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 distal splenorenal shunt (DSRS) was performed in 125 consecutive variceal bleeders. To date, no patients have been lost to follow-up (mean of 79 +/- 20 months). Liver pathology was documented in 85 patients: 45 patients had schistosomal hepatic fibrosis, 17 had nonalcoholic cirrhosis, and 23 had mixed pattern (hepatic fibrosis and cirrhosis). The preoperative data base for these three groups was matched (p greater than 0.05), with a mean follow-up of 79 +/- 20, 70 +/- 14, and 77 +/- 22 months for each population, respectively. The results showed low operative mortality (4.8%), high cumulative patency rate (94.8%) and low recurrent variceal hemorrhage (5.6%). The biochemical data showed significant increase in serum bilirubin (p less than 0.001) and aspartate transaminase (AST) (p less than 0.05) in the nonschistosomal patients. Chronic hyperbilirubinemia was found in 33% of the schistosomal group. Prograde portal perfusion was detected in 94% of the patients, with development of collaterals in 91%. The angiographic pattern of these collaterals was 50% pancreatic, 45% gastric, and 26% colosplenic. Patients with mixed liver disease had a high incidence of Grade III portal perfusion (57%) and more common pancreatic and gastric collaterals (71%). The cumulative survival for all patients was 74.1%, with hepatic cell failure being the leading cause of death (13 patients, 50% of all deaths). The schistosomal patients had a 91.6% incidence, whereas the cirrhotic and mixed groups had survival rates of 75.6% and 65.2%, respectively. Also, of a 15% total incidence of encephalopathy, 4.4% was related to the schistosomal patients, 23.5% to the cirrhotics, and 21.7% to the mixed population. Statistically, the survival rate was significantly better (p less than 0.05) and encephalopathy was significantly lower (p less than 0.05) in the schistosomal population. In conclusion, this data shows that: 1) DSRS has a high patency rate and a low variceal hemorrhage recurrence rate; 2) it maintains some degree of portal perfusion in patients with different nonalcoholic liver diseases, despite development of collaterals; and 3) the schistosomal patients have a better survival rate, with a low incidence of encephalopathy after DSRS, compared with the cirrhotic and mixed populations.
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PMID:Schistosomal versus nonschistosomal variceal bleeders. Do they respond differently to selective shunt (DSRS)? 278 63

We have examined the value of serum type III procollagen amino propeptide (PIIINP) measurement both in evaluation of disease activity and in estimation of prognosis in primary biliary cirrhosis (PBC). 55 paired sera from 32 PBC patients not receiving treatment known to affect PIIINP levels not with non-hepatic inflammatory conditions were used to estimate serum PIIINP by radioimmunoassay. Significant correlations were found between serum PIIINP and serum albumin (P less than 0.001), bilirubin (P less than 0.002) and aspartate transaminase (P = 0.01). The mean serum PIIINP level rose with advancing histological stage (P less than 0.001). In 18 patients in whom more than 1 serum was assayed (mean follow-up 42 months) PIIINP often fell, particularly in patients with established cirrhosis and advanced disease. The independent prognostic value of PIIINP was examined using Cox's proportional hazards model with three other prognostic co-variables (bilirubin, albumin, patient age). Stepwise regression analysis selected albumin (P less than 0.001) and bilirubin (P = 0.002) as the most important prognostic factors. PIIINP did not give independent prognostic information. We conclude that PIIINP is another marker of disease activity in PBC which confers no benefit over existing conventional measurements in routine management of this disease.
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PMID:Is measurement of type III procollagen amino propeptide useful in primary biliary cirrhosis? 280 58

Alcoholic liver cirrhosis is a leading cause of morbidity and mortality in alcohol dependence. A common precursor to cirrhosis is alcoholic hepatotoxicity evident clinically by elevated serum liver enzymes. In this study 50 male patients with significant (greater than two times upper limits of normal) elevation of liver enzymes attending a veterans inpatient alcohol treatment center were matched by age and time since last drink to 50 male veterans without elevated liver enzymes. Patients with elevated liver enzymes were found to be more likely to be daily drinkers, less likely to indulge in binge drinking patterns or have alcoholic blackouts, and showed a trend towards a less severe pattern of alcoholism. Significant gamma glutamyl transferase (GGT) elevations were found in patients consuming an average of 7 beers/day for 5 years, and significant aspartate aminotransferase (AST) elevations were found in patients consuming a threshold of 12 beers/day for 10 years. These findings are consistent with current research suggesting alcoholic cirrhosis is a result of a threshold exposure to alcohol in alcoholics with an additional environmental or genetic risk factor.
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PMID:Risk factors for alcohol hepatotoxicity among male alcoholics. 289 May 7

