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)

The presence of antibody to the hepatitis C virus was determined in 254 alcoholic patients with non-B chronic hepatitis and a titre of antinuclear antibodies of 1/40 or lower. Alcoholic hepatitis was present in 12 patients, steatohepatitis in 20, active chronic hepatitis in 22, cirrhosis in 181, and hepatocarcinoma in 19. Twenty patients had previously received blood transfusion alone or during surgery, 49 had undergone previous surgery without transfusion, a clinical episode of hepatitis could be traced in 14, 4 patients were drug addicts, 41 had received blood transfusion after the diagnosis was made, and 128 presented with alcoholism alone. Anti-hepatitis C antibody was found in 20 out of 2,000 blood donors (1%) in our hospital. Anti-hepatitis C antibody was found in 87 patients (34.2%) in our series, a figure unaltered by past medical history. Patients with anti-HC antibody had higher levels of AST, ALT, total proteins, gamma-globulin, and IgG. The incidence of active chronic hepatitis was higher among patients with anti-HC antibody, whereas the incidence of steatohepatitis was higher among patients without anti-HC. Regarding findings on liver biopsy, the incidence of anti-HC was significantly higher (p less than 0.001) among patients with active chronic hepatitis (72.7%) than in any other group; no significant differences were found between patients with cirrhosis (33.3%), hepatocarcinoma (31.5%), steatohepatitis (15%), or alcoholic hepatitis (16.7%). Among HBsAg-negative patients, the incidence of anti-HC was similar between those with (39.7%) and without other serum markers of HB (32.9%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prevalence and significance of the C virus antibody in chronic hepatopathy not related to B virus in alcoholics]. 131 33

The prevalence of hepatitis virus markers in patients with chronic liver diseases from two countries has been studied: 68 patients (38 alcoholic hepatitis or cirrhosis, 30 chronic HBsAg-positive hepatitis) from Hungary as well as 109 patients (55 alcoholic liver disease, 45 chronic hepatitis or cryptogenic cirrhosis and 9 hepatoma) from Romania were examined for HBsAg, anti-HBs, anti-HBc, anti-HCV and anti-HDV, using the corresponding Abbott Elisa test systems. In alcoholic liver disease HBsAg occurred in 6/38 patients from Hungary and in 22/55 patients respectively, that is HBV markers occurred with significantly higher frequency in alcoholic patients from Romania (p less than 0.05). In the Hungarian group a total of 36 patients were HBsAg positive and out of them 5 had anti-HDV (13.9%), while out of 21 Romania HBsAg carriers 10 patients had anti-HDV (47.6%). Among 9 hepatoma patients 4 had HBsAg, 6 anti-HBs and 7 anti-HBc and 4 had anti-HCV and 3 had anti-HDV. One patient with hepatoma had both HBsAg and anti-HCV plus anti-HDV as well. Results suggest that the infection with hepatitis viruses in alcoholic liver diseases is more common in Romania than in Hungary, and the prevalence of delta virus infection in HBV carriers is also significantly higher in Romania than in Hungary.
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PMID:[Hepatitis virus (HBV, HCV, HDV) markers in chronic liver diseases. Comparative studies in two East-Central European countries]. 132 99

The authors applied a silver colloid technique to identify Argyrophilic Organiser Region (AgNOR) to 8 groups of hepatic lesions: alcoholic hepatitis with dysplasia (3 cases); chronic active hepatitis with dysplasia (4 cases); cirrhosis with dysplasia (5 cases); focal nodular hyperplasia (4 cases) and hepatocellular carcinomas (3 cases of grade I, 3 cases of grade II and 5 cases of grade III of Edmondson). Four cases of non-specific reactive hepatitis were used as control. This work suggests the simplicity and utility of simultaneous application of clumps per cell, AgNORs per clump and total AgNORs counts in the evaluation of neoplastic and preneoplastic lesions of the liver. The results show, in hepatocellular carcinomas, a relationship between the number of clumps, the AgNORs per clump, the total number of AgNORs and the grading of Edmondson. The nodular lesions that can be considered in the differential diagnosis with carcinoma are sufficiently well discriminated using the two parameters AgNORs per clump and total number of AgNORs.
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PMID:Hepatocellular carcinoma and preneoplastic lesions of the liver: evaluation of argyrophilic nucleolar organizer regions (AgNORs). 133 18

The pathogenesis of alcoholic liver disease is unclear. The recent literature on pathogenic factors, including direct effects of ethanol and its proximate metabolite acetaldehyde, associated nutritional factors, the formation of acetaldehyde-protein adducts, associated immune alterations, and the potential for liver injury due to coexisting hepatitis virus infection, is highlighted. The therapy of patients with advanced alcoholic liver injury, especially alcoholic hepatitis, is also controversial. It seems reasonable that all patients should receive adequate nutrition even if parenteral or enteral supplementation is required. Corticosteroid administration may benefit those patients with alcoholic hepatitis who have coexisting spontaneous hepatic encephalopathy and no gastrointestinal bleeding. For patients with complications from end-stage alcoholic cirrhosis, liver transplantation should be considered, as the patient with alcoholic cirrhosis does as well after liver transplantation as those patients with other forms of end-stage liver disease.
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PMID:Modern approach to alcoholic liver disease. 143 70

