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)

In an attempt to determine the frequency of liver injury in adult coeliac disease (A.C.D.) the case records of 74 consecutive patients were examined. In 13 cases histological sections of the liver were available and in 5 of these there were signs of reactive hepatitis. Histological signs of distinct hepatic injury with cirrhosis and/or chronic active hepatitis were found in 7 other patients. In 5 of these serum-IgA was normal, whereas 16 out of 20 control patients with liver cirrhosis not associated with A.C.D. had raised serum-IgA. Serum-aspartate-aminotransferase and serum-alanine-aminotransferase were determined in 53 patients; 29 had raised concentrations. In 19 patients serum-aminotransferases were repeatedly determined before and during the dietary regimen and there was a significant reduction in enzyme concentrations during treatment. The median concentration of serum-alkaline-phosphatase was also reduced during treatment but not significantly. The histological evidence of liver injury in 16% and the abnormal liver-function tests in 39% of the patients indicate that hepatic injury is common in A.C.D. Since liver-function tests or liver biopsy specimens were available for only about two-thirds of the patients, liver damage in A.C.D. may be more common than indicated by these results. The effect of a gluten-free diet on aminotransferase concentrations indicates that the liver injury may be reversible and suggests that in some A.C.D. patients progressive liver damage may be prevented by suitable treatment. Since A.C.D. is not always recognised, the diagnosis should be considered in patients with liver disease of unknown aetiology.
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PMID:Hepatic injury in adult coeliac disease. 6 80

Most forms of liver disease are probably associated with impaired gluconeogenesis, although hypoglycaemia is rarely an important clinical feature. Blood concentrations of the gluconeogenic precursors, lactate, glycerol and alanine are elevated although, in certain situations, alanine levels may be decreased. Abnormal glucose tolerance is present in both acute and chronic liver disease, but is usually not of clinical importance. The mechanism of glucose intolerance remains uncertain, with diminished hepatocyte mass, portal diversion and insulin resistance the major postulates. Indeed, the importance of the liver in disposing of an oral glucose load, is still questioned. Both hyperinsulinism and hypoinsulinism are found in liver disease, with hyperinsulinism common in cirrhosis and acute viral hepatitis. This is accompanied by insulin resistance. The hyperinsulinism is probably due to defective hepatic clearance of insulin rather that to over-production. The cause of the insulin resistance remains to be established. Glucagon levels are raised and may contribute to this resistance. Growth hormone levels are also increased but are associated with low somatomedin levels and the role of growth hormone in insulin resistance is therefore questionable. Future developments include use of new animal models, studies of biopsy specimens and studies of hepatic hormone receptors.
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PMID:Carbohydrate metabolism in liver disease. 79 84

Derangements in glucose, amino acid and protein metabolism in patients with liver cirrhosis were examined with special reference to plasma levels of human growth hormone (HGH). Changes in blood glucose, IRI (immunoreactive insulin), HGH, FFA (free fatty acid) and plasma free amino acid levels were determined in controls and patients following either oral glucose load, protein feeding or intravenous arginine infusion. 1) In patients with liver cirrhosis, incidence of glucose intolerance after glucose tolerance test (GTT) was high and IRI levels were elevated in the fasting state as well as after glucose, protein or arginine loads. 2) Fasting levels of blood HGH were significantly higher in liver cirrhosis than in controls. GTT revealed that blood HGH levels decreased slightly during the rising phase of blood glucose, and conversely, increased during the falling phase of glucose (180 minutes after the glucose load) both in controls and in patients. In cirrhotic patients, marked increases in HGH levels were observed both 120 minutes after the protein load and 60 minutes after the arginine infusion. 3) Fasting levels of serum FFA were significantly higher in liver cirrhosis than in controls. Both controls and patients, however, showed a similar pattern of change in FFA levels following GTT or protein ingestion, i.e. a minimum value 120 minutes after the load and a gradual increase thereafter. 4) Fasting levels of plasma free amino acids were significantly higher in cirrhotic patients than in controls. After the glucose load, however, slight decrease was noted in some amino acid levels. All the amino acid levels examined were elevated following protein ingestion, particularly in cirrhotic patients. 5) A positive correlation was demonstrated in cirrhotic patients between total plasma free amino acids and maximal HGH responses following protein ingestion. Similar significant correlations were observed between the maximal HGH response and the plasma level of several amino acids such as His., Ser., Gly., Thr., Ala., and Ileu., respectively. 6) In cirrhotic patients, negative correlations were demonstrated between fasting levels of serum albumin and total plasma free amino acids or maximal HGH responses, respectively, after the protein ingestion. From these results it was inferred that derangements in the metabolism of protein and amino acids in cirrhotic patients may result in an increase in plasma free amino acid level which in turn stimulates HGH secretion. It was surmised that the HGH levels so elevated in the patients may cause FFA mobilization which in effect results in the glucose intolerance.
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PMID:[Studies on glucose, amino acid and protein metabolism in patients with liver cirrhosis in relation to plasma levels of human growth hormone (author's transl)]. 81 50

