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Biomedical subjects

B Rueff

Publications and source records attributed to B Rueff.

At least 91 records · Page 5Linked to original sources
PubMed1983

Comparison of six treatments of ascites in patients with liver cirrhosis. A clinical trial.

UNLABELLED: A national multicenter study (34 centers) compared six treatments in 328 patients with cirrhotic ascites. Excluded were patients with g.i. bleeding within the last six months, chronic encephalopathy, cancer, tuberculosis or the following complications persisting after three weeks: acute encephalopythy, fever greater than 38 degrees C, infected ascites or biochemical abnormalities: blood urea greater than 8 mmol/l, natremia less than 130 mmol/l, kaliemia less than 2.5 or greater than 5.5 mmol/l, WBC greater than 12000 mm3, total bilirubin greater than 85.5 mumol/l. In each center patients were randomized into two treatment groups, each center using 2 of 6 proposed treatments: (1) Spironolactone and 500 mg Na p.d (77 patients), (2) Spironolactone + furosemide or Moduretic (amiloride + hydrochlorothiazide) and 500 mg Na p.d (80 patients), (3) Spironolactone + Furosemide or Moduretic and unrestricted sodium diet (86 patients), (4) Concentrated ascites reinfusion and 500 mg Na p.d. (36 patients), (5) Unmodified ascites reinfusion and 500 mg Na p.d. (23 patients), (6) Slow ascites drainage and 500 mg Na p.d. (31 patients). Statistical analysis methods were X2, variance analysis and Spotvoll-Stoline and Dunn-Sidak tests. Before treatment, there was no significant difference between the 6 groups. RESULTS: After one month of treatment, no difference was found in the frequency of total or partial regression of ascites, complications of cirrhosis, mortality, acceptability of treatment. Mechanical treatments induced more rapid weight loss but more frequent recurrence; comparison of groups 2 and 3 did not confirm any benefit associated with unrestricted Na diet. Duration of treatment and hospitalization were shorter in group 4 than in groups 3 and 6.

Amiloride↗
PubMed1983

Right-sided endocarditis complicating peritoneovenous shunting for ascites.

We describe two patients with alcoholic cirrhosis in whom staphylococcal right-sided endocarditis developed after insertion of a peritoneovenous shunt (PVS). Massive pulmonary embolism caused early death in one patient. In the other patient, staphylococcal septicemia was cured after shunt removal and antibiotic treatment; recurrent endocarditis due to Corynebacterium xerosis ultimately caused the patient's death. No clinical manifestation of tricuspid valve dysfunction was noted in either patient, and right-sided endocarditis was recognized only at autopsy. The protracted contact of the tip of the venous line of PVS with the atrial wall is likely to be a major factor in the development of right-sided endocarditis in these patients.

Adult↗
PubMed1983

[Warren's anastomosis. Clinical and angiographic results (presentation of a series of 23 cases)].

Twenty-three patients with portal hypertension due to alcoholic cirrhosis were treated by distal splenorenal shunt and gastrosplenic mesenteric disconnection. In the post-operative period, two patients died; in one patient gastro-intestinal bleeding recurred 7 days after surgery and was due to ruptured varices with thrombosis of the splenorenal shunt; ascites developed in 14 patients. Twenty patients were followed up 6 months or more after surgery. Intestinal bleeding occurred in 3 patients with patent shunt. Ascites always disappeared within 3 months after operation. Four patients developed encephalopathy. Seventeen patients were investigated by angiography 3 months or more after surgery. The shunt was patent in 15 and occluded in 2 patients. In all patients with patent shunt a collateral circulation between the portomesenteric to gastrosplenic systems developed. In all patients, the portal flow decreased as suggested by diminution of the diameter of the portal vein. The authors conclude that 3 months after operation, results of distal splenorenal shunt with gastrosplenic disconnection are not hemodynamically different from those of side-to-side portocaval shunt.

