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Biomedical subjects

C Degott

Publications and source records attributed to C Degott.

At least 271 records · Page 15Linked to original sources
PubMed1981

Hepatocytic PAS-positive diastase-resistance inclusions in the absence of alpha-1-antitrypsin deficiency--high prevalence in alcoholic cirrhosis.

The presence of PAS-positive, diastase-resistant inclusions in the cytoplasm of the hepatocytes is characteristic of alpha-1-antitrypsin deficiency. The purpose of this investigation was to determine whether the presence of these inclusions is a specific feature, permitting the recognition of alpha-1-antitrypsin deficiency in patients with liver disease. We examined the liver specimens from 20 patients suffering from alcoholic cirrhosis with the Pi M phenotype, i.e., in whom alpha-1-antitrypsin deficiency was excluded. In seven of these patients, PAS-positive, diastase-resistant inclusions were seen in the hepatocytes; in two patients, these inclusions contained a material antigenically similar to alpha-1-antitrypsin. These inclusions might represent deposits of glycoproteins poorly excreted by the diseased hepatocytes. It is concluded that, in patients with liver disease, the presence of PAS-positive, diastase-resistant inclusions--even containing alpha-1-antitrypsin--in the cytoplasm of the hepatocytes does not permit the hepatic lesions to be ascribed to alpha-1-antitrypsin deficiency.

Amylases↗
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↗
PubMed1981

Invasion of the lumen of the bile ducts by hepatocellular carcinoma.

The purpose of this investigation was to ascertain the prevalence and manifestations of tumorous invasion of the lumen of the bile ducts, a mode of local extension characteristic of hepatocellular carcinoma. In a series of 140 necropsied patients with hepatocellular carcinoma, tumorous invasion of the bile duct was noted in three patients (2.1%). Marked cholestasis was present in these three patients; the other manifestations related to the tumorous invasion of the bile duct were biliary pain in one and gall-bladder enlargement in two patients.

Aged↗
PubMed1981

Chronic active hepatitis and giant multinucleated hepatocytes in adults treated with clometacin.

The authors report the cases of 2 adults who became jaundiced during prolonged administration of clometacin, a new analgesic drug. Jaundice and serum aminotransferase activity progressively increased while the drug administration was continued but quickly decreased when it was eventually interrupted. 1 patient resumed the intake of clometacin and died with jaundice and ascites. In both patients, liver lesions were those of severe chronic active hepatitis with numerous giant multinucleated hepatocytes.

Aged↗
PubMed1981

Unilateral nevoid telangiectasia and chronic liver disease. Report of a case and review of the literature.

Unilateral nevoid telangiectasia was observed on the back of the left hand and wrist in a 19-year old man with chronic liver disease and portal hypertension. Moreover, abnormalities of the elastic fibers of the skin were found. Examination of the liver biopsy showed extensive portal fibrosis with many dilated blood vessels. No usual cause of juvenile cirrhosis was detected. In the comment, the authors suggest that unilateral nevoid telangiectasia and liver disease could be manifestations of a disease involving skin and liver vessels, as in hereditary hemorrhagic telangiectasia.

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

Hepatitis B core antigen in hepatocytes of patients with chronic active hepatitis.

Hepatitis B core antigen was demonstrated in the hepatocytes of 28 of 40 patients with chronic active hepatitis in whose sera hepatitis B surface antigen was not detectable by radioimmunoassay. This finding suggests that in these patients, despite hepatitis B surface antigen being undetectable in serum, the liver disease is the consequence of chronic infection with hepatitis B virus.

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

[Ineffectiveness of corticosteroids in cholestatic forms of chronic active hepatitis].

Four cases of chronic active hepatitis with cholestasis resembling primary biliary cirrhosis are reported. Two patients were women and two were men; their age ranged from 18 to 52 years. They had recurrent jaundice with pruritus, and, in two cases, xanthelasma or xanthomas. All patients had hyperbilirubinemia, a moderate increase in serum aspartate aminotransferase activity, an increase in serum alkaline phosphatase activity and immunoglobulins G levels. Hepatitis B surface antigen was present in one patient. Histological examination of the liver revealed active chronic hepatitis with cholestasis. Moderate doses of prednisone had no effect on clinical or biochemical signs in any of the patients.

Adolescent↗
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↗
PubMed1979

Idiopathic portal hypertension (perisinusoidal fibrosis) after renal transplantation.

We report the cases of two renal transplant recipients suffering from idopathic portal hypertension, a condition characterised by increased portal venous pressure in the absence of both histological lesion of the liver and obstruction of the portal vein. In these two patients, perisnusoidal fibrosis, invisible by light microscopy, was demonstrated by electron microscopy; it is suggested that partial obstruction of hepatic sinusoids by perisinusoidal fibrosis could be the mechanism for increased portal venous pressure in all the patients with idiopathic portal hypertension. In these two patients, who received 6-mercaptopurine and azathioprine, perisinusoidal fibrosis might be the consequence of prolonged administration of these drugs.

Adult↗
PubMed1979

Gold salt-induced cholestasis.

The authors report the case of a patient with transient intrahepatic cholestasis following the administration of a soluble gold salt, sodium aurothiopropanol sulfonate. Other manifestations of intolerance to gold salts included exfoliative dermatitis and eosinophilia.

Aged↗
PubMed1979

Effect of fasting on metabolite-mediated hepatotoxicity in the rat.

Acetaminophen and bromobenzene are transformed in the liver into chemically reactive metabolites that may either bind to glutathione and be detoxified or bind to hepatic proteins and produce liver cell necrosis. Fasting for 42 hr (a) decreased hepatic glutathione concentration, (b) increased the amount of chemically reactive metabolite irreversibly bound to hepatic proteins after administration of 3H-acetaminophen or 14C-bromobenzene, and (c) increased the hepatotoxicity of acetaminophen or bromobenzene. In rats fasted for various lengths of time, there was an inverse relationship between the concentration of glutathione in the liver and the activity of serum glutamic pyruvic transaminases after administration of acetaminophen or bromobenzene. In vitro, there was an inverse relationship between the concentration of glutathione in the incubate and the amount of chemically reactive metabolite bound to microsomal proteins after incubation of 3H-acetaminophen or 14C-bromobenzene with hepatic microsomes. It is concluded that fasting may decrease the inactivation of chemically reactive metabolites by glutathione, increase their binding to hepatic proteins, and enhance the hepatotoxicity of drugs transformed into chemically reactive metabolites that are detoxified by binding to glutathione.

Acetaminophen↗
PubMed1979

Perhexiline maleate-induced cirrhosis.

The authors report the cases of 2 patients who died from cirrhosis after receiving perhexiline maleate, a drug widely used in Europe for the treatment of angina pectoris. Perhexiline maleate had been ingested for 24 and 28 mo, respectively. Manifestations of cirrhosis included jaundice, hepatic encephalopathy, ascites, and portal hypertension. Associated manifestations of intolerance to perhexiline maleate included peripheral neuropathy in 1 patient and marked weight loss in both. Histologic lesions resembled those observed in patients with alcoholic liver disease. Ultrastructural lesions included numerous enlarged lysosomes containing myeloid figures. Histochemical stains demonstrated increased phospholipid content of the hepatocytes. These findings are consistent with the view that prolonged administration of perhexiline maleate may induce both histologic lesions resembling those of alcoholic liver disease and ultrastructural and histochemical lesions resembling those of phospholipidosis.

Aged↗