[Agranulocytosis in acute hepatitis B in an HIV seropositive patient]. / Agranulocytose au cours d'une hépatite B aiguë chez un patient séropositif pour le VIH.

BACKGROUND: During the course of acute hepatitis B, hematology disorders are common though they are generally mild and occur early. Agranulocytosis is exceptional and occurs late in the disease course. CASE REPORT: We report a case of agranulocytosis which developed 3 weeks after onset of acute hepatitis B in an HIV-positive patient. Peripheral and central hematological disorders led to the diagnosis. Agranulocytosis developed during the cytolytic phase of the primary hepatitis B infection and regressed after administration of hematopoietic growth factors. DISCUSSION: It is sometimes difficult to establish the causal effect of hepatitis B in the development of agranulocytosis in patients with an HIV co-infection who are on a multiple drug regimen and subject to multiple bacterial, viral or parasite infections.

Pneumocystis carinii pneumonia in the course of connective tissue disease: report of 34 cases.

OBJECTIVE: To determine the circumstances, the clinical features and the outcome of Pneumocystis carinii pneumonia (PCP) in human immunodeficiency virus (HIV)-free patients with connective tissue diseases (CTD). METHODS: Retrospective analysis of all cases referred 10 medical units in the last 10 years. RESULTS: A total of 34 cases of PCP in patients with CTD were studied (Wegener's granulomatosis, n = 12; systemic lupus erythematosus, n = 6; polyarteritis nodosa, n = 4; poly/dermatomyositis, n = 5; others, n = 7). The majority of patients (25/34 patients; 74%) presented PCP during the first 8 months following the diagnosis of CTD. At the time of diagnosis of PCP, most patients (32/34; 94%) were receiving corticosteroids (mean prednisone equivalent dose: 1.2 mg/kg/day) associated in 24 cases with cytotoxic agents (cyclophosphamide, n = 19; methotrexate, n = 5). Most patients were lymphocytopenic at the onset of PCP: 91% (31/34) of patients had fewer than 1.5 x 10(9)/l circulating lymphocytes and 76% (26/34) had fewer than 0.8 x 10(9)/l. The mean duration of prodromal symptoms was 6 days: this is much shorter than for AIDS associated PCP. Half the patients required intensive care for respiratory failure. Mortality was high (11/34 patients; 32%) although deaths were partly due to infections acquired in intensive care units. Among the 23 survivors, 10 (43%) received secondary prophylaxis for PCP and 13 (57%), received the usual therapeutic regimen. No relapse has been observed in either group with a mean followup of 22 months. CONCLUSION: Although rare, PCP must be considered in patients with any type of CTD and receiving cytotoxic agents and corticosteroids, particularly if they are lymphocytopenic. Thus, bronchoalveolar lavage must be rapidly performed in patients with CTD presenting with fever, pulmonary infiltrates, hypoxemia and lymphopenia.

Activities of lung NADPH-cytochrome C-reductase and of cytochrome P-450 peroxidase during the protection of rat from hyperoxic injury by polyriboinosinic acid-polyribocytidilic acid.

Rats exposed to normobaric oxygen received a single i.p. injection of 2.5 mg/kg of poly I: poly C at various times (-120 to +36 h) before and after the beginning of oxygen exposure. Hyperoxic lung damage and modifications in cytochrome P-450 system components were evaluated. Our results confirmed the protective effect of poly I: poly C on rats exposed to oxygen, reducing the lung edema and the mortality. This effect was only observed when poly I: poly C was injected 48 or 36 h before the beginning of oxygen exposure. Although oxygen exposure per se decreased the total level of lung cytochrome P-450, poly I: poly C per se induced a deeper decrease to levels similar in air- or oxygen-exposed rats. Poly I: poly C did not modify the NADPH-cytochrome c reductase level nor the cytochrome P-450 peroxidase activity in air-exposed rats. The oxygen exposure induced a decrease of these two enzymes, either in the absence or in the presence of poly I: poly C, except when poly I: poly C was injected 48 or 36 h before the beginning of oxygen exposure, times at which poly I: poly C restored the enzymatic values measured in rats exposed to air. Because the times of injection of poly I: poly C were those at which the protective effect was observed, it suggested that the protective effect of poly I: poly C against oxygen toxicity was associated with a lack of oxygen-induced decrease of both the lung NADPH-cytochrome c reductase level and the lung cytochrome P-450 peroxidase activity.