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)

To determine the nature of unexplained chronic serum aspartate aminotransferase elevations of a mild to moderate degree in asymptomatic patients, we performed systematic clinical, biochemical and histologic examinations in 47 individuals who had been screened for virus-, alcohol- or drug-related disease. Serum aspartate aminotransferase levels ranged from 3- to 8-fold normal (mean: 156 +/- 7 units per liter) for at least 6 months (mean: 30 +/- 6 months). Serum alanine aminotransferase levels were also increased but to a lesser degree in most patients. Thirty-four patients (72%) had histologic features of chronic active hepatitis, including 16 with cirrhosis. Ten patients (21%) had steatohepatitis and three (6%) had miscellaneous disorders. Patients with chronic active hepatitis and cirrhosis could not be distinguished from counterparts without cirrhosis by individual clinical or laboratory findings. Antinuclear or smooth muscle antibodies were detected in 18 of the patients with chronic active hepatitis (53%). All patients with steatohepatitis were women, and they had laboratory changes at presentation, including seropositivity for antinuclear antibodies, that overlapped with those of patients with chronic active hepatitis. We conclude that asymptomatic patients with unexplained chronic aspartate aminotransferase elevations of a mild to moderate degree frequently have chronic active hepatitis and that many have cirrhosis. Immunoserologic findings compatible with autoimmune hepatitis are commonly present. Steatohepatitis is the most frequent alternative diagnosis, especially in women, and it is not excluded by the presence of antinuclear antibodies. Differentiation of the disorders is possible only by histologic examination.
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PMID:The nature of unexplained chronic aminotransferase elevations of a mild to moderate degree in asymptomatic patients. 277 13

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

Even though HAV, HBV and HNANB viruses are responsible for most of the viral hepatitis cases, many other viruses have been reported to cause hepatic injury. These viruses may involve the liver, either as part of a systemic illness (e.g. EBV, CMV, HSV) or as the primary target organ (e.g. yellow fever virus, Lassa fever virus, Ebola virus). Clinically overt hepatocellular dysfunction is rare in such viral infections. Biochemical disturbance of hepatic functions shown, for example, by rises in AST and ALT, is a frequent event and indicates hepatic damage. Morphological changes of the liver include varying degrees of hepatic necrosis with a paucity of inflammatory activities. Intranuclear or cytoplasmic inclusion bodies may be characteristic findings in these diseases. Laboratory diagnosis depends upon serology and liver histology. Treatment is still largely supportive in most of these diseases, although recent trials of antiviral agents show promise against some viruses. Chronic sequelae, such as cirrhosis or hepatocellular cancer, are not encountered. More work is needed to elucidate the pathogenesis of hepatic injury in these illnesses.
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PMID:Viral diseases involving the liver. 282 80

The concentration of serum immunoreactive prolyl 4-hydroxylase (S-IRPH) was determined in patients with various liver diseases by the radioimmunoassay developed previously. S-IRPH values were elevated in acute hepatitis (p less than 0.01), hepatocellular carcinoma (p less than 0.05), metastatic liver neoplasm (p less than 0.01) and cholestatic diseases (p less than 0.001), but no significant elevation was seen in chronic hepatitis or liver cirrhosis. The mean value of S-IRPH was highest in cholestatic diseases, and next highest in acute hepatitis. In addition to acute hepatitis, S-IRPH was increased in other conditions of hepatocellular damage such as exacerbation of chronic hepatitis or immediately after transcatheter arterial embolization of hepatocellular carcinoma. In cases of hepatocellular damage S-IRPH varied concurrent with cytoplasmic enzyme (AST, ALT and LDH) levels and in cases of cholestatic diseases with biliary enzyme (Al-P and gamma GTP) levels. These properties appear to be unique among serum enzymes. The characteristics of S-IRPH were considered to be related to its unique subcellular localization within the cell, ie the membrane of rough endoplasmic reticulum.
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PMID:Studies on serum immunoreactive prolyl 4-hydroxylase in liver diseases--its elevation both in hepatocellular damage and cholestatic diseases. 284 41

