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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alcoholic liver disease is associated with abnormalities in circulating levels of thyroid, adrenal and gonadal steroid hormones. The relative importance of ethanol consumption and severity of liver disease in the aetiology of these changes and their relationship to clinical abnormalities are unclear. We studied 31 subjects with alcohol-induced liver disease divided into three groups according to the severity of histological features: fatty change, hepatitis and cirrhosis. Circulating concentrations of thyroid, adrenal and gonadal steroid hormones, together with their major binding proteins, were measured in all subjects, and changes related to histology and tests of liver function, as well as clinical endocrine status. A reduction in circulating free tri-iodothyronine (fT3) was seen in subjects with alcoholic hepatitis and cirrhosis, in association with normal or reduced levels of thyrotrophin (TSH). The absence of abnormalities in subjects with fatty change despite similar ethanol intake to the other groups, and correlations between fT3 and liver function tests, suggest that changes in fT3 reflect the severity of underlying liver disease. Similarly, marked increases in circulating cortisol in the hepatitis and cirrhosis groups, and correlations between cortisol and liver function, suggest that changes largely reflect hepatic disease. The absence of clinical features of hypothyroidism or Cushing's syndrome in these groups, despite abnormalities of fT3 and cortisol, suggest an altered tissue sensitivity to hormone effects. In contrast, increases in circulating oestradiol and reductions in testosterone were found in all three groups in males. These findings suggest that both direct effects of ethanol and hepatic dysfunction determine changes in gonadal steroids in males.
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PMID:Severity of alcoholic liver disease and markers of thyroid and steroid status. 146 52

We report the 10-year survival of 510 patients with a histological diagnosis of alcoholic liver disease. Eight centres in Scotland and North England contributed to this study. Information was available on 92% of the initial cohort. Age was important, with each decade increasing mortality by 55%. A highly significant interaction between sex and histology was observed with a marked survival benefit for males with non-cirrhotic alcoholic liver disease, while in cirrhotic subjects the pattern was reversed. Patients with decompensated liver disease had a relative increase in mortality in excess of 86% while the increase in mortality for alcoholic hepatitis, 'active' cirrhosis and 'inactive' cirrhosis were 52%, 57% and 91% relative to fatty liver. Alcohol intake at the time of diagnosis did not influence outcome. This study emphasises yet again the increased mortality rate of individuals abusing alcohol compared with the general population.
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PMID:A prospective study of alcoholic liver disease and mortality. 148 5

The extracellular matrix (ECM) is a complex of macromolecules that includes collagens, proteoglycans, and complex glycoproteins. In fibrotic liver tissue there is an increase in all of these matrix components, and they increase in serum in the patients with alcoholic hepatitis or liver cirrhosis. These ECM components have been used as a serum marker of hepatic fibrosis. Prolonged obstruction of bile flow results in morphologic and biochemical changes and the development of secondary biliary cirrhosis. In congenital biliary atresia (CBA) there is a close correlation between the degree of the hepatic fibrosis and bile flow after the operation. We estimated that, in CBA, ECM increased in serum, and it would reflect the degree of the hepatic fibrosis. To clarify this we examined the serum procollagen-III-peptide (P-III-P) and laminin in CBA patients. P-III-P was elevated in all preoperative patients but in two of the three postoperative patients whose jaundice disappeared P-III-P was in the normal range. In the all 3 patients whose jaundice continued, P-III-P was in normal range. Serum laminin was elevated in 12 preoperative patients with CBA, but there is no correlation between day of diagnosis and level of laminin. Mean concentration in CBA without jaundice after operation was 3.18 U/mL, 3.226 U/mL in CBA with jaundice and 3.3 U/mL in infantile hepatitis. There were no significant differences among three groups. With the elevation of serum alanine aminotransferase, aspartate aminotransferase, and total bilirubin, serum laminin level was also increased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Laminin and procollagen-III-peptide as a serum marker for hepatic fibrosis in congenital biliary atresia. 150 Oct 26

