PubMed Health⌕ Search

Biomedical subjects

C Degott

Publications and source records attributed to C Degott.

At least 163 records · Page 9Linked to original sources
PubMed1990

Chronic hepatitis in kidney allograft recipients.

98 HBsAg-positive and 31 HBsAg-negative kidney recipients were compared to assess the effect of renal transplantation on chronic liver disease and vice versa. Diagnosis was based on analysis of liver biopsy specimens including semiquantitative evaluation of histological features of chronic hepatitis. Serial specimens were examined: chronic liver disease occurred in 88% of HBsAg-positive patients and 4% of HBsAg-negative patients with normal liver at the time of transplantation. Liver abnormalities in the former were chronic persistent hepatitis (32%), chronic active hepatitis (51%), and cirrhosis (17%). Actuarial patient survival was similar in HBsAg-positive (78%) and HBsAg-negative (87%) patients, as was allograft survival (64% and 71%, respectively). In both HBsAg-positive and HBsAg-negative patients chronic alcohol consumption was more frequent in those with chronic liver disease than those without. These data suggest that renal transplantation may be appropriate for haemodialysis patients with chronic hepatitis whatever their HBV status.

Actuarial Analysis↗
PubMed1990

Recombinant human gamma-interferon in patients with chronic active hepatitis B: pharmacokinetics, tolerance and biological effects.

Pharmacokinetics, tolerance and biological effects of human recombinant gamma-interferon were studied in 12 patients with chronic active hepatitis B. Serum concentrations of gamma-interferon were measured by radioimmunoassay in four patients after a subcutaneous injection of 10 million U (0.5 mg); the peak serum concentration of gamma-interferon (29 +/- 7 U/ml) was reached after 5 to 8 hr and gamma-interferon remained detectable for 24 to 36 hr. Twelve patients received recombinant gamma-interferon, 2.5 to 10 million U daily, for 4 mo. All suffered from a dose-dependent, flulike syndrome similar to that induced by alpha-interferon. Recombinant gamma-interferon induced a marked increase of serum ALT and a significant decrease of serum hepatitis B virus-DNA. Serum hepatitis B virus-DNA disappeared in one patient during administration of recombinant gamma-interferon. Serum hepatitis B virus-DNA disappeared in four additional patients, and HBeAg disappeared in two patients during the 12 mo after administration of recombinant gamma-interferon. These results indicate that subcutaneous injection is suitable for administration of recombinant gamma-interferon and that recombinant gamma-interferon has an antiviral effect in patients with chronic active hepatitis B.

Adult↗
PubMed1990

Clinical course of spontaneous reactivation of hepatitis B virus infection in patients with chronic hepatitis B.

The purposes of this study were (a) to describe the clinical and biochemical manifestations associated with spontaneous reactivation of hepatitis B virus as defined by the reappearance of hepatitis B virus DNA in serum using dot-blot hybridization and (b) to determine whether the clinical and biochemical manifestations associated with hepatitis B virus reactivation were different in patients with and without human immunodeficiency virus-1 infection. During 1 yr, 110 French patients were admitted to Hôpital Beaujon for chronic hepatitis B. Fourteen were found to have hepatitis B virus reactivation; of these, three were anti-human immunodeficiency virus-1-positive. These 14 patients were HBsAg-positive for 60 mo (range = 6 to 180 mo). Clinical manifestations related to reappearance of hepatitis B virus DNA were present in 11 patients. HBeAg/anti-HBe status did not change in nine patients in whom hepatitis B virus reactivation would not have been recognized without hepatitis B virus DNA testing. Cirrhosis was present in nine patients. Four patients, of whom two were anti-human immunodeficiency virus-1-positive, had fulminant liver failure. Two patients died; one was anti-human immunodeficiency virus-1-positive. One patient was given an emergency transplant.

Adult↗
PubMed1990

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↗
PubMed1990

Cholangiographic appearance simulating sclerosing cholangitis in metastatic adenocarcinoma of the liver.

Three patients with liver metastases and clinical and biochemical signs of cholestasis are reported in this study. In the three patients, cholangiography showed shifted and stretched intrahepatic bile ducts and multifocal strictures simulating intrahepatic primary sclerosing cholangitis. In two patients, histological examination showed periductal fibrosis or inflammation. Hepatic metastases should be included among the conditions considered to simulate intrahepatic primary sclerosing cholangitis during cholangiography.