Liver biopsy and liver function tests were performed in 17 obese patients before and 14 months after intestinal shunt operation for obesity. In another 20 patients liver biopsy was performed postoperative only, in 12 patients preoperatively only. Steatosis was present in 85 per cent. of the patients before the operation. After the operation steatosis decreased in half the patients and increased in the other half. In patients with biopsy twice postoperatively there was a significant trend of decreasing steatosis up to 56 months after the operation. No patient developed cirrhosis during the time of observation. Within the first postoperative year there was a substantial and significant increase in serum alanine-aminotransferase and a minor increase in alkaline phosphatases and BSP. There was no correlation between the rate of weight loss and the change in steatosis or liver function.
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PMID:Liver morphology and liver function before and after intestinal shunt operation for obesity. 115 33

In glycogen storage disease type III (glycogen debranching enzyme (DE) deficiency), the activities of serum alanine aminotransferase, aspartate aminotransferase and lactate dehydrogenase may be strikingly elevated during childhood but are low during adult life. To determine the pattern of the elevated serum enzyme activities in relationship to diet, the biochemical subtype and clinical symptoms, 13 patients with DE deficiency were studied. Activities of serum aspartate and alanine transaminases, lactate dehydrogenase, and alkaline phosphatase were markedly elevated during infancy. Continued elevation of enzyme activities during childhood appeared to be related to DE deficiency in liver, but unrelated to DE deficiency in muscle. Activity elevations correlated inconsistently with diet and poorly with childhood growth rate or the presence of hypoglycaemia. The serum enzyme activities declined around puberty concomitantly with a decrease in liver size. Although periportal fibrosis and micronodular cirrhosis indicated the presence of hepatocellular damage during childhood, the decline in serum enzyme activities with age and the absence of overt hepatic dysfunction suggest that the fibrotic process may not always progress.
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PMID:Glycogen debranching enzyme deficiency: long-term study of serum enzyme activities and clinical features. 129 83

We studied the effect of ursodeoxycholic acid in 19 patients with primary biliary cirrhosis, mainly stages III and IV. The dose of UDCA employed was 10-15 mg/kg body weight per day. After 1 yr, 17 patients were still using UDCA, and the mean values of serum alkaline phosphatase, gamma-glutamyltranspeptidase and alanine-aminotransferase had fallen significantly. Serum bilirubin, initially elevated in 7 of the 13 late-stage (III and IV) patients, showed a further increase in 3 of the 7 patients. In 2 of these 3 patients, UDCA had to be withdrawn (dose reduction had no effect). One patient developed a decompensated cirrhosis in spite of UDCA withdrawal. Pruritus worsened in 4 patients, all of whom were late stage patients. Ten late-stage (III-IV) patients showed improvement in liver biochemistry and clinical findings as did all early-stage PBC patients. Thus, UDCA treatment is not beneficial for all PBC patients. Special care should be taken in the early phase of UDCA therapy in later-stage (III-IV) patients: frequent biochemical checks should be carried out, for instance every 2 weeks in the first 2 months after starting UDCA, especially the estimation of bilirubin.
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PMID:Ursodeoxycholic acid treatment in primary biliary cirrhosis with the emphasis on late stage disease. 140 34

In the last decade, the primary, biliary liver cirrhosis was diagnosed in 17 female patients aged between 33 and 72 years. The most frequent complaint were itching and jaundice. Hepatomegaly and itching predominated in the clinical signs Laboratory tests have shown and increase in alkaline phosphatase activity, gamma-glutamyltranspeptidase, and alanine-aminotransferase activities, accelerated ESR and decrease in blood serum albumins. Immunological abnormalities were found in 15 patients, including 12 with antimitochondrial antibodies. Liver biopsy was carried out in all patients enabling to diagnose the primary cirrhosis in 14 of them. Duration of the disease was between 1 and 9 years. Immunosuppressive treatment was carried out in 10 patients, and symptomatic treatment in the remaining 7 patients. No difference in the effect of therapy on actual health state of patients was seen.
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PMID:[Primary biliary liver cirrhosis in patients treated at Szczecin hospitals in 1978-1988]. 166 45

