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Biomedical subjects

C Degott

Publications and source records attributed to C Degott.

At least 253 records · Page 14Linked to original sources
PubMed1983

[Acute rhabdomyolysis in alcoholic patients].

Six episodes of acute rhabdomyolysis were observed within a two-year period in 5 male adult alcoholic patients hospitalised in a hepatology intensive care unit. Painful muscle swelling was discrete of absent in 4 of the 5 patients. Acute rhabdomyolysis was preceded by grand mal seizures in 4 patients, delirium tremens in 1 and high fever with shivers in 3. All cases were rapidly diagnosed on the finding of very high serum creatinine phosphokinase levels. One patient developed acute respiratory failure and recovered after prolonged mechanical ventilation. Three patients had acute renal failure with severe hyperkalemia in one but none required dialysis. Three patients died within 2 to 6 days of the diagnosis, but the deaths were not directly related to rhabdomyolysis. It would appear that in alcoholic patients: the prevalence of rhabdomyolysis is probably underestimated; any muscular hyperactivity as seen in seizures, delirium tremens and prolonged shivers may be a precipitating factor; the condition is easily diagnosed by measuring serum creatinine kinase activity; some cases of acute renal failure in patients with alcoholic cirrhosis might be explained by acute rhabdomyolysis with minimal symptoms.

Acute Disease↗
PubMed1983

Relationship between liver histopathological changes and HBsAg in 111 patients treated by long-term hemodialysis.

We studied liver biopsies performed between January 1972 and June 1980 in 111 patients receiving regular dialysis treatment. Biopsies were performed either because of suspected liver disease (61 patients) or routinely during abdominal surgery or kidney transplantation (50 patients). Repeat biopsies were done in 14 cases. Hepatitis B virus markers, assayed every 3 months during the observation period, were detected at some time in 71 patients (64%); 51 remained persistently positive. Histological examination showed normal liver in 39 cases, lobular hepatitis in 15, chronic persistent hepatitis in 36 and chronic active hepatitis in 21. All patients with chronic active hepatitis were chronic HBsAg carriers, and repeated biopsies showed aggravation only in these patients. The course was remarkably asymptomatic, with lesions leading to fibrosis despite the lack of histopathological patterns of severe necrosis and/or inflammation, which were conspicuously absent in this series.

Biopsy↗
PubMed1983

Non-fatal acute fatty liver of pregnancy.

Four patients are described, admitted during a three-year period, who recovered from acute fatty liver of pregnancy; vomiting and jaundice were the main manifestations of the disease; coma and anuria were absent. During the same period, we observed one patient who died of acute fatty liver of pregnancy. This experience suggests that the non-fatal form of the disorder may be much commoner than the fatal form.

Acute Disease↗
PubMed1983

Dihydralazine hepatitis: report of a case and review of the literature.

The authors report the case of a patient with hepatitis after the administration of dihydralazine, an analogue of hydralazine which is widely used in Europe. Hepatitis occurred during the administration of dihydralazine, quickly improved when the administration of dihydralazine was interrupted, and worsened again when it was resumed. Hepatitis was severe with hepatic encephalopathy and prolonged prothrombin time. There was centrizonal and bridging necrosis. After interruption of the drug administration, the outcome was favorable, but fibrotic sequelae were observed on a follow-up histologic examination.

Biopsy↗
PubMed1983

[Acute hepatitis caused by isaxonine phosphate (Nerfactor)].

We report the cases of four adult patients suffering from acute hepatitis due to isaxonine phosphate (Nerfactor), a drug recently proposed for the treatment of the lesions of peripheral nerves. Hepatitis developed 14 to 166 days after the beginning of the administration of the drug. In all the patients, predominantly centrilobular hepatocytic necrosis was present. In two of our patients, the course of hepatitis was fatal. Hepatitis induced by isaxonine phosphate is likely to be due to an immuno-allergic mechanism.

Acute Disease↗
PubMed1983

[Primary histiocytic lymphoma of the liver. Study of 2 cases and review of the literature].

The authors report two cases of primary histiocytic malignant lymphoma of the liver successfully treated by right hepatectomy. The first case, was free of secondary spread with a follow-up of ten years, although he received no adjuvant therapy. The second patient developed skin, bone and brain metastases, which disappeared after chemotherapy and radiotherapy. He has been free of recurrence for four years. Such primary liver tumors are very rare and are worth knowing because of the efficiency of treatment and of their rather good prognosis. Evolution is different from that observed in histiocytic malignant lymphomas developed in other sites. It is suggested that, in the liver, this tumor might originate and grow from Kupffer's cells. This histologic origin might explain the particular clinical and evolutive features of primary histiocytic malignant lymphomas of the liver.

Adult↗
PubMed1983

[Value of liver puncture-biopsy for diagnosis, classification and treatment of chronic hepatitis].

In the assessment of chronic hepatitis, the liver biopsy serves the following purposes: 1) to confirm the fact that it is chronic. 2) to evaluate its degree of activity. 3) to check if there is cirrhosis or not. 4) to seek morphological proofs for the presence of viral, drug-induced or other aetiological agents. 5) to follow the evolution (in the natural course or during treatment) of the disease by comparing repeated liver biopsies. The initial classification of chronic hepatitis--proposed in 1968--has been reviewed by numerous authors; at the moment, it seems necessary, in order to correlate clinical and histological results better, to emphasize two important facts: 1) the spreading of liver necrosis if there is chronic active hepatitis. 2) the presence--or not--of cirrhosis. Some morphological arguments could be useful in order to diagnose the aetiology of chronic hepatitis. Empirical and specific immunological methods have become available for demonstrating HBsAg. If a chronic active hepatitis with multisystem involvement and/or abnormal serum antibodies is diagnosed, corticosteroid therapy is indicated. In others cases, especially those with virus B disease, the treatment differs according to medical teams.

