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 investigate the prevalence of antibody to hepatitis C virus (anti-HCV) in heavy drinkers with liver disease in Japan, we tested serum samples from 113 heavy drinkers with liver disease and 121 without liver disease. All were negative for HBsAg with no history of blood transfusion. These subjects had consumed more than 80 g of ethanol daily for 5 years or more. Findings for anti-HCV determined by recombinant immunoblot assay testing were positive in 14 (35.9%) of the 39 patients with liver cirrhosis, 14 (58.3%) of the 24 patients with hepatocellular carcinoma and in 8 (53.3%) of the 15 patients with chronic hepatitis. The anti-HCV positive rate in the drinkers with these liver diseases was significantly higher than in those with such disorders as fatty liver (0/10), hepatic fibrosis (0/22), and alcoholic hepatitis (0/3), as well as in the alcoholics without liver disease (5/121, 4.2%). Considering histologic findings in the anti-HCV positive cirrhotics, the occurrence of lymph follicle formation (71.4%), piecemeal necrosis (78.6%) and loose fibrosis (64.3%) were observed to a significantly higher extent than in cirrhotics who were negative for anti-HCV. These findings suggest that advanced chronic liver disease among heavy drinkers in Japan, especially of hepatocellular carcinoma, is closely associated with HCV infection. In the livers of heavy drinkers who were positive for anti-HCV, histologic findings indicated the possibility of viral infection.
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PMID:High prevalence of antibody to hepatitis C virus in heavy drinkers with chronic liver diseases in Japan. 131 67

The prevalence of anti-HCV antibodies in Chinese patients with HBsAg-negative chronic liver diseases was studied retrospectively. Anti-HCV was detected by two different ELISAs. In 97 patients with HBsAg-negative chronic liver disease, 26 (27%) were anti-HCV positive. Of 157 control subjects, only 1 (0.6%) was anti-HCV positive (P less than 0.001). Anti-HCV was detected in 18 of 27 (67%) patients with post-transfusion non-A, non-B (PTNANB) chronic hepatitis or cirrhosis, 5 of 25 (20%) patients with cryptogenic chronic hepatitis or cirrhosis, 2 of 33 (6%) patients with alcoholic liver disease, 1 of 5 (20%) patients with autoimmune chronic active hepatitis (AICAH), none of 4 patients with primary biliary cirrhosis (PBC), and none of 3 patients with fatty liver. The prevalence in this group of patients was lower when compared to reports from other countries. The addition of a urea washing step reduced false-positivity in alcoholic and AICAH groups. The ELISA that employs three recombinant HCV antigens confirmed all positive results by another ELISA with the exception of one weakly positive result in the AICAH group and one in the alcoholic group. One patient in the PTNANB group was detected in addition by the second generation assay. In conclusion, ELISA with a urea wash proved to be useful in reducing false-positivity, and the second generation assay proved to be a sensitive and specific test for anti-HCV antibody.
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PMID:Prevalence of antibody to hepatitis C virus in HBsAg-negative chronic liver disease in Hong Kong using different assays. 132 Dec 25

The present paper is devoted to overview the basic concepts of ethanol-induced hepatic injury and therapeutic modalities by which alcoholic liver disease can be alleviated. The role of alcohol dehydrogenase of both hepatic and gastric origin as well as the importance of the number one metabolite acetaldehyde are discussed, furthermore the effects of microsomal ethanol oxidizing system are also described. The features of the major clinicopathological consequences of alcohol abuse fatty liver, alcoholic hepatitis are briefly outlined, and the basic pathogenetic mechanisms that lead to cirrhosis--cell necrosis, regeneration and fibroplasia--are shown. The understanding of the pathophysiology of alcohol-induced liver injury may improve the therapy with drugs and nutritional factors, and allow successful prevention through the early recognition of heavy drinkers before their social or medical disintegration. In the management of alcoholic liver diseases, among the true hepatoprotective agents a naturally occurring flavonoid silymarin and an active methyl-donor metabolite S-adenosyl-L-methionine seem to be promising. An antifibrotic treatment with colchicine might also be of importance. Further prospective, well-designed, controlled clinical trials are still warranted to evaluate real efficacy of these drugs. The hepatic consequences of alcohol abuse may be treatable, however, prevention would be the true resolution of the major global health problem of alcoholism.
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PMID:Pathogenesis and management of alcoholic liver injury. 134

