanying changes in cytosolic pH. The enzyme inhibitor also altered mphi morphology, leading to the shortening of microvilli and focal loss of surface ruffles. These morphologic effects differed from those produced by altering cytosolic pH by changes in pH(o). The results demonstrate that V-ATPase activity is an important determinant of mphi functioning and structure. Therapeutic use of V-ATPase inhibitors might be expected to compromise the bactericidal activity of alveolar mphi.

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This was a cross-sectional followed by cohort type of study conducted among the pregnant mothers of second trimester in the rural areas of Rajshahi district. Initially 1800 pregnant mothers of second trimester were selected from 18 unions applying 2-stage random sampling. A total of 216 pregnant mothers with asymptomatic bacteriuria were paired among the rest of the healthy pregnant mothers (without bacteriuria) on the basis of age, gravida and economic status for cohort study to relate asymptomatic bacteriuria with the incidence of symptomatic bacteriuria, hypertensive disorders in pregnancy (HDP) and pre-term delivery. The matched paired pregnant mothers were followed monthly interval up to delivery. The prevalence of asymptomatic bacteriuria was 12% among the pregnant mothers in rural Rajshahi. E.Coli was the commonest causative agent of both asymptomatic and symptomatic bacteriuria. The results of this study suggest that asymptomatic bacteriuria were more prone to develop symptomatic bacteriuria, hypertensive disorders in pregnancy and pre-term delivery than that of the healthy mothers (without bacteriuria). Screening of bacteriuria in pregnancy and proper treatment must be considered as an essential part of antenatal care in this rural community.

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