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

Two cases of very probable post-hepatitis cirrhosis are presented. Both were complicated by presinusoidal portal hypertension (P. H. T.), the peroperative portal pressures measured directly being much higher than the wedged hepatic venous pressures. Although post-sinusoidal P. H. T. is the usual complication of most types of cirrhosis, these two cases support recent studies reporting the possibility of pre-sinusoidal P. H. T. in post-hepatitis cirrhosis. The wedged hepatic venous pressure is not a reliable indicator of portal pressure in these cases. The presence of presinusoidal P. H. T. does not exclude the diagnosis of cirrhosis but makes that of alcoholic cirrhosis very unlikely.
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PMID:[Presinusoidal portal hypertension in post-hepatitis cirrhosis]. 641 11

The different sensitivity of the male and the female liver is well established, but there is an obvious difference in male livers as well. One possible explanation for these differences might be the existence of genetic peculiarities among patients with alcoholic cirrhosis. In the early twentieth, Chvostek in Vienna was the first to draw attention to a constitutional element which he believed to be fundamental: Absent body hair, absent or extremely spare hair on the limbs, and pubic hair of the female type, i.e. with horizontal upper border (1) (Fig. 1). Chvostek laid special stress on the fact that these anomalies were of genetic origin and were not a secondary phenomenon do to alcoholism or cirrhosis. The feminine pattern of hair distribution, the so-called "Chvostek's habitus", is a frequently seen condition but the statistical proof of its association with alcoholic cirrhosis in man is still missing. The purpose of our study was to investigate if the feminine pattern of hair distribution in male patients with alcoholic cirrhosis is a genetic characteristic, this anomaly is more frequently encountered in the alcoholic type than in the post-hepatitis type of cirrhosis, the reported discrepancies of HLA frequencies are due to genetic differences.
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PMID:Constitutional factors in alcoholic cirrhosis. 653 37

An assay of serum antigens related to the aminoterminal propeptide of type III procollagen has been suggested for monitoring fibrotic processes in the liver. These antigens were measured here in 61 alcoholics who were divided into four groups on the basis of liver histology: normal light microscopy, fatty liver, alcoholic cirrhosis with hepatitis, and inactive cirrhosis. All the subjects having alcoholic hepatitis with cirrhosis had elevated values in the assay, whereas some of those with either fatty liver or inactive cirrhosis still had normal values. It was, therefore, not possible on the basis of this method alone to distinguish fatty liver from cirrhosis or alcoholic hepatitis, although very high values were suggestive of alcoholic hepatitis. In a follow-up study, the aminopropeptide value decreased slowly during recovery from alcoholic hepatitis and increased rapidly after a new drinking bout. The antigens detected by the assay are heterogeneous in human serum. The proportions of the three main peptide forms varied during recovery from alcoholic hepatitis, the authentic propeptide being the main one at the acute stage, but almost disappearing later. The usefulness of the assay could probably be improved if distinct assays were available for the different antigen forms.
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PMID:Aminoterminal propeptide of type III procollagen in serum in alcoholic liver disease. 660 26

The frequency of cirrhoses drastically increased in the seventies. This increase was predominantly due to an augmentation of alcoholic cirrhosis in men. Cirrhosis is significantly more wide-spread in men than in women. Most of the cirrhoses in women are of unknown origin. Morphologically, the alcoholic cirrhoses are of the micronodular types in their great majority. Combined with HBsAg positivity, the macronodular type is most frequent. The classification in micro- and macronodular cirrhoses do not imply a different etiology but it may indicate different stages in cirrhosis of identic origin. Histologically, the signs of alcoholic hepatitis particularly help to trace back the alcoholic etiology. If HBsAg can be detected and the margins of the pseudolobules are moth- eatenlike , this speaks for a hepatitic origin. The lowest average age was observed in cases of alcoholic cirrhoses, the highest in HBsAg positive cirrhoses of women. Men suffering from cirrhosis die earlier than women. In the case of alcoholic origin, the bulk of the cirrhotic livers are eutrophic while, beside HBsAg positivity, the atrophic livers are prevailing. The two most frequent environmental causes of cirrhosis are alcoholic beverages and hepatitis. Better exploration of the environmental factors and clearing up the origin of cryptogenic cirrhoses are essential tasks of the future.
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PMID:[Importance of environmental factors for the development of liver cirrhosis]. 667 10

