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)

The molar ratio valine + leucine + isoleucine/phenylalanine + tyrosine was determined in the plasma of patients with liver disease of varying aetiology and severity and in an age and sex matched control group. In the control group of 58 subjects the mean ratio was 3.3 +/- 0.5 (ISD). The mean ratio was significantly lowered in groups of 25 patients with alcoholic cirrhosis (P less than 0.001), 25 patients with chronic active hepatitis (P less than 0.001), 23 patients with primary biliary cirrhosis (P less than 0.001), and 11 patients with cryptogenic cirrhosis (P less than 0.001). In a group of 50 patients with cirrhosis, the ratio was significantly lowered (P less than 0.001) irrespective of the presence of hepatic encephalopathy. A good correlation existed between the value of the ratio and the severity of the liver disease as judged histologically, with values of the ratio appearing to reflect histological change irrespective of the patient's clinical condition. There was no significant diurnal variation in the value of the ratio. Lowering of this plasma amino acid ratio appears to be secondary to liver disease and quite independent of the presence of hepatic encephalopathy.
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PMID:Plasma ratio of valine, leucine and isoleucine to phenylalanine and tyrosine in liver disease. 73 76

Serum prolactin levels were determined following stimulation by sulpiride in 20 patients with nonalcoholic liver cirrhosis and 10 normal controls. Prolactin response was essentially the same in the two groups. Only 5 cirrhotics, all with ascites, showed a lower prolactin response after sulpiride stimulation. This was interpreted as a consequence of a rapid prolactin escape from blood into the ascitic fluid, as it was shown to be the case in 2 of these patients. It is concluded that prolactin secretion in nonalcoholic liver cirrhosis is essentially normal. The higher prolactin levels found by others in alcoholic cirrhosis could be the result of a direct effect of alcohol on hypothalamic structures involved in prolactin secretion.
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PMID:Prolactin secretion in nonalcoholic liver cirrhosis. 73 36

Furosemide is frequently used for ascites and causes adverse reactions (AR). In an intensive prospective drug monitoring study of 1,920 patients, 172 (8.9%) had cirrhosis of the liver and received furosemide. Mean age was 53 years, and 66.3% were male; and 87% had alcoholic cirrhosis. Eighty-eight (51.2%) had 221 events that by consensus of the monitoring team and attending physicians were either definitely of probably related to furosemide. No AR was fatal but 24% of patients had severe reactions. Almost all reactions were dose-related (96%). The most common were electrolyte disturbances (23.3% of patients) and volume depletion (14%). Furosemide-induced coma occurred in 20 (11.6%) patients and was more frequent in patients with prior hepatic encephalopathy (p less than 0.0005). Higher total doses (p less than 0.001), hyerbilirubinemia (p less than 0.05), prolonged prothrombin time (p less than 0.02), and longer hospital stay (p less than 0.001) were associated with higher frequencies of AR to furosemide. The frequency of hypokalemia did not decrease when potassium chloride or potassium-sparing diuretics were added to furosemide therapy. Frequdncy of AR did not correlate with age, sex, renal impairment, serum albumin, transaminase, or alkaline phosphatase.
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PMID:Furosemide-induced adverse reactions in cirrhosis of the liver. 75 67

The value of emergency upper gastrointestinal fibre-endoscopy, followed where required by the use of a modified Sengstaken tube, was studied during 84 episodes of acute bleeding in 75 patients who had evidence of portal hypertension with varices. The portal hypertension was due to alcoholic cirrhosis in 80% and to cryptogenic cirrhosis in 9% of the patients. By definition, varices were present in all patients, but in only 66% of episodes were the varices the cause of the bleed. The correct diagnosis of the source of bleeding was made at endoscopy in 89%. A Boyce modification of the Sengstaken-Blakemore tube was passed in 73% of the episodes of variceal bleeding. It effectively stopped the bleeding primarily in 85% of patients but was successful as a final definitive measure only in 46%. Furthermore, only 40% of the patients in whom the tube was passed, survived. Mortality rate could be related to the severity of the bleed and to hepatocellular dysfunction. Survival increased from 23% in those patients with jaundice, ascites, and encephalopathy on admission to 92% in those without these manifestations. The in-hospital survival rate was 52% in patients bleeding from varices and 64% in those bleeding from other causes, with an overall survival rate of 56%, indicating the poor prognosis in cirrhotic patients with gastrointestinal bleeding, irrespective of the cause.
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PMID:Fibreoptic endoscopy and the use of the Sengstaken tube in acute gastrointestinal haemorrhage in patients with portal hypertension and varices. 77 87

The cholesterol-lowering effect of portacaval anastomosis in homozygous familial hypercholesterolemia suggested a study of lipid metabolism in cirrhotic patients after portasystemic anastomoses. Fasting serum cholesterol, triglycerides, insulin, and glucagon levels were obtained in 20 patients with alcoholic cirrhosis and portacaval anastomosis, and in 21 nonshunted subjects with cirrhosis. After 100 g of glucose, given orally, insulin and glucagon levels were measured. In the shunted patients serum cholesterol was higher than in the nonshunted subjects, 240 +/- 15 mg per 100 ml (mean +/- 1 SEM) versus 180 +/- 13 mg per 100 ml, P less than 0.01. Triglycerides were normal in both groups. Fasting insulin was elevated to a greater extent in the shunted patients with cirrhosis (36 +/- 5 muU per ml) than in the nonshunted patients (22 +/- 4 muU per ml), P less than 0.05. Two hours after glucose, insulin levels were also elevated to a greater extent in the shunted subjects (304 +/- 50 muU per ml) than in the nonshunted subjects (167 +/- 29 muU per ml), P less than 0.03. Fasting glucagon (corrected for interference factor) was elevated to a greater extent in the shunted subjects (204 +/- 35 pg per ml) than in the nonshunted subjects (80 +/- 19 pg per ml), P less than 0.01. The explanation for serum cholesterol elevation after surgical shunting in cirrhotics is unknown. Two possible hypotheses--the differential action of insulin and glucagon on cholesterol metabolism and the effects of shunting on the cirrhotic liver--are discussed.
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PMID:Serum lipids, insulin, and glucagon after portacaval shunt in cirrhosis. 83 May 79

