Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019158 (hepatitis)
30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We measured serum levels of carbohydrate deficient transferrin (CDT) in 420 subjects: 100 healthy blood donors, 82 healthy employees, 70 abstaining patients with different chronic nonalcoholic liver disease, 16 abstaining patients with alcoholic fatty liver, 50 abstaining patients with alcoholic liver cirrhosis, 25 abusing patients with alcoholic fatty liver, 41 abusing patients with alcoholic liver cirrhosis, and 36 patients with alcohol dependence syndrome with a daily ethanol consumption of 173 +/- 120 g the last 4 weeks before blood was drawn. In controls the serum level of CDT was significantly higher in females compared with males (17.7 +/- 5.1 and 13.7 +/- 3.8 units/liter, respectively), and the upper normal limit was defined as 27 and 20 units/liter. Sixty-two of 102 (60.8%) abusing patients with alcoholic liver disease had increased levels of CDT compared with 1 of 66 abstaining (1.5%) patients with alcoholic liver disease, and 10 of 70 (14.3%) abstaining patients with nonalcoholic liver disease among them 3 with primary biliary cirrhosis and 2 with chronic autoimmune hepatitis. No correlation was found between serum CDT and gamma-glutamyltranspeptidase (GGT), AST, ALT, and mean red cell volume (MCV). The sensitivity and specificity for serum CDT was 61 and 92%, respectively, compared with 85 and 18% for GGT and 70 and 66% for MCV. No advantage was gained by using the CDT/transferrin ratio. Our study confirms that CDT is a specific marker for chronic alcohol abuse, except in few patients with other chronic liver diseases. Serum CDT seems to be a better indicator of abstention than GGT; AST and MCV in patients with alcoholic liver disease. However, in our hands CDT is not so sensitive for alcohol abuse in patients with liver disease as reported earlier in unselected alcoholics.
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PMID:Serum carbohydrate-deficient transferrin as a marker of alcohol consumption in patients with chronic liver diseases. 848 62

We describe three men and two women, aged 18-50, with an occasional finding of increased aspartate and alanine aminotransferase and gamma-glutamyl transpeptidase levels in the absence of any drug treatment and past or current alcohol abuse. Two patients were overweight (body mass index 29 and 32, respectively) and physical examination was normal in all but one case. Tests for hepatitis A, B and C, Epstein-Barr virus, cytomegalovirus, toxoplasma and autoimmune hepatitis were negative and metabolic diseases (Wilson's disease, haemochromatosis, alpha-l-antitrypsin deficiency) were excluded by specific tests. Ultrasound liver scan revealed massive steatosis in all patients. Liver histology showed diffuse steatosis and parenchymal inflammation in all cases, with concomitant fibrosis and Mallory bodies in three of them. Findings were consistent with non-alcoholic steatohepatitis, a rare condition with potential progression to cirrhosis in a minority of cases. This disease, for which no treatment is currently available, must be considered in all subjects with elevated aminotransferases, in the absence of known causes of liver damage.
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PMID:Non-alcoholic steatohepatitis. Report of five cases and review of the literature. 878 33

