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)

Epidemiological, clinical pathological investigations concerning Balkan nephritis (BN) have revealed some particular aspects which define this condition as a distinct nosologic entity. Its endemic familial character and its occurrence restricted to some limited geographic areas in Bulgaria, Yugoslavia and Romania, are highly unusual. BN leads to chronic impairment of the renal function which is, however, not constantly associated with edema and hypertension. The duration of the disease is prolonged; death takes place from uremia within five to ten years. Gross pathologic changes are consisting of severe bilateral atrophy of the kidneys, with structural changes suggesting a 'renal cirrhosis'. The etiology of the disease is obscure. Investigations carried out by means of electron microscopy and immunofluorescence tests are suggesting that the pathogenesis is rather complex. The role of a persistent tolerated or slow, latent virus infection in certain families, that of some toxic factors, and the implication of autoimmune mechanisms are to be considered.
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PMID:Balkan nephritis. A synthetic view on 50 studied cases. 13 May 42

A simple diagnostic strategy in the diagnosis of insulinoma in adult subjects is proposed based upon the literature and own experiences. It comprises measurement of plasma proinsulin, insulin and C-peptide as well as blood glucose after an overnight fast. When a low or normal proinsulin concentration is found, organic hyperinsulinaemia is very unlikely, while elevated proinsulin, after exclusion of uremia, hepatic cirrhosis, thyreotoxicosis and surreptitious administration of insulin or sulfonylurea drugs, strongly indicates this condition.
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PMID:Strategy in the diagnosis of insulinoma. 22 87

Plasma cortisol levels in 2 normal persons, 2 obese persons, 2 uraemic patients, and 2 patients with cirrhosis of the liver were raised in 4 steps by a combination of iv priming doses and continuous infusions of cortisol. Plasma cortisol levels and transcortin binding were measured as well as plasma clearance rates of labelled and unlabelled cortisol during each of the 5 experimental periods. Plasma cortisol levels increased less and plasma clearance rates of labelled and unlabelled cortisol increased more in obese persons than in normal persons; in patients with disturbed metabolism of cortisol (uraemia, cirrhosis of the liver) the reverse is true. Plasma clearance rates of free cortisol were calculated and differed from an estimated hepatic plasma flow of 0.7 1/min under certain conditions. Since free cortisol is metabolized faster than transcortin-bound cortisol, increasing plasma clearance rates of cortisol are probably due to increasing ratios free/bound cortisol when total plasma cortisol levels are raised. Low plasma clearance rates of cortisol in uraemia and cirrhosis of the liver are thought to be due to endproduct inhibition, respectively reduced liver cell mass.
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PMID:Plasma clearance of cortisol as a function of plasma cortisol levels in normal and obese persons and in patients with uraemia or cirrhosis of the liver. 45 24

Following ureterosigmoidostomy, encephalopathy with hyperammonemia may occur in the presence of cirrhosis, and the same complication was also observed in a few patients without liver damage. This suggests overloading of normal liver ureagenisis by an increased portal ammonia supply. To test this hypothesis and to try to produce an experimental model of chronic hyperammonemia without portal or hepatic damage, ureterocolostomies were performed in rats. These rats were compared with sham operated upon rats and with rats having chronic uremia induced by subtotal nephrectomy. Rats having a ureterocolostomy had chronic, but moderate, systemic hyperammonemia without any histologic hepatic damage and without gross behavioral modifications and slight uremia with only inconstant pyelonephretic lesions. In these rats, hyperammonemia results from hepatic overloading by the increased portal ammonia supply which is a consequence of both intestinal absorption of some urinary ammonia and increased intestinal ammoniagenesis induced by hydrolysis of urinary and circulating urea.
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PMID:Hyperammonemia following ureterocolostomy in the rat. 46 48

Pathologically low serum total triiodothyronine (T3) concentrations are a characteristic finding in patients with severe non-thyroidal illnesses. No adequate explanation has yet been offered for this phenomenon. We have, therefore, investigated the serum concentrations of total thyroxine (T4), total T3 and total 3,3',5'-triiodothyronine (reverse T3)--the metabolically-inactive metabolite of thyroxine--and of TSH in 13 patients with acute myocardial infarction, in 12 patients with compensated liver cirrhosis, in 9 patients with decompensated liver cirrhosis and in 15 patients with chronic renal failure on chronic intermittent haemodialysis by radioimmunoassay. The values obtained were compared to corresponding values of a normal control group (n - 23). According to our results the decrease in serum T3 combined with normal T4 concentrations in severe non-thyroidal illnesses seems to be a consequence of an alteration in thyroxine degradation. Two different possibilities of alteration can be considered: 1. inhibition of the overall deiodinationof T4, leading to low total T3 serum concentrations with concomitant normal to low reverse T3 serum concentrations (chronic uraemia), 2. a shift in the monodeiodination of T4 towards enhanced reverse T3 production, leading also to low total T3 concentrations, but with a concomitant increase in reverse T3 serum concentrations (myocardial infarction, liver cirrhosis). The results obtained in our patients with liver cirrhosis show, moreover, that this alteration of T4 metabolism depends on the severity of the illness.
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PMID:[Serum concentrations of thyroid hormones in severe non-thyroidal illnesses (author's transl)]. 63 38

