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)

Neopterin is a pyrazino-pyrimidine compound which is biosynthesized by macrophages. Increased concentrations of neopterin have been reported in conditions causing a stimulation of cellular immunity, such as viral and other infections, graft versus host disease, autoimmune disease and different malignancies. Recently, urinary neopterin levels have been found increased in patients with acute viral hepatitis and NANB chronic hepatitis. In the present study, neopterin serum levels have been measured in 23 cirrhotic patients (6 HBV related, and 17 cryptogenetic cirrhosis, 7 of them occurring in alcoholic subjects) and in 24 normal subjects. Mean values of serum neopterin were significantly increased in cirrhotics (3.92 +/- 3.28 ng/ml versus 1.24 +/- 0.51 ng/ml in controls, p less than 0.01). Serum neopterin values were not found to be significantly different in cirrhotics assessed in three different clinical classes according to Child's classification and in cirrhotics with and without serological findings of active disease. In fact, in cirrhotic patients, serum neopterin levels did not correlate with the values of serum AST, ALT, ALP, GGT and gamma-globulin. These data show that increased levels of serum neopterin occur in cirrhotic patients, but there is no relation between serum neopterin values and the activity or the clinical severity of the disease. The results are consistent with the hypothesis that activated macrophages are involved in all stages of liver cirrhosis irrespective of its aetiology.
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PMID:Serum neopterin levels in liver cirrhosis. 263 48

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

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

The ratio of the serum aspartate to alanine amino-transferase levels (AST/ALT) is often used as a clue to the etiology of the underlying liver disease. This ratio is usually greater than 2.0 in alcoholic liver disease and less than 1.0 in patients with chronic hepatitis and chronic cholestatic syndromes. We analyzed the AST/ALT ratio in 177 patients with various forms of nonalcoholic chronic liver disease who underwent medical evaluation and percutaneous liver biopsy. In the majority of cases of chronic viral hepatitis, the AST/ALT ratio was less than 1.0. However, there was a statistically significant correlation between the AST/ALT ratio and the presence of cirrhosis. Among 100 patients with chronic type B hepatitis, the mean AST/ALT ratio was 0.59 in those without cirrhosis and 1.02 in those with cirrhosis. Furthermore, the AST/ALT ratio often rose to greater than 1.0 when cirrhosis first became manifest. Thus, the finding of an AST/ALT ratio of greater than 1.0 in a patient with nonalcoholic liver disease should suggest the presence of cirrhosis. In addition, the use of the AST/ALT ratio as a means of separating alcoholic and nonalcoholic liver disease must be tempered with the knowledge that this ratio may be less helpful in the presence of cirrhosis.
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PMID:Ratio of serum aspartate to alanine aminotransferase in chronic hepatitis. Relationship to cirrhosis. 313 26

Twenty-eight patients with biopsy or clinical acute alcoholic hepatitis were prospectively randomized to 21 days of conventional therapy (14 control patients) or, in addition, to 2 L/day of a peripheral iv infusion of a 900 mosmol amino acid-glucose solution (14 patients). Cirrhosis was present in 64% of controls and in 54% of infused patients. There were three deaths in controls and one in the infused group. There were no significant intergroup differences in mortality, clinical findings, liver tests, or functional mass by the galactose elimination capacity either at entry or after completion of the study. In controls, there was intragroup improvement in serum bilirubin (p = 0.033) and AST (p = 0.008) but not in other "liver tests" or in functional hepatic mass by galactose elimination capacity. In infused patients there was improvement in bilirubin (p = 0.001), AST (p = 0.008), and serum albumin (p = 0.016). Improvement in functional mass by galactose elimination capacity was significant at the p = 0.052 level. Hyaline was initially present in six of eight pairs of biopsies in both groups. After treatment, five of six pairs in controls but only one of six pairs in the infused group still had hyaline (p = 0.03). This latter finding, if confirmed in larger groups, may be of considerable clinical importance. It is suggested that 3- to 4-wk trials of such protocols may require a longer duration of follow-up in greater numbers of patients to detect important advantages of amino acid-glucose infusions which are only implicit in these findings.
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PMID:A prospective randomized clinical trial of peripheral amino acid-glucose supplementation in acute alcoholic hepatitis. 330 90

Although copper is believed to be hepatotoxic in Wilson's disease and Indian Childhood Cirrhosis (ICC), the rat shows only minimal hepatic damage on copper-loading. To investigate the possibility that copper deposition may potentiate the effects of a superimposed hepatitis, D-galactosamine (GalN) was given to copper-loaded and control rats. In the non-copper-dosed rats, GalN 0.85 g/kg i.p. produced elevated serum AST (3731 +/- 545 IU/l; normal 64.8 +/- 2.1), ALT (2090 +/- 190 IU/l; normal 18.0 +/- 0.7), and OCT (16.7 +/- 2.6 mmol/min/ml; normal 0.12 +/- 0), and liver cell necrosis with portal infiltration. In rats whose liver copper was elevated to 1298 +/- 169 micrograms/g (control 18.7 +/- 1.7) by oral copper supplementation, GalN produced much smaller increases in AST (825 +/- 122 IU/l), ALT (103 +/- 15 IU/l) and OCT (0.27 +/- 0.02 mmol/min/ml) and minimal histological damage. Viable bacterial cell counts from faecal homogenates showed that the anaerobically cultured bacteria were reduced on copper-dosing of rats. Therefore the protective effect of copper may be due to a decrease in gut-derived endotoxin acting on the liver, or to an impaired prostaglandin synthesis or perhaps to synthesis of acute phase reactants.
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PMID:Copper protects against galactosamine-induced hepatitis. 365 8

A study was carried out to confirm the pathogenetic role of ethanol in the development of chronic active hepatitis (CAH) and to assess if previous or current superimposed hepatitis B virus (HBV) infection could be relevant to the course of alcoholic liver disease (ALD). We examined clinical and laboratory reports of 57 alcoholics with biopsy-proven CAH. Serum and/or tissue HBV markers and the presence or absence of cirrhosis were investigated. Alcohol was the only aetiological factor present in a small group of CAH, with or without histological findings suggestive of alcoholic damage. Age, sex and survival were similar among the subgroups of CAH with and without previous or current HBV infection and among the subgroups of CAH with and without associated histological alcoholic features. Among the laboratory data, the AST/ALT ratio was higher in CAH without previous or current HBV infection. The mean age was comparable in CAH patients with and without cirrhosis, whereas the cumulative 5-year survival was worse in CAH with cirrhosis (87% vs. 49%). These data suggest a difference in alcohol susceptibility in our subjects.
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PMID:Features of chronic hepatitis in alcoholics. A survey in Milan. 369 15


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