Biopsy↗
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

[Nodular regenerative hyperplasia of the liver. Study of 15 cases and review of the literature].

The authors report 15 cases of nodular regenerative hyperplasia (NRH) of the liver observed in 10 women and 5 men during a 9 year period. Gastrointestinal bleeding due to ruptured esophageal varices revealed the liver disease in 11 cases. Hepatomegaly and splenomegaly were noted in 9 cases and ascites in 7. Anicteric cholestasis was demonstrated in 10 cases. Another disease, e. g. myelofibrosis and monoclonal gammapathy, was present in 11 patients. In 10 patients, portal diversion was performed; outcome being favorable with a follow-up of one to six years. The analysis of these cases and of the 113 previously published reports calls for the following comments: 1) In most cases, NRH is characterized by small-sized hepatocytic nodules scattered throughout the entire liver with no surrounding fibrosis; however this histological pattern may vary somewhat, with adjacent normal zones being found adjacent to typical cirrhotic fibrosis; although a precise morphometric study was not performed in our patients, obstruction of the tiny branches of intrahepatic portal veins was not observed. 2) Histological diagnosis of NRH is difficult and in most cases requires surgical biopsy specimens and specific coloration of the reticulin network. 3) NRH must be considered as a new cause of intrahepatic (sinusoidal or presinusoidal) portal hypertension and/or of chronic anicteric cholestasis. 4) A number of various conditions may be associated with NRH, the most frequent being Felty's syndrome and myeloproliferative disorders. 5) The pathogenesis of NRH remains unknown. 6) Portal diversion generally has a favorable outcome in this disease.

Adult↗
PubMed1982

[Anatamo-pathologic aspects of gold-salt induced cholestasis. Report of two cases with ultrastructural study (author's transl)].

The authors report two cases of gold-salt-induced cholestasis. They make a review of the thirteen cases previously related in the literature ; the cholestasis was constant, the hepatocytic necrosis was unusual and the gold-salts were difficult to visualize in the liver biopsy and more especially at the ultrastructural level. The immunological mechanism of hypersensibility is well established ; the possibility of an associated hepatotoxicity is debated.

Aged↗
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↗
PubMed1982

Hepatotoxicity of trichloroethylene-carbon tetrachloride mixtures in rats. A possible consequence of the potentiation by trichloroethylene of carbon tetrachloride-induced lipid peroxidation and liver lesions.

Liver histology was normal 24 h after the administration of trichloroethylene (1 ml . kg-1) in rats. It was normal, or showed necrosis of a few hepatocytes, after the administration of carbon tetrachloride (64 microliters . kg-1). In rats receiving both solvents, there was extensive centrilobular necrosis. In vitro, trichloroethylene did not initiate lipid peroxidation but potentiated that initiated by carbon tetrachloride; a similar potentiating effect was observed for a wide range of trichloroethylene concentrations (0.19-12 mM). In vivo, a wide range of trichloroethylene doses (0.064-1 ml . kg-1) similarly potentiated the hepatotoxicity of carbon tetrachloride. Administration of trichloroethylene (1 ml . kg-1), 5 h earlier, increased carbon tetrachloride-induced lipid peroxidation in vitro, and increased the hepatotoxicity of a subsequent dose of carbon tetrachloride (64 microliters . kg-1). Previous administration of carbon tetrachloride failed to modify lipid peroxidation and to increase the hepatotoxicity of trichloroethylene. We conclude that trichloroethylene potentiates the hepatotoxicity of carbon tetrachloride, possibly by increasing carbon tetrachloride-induced lipid peroxidation.

Animals↗
PubMed1981

Ultrastructural lesions of bile ducts in primary biliary cirrhosis. A comparison with the lesions observed in graft versus host disease.

Intrahepatic bile duct destruction is a characteristic feature of primary biliary cirrhosis and hepatic graft versus host disease. Lymphocytotoxicity against antigens on the surface of biliary cells is one of the cell mediated immune mechanisms debated in the pathogenesis of persistent bile duct destruction during primary biliary cirrhosis. Immune complex injury has also been hypothesized. In graft versus host disease, damage to bile duct cells is also believed to be due to a cytotoxic reaction of the grafted lymphoid cells against the host histocompatibility antigens, and immune complex deposition is likely to occur. The aim in this comparative ultrastructural study of intrahepatic bile ducts in 10 patients with primary biliary cirrhosis and six patients with hepatic graft versus host disease was to investigate whether identical or different ultrastructural lesions were detected in both diseases. Features of conspicuous necrosis of biliary cells, including cytolysosomes, apoptosis, and basement membrane disruption, were observed in both diseases. Numerous lymphocytes established close membrane contacts with biliary cells, especially with the necrotic ones. They had cytoplasmic pseudopods, and some of them displayed a uropod or contained lysosomal vesicles. Abnormalities of the bile duct basement membrane, also observed in both diseases, included thickening or multilayering and numerous lucent areas of rarefaction often containing osmiophilic inclusions. The striking similarity of the ultrastructural lesions in both diseases provides an additional morphological argument to suggest that certain common pathogenic mechanisms might be involved in the destruction of bile ducts in primary biliary cirrhosis as well as in hepatic graft versus host disease.

Adolescent↗