There was an epidemic of non-A non-B hepatitis in a small area of a town in the central part of Japan, which began with an outbreak of several patients in 1981 and then spread extensively with the result that about one third of the inhabitants showed abnormality in serum liver function tests at the health check performed in 1985. We determined histological diagnoses on that occasion for 167 individuals of the abnormal population and recently assayed antibodies against hepatitis C virus (HCV) for most of their sera left available. Histologically, chronic active hepatitis (CAH) was the major pattern, accounting for 59.3% (99 cases) of the total. Others were chronic persistent hepatitis (CPH) (13.2%), chronic lobular hepatitis (CLH) (16.2%), liver cirrhosis (LC) (6.6%) and fatty liver (4.8%). In the serological studies, the newly developed system to detect antibodies against the viral core protein p 22 was found to be much more sensitive than the conventional system to detect anti C 100-3 antibodies. By using these two methods in combination, we found that 82% were antibody-positive, indicating strong implication of HCV in this epidemic. This was further supported by direct detection of the viral genome in patients' sera by polymerase chain reaction following reverse transcription. We further found a strong correlation between the histological inflammatory activity and the antibody prevalence, since nearly all (97.6%) of the CAH cases were antibody-positive by at least either of the antibody assays, while only about 50% were positive in the less active cases such as CPH and CLH.
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PMID:Correlation between detection of anti-viral antibody and histopathological disease activity in an epidemic of hepatitis C. 138 9

The accuracy of ultrasonographic diagnosis of hypoechoic focal fatty change in the 'bright liver' was evaluated in 40 lesions found in 35 patients followed up for a mean period of 37.8 months. Patients with ultrasound and laboratory findings suggesting liver cirrhosis were excluded from the study. All patients underwent a blind liver biopsy in order to verify the diagnosis of diffuse disease suggested by the finding of 'bright liver'. No guided biopsy was performed on the focal lesions in order to establish the accuracy of ultrasound alone in recognizing focal fatty change. Clinical, haematologic and echographic follow-up confirmed the diagnosis in all cases. All histological specimens revealed liver steatosis, indicating a 100% sensitivity of ultrasonography in identifying non-cirrhotic fatty liver with an accompanying focal change. Increased echogenicity and hypoechoic focal changes are reliable indicators of fatty infiltration, making ultrasonography an acceptable, non-invasive method for the diagnosis of liver steatosis.
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PMID:Hypoechoic lesions in the 'bright liver': a reliable indicator of fatty change. A prospective study. 139 27

Previous studies have shown that alpha-tocopherol (vitamin E) pretreatment of experimental animals can protect against acute liver necrosis induced by carbon tetrachloride. In this study we investigated whether the increase of vitamin E liver content by dietary supplementation influences chronic liver damage and cirrhosis induced by carbon tetrachloride in the rat. Our data indicate that vitamin E supplementation did not interfere with the growth rate of the animals and increased about threefold the liver's content of the vitamin. Vitamin E supplementation significantly reduced oxidative liver damage, but it was not effective in protecting against development of fatty liver and did not interfere with metabolic activation of carbon tetrachloride. Moreover, vitamin E-fed animals showed incomplete but significant prevention of liver necrosis and cirrhosis induced by carbon tetrachloride. This has been shown by means of histological examination, analysis of serum parameters and biochemical evaluation of collagen content. These results show that an increased liver content of vitamin E can afford a significant degree of protection against carbon tetrachloride-induced chronic liver damage and cirrhosis.
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PMID:Vitamin E dietary supplementation protects against carbon tetrachloride-induced chronic liver damage and cirrhosis. 139 81

