[Significance of diathermic biopsy in the diagnosis of submucosal mesenchymal gastric tumors].
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Biomedical subjects
Publications and source records attributed to I Kádas.
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Biotransformation capacity was investigated in patients with various degrees of alcoholic liver damage. Aim of the investigation was to study the impairment of biotransformating ability during progression of liver damage. Four groups of patients with various liver diseases (alcoholic fatty liver, chronic persistent hepatitis, chronic active hepatitis, alcoholic cirrhosis) and two groups as controls were studied. The investigations were carried out with exogenous test substances (antipyrine, menthol and sulphadimidine) and by determination of D-glucaric acid excretion. It has been concluded that the depression of biotransformating ability in patients with alcoholic liver diseases is progressing during development of diseases. The changes in various metabolic pathways are different, and they seem to be more marked in the first phase of biotransformation than in the second phases.
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Hepatic angiosarcoma developed in a 46-year-old man, who had had 7-months of arsenic therapy 24 years before. The role of arsenic in the etiology of angiosarcoma of the liver is well know, although rarely has it followed such a brief period of arsenic therapy.
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A gastric tumor was found in a 64-year-old woman who later developed flushing, tachycardia, headache, and lacrymation. The plasma pancreatic polypeptide (PP) level was 700 times normal values, and the majority of the tumor cells were immunoreactive to PP antiserum. Symptoms were alleviated, and PP levels fell after embolization of the hepatic artery for liver metastases. This is the first reported case of gastric PP-producing endocrine tumor.
There are some controversies regarding the effect of (+)-cyanidanol-3 on hepatic drug metabolism. In the present study the effect of (+)-cyanidanol-3 was investigated on the microsomal and mitochondrial enzyme functions (hydroxylation, glucuronide production, D-glucaric acid excretion and acetylation) in alcoholic liver disease. Eight patients with biopsy-proven chronic alcoholic hepatitis were investigated before and after a 10-day, as well as after a further 30-day, treatment with (+)-cyanidanol-3 (Catergen), 3000 mg/day orally. Besides biochemical liver function tests (serum bilirubin levels, GOT, GGT), antipyrine metabolic clearance rate, mentholglucuronide production, urinary D-glucaric acid excretion and sulphadimidine kinetics were determined. Biochemical liver function tests improved markedly after the first period of treatment, at the same time antipyrine metabolic clearance rate decreased. Menthol-glucuronide production and D-glucaric acid excretion decreased significantly only after the second two course of Catergen administration. Sulphadimidine kinetics was not remarkably changed. Our findings suggest that (+)-cyanidanol-3 inhibits the hepatic microsomal drug metabolizing enzyme function in chronic alcoholic hepatitis.
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Thirty-six patients with biopsy-proved chronic active hepatitis (CAH) were randomized. Of these 18 patients, 15 of them HBsAg and/or anti-HBc positive, received (+)-cyanidanol-3 (Catergen, Zyma) in doses of 1.5 g daily for 6 months in addition to the previously started low dose (10-15 mg/day) prednisolone. The other 18 patients, 16 of them HBsAg and/or anti-HBc positive, continued on the former corticosteroid treatment exclusively. After 6 months an overall clinical-biochemical improvement was noted in 10 cyanidanol-treated and in 6 control patients, while the condition deteriorated in 4 drug-treated and 8 control subjects. Serum GPT activity decreased to less than twice the normal in 12/16 drug-treated and in 7/13 control subjects, gamma-GT fell to normal in 7/16 cyanidanol-treated and in 1/10 control patients, IgG fell to normal in 4/8 drug-treated and in 1/9 control patients who all had initially elevated values. The percentage of "active" E-rosette forming cells fell in both groups but the decrease was significant only in the control cases, i.e. cyanidanol inhibited the progressive fall in circulating T cells during the course of the disease. Lymphocyte proliferative response to phytohaemagglutinin stimulation, as measured by 3H-thymidine incorporation, significantly increased in the cyanidanol group. Anti-HBs titres were markedly raised in 7/15 drug-treated and in 2/16 control patients. Thus, cyanidanol had some slight beneficial effect on biochemical liver function tests and the immunological activity in CAH patients. Its use may be recommended as an adjuvant constituent of the complex therapy of the disease.
The biochemical liver function tests form an integral part of diagnostic practice in hepatology. In this study the parameters suited for the estimation of drug elimination and of the induced state of the liver, thus the excretion of D-glucaric acid, of menthol glucuronide and the parameters of antipyrine and sulphadimidine kinetics were correlated with the results of biochemical laboratory tests in patients with chronic liver disease. The aim was to establish universally valid quantitative correlations between the above results. Multiple relationships were revealed, but generally valid correlations for the group of liver diseases occurred only in special relationships (serum albumin level and antipyrine T1/2; serum bilirubin level and sulphadimidine T1/2). The results have been evaluated from the methodological aspect to work out an appropriate dosage regime in liver diseases.