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Biomedical subjects

C Degott

Publications and source records attributed to C Degott.

At least 235 records · Page 13Linked to original sources
PubMed1985

Regulation of renal cytochrome P-450. Effects of two-thirds hepatectomy, cholestasis, biliary cirrhosis and post-necrotic cirrhosis on hepatic and renal microsomal enzymes.

The possibility of a relationship between hepatic and renal cytochrome P-450 contents was assessed in rats with liver disease. In rats killed 3 days after two-thirds hepatectomy (a model for hepatocellular insufficiency), the total microsomal cytochrome P-450 content of the whole liver was decreased by 60% as compared to that in control rats; renal cytochrome P-450 was increased by 30% while the 7-ethoxycoumarin deethylase activity of kidney microsomes was increased by 80%. In rats killed 7 days after bile duct ligation (a model for cholestasis) or 35 days after bile duct ligation (a model for biliary cirrhosis), hepatic cytochrome P-450 was decreased by 60% and 45%, respectively, while renal cytochrome P-450 content was increased by 50% and 150%, respectively. In contrast, in rats killed 15 days after the last dose of carbon tetrachloride, 1.3 ml/kg twice weekly for 3 months (a model for post-necrotic cirrhosis), both hepatic and renal cytochrome P-450 contents remained unchanged. Phenobarbital (80 mg/kg daily for 3 days) was a poor inducer of renal cytochrome P-450 in sham-operated rats but became a potent inducer of renal cytochrome P-450 in rats with two-thirds hepatectomy. We conclude that renal cytochrome P-450 is increased in three models in which hepatic cytochrome P-450 contents are decreased (two-thirds hepatectomy, cholestasis and biliary cirrhosis), but remains unchanged in a model of severe liver pathology, in which hepatic cytochrome P-450 content is not modified (late, post-necrotic cirrhosis). The hypothetical role of endogenous inducer(s) is discussed.

Animals↗
PubMed1985

Pirprofen-induced fulminant hepatitis.

We report the cases of 2 female patients aged 69 and 61 yr, suffering from fulminant hepatitis induced by pirprofen, a new nonsteroidal antiinflammatory drug. The duration of pirprofen administration before the onset of hepatitis was long, 7 and 9 mo, respectively. Hepatitis was not preceded or accompanied by hypersensitivity manifestations. The liver lesion consisted of massive, predominantly centrilobular hepatic cell necrosis and microvesicular steatosis. One patient died of liver failure. Although the risk of fulminant hepatitis is very low, we recommend that, in patients taking pirprofen for more than 2 mo and complaining of asthenia, nausea, or vomiting, serum aminotransferase levels should be measured and administration of the drug should be interrupted as soon as an increased level is noted.

Aged↗
PubMed1985

Myeloid metaplasia, perisinusoidal fibrosis, and nodular regenerative hyperplasia of the liver.

We describe two patients with myeloid metaplasia in whom portal hypertension resulted, not from infiltration of the liver sinusoids by myeloid cells, but from perisinusoidal fibrosis and nodular regenerative hyperplasia of the liver. We hypothesize that myeloid metaplasia induced the development of perisinusoidal fibrosis, which resulted in heterogeneous hepatic tissue blood perfusion, with atrophy of the liver cells in the underperfused areas and nodular regenerative hyperplasia in the normally perfused areas.

Aged↗
PubMed1985

Liver in obesity.

We report on clinical, nutritional, and hepatic histological findings in 50 non-selected obese subjects (mean overweight +74%; range +21-138%). The pathogenesis of the liver damage was assessed with the help of multidimensional analysis of a number of clinical variables. According to the severity of the hepatic lesions, the patients have been ranged in five groups: O (normal liver) 10%; I (fatty liver) 48%; II (fatty hepatitis) 26%; III (fatty fibrosis) 8%; IV (fatty cirrhosis) 8%. The more severe changes (groups III and IV) were constantly associated with excessive alcohol intake. The multidimensional analysis was unable to find a relationship between obesity and the development of fibrosis and cirrhosis whereas it showed that: (a) there was a highly significant correlation between the daily ethanol intake and the degree of overweight, (b) severe fatty metamorphosis was significantly associated with the degree of overweight, the existence of diabetes mellitus, and the amount of alcohol and fat intake, (c) nutritional factors, in particular deficient protein intake, have only an accessory effect in the development of mild inflammation and fibrosis, (d) the consumption of potentially hepatotoxic drugs, very high in the obese (about five drugs per day) could have a role in the development of cirrhosis. In conclusion in our study, there was no evidence that obesity per se could result in severe liver damage.

Adult↗
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

Liver adenomatosis. An entity distinct from liver adenoma?

From 1979 to 1984, we followed the cases of 3 men (aged 13, 31, and 75 yr) and 2 women (aged 38 and 45 yr who had never used oral contraceptives) suffering from liver adenomatosis, an uncommon lesion consisting of numerous benign adenomas in an otherwise normal hepatic parenchyma. During the same period, we observed 20 cases of liver adenoma (one tumor in 18 patients and two tumors in 2 patients). From these cases and the review of previously reported cases of liver adenomatosis and series of liver adenoma, the following distinctive characteristics of these two benign conditions of the liver can be outlined: liver adenomatosis affects men and women, whereas liver adenoma predominantly affects women; liver adenomatosis is unrelated, whereas liver adenoma is closely related, to oral contraceptive use; increases in serum alkaline phosphatase and gamma-glutamyl transpeptidase are common in liver adenomatosis, but are uncommon in liver adenoma.