Considerable clinical and experimental evidence points to the importance of immune responses in the development of alcoholic liver disease. In the present study it was investigated whether circulating antibodies from patients with alcoholic liver disease recognize acetaldehyde-liver protein adducts. Cytosolic and microsomal fractions from livers of Wistar rats or from normal human liver were incubated with acetaldehyde (0.5-2.5 mmol/L) and/or cyanoborohydride (100 mmol/L) then analysed by immunoblotting. Cytosolic fractions that had been incubated with acetaldehyde and cyanoborohydride expressed a 200-kilodalton protein antigen not present in untreated fractions or fractions incubated with acetaldehyde or cyanoborohydride alone. The 200-kilodalton antigen was recognized by immunoglobulin (Ig)A antibodies in a large proportion of sera from patients with alcoholic hepatitis (70%, n = 23), but in significantly smaller proportions of sera from patients with alcoholic cirrhosis without hepatitis (30%, n = 10; P < 0.05), heavy drinkers without overt liver disease (20%, n = 10; P < 0.02), patients with nonalcoholic liver disease (35%, n = 17; P < 0.05), or normal control subjects consuming moderate quantities of alcohol (25%, n = 20%; P < 0.005). These results indicate that IgA antibodies to a 200-kilodalton acetaldehyde-protein adduct are present in a large proportion of patients with alcoholic liver disease and in a significantly smaller proportion of other individuals.
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PMID:Immunoglobulin A antibody to a 200-kilodalton cytosolic acetaldehyde adduct in alcoholic hepatitis. 145 88

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

Nitric oxide, initially described as an endothelial-derived relaxing factor, has recently been recognised as a mediator of macrophage function. We have studied the production of nitric oxide by peripheral blood monocytes from both normal volunteers and alcoholics. This was measured indirectly by assessing nitrite formation. Normal monocytes were found to produce a basal level of nitrite, which could be stimulated more than 6-fold using endotoxin. This effect was abrogated by the addition of nitric oxide synthesis inhibitor, L-n-monomethyl-arginine. A striking difference was observed in the monocytes obtained from alcoholics with and without evidence of alcoholic hepatitis. Whereas the latter behaved in a similar manner to the controls, the former had markedly increased basal levels. In the hepatitis group there was also substantial inhibition of production by L-n-monomethyl-arginine. We believe that these results indicate that nitric oxide derived from monocytes may play a role in the pathogenesis of alcoholic liver disease, especially alcoholic hepatitis.
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PMID:Nitric oxide production by monocytes in alcoholic liver disease. 150 Jun 77

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

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

The work deals with a group of 212 patients suffering from various forms of precirrhotic alcoholic liver disease and includes a period of 8.5 years (January 1981-June 1989). At least two liver biopsies were performed in all patients. according to the histological diagnosis, the patients were distributed into 6 subgroups: simple hepatic steatosis--24 cases (11.3%), hepatic fibrosis--40 cases (18.8%), hepatic steatofibrosis--69 cases (32.5%), acute alcoholic hepatitis--18 cases (8.5%), chronic active hepatitis--43 cases (20.3%) and chronic persisting hepatitis--18 cases (8.5%). The assessed histological parameters included: fatty transformation, hepatic fibrosis, inflammatory infiltrate within the lobules and in the portal spaces, hepatocellular necrosis, cholestasis, proliferation of the bile ductules and modification of the lobular architectonic. The work is aimed at pointing out the precirrhotic hepatic histological lesions induced by alcohol and fraught with an increased risk of progression towards liver cirrhosis. The histological sequential examination of alcoholic hepatic lesions confirm the possibility of progression and installation of the cirrhotic stage for a number of these lesions. Liver cirrhosis developed in 44 patients (20.7%) within a period of 3-7 years, on an average 5.5 years. The progression toward cirrhosis occurred in 12 patients (5.7%) with steatofibrosis, in 11 (5.2%) with hepatic fibrosis, in 14 (6.6%) with an intralobular inflammatory infiltrate, in 17 (8%) with hepatocellular necrosis, in 3 (1.4%) with cholestasis, in 5 (2.3%) with proliferation of the bile ductules and in 10 patients (4.7%) with a modification of the lobular architectonic. In addition, cirrhosis was detected in 8 patients (3.8%) with alcoholic hepatitis and in 13 patients (6.1%) with chronic active hepatitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The criteria of histological activity and the prognosis in precirrhotic alcoholic hepatopathies]. 167 Jan 14


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