For patients with chronic hepatitis B e (HBe)-positive hepatitis, long-term results of pilot studies with lymphoblastoid interferon-alpha, acyclovir, or a combination, and of a randomized controlled trial of interferon/desciclovir combination therapy are presented. HBe seroconversion was observed in more than 40 percent of patients treated with combination therapy, 30 percent with interferon therapy, 18 percent with acyclovir, and 0 percent with no treatment. HBe reactivation occurred in two patients with cirrhosis. Hepatitis B surface seroconversion followed HBe seroconversion in 11 to 30 percent of treated patients. HBe seroconversion was significantly related to initial low levels of viral replication and to transient aminotransferase elevation during the second half of the interferon treatment of 16 weeks. Clinical improvement and persistent normalization of aspartate aminotransferase was observed in all patients with HBe seroconversion. Conversion to a state of virus latency (HBe negative) mostly occurred after therapy, suggesting that the specific immunologic host response had been brought about by the suppression of virus replication through antiviral agents. Recommendations for selection of patients for antiviral combination therapy are made on the basis of these long-term results.
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PMID:Long-term follow-up of antiviral combination therapy in chronic hepatitis B. 304 80

Persistent abnormalities of liver function tests occur in approximately 15% of home parenteral nutrition (HPN) patients and are associated with steatosis, steatohepatitis, and, rarely, fibrosis or cirrhosis. Approximately one-third of patients with gut failure on long-term HPN have low total and free plasma carnitine concentrations, and it has been suggested that a deficiency of L-carnitine may be responsible for the steatosis and steatohepatitis in HPN patients. To determine whether administration of L-carnitine is capable of reversing steatosis in HPN patients, 4 adult women on HPN for a mean of 53 mo (range 21-80 mo) were studied before and after 1 mo of intravenous L-carnitine supplementation (1 g/day). All patients had abnormalities in standard liver function tests and low total and free plasma carnitine values. The mean total and free plasma carnitine concentrations and the mean total hepatic carnitine concentration were reduced before supplementation and rose to normal values after treatment (27.4 +/- 2.3 to 35.5 +/- 3.1 nmol/ml, 19.4 +/- 2.8 to 25.7 +/- 2.5 nmol/ml, and 3.5 +/- 0.65 to 6.5 +/- 1.2 nmol/mg of noncollagen protein, respectively). However, there were no significant changes in mean serum aspartate aminotransferase and alkaline phosphatase levels (65 +/- 21 vs. 54 +/- 12 IU and 429 +/- 220 vs. 472 +/- 224 IU, respectively), plasma free fatty acids, plasma triglycerides, hepatic free fatty acid and triglyceride concentrations, or the grade of hepatic steatosis on light microscopy. These results suggest that carnitine deficiency is not a major cause of steatosis and steatohepatitis in patients receiving HPN.
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PMID:L-carnitine therapy in home parenteral nutrition patients with abnormal liver tests and low plasma carnitine concentrations. 312 32

Plasma levels of the lysosomal enzymes, beta-hexosaminidase and beta-glucuronidase, were analyzed in rats with carbon tetrachloride induced liver cirrhosis. Out of 22 animals, 15 showed cirrhotic and 4 pre-cirrhotic livers. 4 cirrhotic animals exhibited cholestatic features with increased bilirubin, alkaline phosphatase (ALP) and aspartate aminotransferase (ASAT) in plasma. The remaining 15 pre-cirrhotic and cirrhotic rats showed clear significant changes only in ASAT levels. These 15 rats showed no consistent increase in plasma, spleen or liver lysosomal enzyme activities, whereas the 4 rats with cholestatic features exhibited considerable increases of lysosomal enzymes. The increased activities might be attributed to decreased biliary excretion and/or increased production of lysosomal enzymes by activated macrophages.
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PMID:Lysosomal enzymes in plasma, liver and spleen from rats with carbon tetrachloride-induced liver cirrhosis. 315 68

Selenium deficiency has been implicated as contributing to hepatic injury in alcoholics. The mechanism by which this occurs is most likely lipoperoxidation secondary to decreased activity of the selenoenzyme glutathione peroxidase. To further assess this relationship, we measured selenium content in autopsy livers in 12 patients with alcoholic cirrhosis compared to 13 patients matched for age and sex dying from other causes, mostly with cardiopulmonary diseases. The mean (+/- SEM) hepatic selenium content in cirrhosis was 0.731 +/- 0.077 microgram/g dry weight versus 1.309 +/- 0.166 microgram/g in controls (P less than 0.005; Student's t test). Clinical and biochemical indices of significant hepatic dysfunction, including encephalopathy, ascites, and elevations of serum bilirubin or prothrombin time, were only present in the cirrhotic group. A significant inverse correlation between hepatic selenium content and the prothrombin time was noted (r = -0.50; P less than 0.02). No significant relationships between hepatic selenium and the abnormalities of bilirubin, albumin, or aspartate aminotransferase were found. We conclude that significantly decreased hepatic selenium stores are present in patients with severe alcoholic cirrhosis compared to controls. The magnitude of that selenium deficit does correlate with some indices of hepatic function, specifically the prothrombin time. These data lend further support to a true selenium deficiency state in alcoholic cirrhosis. It is highly possible that selenium deficiency represents an important link, synergistically joining the nutritional and hepatotoxic backgrounds of alcoholic liver injury and cirrhosis.
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PMID:Decreased hepatic selenium content in alcoholic cirrhosis. 316 92