We administered ursodeoxycholic acid (UDCA) orally, at a daily dose of 600 mg, for 4 months to 36 patients with chronic viral hepatitis C. Another 36 patients with chronic viral hepatitis C, treated with placebo for 4 months, served as controls. None of the patients were alcoholics and none suffering from autoimmune hepatitis. Of the 36 patients in the UDCA-treated group, 13 had high levels of serum gamma-glutamyltranspeptidase (GGT), i.e., exceeding 150 U/l (normal < 50 U/l). Histological examination of liver biopsy specimens obtained from 10 patients in this group before treatment suggested that damage of the interlobular bile ducts was prominent in patients with higher levels of serum GGT. After 1 month of UDCA treatment, significant decreases in the levels of serum GGT, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were observed (P < 0.05 for GGT and AST), and the decreases continued for the 4-month treatment period. The reduction of GGT levels was the most prominent change in the liver function indices; the percent change in the GGT level was -25.2 +/- 4.4 (mean percent change +/- SE) at 1 month and -38.0 +/- 5.0 at 4 months. A significant correlation was observed between the serum delta GGT level (GGT value before treatment minus value after 3 months of treatment) and the total score for morphological injury of the bile ducts (P < 0.05). These results suggested that UDCA has the potential to reverse hepatocellular damage in patients with chronic viral hepatitis C, in whom high GGT levels may be due, in part, to a damaged interlobular bile duct. UDCA may be useful for the treatment of chronic viral hepatitis C, especially in patients exhibiting a high level of GGT.
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PMID:Efficacy of ursodeoxycholic acid therapy in chronic viral hepatitis C with high serum gamma-glutamyltranspeptidase levels. 880 32

We have evaluated the diagnostic efficacies of ultrasonography and hepatitis C virus (HCV) antibody measurement to differentiate pathogenesis of liver dysfunction in the asymptomatic adults with elevated ALT value. Among 4256 visitors to PL Tokyo Health Control Center for their health examination, 463 cases (11%) showed abnormal liver function including elevation of ALT value. Ultrasonography and HCV antibody measurement using the second generation reagent had been applied to 362 cases in order to screen the etiology of liver dysfunction. The ultrasonography succeeded to establish the diagnosis of fatty liver in 137 cases (38%) and 41 cases (11%) demonstrated positive HCV antibody. There were 4 cases with positive HBs antigen, however, it was found that their abnormal liver function was attributed to other etiology such as fatty liver and alcoholic liver dysfunction rather than chronic type B hepatitis. HCV antibody-positive cases showed higher levels of total protein, ZTT, AST, ALT, and lower levels of albumin, A/G, total cholesterol, triglyceride, gamma-GT and cholinesterase value than other cases. HCV antibody titers were not correlated to hepatic parenchymal damage estimated by ALT or cholinesterase value. Only a little correlation was observed between HCV antibody titers and HCV-RNA amounts determined by the competitive reverse transcription-polymerase chain reaction (RT-PCR) method. These results indicate sufficient diagnostic efficacies of ultrasonography and HCV antibody measurement for a pathogenesis differentiation in the asymptomatic patients with liver dysfunction, and these examinations should be employed as the first-step screening tests for the etiology determination of liver diseases in the primary care medicine.
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PMID:[Pathogenesis-screening tests for liver dysfunction in the asymptomatic patients with elevated ALT values and their diagnostic efficacies in primary care medicine]. 885 69

We report the case of a young HIV seropositive patient with severe hemophilia A who presented rapid liver failure related to his chronic C hepatitis. The patient had been receiving factor VIII:C clotting factor concentrates (mean 60,000 U/year) since 1975. In 1984 alanine aminotransferase presented abnormal levels. The CD4 lymphocyte count in 1991 was normal and ultrasonographic scan showed normal liver morphology. In 1991 the patient were found to be seropositive for HCV antibodies as detected by the ELISA method and confirmed by the RIBA method. One year later, a progressive increase in policlonal gamma-globulin and a decrease in the CD4+ lymphocyte count to below 500/muL were detected in concomitance with ultrasonographic evidence of a progressive increase in the longitudinal diameters of the liver and spleen and signs of liver inhomogeneity. A significant inverse correlation was observed between the increase in the longitudinal diameter of the liver and the decline in albumin levels, and between the increase in the longitudinal diameter of the liver and the drop in platelet count. Elevated levels of ammonemia, gamma-glutamyl transpeptidase, alkaline phosphatase and IgA were detected. Moreover, decreased levels of the C4 and C3 complement fractions were documented. At this time (1994), esophagogram and esophagogastroscopy evidenced varicosities in the lower esophageal section (stage F1). The patient died in 1995 March at the age of 29 years of sudden septic shock related to Pseudomonas aeruginosa infection.
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PMID:Rapid liver failure related to chronic C hepatitis in an HIV seropositive hemophilic patient with severe immunodepression. 887 Mar 78