Using a monoclonal antibody to bromodeoxyuridine, we studied the cell kinetics of human hepatocellular carcinoma, liver cirrhosis, chronic active hepatitis and alcoholic liver fibrosis. Specimens were taken either by biopsy or surgery and immediately incubated with 0.1% bromodeoxyuridine solution at 37 degrees C for 45 min. After in vitro labeling, the bromodeoxyuridine taken up by the nuclei of S-phase cells was determined by the avidin-biotin-peroxidase complex method, using an anti-bromodeoxyuridine monoclonal antibody as the first antibody. The number of positive nuclei in 1,000 hepatic cells was counted, and the bromodeoxyuridine labeling index was expressed per thousand. The mean bromodeoxyuridine labeling index +/- S.D. of the cancerous portion of hepatocellular carcinoma, the noncancerous portion of hepatocellular carcinoma, liver cirrhosis, chronic active hepatitis and alcoholic liver fibrosis were 64.1 +/- 31.3, 33.6 +/- 14.4, 23.2 +/- 20.8, 9.1 +/- 6.1 and 21.6 +/- 13.0, respectively. The mean bromodeoxyuridine labeling index of the hepatocellular carcinoma cancerous portion was statistically higher than that of any other group. There was no statistical difference by the t test or the Wilcoxon test between the noncancerous portion of hepatocellular carcinoma and liver cirrhosis, and these two groups were proved interdependent by chi 2 test (Fisher's exact test), whether they were subdivided by bromodeoxyuridine labeling index greater than or equal to 10 or not. Bromodeoxyuridine labeling index was not significantly correlated with the usual biochemical parameters such as serum AST, ALT, gamma-GTP, alkaline phosphatase, lactate dehydrogenase, cholinesterase, albumin, and alpha-fetoprotein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:S-phase cells in diseased human liver determined by an in vitro BrdU-anti-BrdU method. 284 68

The repeated observation of a fall in serum enzymes at midmenstrual cycle in an untreated patient with primary biliary cirrhosis stimulated a study of estrogen administration in five patients with primary biliary cirrhosis. One patient was premenopausal, one patient was postmenopausal and three had had oophorectomy. After 2 weeks of ethinyl estradiol, AST was under 100 IU per dl in all and had decreased by 50% or more in 4 of 5 patients. gamma-glutamyltransferase and alkaline phosphatase fell by 50 and 30% or more, respectively, in all patients. The decreases in serum enzymes were statistically significant in all patients for gamma-glutamyltransferase, in 4 of 5 for AST and in 3 of 5 for alkaline phosphatase. One patient developed increased icterus leading to withdrawal of estradiol. Withdrawal of estradiol was followed by return toward control values over variable periods, usually 1 to 4 weeks. Repeated courses of estradiol reproduced these enzyme changes. These observations indicate that estradiol in the doses used (0.05 mg per day) reversibly lowers serum enzyme values in biliary cirrhosis. The mechanism of the effect is unexplained, but an immune system alteration may be responsible.
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PMID:Effect of estradiol upon serum enzymes in primary biliary cirrhosis. 288 13

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

Copper is believed to be hepatotoxic in Indian Childhood Cirrhosis and Wilson's disease. However, copper-loading causes only minimal hepatic damage in animal models. The hypothesis was therefore proposed that a second hepatic insult may precipitate or perpetuate liver injury in a copper-laden liver. In non-copper-dosed rats CCl4 (10 mmol/kg, i.p.) produced elevated serum AST (809 +/- 298 IU/l, normal 20 +/- 5) and ALT (295 +/- 157 IU/l, normal 6 +/- 1) and extensive liver cell necrosis, portal tract inflammation, fat deposition, and perilobular hepatocyte ballooning. In rats whose liver copper was elevated from 75 +/- 13 to 461 +/- 13 micrograms/g by oral copper supplementation, CCl4 produced much smaller increases in AST (492 +/- 80 IU/l) and ALT (172 +/- 57 IU/l) and mild focal liver cell necrosis. Fat deposition and perilobular vacuolation were not reduced. Prior copper-loading of rats unequivocally protected against the CCl4-induced liver injury. Triglyceride accumulation, however, was apparently unaffected. The possible interactions of copper with prostaglandin-mediated inflammation and with free-radical-induced liver damage are discussed.
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PMID:The effect of carbon tetrachloride on the copper-laden rat liver. 292 91

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


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