Transvenous biopsy of orthotopic liver grafts--feasible and effective.
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Biopsy↗
Biomedical subjects
J Bernuau
Publications and source records attributed to J Bernuau.
[Fulminant and subfulminant viral hepatitis].
The adjectives fulminant and subfulminant apply to those forms of acute hepatitis where the prothrombin level falls below 50 p. 100 of its normal value and which is complicated by clinical hepatic encephalopathy. The most frequent cause is an acute viral hepatitis, notably that due to the B virus. Beside jaundice and encephalopathy, the most striking manifestations consist of low factor V level, cardiocirculatory hyperkinesia, acute renal failure due to hypovolaemia, respiratory alkalosis and sometimes hypoglycaemia or hypophosphataemia. The mortality rate, which is 75 p. 100 overall, varies with the causative virus. The prognosis is based on the degree of factor V decrease rather than on the severity of the encephalopathy. Coagulant fractions and nervous sedatives may obscure the prognosis and should not be administered. With emergency liver transplantation, 60 p. 100 of the patients who would have died survive. Early hospitalization of patients with severe acute hepatitis (prothrombin level below 50 p. 100 of its normal value, but no hepatic encephalopathy) is associated with much lower mortality rates and could be used to prevent transformation into fulminant or subfulminant hepatitis.
Acute Disease↗
Fulminant hepatitis after lisinopril administration.
A case of fulminant hepatitis in a patient taking lisinopril for 5 weeks for arterial hypertension is reported. Jaundice, fever, myalgia, and marked increase in serum aminotransferase activities occurred after 2 weeks of treatment. Continuation of lisinopril administration for 3 weeks after the onset of jaundice was associated with the development of grade III encephalopathy and a marked decrease in prothrombin and proaccelerin levels. This case strongly suggests that lisinopril may induce acute hepatitis and that continuation of the treatment after the onset of jaundice can lead to life-threatening hepatic failure.
Angiotensin-Converting Enzyme Inhibitors↗
Acute hepatitis after tetrahydroaminoacridine administration for Alzheimer's disease.
Tetrahydroaminoacridine administration has been proposed as a treatment for Alzheimer's disease. Although recent studies have shown that tetrahydroaminoacridine administration can be associated with mild or moderate liver dysfunction, to our knowledge, no case of symptomatic hepatitis with severe liver lesions has heretofore been reported. We describe a patient who developed jaundice after receiving tetrahydroaminoacridine for three weeks. Histologic examination showed extensive hepatocellular necrosis. Tetrahydroaminoacridine withdrawal was followed by the disappearance of jaundice within a few days and complete recovery within 5 weeks. This case shows that tetrahydroaminoacridine administration can induce marked liver cell necrosis resulting in symptomatic acute hepatitis.
Acute Disease↗
Anti-liver endoplasmic reticulum autoantibodies are directed against human cytochrome P-450IA2. A specific marker of dihydralazine-induced hepatitis.
Sera from patients with dihydralazine-induced hepatitis were shown to contain anti-liver microsomal autoantibodies (anti-LM) by indirect immunofluorescence. These anti-LM antibodies were different from anti-liver/kidney microsomes (anti-LKM) 1 or 2 autoantibodies which have been previously described. Sera recognized a single 53,000 = Mr polypeptide in human liver microsomes as judged by immunoblotting, and the target antigen was identified as cytochrome P-450IA2 (P-450IA2) by (a) comparison of immunoblotting patterns with anti-human P-450IA2 and anti-rat P-450IA2 and with five anti-LM sera, and (b) specific immunoinhibition of microsomal ethoxyresorufin and phenacetin O-deethylation activities (both P-450IA2 supported reactions) by anti-LM antibodies. Finally, purified human P-450IA2 was recognized by these anti-LM sera. The anti-LM antibodies are specific for the disease because none of the other antisera tested behaved in the same manner as anti-LM, even those from patients treated with dihydralazine and without hepatic disease. A possible role of P-450IA2 in the metabolism of dihydralazine was suggested by competitive inhibition of ethoxyresorufin-O-deethylase observed in microsomal incubations. Thus, a new example is presented in which a cytochrome P-450 may be a target for autoantibodies in drug-induced hepatitis.