Adenocarcinoma↗
PubMed1990

Antinuclear antibodies directed to a 200-kilodalton polypeptide of the nuclear envelope in primary biliary cirrhosis. A clinical and immunological study of a series of 150 patients with primary biliary cirrhosis.

Antinuclear antibodies giving a perinuclear fluorescence and directed to a 200-kilodalton polypeptide of the nuclear envelope have been described in primary biliary cirrhosis. The purpose of this study, based on a series of 150 patients with primary biliary cirrhosis, was to ascertain the prevalence of these antibodies and to compare patients with and without these antibodies. Antinuclear antibodies giving a perinuclear fluorescence were demonstrated in 43 of the 150 patients (29%); antibodies directed to the 200-kilodalton polypeptide of the nuclear envelope were found in 40 of these 43 patients. Asthenia, arthralgia, associated extrahepatic diseases, Raynaud's phenomenon, and other antinuclear specificities were significantly less common, and titers of antimitochondrial antibodies were significantly lower in patients with antibodies directed to the 200-kilodalton polypeptide of the nuclear envelope than in patients without these antibodies. Clinical outcome, liver tests, and histological lesions did not significantly differ in patients with and without these antibodies.

Antibodies, Antinuclear↗
PubMed1990

Microvesicular steatosis of the liver.

The term "microvesicular steatosis of the liver" refers to a variant form of hepatic fat accumulation whose histologic features contrast with the much more common macrovesicular steatosis. Microvesicular steatosis of the liver was originally described in association with conditions who share a number of biochemical and a limited number of clinical features: acute fatty liver of pregnancy, Reye's syndrome, Jamaican vomiting sickness, sodium valproate toxicity, high-dose tetracycline toxicity and certain congenital defects of urea cycle enzymes; they were thought to constitute an entity of "microvesicular fat diseases". In recent years the disease has been described in a wide variety of conditions: alcoholism, toxicity of several medications, delta hepatitis in South America and Central Africa, sudden childhood death, congenital defects of fatty acid beta oxidation, cholesterol ester storage disease, Wolman disease and Alpers syndrome. Not much is known regarding the pathogenesis of microvesicular steatosis but in many instances the primary defect could be a mitochondrial lesion, and inhibition of the mitochondrial beta oxidation of fatty acids has been the most frequently implicated defect. The different conditions associated with microvesicular steatosis are heterogenous in many aspects. Maintaining the concept of "microvesicular fat diseases" as a unique entity seems no longer justified.

Fatty Liver↗
PubMed1990

Membranous obstruction of the inferior vena cava and hepatocellular carcinoma in a Caribbean patient.

Membranous obstruction of the inferior vena cava has been reported mainly in South Africa, Japan, and India; in 20-40% of patients the disease is complicated by hepatocellular carcinoma. We report a case of membranous obstruction of the inferior vena cava with hepatocellular carcinoma in a 43-year-old Caribbean man of Indian origin. The Caribbean islands may constitute another geographical area where the population is at risk for the development of membranous obstruction of the inferior vena cava and subsequent hepatocellular carcinoma.

Adult↗
PubMed1990

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↗
PubMed1990

Stereoselective and nonstereoselective effects of ibuprofen enantiomers on mitochondrial beta-oxidation of fatty acids.

The effects of the R-(-) and S-(+)ibuprofen enantiomers were first studied in vitro with mouse liver mitochondria incubated in the presence of various concentrations of exogenous coenzyme A. In the presence of a low concentration of coenzyme A (2.5 microM), the R-(-)enantiomer (which forms an acylcoenzyme A) inhibited stereoselectively the beta oxidation of [1-14C]palmitic acid but not that of [1-14C]palmitoyl-L-carnitine (which can directly enter the mitochondria). In the presence, however, of a concentration of coenzyme A (50 microM) reproducing that present in liver cell cytosol, both enantiomers (2 mM) slightly inhibited the beta oxidation of [1-14C]palmitic acid and markedly inhibited the beta oxidation of [1-14C]octanoic acid and [1-14C]butyric acid. In vivo, both enantiomers (1 mmol.kg-1) similarly inhibited the formation of [14C]CO2 from [1-14C]fatty acids. Both enantiomers similarly decreased plasma ketone bodies. Both similarly increased hepatic triglycerides, and both produced mild microvesicular steatosis of the liver. We conclude that both ibuprofen enantiomers inhibit beta oxidation of fatty acids in vitro and in vivo. In addition, the R-(-)enantiomer may stereoselectively sequester coenzyme A; at low concentrations of coenzyme A in vitro, this may stereoselectively inhibit the mitochondrial uptake and beta oxidation of long chain fatty acids.

