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)

Patients attending a clinic for diseases of the liver were tested for blood-ethanol by a gas chromatographic technique sensitive to about 5 mg/dl (1 mmol/1). Of 172 patients (51 men, 121 women) 36% gave a history of heavy drinking (greater than 80 g ethanol/day; equivalent to 8 fl oz of whisky or 1 litre of wine) and 13% had ethanol in the bloodstream at values of 8-400 mg/dl. 42 patients (24%) had the liver-biopsy changes of alcoholic liver disease, and 17 of these had ethanol in the blood at one time or another. Nearly half (22/49) of all patients admitting heavy drinking also had detectable blood-ethanol. In all cases but 1 where blood-ethanol was found, a drinking history was admitted on first attendance, and alcoholic liver disease was nearly always found on subsequent biopsy. Blood-ethanol and admission of drinking were most constantly found in association with alcoholic steatosis and hepatitis. Both features were less commonly present in cases of alcoholic cirrhosis. Only 1 patient of 22 with "cryptogenic" cirrhosis on biopsy was found to have both ethanol in the blood and an alcoholic history, although 5 had an alcoholic history alone. The value of serial blood-ethanol estimations in the treatment of alcoholics and the detection of relapses is demonstrated. The findings confirm the relatively low frequency of alcoholism as a contributor to cirrhosis in the United Kingdom. Alcohol does not seem a major cause of cryptogenic cirrhosis. Casual blood-ethanol estimation is a useful and objective adjunct to techniques of investigating diseases of the liver.
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PMID:Casual blood-ethanol estimations in patients with chronic liver disease. 5 Nov 46

45% of 65 Gambian patients with cirrhosis, and 53% of 63 patients with primary liver cancer were found to have hepatitis-associated antigenaemia, re-inforcing the possible aetiological role of hepatitis in these two common diseases of Africa.
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PMID:Hepatitis associated antigen, cirrhosis and primary carcinoma of the liver in the Gambia. 5 11

Peripheral blood and hepatic tissue T- and B-lymphocyte distributions, serum alpha fetoprotein (AFP) concentrations, and hepatic AFP were studied in 46 patients undergoing diagnostic percutaneous liver biopsy. The patients included 26 with alcoholic liver disease, 13 with nonalcoholic hepatitis or cirrhosis, and 7 with either normal histology or minor nonspecific changes. Serum AFP was determined by radioimmunoassay and hepatic tissue AFP by indirect immunofluorescence. Peripheral blood T lymphocytes were identified by the sheep red-cell rosette technique; and B lymphocytes by fluoresceinated anti-immunoglobulin antisera and IgG aggregates. Tissue identification of T lymphocytes was accomplished using an extensively absorbed rabbit antihuman thymocyte antiserum and indirect immunofluorescence; tissue B lymphocytes were identified using pepsin F (ab')2 fragments of rabbit IgG antibodies to human immunoglobulins. T lymphocytes predominanted in hepatic lymphoid infiltrates from patients with alcoholic liver disease (91+/-4%), whereas in patients with chronic active or chronic persistant hepatitis, viral hepatitis, or cryoptogenic cirrhosis proportions of T and B lymphocytic infiltrates were similar (50+/-15%). Hepatic tissue AFP was detected in 9 of 18 patients with alcoholic hepatitis; serum AFP concentration was increased in only 1 of these 9 patients. Tissue AFP was not observed in the remaining biopsy material nor were serum AFP concentrations increased. Peripheral blood T-cell numbers were significantly decreased in patients with alcoholic liver disease (P less than 0.01) and in nonalcoholic hepatitis or cirrhosis (P less than 0.025). A close relationship between peripheral blood T-lymphocytopenia and hepatic T-cell infiltrates was observed in patients with alcoholic liver disease; this relationship was less apparent in patients with nonalcoholic hepatitis or cirrhosis.
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PMID:Localization of T and B cells and alpha fetoprotein in hepatic biopsies from patients with liver disease. 5 55

Results of biochemical tests in 61 patients with acute viral hepatitis resp. 63 patients with subacute hepatitis were compared with laboratory findings of 27 patients with liver cirrhosis in the stage of severe activity of the disease. In acute and subacute viral hepatitis was the activity of GPT and CHE significantly higher than in active cirrhosis of the liver. In contrast to these findings was the activity of GLDH and the blood level of bilirubin in both groups of patients similar and for the differential diagnosis of no importance. Low albumin, high gammaglobulin and significant increase of IgG and IgA fractions of immunglobulins in serum are additionally to the results of the activity of some serum enzymes for the diagnosis of active liver cirrhosis in comparison to acute and subacute viral hepatitis of greatest value.
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PMID:[Differential diagnosis of acute viral hepatitis and liver cirrhosis with severe activity (author's transl)]. 5 26

