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Biomedical subjects

F Lellouche

Publications and source records attributed to F Lellouche.

At least 19 recordsLinked to original sources
PubMed2006

Adults with spontaneous aerobic Gram-negative bacillary meningitis admitted to the intensive care unit.

The characteristics of spontaneous aerobic Gram-negative bacillary meningitis (AGNBM) were determined in 40 adults requiring admission to an intensive care unit (ICU) during a 16-year period in ten French ICUs. Eight infections were hospital-acquired and most patients had predisposing factors, mainly chronic alcoholism and an immunocompromised status. Three immunosuppressed patients had disseminated strongyloidiasis. Gram's stain, cerebrospinal fluid and blood cultures were positive for 85%, 98% and 80% of cases, respectively. Escherichia coli (57%) and Klebsiella pneumoniae (17%) were the most frequent pathogens. In-ICU mortality was 38%. Spontaneous AGNBM is a rare complication of bacteraemia in adults. The severity of predisposing underlying diseases might explain the poor prognosis despite appropriate antimicrobial therapy.

Adult↗
PubMed2004

Successful treatment of brain aspergillosis with voriconazole.

Until recently, brain aspergillosis was almost always fatal, with a response rate to amphotericin B of < 10%. This study describes a retrospective analysis of eight consecutive cases of brain aspergillosis. All patients were immunosuppressed and five required mechanical ventilation. Antifungal treatment included amphotericin B (n = 7), itraconazole (n = 3), voriconazole (n = 2) and flucytosine (n = 1). Three (38%) patients survived following prolonged azole therapy after initial amphotericin B treatment, combined with a reduction in their immunosuppressive treatment. The prognosis of brain aspergillosis might be improved if immunosuppression could be reduced and prolonged oral azole therapy used.

Adult↗
PubMed1998

Allele frequencies of hereditary hemochromatosis gene mutations in a local population of west Brittany.

Hereditary hemochromatosis (HH) gene mutations, C282Y and H63D, have been screened in a cohort of 254 presumably healthy persons originating from a western region of France. The carrier frequencies of these mutations and the incidence of HH have been estimated and compared with those of other studies. This cohort contains two C282Y/C282Y genotypes and has the highest C282Y heterozygosity frequency (17.46%) ever reported.

Adult↗
PubMed1993

A chronic hypercoagulable state and life-long platelet activation in beta thalassemia major.

Increased frequency of thromboembolic events has been recently observed in patients with thalassemia major (TM), causing hypoxemia and cor pulmonale. Autopsy findings demonstrated "old" and recent pulmonary and renal infarcts as well as premature atherosclerosis. Studies to determine hypercoagulability showed: impaired platelet aggregation, increased circulating platelet aggregates, shortened platelet survival, enhanced excretion of urinary metabolites of thromboxane A2 (TXA2) and prostacyclin and decreased plasma levels of Protein C, Protein S or anti-thrombin III. Erythrocytes from TM patients enhanced thrombin formation in a "prothrombinase" assay (using a chromogenic substrate). Chronic anti-thrombotic therapy may be indicated in thalassemic patients to prevent the cardiac and pulmonary complications.

Blood Platelet Disorders↗
PubMed1992

Increased production of platelet-derived thromboxane in patients with lupus anticoagulant.

The in vivo production of thromboxane A2 and prostacyclin was assessed in 31 samples from 25 patients with lupus anticoagulant and in 32 controls. The urinary excretion of 11-dehydro-thromboxane B2 (a major thromboxane metabolite of platelet origin) was very significantly increased (p less than 0.0003) in the patients contrasting with a lesser increase of urinary 2,3-dinor-6-keto-prostaglandin F1 alpha reflecting the vascular production of prostacyclin (p less than 0.02). Our study shows that in patients with lupus anticoagulant, platelet activation may occur without a compensatory increment in the vascular biosynthesis of prostacyclin suggesting an increased risk for thrombosis.

Adult↗
PubMed1991

Imbalance of thromboxane/prostacyclin biosynthesis in patients with lupus anticoagulant.

The mechanism involved in the association between antiphospholipid antibodies and thrombosis or fetal loss remains unclear. We assessed the biosynthesis of thromboxane A2 and prostacyclin in 31 samples from 25 patients with lupus anticoagulant and in 32 controls. The urinary excretion of the major thromboxane metabolite of platelet origin (11-dehydrothromboxane B2) was very significantly increased (P less than .0003) in the patients. In contrast, the urinary metabolite reflecting the vascular production of prostacyclin (2,3-dinor-6-keto-prostaglandin F1 alpha) was much less increased (P less than .02). We found no correlation between the levels of anticardiolipin antibodies and the urinary excretion of 11-dehydro-thromboxane B2. Six patients with elevated urinary 11-dehydrothromboxane B2 were treated with low-dose aspirin (20 mg/d during 7 days). In these patients, there was a close relationship between the extent of inhibition of the thromboxane urinary metabolite (72%) and serum thromboxane B2 (79%). In contrast, the urinary excretion of 2,3-dinor-6-ketoprostaglandin F1 alpha was nearly unchanged (13% reduction). In addition, the F(ab')2 fragments isolated from six patients presenting increased urinary 11-dehydro-thromboxane B2 enhanced the generation of thromboxane B2 (P = .04) and the release of 14C serotonin (P = .009) by normal washed platelets, as compared with F(ab')2 from controls. In summary, our study shows that in patients with lupus anticoagulant, platelet activation may occur without a compensatory increment in the vascular biosynthesis of prostacyclin. This observation may be crucial to cause or reflect an increased risk for thrombosis. In addition, our results may suggest a rationale for antiplatelet agents for the prophylaxis of thrombosis in many patients with the antiphospholipid syndrome.

Autoantibodies↗
PubMed1991

In vivo platelet activation in beta-thalassemia major reflected by increased platelet-thromboxane urinary metabolites.

Increased frequency of thromboembolic events has been recently observed in patients with beta-thalassemia major (TM). Platelet function anomalies including impaired aggregation, increased circulating aggregates, and our finding of shortened platelet survival indicate that platelets may be involved in the hypercoagulability in thalassemia. Consequently, we used a technique based on thin layer chromatography purification and enzyme immunoassay to measure urinary metabolites of thromboxane A2 (TXA2) and prostacyclin (PGI2) in nine splenectomized patients with beta-TM regularly transfused, five non-splenectomized patients with beta-thalassemia intermedia (TI), and 20 healthy individuals. A significant 4- to 10-fold increase was observed in the urinary excretion of 2,3-dinor-TXB2, 11-dehydro-TXB2 and 2,3-dinor-6-keto-PGF1 alpha in patients with TM and TI as compared with healthy controls. No significant differences were found in the concentrations of these metabolites between TM and TI patients. Six TM patients received a very low dose of aspirin (20 mg/day) for 7 days. A significant decrease was observed in the urinary concentrations of 2,3-dinor-TXB2 and 11-dehydro-TXB2 derived from platelets. However, the levels of urinary 2,3-dinor-6-keto-PGF1 alpha reflecting vascular production and TXB2 and 6-keto-PGF1 alpha originating from the kidney were not significantly changed. These results are consistent with those of increased in vivo production of TXA2 because of endogenous platelet activation.

6-Ketoprostaglandin F1 alpha↗