Animals↗
PubMed1990

Amiodarone inhibits the mitochondrial beta-oxidation of fatty acids and produces microvesicular steatosis of the liver in mice.

Amiodarone has been shown to produce microvesicular steatosis of the liver in some recipients. We have determined the effects of amiodarone on the mitochondrial oxidation of fatty acids in mice. In vitro, the formation of 14C-acid-soluble beta-oxidation products from [U-14C]palmitic acid by mouse liver mitochondria was decreased by 92% in the presence of 125 microM amiodarone and by 94% in the presence of 125 microM N-desethylamiodarone. Inhibition due to 100 or 150 microM amiodarone persisted in the presence of 5 mM acetoacetate, whereas acetoacetate totally relieved inhibition due to 15 microM rotenone. In vivo, exhalation of [14C]CO2 from [U-14C]palmitic acid was decreased by 31, 40, 58 and 78%, respectively, in mice receiving 19, 25, 50 and 100 mg.kg-1 of amiodarone hydrochloride 1 hr before the administration of [U-14C]palmitic acid. One hour after 100 mg.kg-1, the exhalation of [14C]CO2 from [1-14C]palmitic acid, [1-14C]octanoic acid or [1-14C]butyric acid was decreased by 78, 72 and 53%, respectively. Exhalation of [14C]CO2 from [1-14C]palmitic acid was normal between 6 and 9 hr after administration of 100 mg.kg-1 of amiodarone hydrochloride, but was still inhibited by 71 and 37%, 24 and 48 hr after 600 mg.kg-1. Twenty four hours after the latter dose of amiodarone, hepatic triglycerides were increased by 150%, and there was microvesicular steatosis of the liver. We conclude that amiodarone inhibits the mitochondrial beta-oxidation of fatty acids and produces microvesicular steatosis of the liver in mice.

Amiodarone↗
PubMed1990

[Hepatic adenoma and hepatocellular carcinoma in 3 brothers with type I glycogenosis].

We report 2 cases of type I glycogen storage disease (Von Gierke's disease) discovered in 2 brothers at the age of 7 and 5 years, respectively. Both developed hepatic adenoma at the age of 19 and 17. Hepatocellular carcinoma occurred in the older brother the discovery of adenoma 4 years after. The frequency of these tumors in patients with type I glycogen storage disease raises problems concerning the treatment and modality of regular surveillance of the liver in these patients. The policy for the detection and treatment of these tumors, and particularly the indications for liver transplantation are discussed.

Adenoma↗
PubMed1990

[Primary biliary cirrhosis: current modes of presentation. Clinical, biochemical, immunologic and histologic study of 206 patients seen from 1978 to 1988].

The aim of this study, based on a series of 206 patients (186 women and 20 men) with primary biliary cirrhosis seen from 1978 to 1988, was to assess the current modes of presentation of the disease. In approximately 30 percent of patients, primary biliary cirrhosis was recognized at an asymptomatic stage. Two thirds of these patients remained asymptomatic: they were older (mean age 57 years) and had less severe histological lesions than the patients who became symptomatic (mean age 45 years). The modes of presentation were not markedly different in the male and female patients of our series. The prevalence of cholelithiasis seemed to be particularly high (more than 20 percent in our patients). Complications of portal hypertension (bleeding esophageal varices or ascites) were the initial manifestations of primary biliary cirrhosis in 8 percent of our symptomatic patients. Alkaline phosphatase level was normal or only slightly increased in 15 percent of our patients: a normal level or a slight increase in alkaline phosphatases is not an argument against the diagnosis of primary biliary cirrhosis. Antinuclear antibodies with perinuclear fluorescence were demonstrated in 26 percent of our patients; in most of these patients, an antibody to a 200 kD protein of the nuclear envelope was present; in patients with this antibody, asthenia, arthralgias and associated extrahepatic diseases were less common and the titers of antibodies to mitochondria were lower than in the patients without this antibody.