A herd of 650 Holstein cows was examined for skin disease. Approximately 400 of the lactating adults were affected, but heifers, calves, and nonlactating cows were clinically normal. The condition was characteristic of primary photosensitization. Milk production of the affected cows was normal. Affected cows did not appear to be ill, and none of the cows was icteric. Three of 7 cows had high serum gamma-glutamyltransferase activities, but in the other 4 cows, activity was within the reference range. Serum activities of other hepatic enzymes were within reference ranges in the 7 cows that were examined. Hepatic biopsy specimens from 3 cows were normal. Specimens from 4 other cows had changes that ranged from minimal to mild, chronic, lymphoplasmacytic periportal hepatitis to acute, random, necrotizing hepatitis. Development of photosensitivity was related to ingestion of alfalfa silage. Acetone extracts of the alfalfa silage, but not of other feedstuffs, were found to inhibit growth of Candida albicans under ultraviolet light. Cows experimentally fed a diet composed exclusively of the alfalfa silage developed skin lesions after 6 days, but did not have detectable serum concentrations of phylloerythrin.
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PMID:Primary photosensitization related to ingestion of alfalfa silage by cattle. 889 27

In order to investigate the possibility of early discrimination of extrahepatic biliary atresia from other cholestatic diseases, a series of results of liver function tests in infants with cholestatic diseases were reviewed. The results of routine liver function tests (LFT) recorded in patients' charts were reviewed within 12 weeks after birth in 47 infants with extrahepatic biliary atresia (BA), 10 infants with neonatal hepatitis (NH) and 130 age-matched control infants (CO) without cholestatic diseases. The mean of each test value for each week after birth was derived from the actual data examined in each infant. No differences were observed between BA and CO in the levels of aminotransferases within 2 weeks after birth. Total bilirubin and direct bilirubin levels were significantly different between BA and CO within 1 week after birth (16.1 +/- 3.2 mg/dL vs 11.1 +/- 4.5 mg/dL, 4.6 +/- 2.6 mg/dL vs 0.7 +/- 0.3 mg/dL, respectively). The direct bilirubin-total bilirubin ratio exceeded 25% within the first week in BA. The individual values of direct bilirubin (DB) exceeded 2 mg/dL within the first week in all infants with BA, while none of the individual values exceeded 1.6 mg/dL in CO. Gamma-glutamyl transpeptidase levels were significantly different between BA and CO at 4 weeks (432 +/- 272 IU/L vs 79 +/- 43 IU/L) and thereafter; and were significantly different between BA and NH at 6 weeks (314 +/- 232 IU/I vs 69 +/- 58 IU/L) and thereafter. These data suggest that the determination of direct bilirubin within 1 week after birth can detect extrahepatic biliary atresia patients from those with physiologic jaundice, and gamma-glutamyl transpeptidase levels may discriminate BA from NH at no later than 6 weeks of age.
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PMID:Pre-operative time course changes in liver function tests in biliary atresia: its usefulness in the discrimination of biliary atresia in early infancy. 894 12