Adult↗
PubMed1982

Transvenous liver biopsy: an experience based on 1000 hepatic tissue samplings with this procedure.

Transvenous liver biopsy was attempted 1033 times in 932 patients in whom percutaneous liver biopsy was contraindicated. A hepatic tissue specimen was obtained in 1000 out of these 1033 attempts. The specimen was unfragmented and/or large enough to allow correct evaluation of liver architecture in 518 of the 807 successful biopsies (64.2%) in patients with liver fibrosis or cirrhosis and in 191 of the 193 successful biopsies (98.9%) in patients with nonfibrotic lesion of the liver. Transvenous liver biopsy was followed by no or minor complication in all our patients except for one who suffered fatal intraperitoneal bleeding due to perforation of the liver capsule. It is concluded that transvenous liver biopsy is a workable, efficient, safe procedure for obtaining hepatic tissue specimens and that this method is essential in a department of hepatology.

Biopsy↗
PubMed1981

Hypoglycemia. A common complication of septicemia in cirrhosis.

Asymptomatic hypoglycemia was demonstrated in 15 of 30 cirrhotic patients with septicemia. Blood glucose levels were measured daily in these patients. Severe circulatory failure was present in the 15 patients with hypoglycemia and was absent in the 15 patients with normal blood glucose levels. Hypoglycemia is a common complication of septic shock in patients with cirrhosis, and blood glucose levels should be systematically measured in cirrhotic patients with septicemia or shock. Septicemia should be considered in any cirrhosis patient with a low blood glucose level.

Blood Glucose↗
PubMed1981

Non-inflammatory herpes simplex hepatitis in an adult with chronic neutropenia.

We report the case of a young woman with chronic neutropenia, in whom hepatitis, extensive herpetic eruption and herpes simplex viremia developed after genital herpetic ulceration. Although severe liver necrosis was present, the patient's death did not result from hepatic failure. No inflammatory cell infiltration was found circumscribing the multiple necrotic foci in the liver. This absence of inflammatory cell infiltration reflects the host's inability to normally restrain herpes simplex virus dissemination and, in this patient, might be the consequence of chronic neutropenia.

Adult↗
PubMed1980

Fulminant hepatic failure due to transient circulatory failure in patients with chronic heart disease.

Heart failure is a recognized, although uncommon, cause of massive liver cell necrosis, the clinical consequences of which are intermingled with those of cardiac insufficiency in most cases. We report the cases of six patients suffering from chronic heart failure in whom an episode of acute circulatory failure resulted in massive liver cell necrosis and fulminant hepatic failure. The manifestations of fulminant hepatic failure, ie, hepatic encephalopathy, jaundice, and marked increase in prothrombin time, developed after an interval of one to three days, after the episode of acute circulatory failure, while the patiens' hemodynamic condition had returned to the previous basal status.

Adult↗
PubMed1980

Is renal transplantation involved in post-transplantation liver disease? A prospective study.

Various lesions of the liver commonly observed in renal transplant recipients are usually considered as a consequence of the transplantation procedures (immunosuppression, drug toxicity, alteration of immune responses to various viruses). A group of 64 patients all treated with corticosteroids and azathioprine was studied prospectively, and serial liver biopsies were performed on the day of transplantation and at 1 and 3 years after transplantation. Chronic hepatitis was already present in 40% of the patients on the day of transplantation and an increase of only 15% in the frequency of this condition was observed 3 years later. The presence of HBsAg in 45% of the patients at the time of transplantation was significantly associated with liver lesions. In about 3% of the cases, transplantation was directly responsible for a liver disease (peliosis hepatitis). During the followup period an evolution from chronic persistent hepatitis to chronic active hepatitis was observed with an abnormally high frequency (25%). We conclude that most of the liver diseases observed in transplant recipients are the consequence of events before transplantation and probably related to hemodialysis.

