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Biomedical subjects

B Rueff

Publications and source records attributed to B Rueff.

At least 37 records · Page 2Linked to original sources
PubMed1990

[Prevalence of alcoholic diseases. At a teaching hospital of the Paris suburbs].

During the last 15 days of January 1989, the 757 patients admitted for more than 48 hours in any of the departments of Hôpital Beaujon (Clichy) were investigated for diseases that were certainly or probably related to alcoholism, and in order to detect drinkers at high risk, the amount of alcohol consumed in a week was recorded. The prevalence of alcohol-related diseases was 14.7 per cent (range: 12.2 per cent-17.2 per cent) and that of alcohol consumers at high risk was 4.2 per cent (range: 2.8 per cent-5.6 per cent).

Adult↗
PubMed1989

[Detection of alcoholic patients using the systematic CAGE autoquestionnaire. In out patients].

A French adaptation of the CAGE questionnaire was used as a self-administered test in 200 outpatients (heart clinic 100, gastroenterology clinic 100) from a French University Hospital. People with two positive items or more were regarded as potential "alcoholics", i.e. indulging in excessive alcohol consumption without being alcohol-dependent. With a 9.5 per cent prevalence of "alcoholics", 95.5 per cent of out-patients were correctly classified.

Adult↗
PubMed1989

Portal hypertension and ascites in acute hepatitis: clinical, hemodynamic and histological correlations.

We attempted to ascertain the mechanism of portal hypertension and ascites complicating acute hepatitis in 66 patients who underwent transvenous liver biopsy and measurement of hepatic venous pressure gradient. Increase in hepatic venous pressure gradient was related to the severity of acute hepatitis, as indicated by the significant correlation between the values for hepatic venous pressure gradient and serum bilirubin, serum albumin or coagulation factor V, and by its higher value in patients with, than in patients without, encephalopathy. Hepatic venous pressure gradient was higher in patients with, than in patients without, ascites (12.5 +/- 3.4 vs. 8.4 +/- 3.6 mmHg, respectively; p less than 0.001). No ascites was clinically detectable in the patients in whom hepatic venous pressure gradient was below 6 mmHg. We tested the hypothesis that sinusoidal collapse due to liver cell dropout was a major factor in portal hypertension. Semiautomatic determination of the fractional area of sinusoidal collapse on chromotrope-stained sections and automatic measurement of Sirius red-stained collagen fiber density were performed. Hepatic venous pressure gradient significantly correlated with fractional sinusoidal collapse area (r = 0.61, p less than 0.001) and with Sirius red-stained collagen fiber density (r = 0.43, p less than 0.01). We conclude that portal hypertension in the course of acute hepatitis is related to the severity of liver damage and is a major factor in the development of ascites. Portal hypertension is mainly determined by intrahepatic vascular space being reduced by the collapse of sinusoids.

Acute Disease↗
PubMed1989

Successful endoscopic obturation of gastric varices with butyl cyanoacrylate.

In 27 patients who had bled from esophagogastric varices, large-sized and/or actively bleeding gastric varices were endoscopically obturated with the tissue adhesive butyl cyanoacrylate. Active bleeding was stopped in six patients. Rebleeding occurred in 10 patients; in four patients, rebleeding was due to ruptured gastric varices, occurred early and was successfully treated by reinjection of gastric varices; in one patient, rebleeding was attributed to ulceration on an injected gastric varix. Eight patients died: two of rebleeding (from esophageal varices or undetermined source), four of sepsis and/or liver failure and two at home of undetermined cause. No specific complication due to injection of gastric varices was observed. The results obtained in this series of patients with gastric varices obturated by injection of butyl cyanoacrylate are much more satisfactory than those obtained in previously published series of patients with gastric varices treated by injection of sclerosants.

Adult↗
PubMed1989

Fatal liver failure due to disulfiram.

We present the case of a 30-year-old man with disulfiram-induced hepatitis complicated by fatal liver failure. The disease followed a protracted course with an interval of 25 days between the onset of jaundice and the onset of encephalopathy. In this patient, the severity of the liver disease might have been due to reingestion of disulfiram shortly after the onset of jaundice.

Acute Kidney Injury↗
PubMed1989

A randomised controlled study of propranolol for prevention of recurrent gastrointestinal bleeding in patients with cirrhosis.

74 cirrhotic patients with a history of variceal or gastric bleeding were randomly assigned to treatment with propranolol (40 to 360 mg/day) or placebo. The patients were all in good condition and doses of propranolol were titrated until a 25% reduction in heart rate was achieved. After 2 years, the cumulative percentage of patients free from rebleeding was significantly greater among the patients receiving propranolol (79%) than in the placebo group (32%; p less than 0.0001). Similarly, the percentage of surviving patients was significantly greater with propranolol (90%) than with placebo (57%; p less than 0.02) after 2 years. It was concluded that in cirrhotic patients in good condition, propranolol reduced both the risk of recurrent gastrointestinal haemorrhage and the mortality rate during a 2-year period of continuous administration of the drug.

Adult↗
PubMed1989

[Polyuria and polydipsia in acute fatty liver of pregnancy. Discussion based on a case].

We report the case of a 25-year-old nullipara in whom polyuria and polydipsia occurred 8 weeks before the first symptoms of acute fatty liver of pregnancy and disappeared a few days after delivery. This time course suggests that polyuria and polydipsia were closely related to acute fatty liver of pregnancy. Thus, this diagnosis should be envisaged in any woman with normal blood levels of glucose and calcium, and complaining of polyuria and polydipsia in the third trimester of pregnancy.

Adult↗
PubMed1988

Chronic Q fever hepatitis complicated by extensive fibrosis.

