[Ultrasound-guided puncture-biopsy of the liver could replace blind puncture-biopsy in diffuse hepatopathies. Retrospective study of 1293 patients]. / La ponction-biopsie hépatique échoguidée pourrait remplacer la ponction-biopsie à l'aveugle dans les hépatopathies diffuses. Une étude rétrospective chez 1,293 patients.

OBJECTIVES: The aim of this retrospective study was to compare the efficiency and complications of percutaneous hepatic biopsy either guided by ultrasonography in the left lobe, or blindly by the intercostal route in the right lobe, in the diagnosis of diffuse liver diseases. PATIENTS AND METHODS: Liver biopsy was performed in 1,293 patients for 5 years. In group 1 (289 patients, including 140 out-patients), liver biopsy was guided by ultrasound. In group 2, blind intercostal liver biopsy was performed in 1,004 patients. Patients were observed for 6 hours after biopsy in both groups. RESULTS: The failure rate of liver biopsy was significantly lower in group 1 (1.7%) than in group 2 (9.25%, P < 0.01). The prevalence of the histological lesions was similar in both groups. No related-biopsy death occurred. Complications were more serious after blind biopsy (1 acute pancreatitis with a hematoma of the liver, 1 bile leakage around the gallbladder, 1 hemoperitonitis, 1 large intrahepatic hematoma), than after guided biopsy (1 small hematoma of the liver, 1 acute biliary pain on the 10th day). CONCLUSION: Hepatic biopsy guided by ultrasonography could replace blind biopsy in the diagnosis of diffuse liver diseases.

[Bronchial infection and brain abscess caused by Pasteurella multocida]. / Infection bronchique et abcès cérébral à Pasteurella multocida.

The authors report a case of pasteurellosis with abscess of the brain consecutive to a bronchopulmonary infection in a woman with old-standing bilateral bronchiectasis. The prevalence of respiratory infections caused by Pasteurella multocida is low, but it is certainly underestimated. Bronchial and/or pleuro-pulmonary infections occur in subjects with reduced local and/or systemic defences. The respiratory system is colonized by direct or indirect contagion, usually in contact with pet animals carrying the organism.

Assessment of asymptomatic liver fibrosis in alcoholic patients using fibroscan: prospective comparison with seven non-invasive laboratory tests.

BACKGROUND: Systematic screening for liver fibrosis in heavy-drinking patients is a challenge. Aims To assess Fibroscan for non-invasive diagnosis of asymptomatic liver fibrosis in alcohol abuse patients, to determine diagnostic liver stiffness cut-off values and to compare performance of Fibroscan with seven non-invasive laboratory tests. METHODS: One hundred and three alcoholic patients were studied. Liver fibrosis was staged by METAVIR system. Fibroscan, Fibrotest, Fibrometer, Hepascore, APRI, PGA, PGAA and hyaluronic acid tests were performed. Liver stiffness cut-offs were determined using receiver-operating characteristic (ROC) curves. RESULTS: Liver stiffness was correlated with fibrosis (r = 0.72, P < 0.014), with median at 5.7, 6.3, 8.4, 15 and 47.3 kPa for F0 (n = 8), F1 (n = 18), F2 (n = 24), F3 (n = 20) and F4 (n = 33) stage fibrosis respectively. For Fibroscan, areas under ROC curves (AUROCs) were 0.84 (95% CI: 0.73-0.95) (F > or = 1), 0.91 (0.85-0.98) (F > or = 2), 0.90 (0.82-0.97) (F > or = 3) and 0.92 (0.87-0.98) (F = 4), yielding diagnostic stiffness cut-offs of 5.9 (F > or = 1), 7.8 (F > or = 2), 11 (F > or = 3) and 19.5 (F4) kPa. Sensitivity, specificity, PPV and NPV were 80%, 90.5%, 93% and 70% for F > or = 2, and 85.7%, 84.2%, 68.6% and 87.9% for F = 4. Performance of Fibroscan was higher than seven laboratory tests, for which AUROCs ranged from 0.66 to 0.77 (F > or = 1), from 0.54 to 0.82 (F > or = 2), from 0.43 to 0.88 (F > or = 3) and from 0.56 to 0.89 (F = 4), with significant difference only vs. APRI (P < 0.001) and Hepascore (P = 0.04). Combining Fibroscan with each tests did not improve performance. CONCLUSIONS: Fibroscan is effective to assess liver fibrosis in alcoholic patients. Instant screening of liver fibrosis in heavy drinkers is feasible without liver biopsy.

Cirrhosis: a new, but expected cause of biliary sludge.

BACKGROUND/AIMS: Biliary sludge is increasingly recognized as a natural stage in gallstone formation. Logically, cirrhosis, a well-documented cause of black pigment cholelithiasis, should be another condition predisposing to the development of sludge. The aim of this study was to assess the prevalence of biliary sludge in an unselected population and to test the hypothesis that cirrhosis could be one of the causes of sludge. METHODS: We reviewed the clinical findings and ultrasonograms of 2138 patients, hospitalized or not, consecutively seen in our department between January 1993 and December 1994. Sonograms showing biliary sludge mixed with stones were excluded. Three hundred and eighty-eight of the 2138 were cirrhotic patients. RESULTS: The overall prevalence of biliary sludge was 4%. Sludge was found in 44 of 388 (11%) of the cirrhotic patients (alcoholism, n = 39; chronic viral B hepatitis, n = 3; hemochromatosis, n = 1; and cryptogenic, n = 1), compared with 42 of 1750 (2%) noncirrhotic patients (p < 0.000001). Thirteen cirrhotic patients received intravenous alimentation for 2 to 17 days, 8 were given somatostatin for variceal bleeding, and 7 have previously had 1 to 5 sessions of endoscopic sclerotherapy of esophageal varices with polidocanol. CONCLUSIONS: This study convincingly demonstrates that cirrhosis must be added to the growing list of conditions associated with biliary sludge.