Alanine Transaminase↗
PubMed1980

Portal hypertension in fulminant viral hepatitis.

The gradient between wedged and free hepatic venous pressures were measured in 10 unselected adult patients suffering from fulminant viral hepatitis. The gradient was increased in all the studied patients, ranging from 0.9 to 2.1 kPa; this finding indicates that portal hypertension was present in all these cases. Ascites was present in all the five patients having a gradient about 1.5 kPa and affected only two of the five patients having a gradient below 1.5 kPa; this observation suggests that portal hypertension plays a role in the mechanism of ascites in fulminant viral hepatitis. Portal hypertension in fulminant viral hepatitis is likely to be the consequence of an intrahepatic block due to massive necrosis of the liver cells.

Adult↗
PubMed1980

Portal hypertension, size of esophageal varices, and risk of gastrointestinal bleeding in alcoholic cirrhosis.

We studied the relationship between the degree of portal hypertension measured by the gradient between wedged and free hepatic venous pressures, the size of esophageal varices, and the risk of gastrointestinal bleeding in a series of 100 unselected patients with alcoholic cirrhosis. The degree of portal hypertension was not different in patients with no visible, in those with small-sized, and in those with large-sized, esophageal varices. The degree of portal hypertension was not different in patients without and with gastrointestinal bleeding, whether the source of hemorrhage was ruptured varices or acute gastric erosions. The risk of gastrointestinal bleeding, whether due to ruptured varices or acute gastric erosions, was significantly higher in patients with large-sized, than in those with no visible or small-sized, esophageal varices. It is concluded that, in patients with alcoholic cirrhosis, (a) the degree of portal hypertension has no predictive value for the risk of gastrointestinal bleeding and (b) large-sized esophageal varices are associated with a high risk of occurrence or recurrence of gastrointestinal bleeding and could be taken into account for a better selection of patients for portacaval shunt.

Blood Pressure Determination↗
PubMed1979

[Alcoholic ketoacidosis (author's transl)].

Chronic alcoholism is a frequently unrecognized cause of ketoacidosis in nondiabetic patients. Seven episodes of alcoholic ketoacidosis were observed in three patients. No consciousness disturbances were present. Semi-quantitative tests for ketones were strongly positive in urine, weakly positive in serum. The anion gap was between 25 and 41 mEq/l; serum lactate was between 0.9 and 9.0 mEq/l, and, in all cases, below the anion excess. Blood glucose ammonia was increased. Massive fatty liver was documented in all patients. All ketosis episodes followed an increase of alcohol ingestion associated with one to four week-starvation and vomiting; however, at the time of admission, alcohol was weakly increased in blood. In the four episodes where diagnosis was correct, ketoacidosis was rapidly corrected without insulin administration. In conclusion, in some nondiabetic subjects, the occurence of alcohol prolongated ingestion together with starvation and vomiting is responsible for ketoacidosis; because alcoholic ketoacidosis has often a mild clinical expression, its true prevalence is underestimated; insulin administration is not required.

Acidosis↗
PubMed1979

[Acute fatty infiltration of the liver in pregnancy. One case (author's transl)].

Acute fatty infiltration of the liver in pregnancy is characterised by microvacuolar fatty infiltration, without necrosis, occuring at the end of pregnancy. This syndrome, defined by Sheehan in 1940, remains rare. The authors were able to find 62 authentic cases in the french, english and german literature. The course is fatal in 75% of cases for the mother and 70% for the child. The gravity is related to hepatocellular failure, but also to extra-hepatic complications (renal failure, haemorrhagic syndrome, infectious complications, acute haemorrhagic and/or necrosing pancreatitis). When the course is favourable, the hepatic lesions disappear in a few weeks and there is no recurrence during subsequent pregnancies. The histological lesions of acute fatty infiltration of the liver in pregnancy are identical to those of fatty infiltration of the liver induced by cyclines and of Reye syndrome.

Acute Disease↗