Adenoma↗
PubMed1984

Protective effect of 16,16-dimethyl prostaglandin E2 on the hepatotoxicity of bromobenzene in mice.

It has been suggested that 16,16-dimethyl prostaglandin E2 may have a cytoprotective effect in the liver. To assess this hypothesis, we determined the effects of this prostaglandin on the metabolism and toxicity of bromobenzene in mice. Administration of 16,16-dimethyl prostaglandin E2 (50 micrograms/kg s.c., 30 min before, and every 6 hr after, the administration of bromobenzene) did not modify the disappearance curves of unchanged bromobenzene from plasma and liver, and did not modify the amount of bromobenzene metabolites covalently bound to hepatic proteins 1-24 hr after the administration of a toxic dose of bromobenzene (0.36 ml/kg i.p.). The prostaglandin, however, markedly reduced serum alanine aminotransferase activity, the extent of liver cell necrosis, the depletion of glutathione, and the disappearance of cytochrome P-450 after administration of this toxic dose of bromobenzene (0.36 ml/kg i.p.). It also markedly reduced mortality after administration of a lethal dose of bromobenzene (0.43 ml/kg i.p.). We conclude that 16,16-dimethyl prostaglandin E2 can prevent hepatic necrosis without decreasing the covalent binding of bromobenzene metabolites to hepatic proteins. The mechanism for this dissociation between covalent binding and toxicity remains unknown.

16,16-Dimethylprostaglandin E2↗
PubMed1984

Recurrent jaundice caused by recurrent hyperemesis gravidarum.

The existence of jaundice induced by hyperemesis gravidarum is controversial. We report the case of a woman who suffered from three episodes of jaundice during the first trimester of three consecutive pregnancies, a few days after the onset of hyperemesis gravidarum. Jaundice was caused by conjugated hyperbilirubinaemia. Serum alanine aminotransferase activity was increased and scarce necrotic hepatocytes were shown on light and electron microscopic examinations. Cessation of vomiting was rapidly followed by complete recovery. This observation supports the view that severe vomiting can cause jaundice in pregnant women.

Adult↗
PubMed1984

Amitriptyline-induced fulminant hepatitis.

The authors report the case of a patient who received amitriptyline on 2 occasions. On both occasions, she had fever and jaundice. On the second episode, hepatitis was severe with hepatic encephalopathy, ascites, increased prothrombin time, and massive hepatic necrosis. After interruption of the drug administration, the patient made a slow but complete recovery.

Amitriptyline↗
PubMed1984

Mechanism for isaxonine hepatitis. II. Protective role of glutathione and toxicological studies in mice.

Coincubation of 0.4 mM [3H]glutathione with 4 mM isaxonine , an NADPH-generating system, glutathione S-transferase and mouse liver microsomes, followed by thin-layer chromatography of the incubation mixture, resulted in the appearance of a 3H-labeled peak with characteristics consistent with a glutathione- isaxonine metabolite adduct: this peak was absent if either isaxonine or the NADPH-generating system was omitted and was decreased if the transferase was omitted. In vivo, the concentrations of hepatic glutathione and glutathione disulfide were markedly decreased 2.5 hr after administration of isaxonine (4 mmol X kg-1 i.p.); this depletion of glutathione was prevented essentially by pretreatment with piperonyl butoxide. In vitro, addition of 4 mM glutathione decreased markedly the amount of [14C] isaxonine metabolite that bound to microsomal proteins during incubation of 1 mM [2-14C] isaxonine with hepatic microsomes and an NADPH-generating system. In vivo, pretreatment with diethylmaleate decreased further hepatic glutathione concentration and markedly increased the amount of [14C] isaxonine metabolite covalently bound to hepatic proteins, 2.5 hr after administration of [2-14C] isaxonine (4 mmol X kg-1 i.p.). Administration of isaxonine (4 mmol X kg-1 i.p.) decreased hepatic cytochrome P-450 concentration, but failed to produce liver cell necrosis, even in mice pretreated with phenobarbital, 3-methylcholanthrene or diethylmaleate, despite high levels of in vivo covalent binding in pretreated animals. We conclude that the reactive metabolite of isaxonine may be conjugated with glutathione or may covalently bind to hepatic proteins. The metabolite, however, has limited hepatotoxic potential in mice.

Animals↗
PubMed1983

[Hepatic biopsy by transvenous approach in hemopathies with coagulation disorders].

Percutaneous liver biopsy is often contra-indicated in patients with blood diseases associated with disorders of coagulation. Transvenous liver biopsy was performed in 36 such patients who also presented with unexplained hepatic abnormalities. In 31 patients liver tissue sampling was sufficient for adequate evaluation of liver damage: malignant infiltration was confirmed in 21, and associated hepatic disorder was diagnosed in 10. Five patients had a histologically normal liver. This study shows that in patients with blood disease enough liver tissue can be obtained by transvenous biopsy for a diagnosis to be made.

Biopsy↗