Resting energy expenditures (REEs) were measured in 40 alcoholic cirrhotic (AC) patients by indirect calorimetry and corrected for 24-h urinary creatinine and excretion. These REEs were compared according to the stage of severity of the cirrhosis, the nutritional status, and the presence or absence of alcoholic hepatitis (AH). Mean REE was not significantly different between the Child class A, B, and C patients, even when corrected for 24-h urinary creatinine. Mean REE was significantly less in malnourished AC than in well-nourished patients (1308 +/- 285 vs. 1531 +/- 255 kcal, p less than 0.02). However, when measured energy expenditure was corrected for 24-h urinary creatinine, the difference between the two groups of patients disappeared (1800 +/- 540 kcal/g creatinine in malnourished patients vs. 1890 +/- 780 kcal/g creatinine in well-nourished patients). Finally, there was no significant difference between the REE, corrected or not, for the 24-h urinary creatinine in AC with or without AH. Thus, when REE is normalized to lean body mass, represented by 24-h urinary creatinine, the metabolic activity in AC is not dependent on the severity of the cirrhosis, nutritional status, or existence of AH.
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PMID:Relationship of resting energy expenditure with liver function and nutritional status in patients with alcoholic cirrhosis. 156 84

Forty Japanese patients with alcoholic liver disease (nonspecific change, 9; fatty liver, 5; hepatic fibrosis, 4; chronic hepatitis, 12; alcoholic hepatitis, 5; liver cirrhosis, 5) were followed for 3-17 yr (average 8 yr) with repeated liver biopsies (2-5 times; average 2.5 times) at intervals of more than 3 yr. All of the patients continued to consume alcohol during this observation period. Five out of 12 patients with chronic hepatitis and 2 of 5 patients with alcoholic hepatitis eventually progressed to cirrhosis, while none of the 4 patients with hepatic fibrosis became cirrhotic. Anti-hepatitis C virus antibody was positive in 2 patients with liver cirrhosis among 12 patients whose sera were available. Two patients with cirrhosis died of hepatic failure and one patient died of hepatocellular carcinoma. These data suggest that the long-term prognosis of alcoholic liver disease is not necessarily poor, but patients with chronic hepatitis or alcoholic hepatitis can be at risk of progression to cirrhosis.
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PMID:Long-term histologic follow-up study of alcoholic liver disease. 156 40

Excessive consumption of ethanol results in reversible redox changes in the liver that are mainly responsible for the accumulation of triglycerides and the fatty liver of the alcoholic patient. In spite of continuing alcohol abuse, only a fraction of all alcoholics will develop alcoholic hepatitis and eventually cirrhosis. Genetic predisposition and environmental factors (in particular the often poor nutrition of the alcoholic) probably play an important role in the evolution of these complications. The generation of reactive oxygen species increases during the metabolism of ethanol, but their pathogenetic role in alcoholic liver disease in man is not clear. Acetaldehyde, a metabolite of ethanol, can react with proteins and form stable adducts. Such neoantigens may elicit an immunologic response which could in part be responsible for the liver cell damage associated with excessive alcohol consumption. Since no satisfactory animal model for alcoholic liver disease exists, the relative importance of the various factors involved in alcoholic liver disease is difficult to assess.
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PMID:[Pathogenesis of alcoholic liver disease]. 158 33

