ABSTRACT
(+)-Cyanidanol-3 is considered to have cytoprotective effect in toxic liver injury. A randomized clinical trial was carried out in alcoholic precirrhotic patients and in chronic active hepatitis with (+)-cyanidanol-3 versus placebo. The daily dose of the drug was 1.5-2.0 g for a one-year period. A: Toxic alcoholic precirrhotic liver disease: 38 patients were treated with (+)-cyanidanol-3, 36 with placebo. We found significant improvement in the subjective symptome like asthenia and anorexia, and in serum aspartate-transaminase (GOT) levels. However, it is possible that the improvement was in part due to abstinence from alcohol. B: Chronic active hepatitis: previously introduced continuous prednisolone therapy (10-15 mg/day) was combined with (+)-cyanidanol-3 in 13 patients and with placebo in 12 controls. The results showed a more favourable, but not significantly better response in patients receiving (+)-cyanidanol-3 versus placebo. We concluded that the drug might be of benefit in some cases with chronic active hepatitis as an adjunct to corticoid therapy.
Subject(s)
Benzopyrans/therapeutic use , Catechin/therapeutic use , Hepatitis, Alcoholic/drug therapy , Hepatitis, Chronic/drug therapy , Liver/drug effects , Adult , Aged , Clinical Trials as Topic , Drug Therapy, Combination , Humans , Liver Function Tests , Middle Aged , Prednisolone/therapeutic useABSTRACT
Changes in oral glucose-tolerance have been studied in patients subjected to endoscopic retrograde pancreatography. Glucose tolerance is impaired 72 hours after ductography, and significant changes can still be seen even after one month; glucose tolerance returns to normal six to 12 months after pancreatography. In an attempt to discover the mechanism underlying impaired tolerance serial measurements were made of plasma insulin and glucagon levels. The observation that the ratio I/G decreased in these patients indicates that enhanced glucagon release, probably due to mechanical and/or osmotic injury, may be responsible for the hyperglycaemia that is observed.
Subject(s)
Cholangiopancreatography, Endoscopic Retrograde/adverse effects , Hyperglycemia/etiology , Amylases/blood , Blood Glucose/analysis , Contrast Media , Follow-Up Studies , Glucagon/blood , Glucose Tolerance Test , Humans , Insulin/bloodSubject(s)
Pancreas/diagnostic imaging , Pancreatitis/etiology , Somatostatin/therapeutic use , Amylases/blood , Endoscopy/adverse effects , Glucagon/blood , Humans , Hydrocortisone/blood , Insulin/blood , Pancreatitis/prevention & control , Radiography/adverse effects , Somatostatin/administration & dosageABSTRACT
Glutamate dehydrogenase (GDH) and glutaminase activity in the rat brain was altered by chronic ammonia intoxication, subacute liver injury induced by CCl4 or digalactosamine, and the combination of them. GDH activity was found to increase considerably in ammonia intoxication without liver damage, probably as a result of enzyme induction. GDH activity failed to increase, while glutaminase was appreciably elevated. when ammonia intoxication was associated with hepatic injury. Toxicological studies have indicated that these changes in brain enzyme levels may be involved in the mechanism of ammonia neurotoxicity.