Six patients with chronic uremia in whom ascites developed during maintenance hemodialysis are described. Their clinical and biochemical findings are reviewed and compared with data of 10 hemodialyzed patients without ascites. Liver cirrhosis was the origin of ascites in only one case. Hypoalbuminemia, liver cirrhosis, congestive heart failure, peritonitis, peritoneal tuberculosis and carcinomatosis were uniformly absent in the other patients. Long-term and marked overhydration seems to be at the origin of ascites. Lack of peripheral edema, probably due to ascites compartmentalization, was a constant finding in every noncirrhotic patient with ascites. When long-term overhydration was stopped after successful kidney transplantation or by means of diminished water and salt ingestion, reversal of the syndrome was attained. Nevertheless, ascites because of liver cirrhosis was not influenced by means of kidney transplantation. In three patients with ascites who did not receive a transplant, a significant reduction in water and salt ingestion was reached after intensive psychotherapy which led to reversal of the ascitic syndrome. In one anephric patient ascites did not develop despite water overloading. Survival has not been influenced by the formation of ascites. Further research is needed to determine the mechanism of sodium transfer across the peritoneal membrane. Influence of humoral factors can be considered, if an active transport mechanism could be demonstrated.
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PMID:Ascites in patients undergoing maintenance hemodialysis. Report of six cases and physiopathologic approach. 78 11

A 62-year-old woman gave clinical manifestation of liver cirrhosis. Urinary protein was false positive, no uremia was found and renal changes were entirely overlooked. Deposition of abundant lipids (globoside and ceramide trihexoside) was found in the kidneys; essentially degenerative changes of the tubular epithelia were noted. These renal changes were compared with those in Fabry's disease.
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PMID:Renal accumulation of glycosphingolipids. Report of a case and a review of literature. 80 60

Five hundred patients with the isomorphic pattern of the isoenzymes of serum lactate dehydrogenase (LDH) were surveyed. The isomorphic pattern of LDH isoenzymes is defined as a significant increase of total LDH with normal or low percentage of individual fractions, but with the LDH1:2 ratio less than unity. Diagnoses were, in descending order of frequency, cardiorespiratory diseases, malignancy, fracture, diseases of the central nervous system, infection/inflammation, hepatic cirrhosis and/or alcoholism, trauma without fracture, infectious mononucleosis, hypothyroidism, uremia, necrosis, pseudomononucleosis, viremia and intestinal obstruction. Incidence of increased serum activity in individuals without evidence of disease or drug explanation was 3 percent. Low PaO2 was observed in 88 percent of the 67 patients in whom it was measured.
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PMID:Clinical significance of the isomorphic pattern of the isoenzymes of serum lactate dehydrogenase. 90 Aug 65

A new low molecular weight protein was purified from the urine of uraemic patients. The protein was found to be glycoprotein with a molecular weight of 31 500, determined by SDS-polyacrylamide gel electrophoresis, and a carbohydrate content of 19%. It was electrophoretically heterogenous and migrated in the slow alpha1-region. The mean serum level in 20 apparently healthy individuals was 32+/-10 mg/1. The serum level was normal in 5 patients with severe reduction of plasma protein synthesis caused by cirrhosis of the liver but elevated in patients with a decreased glomerular filtration rate. The mean urinary excretion in 5 healthy individuals was 1.3 mg/24 h. Increased excretion was seen in 10 patients with varying degrees of uraemia.
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PMID:alpha1-Microglobulin, a new low molecular weight plasma protein. 100 Aug 59

Changes in brain serotonin and tryptophan concentrations probably represent one of the most important mechanisms in the regulation of eating behavior both in experimental animals and in humans. Anorexia, which accompanies numerous diseases, e.g., cancer, liver cirrhosis, and uremia, may recognize an increased brain availability of tryptophan as a common pathogenic mechanism. This will lead to a rise in brain serotonin synthesis, which, in turn, is responsible for a reduction in food intake. According to this hypothesis, the anorexia observed in various diseases could be improved either by a decrease in the cerebral synthesis of serotonin or by a reduction in the entry of tryptophan into the brain.
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PMID:Increased availability of tryptophan in brain as common pathogenic mechanism for anorexia associated with different diseases. 180 75


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