We studied a consecutive series of 204 patients who were admitted to a hospital for addictive diseases during 40 months and who had a liver biopsy. Parenteral drug abusers (n = 34) were significantly younger than alcohol abusers (n = 23) or abusers of both (n = 147) and had lower levels of serum alkaline phosphatase, total bilirubin, and aspartate aminotransferase than the other two groups. Chronic active hepatitis and chronic persistent hepatitis were more frequent (p less than 0.001) in abusers of parenteral drugs alone, whereas cirrhosis was found most often (p less than 0.001) in abusers of both alcohol and parenteral drugs. Cirrhosis was present in 10 of 39 (26%) simultaneous abusers of alcohol and parenteral drugs compared with 58 of 96 (60%) alcohol-abusing former parenteral drug abusers (p less than 0.001). Methadone maintenance treatment was not associated with cirrhosis. Thus, methadone-maintained patients who abuse alcohol and develop cirrhosis should remain in methadone maintenance treatment and receive concomitant alcoholism treatment. Also, these data further support the hypothesis that abusers of both alcohol and parenteral drugs have an increased risk of developing cirrhosis.
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PMID:Chronic liver disease in abusers of alcohol and parenteral drugs: a report of 204 consecutive biopsy-proven cases. 354 73

We measured the activity of carnosinase, a prominent hepatic peptidase, in sera from 69 patients with liver disorders. Mean values (and SDs) for those with liver cirrhosis (17 cases) and hepatoma (seven cases) were 0.51 (0.28) and 0.68 (0.21) mumol/mL per hour, respectively--clearly less than for normal adults: 4.19 (0.95) mumol/mL per hour. Samples from 17 cases of chronic hepatitis also showed moderately decreased activity, 1.41 (0.97) mumol/mL per hour. In contrast, 14 cases of acute hepatitis generally showed values falling within the normal limits: 3.41 (1.97) mumol/mL per hour. Our results for carnosinase correlated with those for cholinesterase (r = 0.70) and with the concentration of albumin in serum (r = 0.59), but not with the activity of either creatine kinase, aspartate aminotransferase, or alanine aminotransferase in serum. Carnosinase values differed more among groups of disorders than did the values for cholinesterase or albumin. Measurement of serum carnosinase activity may be of clinical value in assessing the severity of chronic liver-cell damage, but not in differentiating liver disease from nutritional, muscle, or endocrine disorders.
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PMID:Decreased activity of carnosinase in serum of patients with chronic liver disorders. 373 53

Serum mitochondrial aspartate aminotransferase activity was measured using an immunochemical method in 251 subjects, of whom 140 were chronic alcoholics. The alcoholic patients included 37 with normal liver routine tests (Group I), 61 with noncirrhotic alcoholic liver disease (Group II) and 42 with cirrhosis (Group III), of whom 21 had been abstainers for at least 2 months. All of the remaining 111 subjects were nonalcoholic: 61 had various types of liver disease (Group IV) and 50 were healthy controls. A second assay of serum mitochondrial aspartate aminotransferase activity was performed in 76 alcoholics after a period of abstinence of about 7 days. In addition, serial mitochondrial aspartate aminotransferase determinations were performed in four nonalcoholic volunteers prior to, during and following an alcohol bout. Mean mitochondrial aspartate aminotransferase and mitochondrial aspartate aminotransferase/total aspartate aminotransferase ratio were significantly increased in the alcoholics whatever their liver status, with a sensitivity of the ratio of 81, 85 and 66% for Group I, Group II and the 21 drinkers of Group III, respectively. Only 1 of the 21 cirrhotic abstainers had an increased ratio. Among the 61 nonalcoholic patients with liver disease, 11 had an increased mitochondrial aspartate aminotransferase/total aspartate aminotransferase ratio, specificity of which was 82%. After drinking had been stopped for about 1 week, mitochondrial aspartate aminotransferase decreased by more than 50% and therefore appears as a reliable tool to assess abstinence. In the four cases of alcohol bouts, no significant modifications in mitochondrial aspartate aminotransferase serum values were observed, thus suggesting that mitochondrial aspartate aminotransferase is indeed a marker of chronic, but not of acute, alcohol intake.
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PMID:Serum mitochondrial aspartate aminotransferase as a marker of chronic alcoholism: diagnostic value and interpretation in a liver unit. 373 96


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