A prospective unblinded, randomized trial of treatment for chronic aggressive hepatitis and non-alcoholic cirrhosis involving 154 patients chosen by predefined histological criteria showed no difference with regard to survival between patients receiving 100 mg of azathioprine and those receiving 10-15 mg of prednisone daily. Survival was unrelated to initial biochemical activity. In the initially most active cases biochemical activity was significantly reduced (p = 0.02), more often by prednisone than by azathioprine. The reduced activity was not reflected in subjective complaints or in the working capacity of the patients. Side effects were more frequent in the azathioprine group. Hematological side effects were exclusively found among azathioprine-treated patients. Prognosis was worst in patients who initially had high values of serum bilirubin and alkaline phosphatases and low values of serum albumin and prothrombin. The follow-up study is being carried out to obtain long-term observations.
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PMID:Azathioprine versus prednisone in chronic active hepatitis and non-alcoholic cirrhosis. Effect on survival and activity. 676 Mar 78

Using direct immunofluorescence, a nuclear antigen was found in liver of chronic hepatitis patients with circulating NANBe Ag or anti-NANBe, and selected sera from either group were used as source of conjugates. The new Ag/Ab system was designated NANBc Ag and anti-NANBc since it behaved like the core Ag of HBV . NANBc Ag was detected in coded frozen liver biopsies from patients with chronic persistent 15/25 (60%) or active 27/50 (54%) hepatitis and cryptogenic cirrhosis 16/30 (53.3%) devoid of HBV markers. Only 2/30 alcoholic cirrhosis cases (7%) used as controls were positive (p less than or equal to 0.001). The homologous anti-NANBc antibody was always detectable by indirect immunofluorescence in the patients' serum when NANBc Ag was found in the liver. It was also found in 11/135 (8%) additional cases without any other NANB marker. A correlation was observed between coded detection of the NANBc Ag/Ab system by immunofluorescence and demonstration of NANBe Ag or anti-NANBe by immunodiffusion. In acute post-transfusion NANB hepatitis, anti-NANBc was first detectable 14 days after transfusion and persisted as long as ALT remained elevated, or longer. IgM anti-NANBc present at onset became associated with an increasing proportion of IgG after the 28th day. The prevalence of anti-NANBc in sporadic NANB hepatitis (11/50 = 22%) was significantly lower (p less than or equal to 0.001) than in cases with parenteral exposure such as post-transfusion, occupational or drug addict hepatitis (47/72 = 65%). Immunofluorescent tests for NANBc Ag and Ab are promising assays for the serological diagnosis of NANB hepatitis.
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PMID:Detection by immunofluorescence of a new "core-like" Ag/Ab system in liver and serum of patients with NANB hepatitis. 681 8

Blood-lead concentrations (Pb-B) were measured in 318 adult inpatients with chronic liver diseases. The Pb-B was highest (387 +/- 96 micrograms/l) in 102 patients with alcoholic liver disease without cirrhosis. The Pb-B was still high, but significantly lower in 60 patients with compensated alcoholic cirrhosis (342 +/- 100 micrograms/l) and in 72 patients with decompensated alcoholic cirrhosis (312 +/- 97 micrograms/l). This difference was in part due to a significant decrease of the hematocrit which fell from 44.4 +/- 4.9% to 42.4 +/- 27.2% and to 39.2 +/- 7.4% respectively. In patients with viral or cryptogenic liver diseases the Pb-B was 211 +/- 69 micrograms/l in 11 patients with chronic persistent hepatitis, 219 +/- 72 micrograms/l in 19 with chronic active hepatitis, 206 +/- 94 micrograms/l in 28 with compensated cirrhosis, and 226 +/- 98 micrograms/l in 26 with decompensated cirrhosis, without any significant difference. The Pb-B of the male patients showed no correlation to age, with the exception of 25 male patients with chronic persistent and active hepatitis (r = 0.626, P less than 0.001).
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PMID:Blood-lead levels in patients with chronic liver diseases. 687 92