Adult↗
PubMed1990

[An increase of choleresis in secondary biliary cirrhosis in rats is caused by bile duct secretion].

Bile flow may be considerably increased in human cirrhosis. The mechanism of this increase has not been established. Two mechanisms have been proposed: a) increased canalicular filtration because of sinusoidal hypertension, or b) secretion by proliferated bile ductules. To distinguish between these two possibilities, we examined the determinants of bile secretion in rats with secondary biliary cirrhosis after bile duct obstruction. Sham-operated animals served as controls. Four weeks after bile duct ligation, all animals had cirrhosis. Bile flow was significantly higher and bile salt secretion significantly lower in cirrhotic animals than in controls. Biliary bicarbonate concentration was significantly higher in cirrhotic animals than in controls. Bile-to-plasma concentration ratio of erythritol was significantly lower in cirrhotic animals than in controls, suggesting a dilution of erythritol by a secretion distal to bile canaliculi. Bile-to-plasma ratio of sucrose was not significantly different in cirrhotics and controls, suggesting that paracellular permeability was not modified. Secretin, at the dose of 3 clinical units/100 g, induced an increase of approximately 75 percent in bile flow, and 70 percent in biliary bicarbonate concentration in cirrhotics. In conclusion, bile flow was increased in biliary cirrhosis in rats. The dilution of erythritol, the increase in biliary bicarbonate concentration and the increased response to secretin strongly suggest that increased choleresis was due, at least in part, to secretion by bile ductules or ducts. These results confirm that secondary biliary cirrhosis is a good experimental model for the study of alterations of bile secretion in cirrhosis.

Animals↗
PubMed1990

[Fatal fulminant hepatitis in 2 women taking toloxatone (Humoryl)].

We report two cases of fulminant hepatitis which might be due to toloxatone, a new type-A monoamine oxidase inhibitor. Hepatitis occurred 20 days after the beginning of toloxatone administration in the first case and 138 days after the reintroduction of treatment in the second case. Clinical features included vomiting and jaundice, followed by asterixis and coma. Histologically, hepatic cell necrosis was predominant in the centrilobular area in the first case, and affected the entire lobule in the second case. Both patients died despite emergency liver transplantation.

Acute Disease↗
PubMed1989

Metabolic activation of the antidepressant tianeptine. II. In vivo covalent binding and toxicological studies at sublethal doses.

Administration of [14C]tianeptine (0.5 mmol/kg i.p.) to non-pretreated hamsters resulted in the in vivo covalent binding of [14C]tianeptine metabolites to liver, lung and kidney proteins; this very high dose (360-fold the human therapeutic dose) depleted hepatic glutathione by 60%, and increased SGPT activity 5-fold. Lower doses (0.25 and 0.125 mmol/kg) depleted hepatic glutathione to a lesser extent and did not increase SGPT activity. Pretreatment of hamsters with piperonyl butoxide decreased in vivo covalent binding to liver proteins, and prevented the increase in SGPT activity after administration of tianeptine (0.5 mmol/kg i.p.). In contrast, pretreatment of hamsters with dexamethasone increased in vivo covalent binding to liver proteins, and increased SGPT activity after administration of tianeptine (0.5 mmol/kg i.p.). Nevertheless, liver cell necrosis was histologically absent 24 hr after the administration of tianeptine (0.5 mmol/kg i.p.) to non-pretreated or dexamethasone-pretreated hamsters. In vivo covalent binding to liver proteins also occurred in mice and rats, being increased by 100% in dexamethasone-pretreated animals. In vivo covalent binding to liver proteins was similar in untreated female Dark Agouti rats and in female Sprague-Dawley rats. These results show that tianeptine is transformed in vivo by cytochrome P-450, including glucocorticoid-inducible isoenzymes, into chemically reactive metabolites that covalently bind to tissue proteins. The metabolites, however, exhibit no direct hepatotoxic potential in hamsters below the sublethal dose of 0.5 mmol/kg i.p. The predictive value of this study regarding possible idiosyncratic and immunoallergic reactions in humans remains unknown.

Alanine Transaminase↗