Biomedical subjects
Publications and source records attributed to D Neau.
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Recombinant hepatitis B vaccine is usually well tolerated. Clinical and laboratory test manifestations with immunologic mechanisms have nonetheless been described following use of this vaccine. We retrospectively report 7 cases of thrombocytopenia occurring within 3 months (7 weeks on the average) of 1 or following injections of recombinant hepatitis B vaccine. Four boys and 3 girls, average age 12 y, were involved. Three had a history of immune thrombocytopenic purpura. Four had haemorrhagic manifestations. The haemogram showed thrombocytopenia (24 x 10(9)/l on the average) without alterations of the other lines. Infectious and immune aetiologies were excluded in all cases. The course varied after treatment by corticosteroids, high-dose intravenous immunoglobulin, or both. After describing the different manifestations subsequent to recombinant hepatitis B vaccination, we discuss post-vaccinal thrombocytopenias (vaccines in question, mechanisms) and the reality of this entity.
Relationships were sought between specific anti-HIV cytotoxic T lymphocyte (CTL) responses (against structural and regulatory proteins of the HIV-1 LAI isolate) and plasma and cellular viral loads (VLs) in 17 recently HIV-1-infected patients including 3 displaying asymptomatic primary infection (PI) followed up for 12 months. Plasma VL was correlated directly with CD8 counts and inversely with CD4 counts. Cytotoxic reactions were observed in all patients and directed mainly against structural proteins. The earliest CTL responses were against Gag and Env proteins detected in 87 and 75% of the subjects, respectively, within the first month following PI. Anti-Env and Gag cytotoxic responses were inversely correlated with the plasma VL. Reactions against the pol gene products were thought to be either less involved in or less efficient for the initial decrease of viremia. Responses against regulatory gene products were weak and variable, apart from Nef, which was recognized by half of the subjects. Neutralizing antibodies were not detected before month 3, and were found only in six patients at subsequent times. Two of three patients with asymptomatic PI had a low viral burden and either a delayed response or one limited to a few protein CTL responses, suggesting that the magnitude of the CTL response depends on the initial plasma VL. The third patient displayed viral and CTL parameters identical to those of the patients with symptomatic PI. However, two subjects with symptomatic PI exhibited similarly low plasma VL and moderate CTL responses. Overall, the results suggest that the CTL response may not be the sole factor controlling viremia.
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HIV-1 primary infection is characterized by a short high titer viremia, which rapidly declines as the immune response emerges. The role of autologous neutralizing antibodies in the decline of viral replication was evaluated in 12 patients with primary or recent HIV-1 infection. Neutralizing antibodies detected for each patient could not generally be observed before several months after isolation of the first obtained HIV isolate. The plasma viral load, as measured by quantitation of the HIV-1 RNA, underwent a global decrease during the first 6 months of the infection, but this decrease did not seem to be associated with the emergence of neutralizing antibodies. The proviral load in peripheral blood mononuclear cells, which was studied by quantitative DNA polymerase chain reaction, exhibited fluctuations and was not as well curtailed as the plasma viremia in the majority of patients.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
The authors report the case of a 16 year-old boy admitted for the seventh acute occurrence in 18 months of abdominal pain associated with hypereosinophilia. Each episode was identical in nature and receded spontaneously after 5 or 6 days. Biopsy of a fiber colonoscopically obtained specimen of small intestine was performed. The diagnosis of eosinophilic gastroenteritis was based upon an infiltration of the digestive mucosa by eosinophils, the absence of elements in favor of other types of digestive-tract disease (parasitic, allergic, hematologic, or inflammatory), and the absence or other illness outside the digestive system. However, the incidental discovery of a distal dilation of both of the patients ureters during one such episode, that disappeared with the other symptoms, raises the possibility of a bladder location as well, and thus of a hypereosinophilic syndrome. Corticoids were administered then tapered down. A relapse occurred 2 months later. Currently, he is taking 20 mg of a corticoid every other day and has presented no manifestations over the last 9 months.
Sweet's syndrome is an acute febrile neutrophilic dermatosis. Although it frequently appears as an idiopathic disorder, it may occur in association, often as presenting sign, with malignancy or more rarely with infections. We report two cases of Sweet's syndrome preceded by digestive infection due to Yersinia enterocolitica, affirmed by significant rises in serum antibody titers. Other nongastrointestinal manifestations of such infections are known, predominantly arthritis and erythema nodosum. Sweet's syndrome is a rare complication of these infections. Treatment with systemic steroids, usually effective, can be replaced by antibiotics with apparently favorable results. The search of an infectious origin should be systematic in cases of Sweet's syndrome that appear to be idiopathic.
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OBJECTIVES: Cerebral toxoplasmosis is the most frequent opportunistic infection in patients with acquired immune deficiency syndrome in France. We evaluated the effect of adding folic acid to the standard treatment (including pyrimethamine) on preventing induced cytopenia in order to determine the optimal dose. METHODS: From January to September 1990, pyrimethamine (50 mg 3 times per week) was given as primary prophylaxis against toxoplasmosis to 30 patients who were positive for human immunodeficiency virus (CDC classes II or II, CD4 counts < 200/mm3). The patients were randomly divided into three groups given 5, 25 and 0 mg folic acid 3 times per week. Associated treatments were the same in all patients (zidovudine 600 mg/d, pentamidine isethionate aerosol, 300 mg, once a month). Blood cell counts and lymphocyte subset counts were made on days 0, 30, 90 and 180. RESULTS: Two patients were lost to follow-up and between day 90 and 180, 3 were excluded due to other opportunist infection and 1 due to zidovudine induced anaemia. Between the groups, there was no difference in haemoglobin level or cell counts on day 0. No haematologic toxicity was observed at day 90. Haemoglobin was significantly reduced in the control group (0 mg folic acid) on day 180 (mean haemoglobin on day 180, 13.8, 13.1 and 12.1 g/dl in groups 1, 2 and 3 respectively). No variation in polynuclear neutrophil counts was observed. CONCLUSION: These findings suggest that folic acid has a moderate beneficial effect on preventing haematologic disease in patients treated with pyrimethamine. There was no observed dose effect.
Three cases of long QT-interval due to halofantrine were documented in 1992 in France. Two of them had a congenital long QT-interval (Romano-Ward syndrome). We performed a prospective study of cardiac monitoring in 20 patients taking halofantrine. Minimal ECG changes were noted with lengthening of the QT-interval. Systematic ECG is necessary before giving halofantrine.
Human Parvovirus B19 (PB19) may cause joint manifestations. We report eight cases of polyarthritis associated with PB19 IgM: six cases of acute polyarthritis spontaneously resolving within a few days, and two other cases suggesting that PB19 should be responsible for accutisation of chronic disease (lupus with Kikuchi's disease and HLA B27 related arthritis).
Gaucher's disease is a sphingolipidosis transmitted as an autosomal trait. Bone lesions are frequent in type 1 of the disease (i.e. the adult type without neurological manifestation). We report the case of a 70-year old woman suffering from spinal lesions with vertebral collapse and spinal cord compression. Our diagnosis was based on the finding in bone samples of Gaucher cells looking like large macrophages, and on the enzymatic assay of glucocerebrosidase. New treatments, such as replacement of the deficient enzyme by placental glucocerebrosidase, are currently being evaluated.