In view of the widespread use of serum thyroglobulin determination in the follow-up of patients with differentiated thyroid carcinoma, the influence of acute and chronic liver disease on serum thyroglobulin concentration was investigated in thirty-seven consecutive patients with histologically proven alcoholic liver cirrhosis and twenty-three patients with acute non-alcoholic hepatitis. Seventy-four healthy volunteers served as controls. Serum thyroglobulin concentration was significantly elevated in cirrhosis: median 29.5 micrograms/l, (range 4.3-94.0 micrograms/l) compared to controls: median 16.0 micrograms/l, (range 4.8-89.6 micrograms/l), (P less than 0.001). Serum thyroglobulin concentration in patients with acute hepatitis: median 16.2 micrograms/l, (range 7.9-70.0 micrograms/l) was not significantly different from controls. The level of free-T3-index was significantly reduced and the level of free-T4-index was significantly elevated in both cirrhosis and hepatitis compared to controls. Serum TSH concentration was significantly elevated in cirrhosis compared to hepatitis and controls. Serum thyroglobulin levels were positively correlated to levels of free-T3-index (r = 0.35, P less than 0.05) and T3/T4-ratio (r = 0.40, P less than 0.05) but not to levels of serum TSH or free-T4-index or any of the liver function tests in any of the groups. In conclusion, our results do not clearly indicate whether the elevated serum thyroglobulin level in cirrhosis was caused by an impaired elimination and/or an increased secretion from the thyroid gland. The increase in serum thyroglobulin concentration in chronic alcoholic liver disease was not of a magnitude likely to cause misinterpretation of results obtained during the follow-up of patients with differentiated thyroid carcinoma.
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PMID:Serum thyroglobulin in acute and chronic liver disease. 688 38

Acetaldehyde in non-toxic doses (15.6 micrograms per start) causes in the inhibition test of the migration of leucocytes an inhibition of the migration in 6/13 of the patients with alcoholic hepatitis, a stimulation of the migration in 6/11 of alcohol cirrhoses. Healthy (n = 16) persons, patients with alcoholic fatty degeneration of the liver (n = 3) as well as non-alcoholic liver diseases (chronic persisting hepatitis, n = 11; chronic active hepatitis, n = 8, cirrhosis, n = 7) did not show this cellular immune reagibility. The inhibition of the migration and the stimulation of the migration, respectively, might develop by hapten autoantigen complexes (altered cytoskeleton?) with release of the factors of inhibition of migration and stimulation of migration, in which case the role of a hapten belongs to acetaldehyde. The results of the tests did not correlate with functional and histological findings of the liver, with the actual consumption of alcohol and also not with haptoglobin phaenotypes. When it is postulated that by acetaldehyde also the release of further lymphokines is mediated, origin and progression of alcoholic hepatitis and alcoholic cirrhosis might be explained immunopathogenetically.
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PMID:[Acetaldehyde-induced leukocyte migration inhibition in alcoholic liver diseases]. 712 38

The real prevalence of liver cirrhosis within the total population is unknown. Our own statistic evaluations of the mortality from liver cirrhosis in relation to the death rate and investigations in fatal accidents may suppose a real prevalence of nearly 1% in the population of the GDR. Investigations of trends have shown a rising rate of incidence and mortality from liver cirrhosis in the GDR, mainly caused by alcoholic cirrhosis. There are positive correlations with the increasing alcohol consumption and negative ones with hepatitis incidence. Liver cirrhoses are accompanied by a high percentage of secondary diseases especially by gastroenterologic, cardiologic and metabolic disorders. The increase of alcoholic cirrhoses in the age group 20-40 years from 35% 1970 to 63% 1978 with the peak for men between 30-50 years will be of economic importance. Main topics for the epidemiologic research of liver cirrhosis have been discussed.
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PMID:Contributions to the epidemiology of liver cirrhosis and chronic hepatitis. 712 17


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