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Biomedical subjects

E Bercoff

Publications and source records attributed to E Bercoff.

At least 73 records · Page 4Linked to original sources
PubMed1985

Ketoconazole-induced fulminant hepatitis.

We report the cases of two adult patients in whom fulminant hepatitis developed after 17 and 103 days of ketoconazole administration. Histologic administration showed massive, predominantly centrilobular necrosis. Clinical manifestations of hypersensitivity and eosinophilia were absent in both patients, which suggests that ketoconazole hepatotoxicity is not mediated through an immunoallergic mechanism.

Adult↗
PubMed1985

[Glomerulonephritis secondary to ventriculo-atrial shunts].

The authors report the case of a 45 year old man who had undergone a ventriculo-atrial CSF shunt procedure 5 years previously for normal pressure hydrocephalus and who had several unexplained episodes of infection over a 12 months period and has now developed a mixed nephrotic syndrome associated with a septicaemia. Corynebacterium commensale and Staphylococcus epidermis were isolated from the valve culture. Ablation of the valve resulted in clinical cure with minimal functional renal sequellae. The initial renal biopsy showed type I proliferative glomerulonephritis with subendothelial deposits of complement and immunoglobulins, which did not completely regress after 3 months' evolution. The serum complement fractions suggested activation of the alternate pathway and the possible pathogenic role of circulating immune complexes.

Antigen-Antibody Complex↗
PubMed1984

Effects of propranolol on renal blood flow and renal function in patients with cirrhosis.

Systemic and splanchnic hemodynamics, renal blood flow, and renal function were studied in 13 patients with cirrhosis both before and 1 h after oral administration of 40 mg of propranolol (acute administration) and 1 mo after continuous administration of this substance at doses reducing the heart rate by 25% (chronic administration). Cardiac output and the gradient between wedged and free hepatic venous pressures significantly decreased after acute and chronic administration of propranolol; mean arterial pressure did not change significantly and systemic vascular resistance significantly increased. Renal blood flow and renal vascular resistance did not change significantly after acute administration of propranolol and renal function did not change significantly after acute or chronic administration of propranolol. We conclude that propranolol does not alter renal function in patients with cirrhosis who are in good physical condition.

Aldosterone↗
PubMed1984

Discrepancy between wedged hepatic venous pressure and portal venous pressure after acute propranolol administration in patients with alcoholic cirrhosis.

In patients with alcoholic cirrhosis, wedged hepatic venous pressure closely reflects portal venous pressure. This study was carried out to determine if propranolol-induced reductions in portal venous pressure are accurately evaluated by the measurement of wedged hepatic venous pressure. Hepatic venous cannulation and percutaneous transhepatic catheterization of the portal vein were simultaneously performed in 7 patients with alcoholic cirrhosis. One hour after oral administration of 40 mg of propranolol, wedged hepatic and portal venous pressures significantly decreased from 24.3 +/- 3.5 (mean +/- SD) to 19.0 +/- 3.0 mmHg, and from 24.7 +/- 3.9 to 22.4 +/- 3.6 mmHg, respectively. Although no significant difference was found between baseline wedged hepatic and portal venous pressures, a significant difference was found between these pressures after propranolol administration. We concluded that during acute administration of a drug acting on the splanchnic circulation, the measurement of wedged hepatic venous pressure may not provide a reliable estimation of the magnitude of the changes in portal venous pressure. There is, however, no evidence that the direction of the changes might not be adequately assessed by wedged hepatic venous pressure measurement.

Aged↗
PubMed1984

[Systemic circulatory hyperkinetic syndrome in patients with cirrhosis. Relation with hepatocellular failure and portal hypertension].

Hyperkinetic circulatory state is common in patients with cirrhosis but the cause of this syndrome has not been clearly elucidated. Systemic hemodynamic changes and their relationship to liver failure and splanchnic hemodynamics were studied in 100 patients with cirrhosis and were compared to a group of 15 patients without portal hypertension. Cardiac output was significantly higher and systemic vascular resistance was significantly lower in cirrhotic patients than in control patients. Multivariate analysis revealed that among different clinical, biochemical and splanchnic hemodynamic data, serum albumin, serum bilirubin, plasma prothrombin, and gastrointestinal bleeding significantly and independently explained the variation of cardiac output and systemic vascular resistance. No relationship was found between hepatic venous pressures or the presence of ascites and the hyperkinetic syndrome. From these results, it is concluded that in patients with cirrhosis liver failure is partly responsible for the hyperkinetic state.

Adult↗
PubMed1983

Propranolol does not further decrease the clearance of antipyrine in patients with alcoholic cirrhosis.

We determined the clearance of antipyrine before, and during, the administration of propranolol in eight male patients with alcoholic cirrhosis and a recent episode of gastrointestinal bleeding. The clearance of antipyrine in these patients was markedly reduced as compared with that in eight male, age-matched control subjects but was not further decreased after 1 month of propranolol administration. Antipyrine is the prototype of a drug with a low hepatic clearance. We suggest that the hepatic metabolism of some low clearance drugs may not be further decreased when patients with alcoholic cirrhosis are placed on propranolol therapy for the prevention of recurrent gastrointestinal bleeding.

Adult↗