The serum immunoglobulin (Ig) G, A, and M levels were investigated with respect to their differential diagnostic significance, pathogenesis and estimation of prognosis of different forms of liver disease. The sera of 204 patients with acute hepatitis, fatty liver I and II, and cirrhosis, and of 110 healthy adutls were quantitatively determined for immunoglobulins. 1. IgG- and IgA-concentrations higher than 2000 mg% and 330 mg%, respectively, indicate chronic aggressive hepatitis or cirrhosis, and exclude all other groups. 2. A clear correlation between HBsAG (Australia Antigen) and immunoglobulin content could not be demonstrated in any group; 3. A significantly elevated level of IgA was observed in alcoholic cirrhosis when compared to non-alcoholic cirrhosis. No such differences were found inhe other groups. 4. Acute and chronic persistent hepatitis show a similar increase of immunoglobulins. Thus persistent high levels of Ig following acute hepatitis indicate the development into a chronic hepatitis. 5. A relative increase of IgA rather than IgG corresponds to the degree of inflammatory activity of a liver process.
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PMID:[Quantitative serum immunoglobulin determination: differential diagnostic significance for liver disease (author's transl)s]. 84 Jan 24

The process of fibrin formation was systematically in 25 patients with severe alcoholic cirrhosis. Results of functional tests are reported. A significant lengthening of the thrombin time was found which could not be completely attributed either to hypofibrinogenaemia or to an increase in physiological anticoagulants or to the presence of pathological antithrombins. A defect in fibrin polymerization was seen in the absence of significant levels of antipolymerizing agents. Indirect evidence pointed to an abnormal fibrinogen function. This was mainly suggested by the "polymerization curves" of mixtures of normal and pathological plasmas and the changes in physico-chemical properties of the clot (optical and elastic properties; tensile strength). Altered synthesis in hepatocytes may lead to an "acquired dysfibrinogenaemia" in the late stages of liver cirrhosis, although alteration of a normal fibrinogen molecule after secretion cannot be definitely excluded.
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PMID:Impaired fibrin formation in advanced cirrhosis. 86 94

1. Mitochondria and microsomal fractions have been isolated from liver biopsies from patients with alcoholic cirrhosis, cryptogenic cirrhosis or chronic aggressive hepatitis. 2. Cirrhotic livers yieled fewer mitochondria than normal liver. 3. The most significant change was a decrease in mitochondrial respiratory control. Cirrhotic microsomal fractions had a 50% diminution in cytochrome b5 and cytochrome P-450 content. 4. The two patients with chronic aggressive hepatitis showed similar mitochondrial and microsomal changes.
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PMID:Mitochondrial functions and content of microsomal and mitochondrial cytochromes in human cirrhosis. 88 31

Serial measurements of complement components were performed in fifty-nine patients with acute, uncomplicated hepatitis and twelve with alcoholic cirrhosis. Thirty-one of the former group had detectable hepatitis B antigen. Abnormal complement profiles were observed in nine patients with hepatitis B and seven with antigen-negative hepatitis. Low levels of C4, C3 and factor B were common in the subjects with cirrhosis and confined to those cases with severe reduction in serum albumin and/or prothrombin index. By contrast, the complement changes in the patients with hepatitis occurred without significant alteration in these parameters; certain subjects also had reduction in C1q and C5 and a significant number had C3d detectable in fresh plasma. The pattern of abnormality suggests predominant involvement of the classical pathway and it is concluded that this results, at least in part, from an immune process evident only in the early clinical phase of hepatitis. Such gross changes in complement are likely to reflect immune-complex activity and it is proposed that these complexes may be important in the clearance of virus material. The data supports a previous suggestion that recovery from acute hepatitis is primarily dependent on host immune competence rather than viral cytotoxicity or generation of immune complexes.
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PMID:Acute hepatitis: significance of changes in complement components. 89 Oct 25

Survival rates were compared in 82 patients who underwent therapeutic portacaval shunt. All patients were followed for at least 5 years after shunt or until death. Survival rates were calculated by Life Table methods. Based on a combination of currently accepted histological and clinical criteria, there were 45 patients with Laennec's cirrhosis, 29 patients with postnecrotic cirrhosis, 11 of whom had histological evidence of chronic active hepatitis, and 8 patients with primary biliary cirrhosis. Survival rates were similar in all three groups, alcoholic cirrhosis, postnecrotic cirrhosis, and primary biliary cirrhosis. Hepatic reserve, as defined by Child's classification, provided the best criteria for predicting survival. The type of shunt, end-to-side, side-to-side, or splenorenal, did not influence survival. Histological evidence of chronic active hepatitis adversely affected survival in patients with postnecrotic cirrhosis. However, histological evidence of ongoing alcoholic hepatitis in patients with Laennec's cirrhosis did not influence survival adversely. The data indicate that once a patient with cirrhosis has bled from esophageal varices, the etiology of the cirrhosis is not a major factor in determining survival after a therapeutic portacaval shunt.
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PMID:Survival in patients with postnecrotic cirrhosis and Laennec's cirrhosis undergoing therapeutic portacaval shunt. 89 71


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