Autoantibodies↗
[Treatment of hypovolemia after upper digestive hemorrhage caused by portal hypertension in cirrhosis].
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Animals↗
[Fatal hepatitis probably caused by exifone (Adlone)].
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Aged↗
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↗
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↗
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↗
Extent of hepatectomy in the rat. Evaluation of basal conditions and effect of therapy.
In the present study, subtotal hepatectomy was evaluated as a model of acute liver failure in the rat. Sprague-Dawley rats, weighing 250-300 g, underwent hepatectomy under varying basal conditions of temperature and glucose administration. Rats operated and maintained postoperatively at ambient temperature (25 degrees C external environment) developed hypothermia with a rate of return to normal temperature which was related to the extent of hepatectomy and the availability of glucose postoperatively. However, no significant difference in survival was observed between groups maintained at ambient temperature and those whose core temperature was maintained at 37 degrees C by passive external warming. Severe hypoglycemia was observed in rats undergoing 90 and 95% hepatectomy without glucose postoperatively. With 20% glucose available in drinking water the mortality of 90% hepatectomy was reduced from 95 to 40% (p less than 0.0001). With increase of the hepatectomy to 95%, 90% mortality was observed despite glucose support. Transplantation of 4 x 10(7) isolated syngeneic hepatocytes intraperitoneally at the time of hepatectomy did not increase survival after 90 or 95% hepatectomy; addition of testosterone therapy did not improve survival either alone or with hepatocyte transplantation. In this study, hepatectomy exceeding 90% was lethal and did not respond to the supportive measures provided. Hepatocyte transplantation and testosterone pretreatment, both therapies which are thought to increase regeneration, were ineffective in improving survival in this resection model.
Animals↗
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↗
[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↗
[The HELLP syndrome: a special form of hypertension in pregnancy].
The HELLP syndrome--H for haemolysis, EL for elevated liver enzymes and LP for low platelet count, is a serious complication of hypertension of pregnancy. We report five cases of this syndrome. The haemolysis, which is the consequence of a microangiopathic haemolytic anemia, is not always present: we report four such cases. The recognition of the HELLP syndrome even in the absence of hypertension is important and must be thought of when epigastric or dorsal pain occur in the second half of pregnancy. No liver biopsy was done in this small series.
Adult↗
Fulminant hepatitis due to reactivation of chronic hepatitis B virus infection after allogeneic bone marrow transplantation.
A case of hepatitis B reactivation following bone-marrow transplantation for leukemia in a previously healthy HBsAg carrier is reported. A number of changes in HBV serum markers were contemporary to the acute episode. All of them (increase of HBsAg concentration, conversion from anti-HBe to HBeAg, appearance of anti-HBc IgM and of serum HBV-DNA) were suggestive of a "switching-on" of viral replication. Institution of corticosteroid treatment at the onset of the acute phase did not prevent the fatal outcome.
Adult↗
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↗
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↗
Liver transplantation for protoporphyria. Evidence for the predominant role of the erythropoietic tissue in protoporphyrin overproduction.
Protoporphyria is an inherited disorder of heme biosynthesis characterized by an overproduction of protoporphyrin in the erythropoietic and hepatic tissues, the relative contribution of which in the metabolic disorder has not been directly quantitated. Excess protoporphyrin is eliminated solely by the liver into the bile and feces. We describe the case of a patient with protoporphyria complicated by severe cirrhosis in whom liver transplantation was performed and resulted in almost complete disappearance of skin photosensitivity manifestations and reduction in the level of protoporphyrin in erythrocytes. However, the level of protoporphyrin in feces was not markedly different before and after liver transplantation, which suggests that overproduction of protoporphyrin was unchanged. These findings are consistent with the view that the diseased liver and ensuing low hepatic clearance of protoporphyrin contributed to accumulation of protoporphyrin in the body and that, at least in this patient, the role of the hepatic tissue in the overproduction of protoporphyrin was small in comparison with that of the erythropoietic tissue.
Adult↗