We tested the sera of 67 consecutive patients for hepatitis G virus (HGV) RNA by reverse transcriptase-polymerase chain reaction (RT-PCR). These patients (42 males and 25 females, median age 35 years, range 13-64 years) had liver disease of unknown aetiology and were without markers of hepatitis (A-E) viruses or signs of genetically determined, autoimmune, alcoholic or drug-induced liver disease. The controls in this study were 110 patients (50 females and 60 males, median age 45 years, range 9-65 years) with chronic hepatitis B virus (HBV) infection (19 patients) or hepatitis C virus (HCV) infection (91 patients). Ten of 67 (14.9%) patients with cryptogenic disease were positive for HGV RNA by at least three separate tests; HGV RNA was also detected in one of 19 (5.3%) hepatitis B surface antigen (HBsAg) carriers and in nine of 91 (16.6%) patients with antibody to HCV. These data suggest that HGV occurs as frequently in HCV-infected patients as in those with cryptogenic disease. Elevated serum gamma glutamyl transpeptidase (gamma-GT) (higher than twice the normal value) and alkaline phosphatase levels were found in eight of 10 (80%) HGV RNA positive patients and in six of 57 (10.5%) HGV RNA negative patients (P < 0.0001). Five (50%) HGV RNA positive patients had non-specific inflammatory bile duct lesions. A statistically significant difference was observed between HGV RNA positive and negative patients with chronic HBV or HCV infections (P < 0.029). Therefore, the spectrum of liver disease associated with HGV is wide, but a characteristic lesion of the bile duct leading to elevation of cholestatic enzymes might be specific for this virus.
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PMID:Hepatitis G virus RNA in the serum of patients with elevated gamma glutamyl transpeptidase and alkaline phosphatase: a specific liver disease? [corrected]. 894 81

When administered with D-galactosamine, lipopolysaccharide endotoxins produce a good experimental animal model of hepatitis. This galactosamine plus endotoxin model has been used widely, but the acute effect of this fixed combination of two chemicals on hepatic and extrahepatic biotransformation has not been determined. Therefore, either 2 or 4 hr after a single intraperitoneal dose of 300 mg/kg galactosamine plus 30 micrograms/kg lipopolysaccharide was administered, serum, liver, kidney, intestine, and spleen were collected. Serum enzymes (alanine and aspartate aminotransferases, sorbitol dehydrogenase, and gamma-glutamyltranspeptidase) were elevated dramatically 2 and 4 hr after treatment. Cytochrome P450 monooxygenase activity toward benzo-[a]pyrene was increased in kidney 4 hr after treatment, whereas dealkylation of 7-methoxycoumarin or 7-ethoxyresorufin was unchanged in any tissue at either time point. An increase in UDP-glucuronosyltransferase activity toward 4-methylumbelliferone and 4-hydroxybiphenyl was noted in the intestine. Conjugation of 1-chloro-2,4-dinitrobenzene with glutathione was increased in intestine and spleen 2 hr after treatment. gamma-Glutamyltranspeptidase activity was unaltered in all tissues studied. Reduced glutathione concentrations were increased significantly by different amounts depending on which organs were studied 2 or 4 hr after treatment. These results indicate that galactosamine/lipopolysaccharide-induced liver injury is not accompanied by major effects on the examined biotransformation reactions.
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PMID:Minimal effect of acute experimental hepatitis induced by lipopolysaccharide/D-galactosamine on biotransformation in rats. 895 52

We describe a 43-year-old woman with clinical features compatible with autoimmune cholangiopathy recently reported by Ben Ari et al. She was negative for anti-mitochondrial antibody, positive for high titer anti-nuclear antibody with homogeneous pattern, high levels of serum immunoglobulin G and nearly normal levels of serum immunoglobulin M for more than five years. In the early stages of the disease, the elevations of serum transaminase, alkaline phosphatase and gamma-glutamyl transpeptidase were well controlled by the administration of ursodeoxycholic acid. After five years of follow-up, she showed the second exacerbation of liver function tests, which then rapidly improved by prednisone administration. To analyze the antigen diversity recognized by T-cells in the liver, T-cell receptor repertoire was examined by immuno-histochemistry. The liver biopsy obtained in the early stage showed clonal accumulation of V beta 5.1-positive cells in portal areas, which was found in patients neither with primary biliary cirrhosis nor autoimmune hepatitis. In conclusion, these data suggest that T-cell response in autoimmune cholangiopathy is different from those two autoimmune liver diseases, which may imply a distinct entity of the disease.
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PMID:Clonal accumulation of V beta 5.1-positive cells in the liver of a patient with autoimmune cholangiopathy. 906 73


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