Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum catalase activity was moderately increased in fatty liver, acute alcoholic hepatitis and in the decompensated form of cardiac circulatory failure. It showed significant increase in acute yellow atrophy and in toxic hepatitis while no changes were detected in liver cirrhosis and viral hepatitis. Serum catalase activity showed a good correlation (r = 0.820) with the serum glutamate dehydrogenase activity. In accordance with our results, the inexpensive assay of serum catalase activity is suggested for the detection of severe liver cell damage.
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PMID:Serum catalase enzyme activity in liver diseases. 345 88

Vaquez and Aubertin advance three theories in explanation of the adrenal hyperplasia; first, that it may not be the cause of hypertension but "an antitoxic hyperplasia" caused by the retained products of metabolism which may be responsible also for the hypertension; second, that it may be the cause of hypertension but secondary to the renal lesion; third, that it may be the cause of hypertension but may antedate the renal lesion or be entirely independent of it. They, as well as other French writers, insist that this hyperplasia is almost constantly associated with chronic nephritis of the interstitial type and it is seldom found with the parenchymatous type of nephritis, or with other lesions. Hyperplasia of the adrenal, as far as my material enables one to judge, does not occur during the first and second decades. In the third decade it is relatively frequent in the absence of chronic arterial and renal disease but reaches the maximum in association with such disease after the fourth decade. It is an almost constant lesion in arteriosclerosis associated with chronic interstitial nephritis and left-sided heart hypertrophy, but occurs with almost equal frequency in arteriosclerosis with chronic nephritis of the parenchymatous type. It is a relatively frequent lesion of arteriosclerosis without chronic nephritis and of the latter without arteriosclerosis also. As the result of this analysis one is led to the view that while hyperplasia of the adrenal is a very frequent concomitant of chronic renal and arterial disease it is not exclusively a feature of either type of nephritis or yet of chronic vascular disease; but it probably represents the effect of some factor operating in that period of life in which chronic renal and arterial affections are most frequent. Worthy of special emphasis is the observation that the characteristic lesion of an adrenal, the seat of local arteriosclerosis, is of the type of the chronic productive inflammation seen in arteriosclerosis of the pancreas and kidney; that is, thickening of the vessels, increase of connective tissue and round cell infiltration. Associated with these changes is a hyperplasia which is very constant, and which may be, in part, of the nature of a compensatory hyperplasia similar to that seen in the liver of cirrhosis and acute yellow atrophy. A hyperplasia of this type, as has been shown, may occur in destructive lesions of the gland. This, however, does not explain hyperplasia in the absence of local vascular changes which fact is, possibly, as suggested by Landau, evidence, not of a correlation between kidney and adrenal, but of a vicarious hypertrophy depending upon lesions of some other organ of the body than the kidney, possibly some other ductless gland, affected by arteriosclerosis or other disease.
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PMID:THE RELATION OF LESIONS OF THE ADRENAL GLAND TO CHRONIC NEPHRITIS AND TO ARTERIOSCLEROSIS; AN ANATOMICAL STUDY. 1986 60

Experimental dietary hepatic injury (diffuse or focal necrosis and cirrhosis in rats, with or without ascites and pleural and pericardial effusion) is determined by the dietary factors instrumental also in the production of fat infiltration of the liver and thus opposed to the lipotropic activity of casein. Accordingly, rats maintained on a diet low in casein with a moderately high or high content of fat and without choline regularly exhibited hepatic injury after between 100 and 150 days. Supplements of l-cystine had an aggravating effect on the production of cirrhosis of the liver, whereas a supplement of choline alone reduced the severity and the incidence of hepatic injury, although not decisively. The combined administration of l-cystine plus choline or of dl-methionine in adequate doses, however, proved to be highly effective in preventing injury to the liver. These conclusions have been corroborated by the use of different modifications of the basal diet. Rats with dietary hepatic injury exhibit, in sequence, changes that vary from diffuse necrosis resembling human acute or subacute yellow atrophy to advanced portal cirrhosis. Diffuse necrotizing nephrosis was a frequent accompaniment of the hepatic injury. Cystine again, proved to be a factor which aggravated this condition.
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PMID:OBSERVATIONS ON THE CONDITIONS OF DIETARY HEPATIC INJURY (NECROSIS, CIRRHOSIS) IN RATS. 1987 Nov 89