Serum CA 19-9 and alpha-fetoprotein (AFP) levels were determined in 211 patients with liver cirrhosis and 27 with primary hepatocellular carcinoma (HCC) associated with liver cirrhosis. This was done to determine the usefulness of CA 19-9 level with respect to AFP level in distinguishing between these two illnesses, and to assess the influence of some clinical and biochemical variables on these tests in patients with liver cirrhosis with or without primary HCC. Pathologic AFP values were found in 23 of 27 (sensitivity, 85%) patients with HCC; CA 19-9 levels increased in only 12 of 27 (sensitivity, 44%) HCC patients, the values being comparable with those of patients with liver cirrhosis. In liver cirrhosis a substantial number of false-positive values was found for both markers, although they were higher for CA 19-9 (50 of 211 versus 39 of 211). In liver cirrhosis correlations were found between AFP level and alanine amino-transferase level; and between CA 19-9 level and (1) total bilirubin value, (2) alkaline phosphatase level, and (3) pseudocholinesterase level. The authors conclude that CA 19-9 level is a poor biochemical marker, inferior to AFP level, in the detection of a carcinomatous transformation of liver cirrhosis. The finding of false-positive AFP values in liver cirrhosis seems mainly attributable to cellular proliferation and necrosis. Cholestasis seems to greatly affect serum CA 19-9 level variations, probably by reducing its liver metabolism.
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PMID:Serum CA 19-9 and alpha-fetoprotein levels in primary hepatocellular carcinoma and liver cirrhosis. 138 Dec 71

In the post-absorptive stage L-alanine is the main source of alpha-amino-nitrogen reaching the liver as glucose precursor. This aminoacid has been used as a measure of urea synthesis capacity in several pathologic conditions, but it has not been employed sistematically in patients with liver cirrhosis. We tried to address this issue by evaluating: a) L-alanine plasma levels, b) urea extraformation (UE), and c) ammoniogenesis after oral L-alanine (0.25 and 0.50 g/kg b wt) in healthy control subjects and in patients with nonalcoholic compensated (Child-Pugh's A class) and decompensated (Child-Pugh's B and C) liver cirrhosis. L-alanine plasma levels after oral load were higher and lasted longer in cirrhotics as compared to controls. Furthermore, after L-alanine oral load, significantly higher ammonia plasma levels were observed in cirrhotics than in controls. Changes in the urea extraformation were comparable in cirrhotics and controls. Both delayed L-alanine elimination from plasma and L-alanine-induced hyperammoniemia were more evident in decompensated cirrhotics and related to L-alanine dose.
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PMID:L-alanine plasma levels after oral loads in non-alcoholic liver cirrhosis: relationship with urea extraformation and ammoniogenesis. 174 21

Four hundred and four patients (273 men, 131 women) aged 3 to 85 years with chronic Hepatitis B virus (HBV) infection seen during a five year period were analysed. At presentation, 177 patients (44%) were Hepatitis B e Antigen (HBeAg) positive (mean age 32 years) and 217 patients (54%) were anti-HBe-positive (mean age 40 years). Ten patients (2%) were negative for HBeAg and anti-HBe. Serum HBV-DNA was detected in 169 patients (42%). 85% of the HBeAg-positive patients had detectable serum HBV-DNA and 9% of the HBeAg-negative patients were positive for serum HBV-DNA. The mean serum Alanine amino-transferase (ALT) and Aspartate amino-transferase (AST) levels were higher in HBeAg-positive patients (75 and 52 iu/l) than in HBeAg negative patients (46 and 37 iu/l) (P less than 0.001). Liver biopsies were performed in 135 patients. Fifty-three (39%) had minimal changes, 61 (45%) chronic hepatitis (CPH, CLH & CAH) and 21 (16%) cirrhosis. There was no significant difference in the histologic distribution between HBeAg-positive and HBeAg-negative groups. Two hundred and fifty eight patients were followed up for a mean duration of 2 years (range 3 to 108 months). The cumulative probability of clearing HBeAg at the end of the first, second and third year were 14%, 16% and 18% respectively. Of these, the cumulative probability of developing anti-HBe over one, two and three years were 8%, 9% and 11% respectively. Reversion to HBeAg occurred in 1.5% of patients who were HBeAg-negative at presentation and 11% of HBeAg-positive patients who cleared HBeAg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic hepatitis B infection in Singapore. 179 64


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