Alcohol can induce a wide spectrum of histological changes in the liver. Three morphologic patterns of alcoholic liver injury are now generally accepted, i.e. fatty change, alcoholic hepatitis and alcoholic cirrhosis, but a broad array of lesions has been added to this list in recent years. These damage patterns differ considerably in their significance as to indication and diagnostic power of liver biopsies. Liver biopsy is recommended in patients with clinically suspected alcoholic liver disease for diagnostic and prognostic reasons. Moreover, clinicians want to exclude nonalcoholic liver diseases that might otherwise be missed. Alcoholic hepatitis, which is associated with increased morbidity and mortality, has the highest degree of diagnostic specificity in biopsies, because its features are well-defined and are mimicked by a rather small group of other causes. When associated with perivenular and pericellular fibrosis, it may provide prognostic parameters. In contrast, fatty liver, which may be induced by alcohol as well as other etiologies, usually does not need liver biopsy, with some exceptions. It may lead to cholestasis severe enough to mimic obstructive jaundice, or may result in abnormal imaging studies suggesting metastases. Verification of histological findings may be important when these circumstances arise. Cirrhosis is easily verified in biopsies of appropriate quality; however, advanced cirrhosis is a morphologically nonspecific alteration, because cirrhotic tissue patterns converge irrespective of their cause. Liver biopsy may help to identify nonalcoholic liver disease in patients suspected of harboring alcoholic liver disease. In fact, up to 20% of biopsies may show other, potentially treatable disorders, thus extending the indication for liver biopsy in situations of complex clinical and laboratory patterns.
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PMID:[Liver biopsy in suspected alcoholic liver damage]. 162 Dec 36

The hepatitis B virus (HBV) markers were studied by Sorin RIA kits in the sera of 390 patients suffered from histologically confirmed chronic liver disease. On the base of HBsAg, anti-HBs, anti-HBc seronegativity the HBV infection was excluded in 235 cases. In most HBV negative cases the diagnosis was fatty liver and alcoholic hepatitis (52%), while chronic active hepatitis and/or liver cirrhosis occurred only in 21.7% of patients. Past or present HBV infection was proved in 155 patients. The diagnosis of 52.9% of cases in this group was chronic active hepatitis and/or liver cirrhosis, while fatty liver and alcoholic hepatitis occurred in 27.7%. The detailed HBV marker analysis was performed in 76 patients. Previous infection without replication (anti-HBs and/or anti-HBc and/or anti-HBe positivity) was proved in 48 cases, 12 patients have active HBV infection (HBsAg, HBe, IgM anti--HBc, positivity), while in 16 cases integrated HBV infection (HBsAg, anti-HBc, anti-HBe positivity) was proved. The HBsAg--IgM complex seropositivity was detected in every case with active HBV replication. Because of therapeutic, prognostic and epidemiologic significances the detailed HBV serology in chronic liver diseases is stressed.
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PMID:[Significance of detailed Hepatitis B virus marker studies in chronic liver diseases]. 163 Aug 8

Malondialdehyde (MDA) level was determined spectrophotometrically with thiobarbituric acid method on 50 healthy persons and 160 patients with alcoholic and nonalcoholic liver diseases. Alcoholics without liver damage show normal plasma MDA values. Alcoholic fatty liver, alcoholic hepatitis and alcoholic liver cirrhosis cause an increase of MDA values. The highest concentrations of MDA were found on patients with acute virus hepatitis. Also noninfectional hepatitis and nonalcoholic liver cirrhosis showed an elevated MDA-Level. Liver damage and lipid peroxidation are considered as closely connected processes.
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PMID:[Malondialdehyde concentration in blood plasma of patients with liver diseases]. 164 26

An enzyme immunoassay (Ortho-HCV ELISA) for antibodies against the hepatitis C virus was used to test serum samples from 39 patients with alcoholic cirrhosis and 34 patients with alcoholic hepatitis or fatty liver. The frequency of a positive result in the cirrhotics was significantly higher than in the alcoholics without cirrhosis (38.5% vs 8.8%, P less than 0.01). However, the positive results in the cirrhotics were associated with high gammaglobulin concentrations, and optical density values in the assay correlated closely with serum globulin (r = 0.73, P less than 0.01). The findings suggest that serum from patients with alcoholic cirrhosis may contain a component that give false-positive results in the assay.
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PMID:High incidence of antibodies to hepatitis C virus in alcoholic cirrhosis: fact or fiction? 165 49


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