Liver involvement is common in acute and chronic Q fever and consists of nonspecific hepatitis and granulomas without fibrosis. We report the case of a patient suffering from chronic Q fever with nonspecific hepatitis and granulomas, in whom progressive development of extensive liver fibrosis was documented by repeated biopsies.

Aged↗
PubMed1988

Liver hypermetabolism during alcohol withdrawal in humans. Role of sympathetic overactivity.

Catecholamines, which are elevated during alcohol withdrawal, can alter hepatic blood flow and increase hepatic oxygen consumption. We hypothesized that, in the withdrawal state, hepatic oxygen consumption and delivery could be altered in relation to an increased sympathetic activity. Thirteen chronic alcoholics were studied 34-72 h after withdrawal and 10 days later (control period) using conventional hemodynamic methods. As compared with the control period, splanchnic oxygen uptake was elevated at withdrawal (74.5 +/- 27.1 vs. 59.2 +/- 16.8 ml/min, p less than 0.025) and its variation was correlated with that of plasma epinephrine (r = 0.70, p less than 0.01). The hepatic venous oxygen content was reduced at withdrawal (113 +/- 22 vs. 126 +/- 21 ml/L, p less than 0.025) and correlated inversely with plasma norepinephrine levels (r = 0.56, p less than 0.01). We conclude that, during alcohol withdrawal in humans, hepatic energy expenditure may be elevated in relation to epinephrine secretion and that sympathetic overactivity may hinder the adaptive response in hepatic blood flow. The wide range in sympathetic nervous response to alcohol withdrawal could explain some differences in individual susceptibility to liver damage caused by alcohol.

Energy Metabolism↗
PubMed1988

Etiology of portal vein thrombosis in adults. A prospective evaluation of primary myeloproliferative disorders.

In a prospective study of 33 adults with portal vein thrombosis unrelated to a liver tumor, we have assessed the prevalence of primary myeloproliferative disorders using conventional criteria and cultures of bone marrow progenitor cells. A primary myeloproliferative disorder was documented in 14 patients investigated at the time of recognition of portal vein thrombosis. Among these 14 patients, the main clue to the presence of the myeloproliferative disorder was (a) the observation of suggestive abnormalities of peripheral blood cell counts in 4 patients; (b) characteristic findings at bone marrow biopsy or determination of total red cell volume in 3 patients; and (c) formation of "spontaneous" erythroid colonies in cultures of bone marrow progenitor cells in erythropoietin-poor medium in 7 patients. In 2 other patients, agnogenic myeloid metaplasia with myelosclerosis of apparently recent onset developed 5 yr after recognition of portal vein thrombosis. In conclusion, primary myeloproliferative disorders--in a full-blown or latent form, or at an early stage--are a major cause of portal vein thrombosis.

Blood Cell Count↗
PubMed1988

Quinidine phenylethylbarbiturate-induced fulminant hepatitis in a pregnant woman. A case report.

We report the case of a 19-year-old Laotian patient affected by fulminant hepatitis during the third trimester of her pregnancy after a 1-month administration of quinidine phenylethylbarbiturate. After delivery, the patient underwent orthotopic liver transplantation. The patient was in good condition 16 months after liver transplantation. Quinidine itself or phenylethylbarbiturate may be responsible for fulminant hepatitis in this patient.

Adult↗
PubMed1988

Amodiaquine-induced fulminant hepatitis.

Three patients suffered from fulminant hepatitis within 23, 59 and 22 weeks after having ingested a total dose of 16, 26 and 15 g, respectively, of amodiaquine for the prophylaxis of malaria. Amodiaquine administration was continued for 44, 21 and 25 days after the onset of jaundice, respectively. One patient underwent emergency orthotopic liver transplantation and survived. The other two died. Fulminant hepatitis threatens patients in whom amodiaquine administration is protracted for several months and not interrupted when jaundice occurs.

Adolescent↗
PubMed1988

Nadolol for prophylaxis of gastrointestinal bleeding in patients with cirrhosis. A randomized trial.

This controlled trial was designed to evaluate the prophylactic effect of nadolol on gastrointestinal bleeding in cirrhotic patients with large oesophageal varices who had never bled. Nadolol or placebo was given randomly to two groups of 53 patients. The percentage of patients free of gastrointestinal bleeding 1 year after inclusion in the study was 83 +/- 6% (mean +/- S.D.) in the nadolol group and 80 +/- 6% in the placebo group. In the nadolol and placebo groups, 40 and 47 patients, respectively, were compliant, i.e., took nadolol or placebo continuously. The percentage of patients who were free of bleeding 1 year after inclusion was 97 +/- 3% in the subgroup of compliant nadolol patients. This percentage was significantly higher than that of patients who were free of bleeding in the placebo group (P less than 0.03) as well as in the subgroup of compliant placebo patients (77 +/- 6%; P less than 0.02). We concluded that, although there was no overall significant effect of nadolol on the risk of bleeding in cirrhotic patients in good condition with large oesophageal varices, this study suggests that nadolol reduced the risk of bleeding in compliant patients.

Clinical Trials as Topic↗
PubMed1988

Portal vein thrombosis with ruptured oesophageal varices as presenting manifestation of hereditary protein C deficiency.

The protein C system is essential in limiting the activation of coagulation in vivo. We report the case of a 45 year old man with portal vein thrombosis complicated by ruptured oesophageal varices. Low concentration of plasma protein C was found in the patient and subsequently in one brother with a history of venous thromboembolism, and also in one son and one nephew who were asymptomatic. Hereditary protein C deficiency should be considered in patients with portal hypertension due to portal vein thrombosis.

Esophageal and Gastric Varices↗