We present pathologic findings for 52 livers (51 autopsy specimens and one wedge biopsy specimen) from patients with systemic lupus erythematosus (SLE). Hepatic congestion was the most common disease (40 livers), followed by fatty liver (38), arteritis (11), cholestasis (nine), peliosis hepatis (six), chronic persistent hepatitis (six), nonspecific reactive hepatitis (five), cholangiolitis (four), nodular regenerative hyperplasia of the liver (three), and hemangioma (three). The data obtained here suggest that arteritis of the SLE liver is more common than has been recognized previously. One patient had hepatic infarction complications induced by arteritis. On the basis of the findings in the present study and a review of the literature, we suggest that hepatic infarction resulting from arteritis is rare in SLE. On the other hand, while occurrence of nodular regenerative hyperplasia of the liver in SLE patients has been considered to be rare, our findings suggest that it may be more common than has been recognized previously. Although congestion and cholestasis may be acute terminal illnesses, fatty change is considered to be specific to the SLE liver. Statistical analysis indicates that exposure to a large dosage of glucocorticoids is a significant factor in the etiology of severe fatty liver. In addition, our review of Japanese autopsy registry data for 1,468 patients with SLE indicates that the incidence of chronic liver diseases in SLE autopsy cases is as follows: chronic hepatitis, 2.4%; cirrhosis, 1.1%; and liver fibrosis, 0.8%.
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PMID:The liver in systemic lupus erythematosus: pathologic analysis of 52 cases and review of Japanese Autopsy Registry Data. 139 43

Four markers for hepatic fibrosis--N-terminal peptide of Type III procollagen (PIIIP), Laminin P1 (laminin), Type IV collagen (Type IV-C), and 7S domain (7S)--were measured in the sera of 90 patients with various chronic liver diseases diagnosed by liver biopsy--fatty liver (FL), chronic inactive hepatitis (CIH), chronic active hepatitis (CAH), and liver cirrhosis (LC)--and in the sera of 20 healthy controls. The values of markers were compared with the grade of histologic findings of the liver. Four markers were significantly raised in the CAH group and the LC group, and they were considered to be indicators of hepatic fibrosis. PIIIP reflected necrosis and inflammation as well as fibrosis of the liver. Laminin, Type IV-C, and 7S reflected severe fibrosis. 7S was considered to be useful marker for liver cirrhosis.
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PMID:[Clinical significance of measurement of PIIIP, laminin P1, type IV-C and 7S in patients with chronic liver diseases--with special reference to histological findings]. 140 88

Serum levels of monomeric, dimeric and tetrameric pseudocholinesterases were measured by means of enzyme-linked immunosorbent assay in patients with various liver diseases and normal controls in order to evaluate their clinical significance. In patients with liver cirrhosis, serum levels of monomeric, dimeric and tetrameric were significantly lower than those in normal controls, patients with fatty liver and chronic hepatitis. The ratio of monomeric and dimeric to tetrameric in patients with liver cirrhosis was also significantly lower than that in normal controls, patients with fatty liver and chronic hepatitis. Serum levels of tetrameric, dimeric and monomeric were not significantly higher in the patients with fatty liver than in normal controls, but the ratio of monomeric and dimeric to tetrameric was significantly higher in patients with fatty liver than that in normal controls, patients with chronic hepatitis and liver cirrhosis. These findings suggest that the selective determinations of serum levels of monomeric, dimeric and tetrameric pseudocholinesterases are useful to estimate the metabolism of fat and protein in various liver diseases.
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PMID:[Clinical evaluation of serum levels of monomeric dimeric and tetrameric pseudocholinesterases in patients with various liver diseases]. 140 89

Opsonic glycoprotein, alpha 2-HS-glycoprotein concentration was studied in the serum of 753 patients with various hematological, malignant, immunological, metabolic, endocrine and liver diseases and 68 healthy controls. Decreased serum alpha 2-HS-glycoprotein levels were detected in patients with acute leukemias, chronic granulocyte and myelomonocyte leukemias, lymphomas, myelofibrosis, multiple myeloma, metastatizing solid tumors, systemic lupus erythematosus, rheumatoid arthritis, acute alcoholic hepatitis, fatty liver, chronic active hepatitis, liver cirrhosis, acute and chronic pancreatitis, and Crohn's disease. Elevated levels were measured in patients with B and NANB/C hepatitis. Further decreased levels were observed in some groups with secondary infections. Serum alpha 2-HS-glycoprotein levels are affected by many factors, influencing the synthesis and elimination of the protein. The detection of serum alpha 2-HS-glycoprotein concentration has no specific diagnostic value as a marker for tumors or other diseases, however, its determination can be useful for the assessment of a non-specific regulator of the host defence.
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PMID:[Diagnostic value of the determination of serum alpha2-HS-glycoprotein]. 140 55


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