The frequency distribution of HBs Ag in different parts of the world reveals a relatively high frequency among healthy members of population groups inhabiting areas of high incidence of liver cell carcinoma. Similar high frequencies of HBs Ag are also found in those areas where macronodular cirrhosis is relatively common and is usually complicated by liver cell carcinoma. In geographic areas with low incidence of liver cell carcinoma and macronodular cirrhosis, a relatively low frequency of HBs Ag is usually encountered in the population. The frequency of HBs Ag is relatively higher in patients with liver cell carcinoma with or without cirrhosis than in comparable controls. The subtypes of the antigen do not correlate with the incidence of liver cell carcinoma and there is also no correlation between alpha fetoprotein and HBs Ag in the presence of liver cell carcinoma. HBs Ag is very rarely detected in patients with micronodular cirrhosis or in liver cell carcinoma which may be its complication. It would appear that HBs Ag is necrogenic in the liver and is capable of producing hepatic necroses or hepatitis which may progress to macronodular cirrhosis. The areas of hepatic necroses may either progress to liver cell carcinoma or the resultant macronodular cirrhosis may be complicated by carcinoma. The oncogenic potential of HBs Ag requires further studies.
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PMID:Hepatitis B surface antigen and liver cell carcinoma. 5 11

Chronic liver disease developing after acute hepatitis type B is well documented, but is not thought to occur after acute hepatitis due to other viruses. However, follow-up of 29 patients in a haemodialysis unit who contracted HBsAg-negative acute hepatitis during 1968-70 revealed 8 cases with raised serum-aminotransferase levels dating from that time. Liver biopsy in 7 of these disclosed chronic aggressive hepatitis in 3, of whom 2 had already progressed to advanced cirrhosis. Chronic persistent hepatitis was present in 2 others, and the remaining 2 had non-specific hepatitis in association with massive iron overload. Immunological studies demonstrated a higher frequency of cellular immunity to HBsAg in those who had previously had acute hepatitis than in those who had not, although the prevalence of humoral antibody was similar in the two groups. One possible explanation for these findings is the presence of immunological cross-reaction at a cellular level between the hepatitis B virus and that responsible for the initial outbreak.
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PMID:Chronic liver disease developing after outbreak of HBsAG-negative hepatitis in haemodialysis unit. 5 71

"e" is a serum antigen associated with type-B hepatitis. It is found only in hepatitis B surface antigen (HBsAg) positive sera, but is antigenically distinct from HBsAg. e antigen was not detected in the serum of any of 99 cases of acute type-B hepatitis who recovered normally. Its antibody, anti-e, was found in 14 (14%). The antibody usually appeared before clearance of HBsAg and before appearance of HBsAb. Serum e was not detected in any of 29 symptom-free carriers of HBsAg, but 21 (73%) showed anti-e. Serum e was found in chronic active hepatitis (44%) and chronic persistent hepatitis (31%). The antibody, however, was detected in only 2 of 79 patients with chronic active hepatitis but in 7 (44%) of chronic persistent hepatitis. Serum e was not found in 5 patients with primary liver-cell carcinoma or 5 with inactive HBsAg-positive cirrhosis. The antibody was, however, found in all 5 of those with inactive cirrhosis and in 4 of the 5 with primary cancer. These results suggest that the presence of e antigen is associated with active and usually continuing liver disease. Anti-e, however, is associated with inactive liver disease and asymptomatic carriage of HBsAg, and its presence must be regarded as a valuable sign in predicting those who will escape progressive chronic liver disease.
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PMID:Incidence and clinical significance of e antigen and antibody in acute and chronic liver disease. 5 57

Follow-up study of 40 children suffering from chronic hepatitis. The diagnosis was made by liver needle biopsy with the Menghini method, when clinical signs or laboratory data of liver disease had lasted for more than 6 months. 24 patients showed the histological pattern of the aggressiv type of chronic hepatitis according to the definition of the European Association for the Study of the Liver (1968). In this group only 5 children had autoantibodies in the serum (so-called lupoid hepatitis). The HBAg positive courses played the most important part in the chronic persistent group as well as in the aggressive one. According to literature only the patients with the aggressive type have been treated with prednison, because chronic persistent hepatitis has a good prognosis without any treatment. In nearly all cases high transaminases and gammaglobulin levels decreased during the treatment with prednison, whereas the histological signs of inflammation seldom changed. Cirrhosis of the liver has developed in 2 HBAg positive patients of the aggressive group, who had not consequently received their daily dose of prednison.
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PMID:[Studies on juvenile chronic hepatitis]. 5 74

Laparoscopy was technically successful in 73 of 75 patients in whom liver disease was suspected but not accurately diagnosed after medical investigation. In 46 patients (63%) the final histological diagnosis was either diffuse parenchymatous disease (cirrhosis/hepatitis) or metastatic malignant disease; 2 had a curable medical disease (tuberculous ascites); and 6 had a curable surgical disease (5 with gallstones and 1 with an ectopic adrenal tumour). There were no deaths and no serious complications. With increasingly accurate non-invasive techniques for localising lesions in the liver, laparoscopy, with directed biopsy, should help to provide correspondingly accurate histological confirmation.
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PMID:Laparoscopy in liver disease. 5 94

In a prospective study 148 consecutive patients with biopsyproved acute viral hepatitis were observed serially and followed for 5 years. They were divided into three groups on the basis of being treated with high or low doses of gamma globulin and compared with a control group, not treated. As the efficacy of gamma globulin for the prophylaxis or modification of infectious hepatitis has been well documented by many investigators during the past 25 years, we were interested in evaluating the therapeutic effect of gamma globulin on the course of viral hepatitis. The purpose of the study was to determine the comparative efficacy of various doses of gamma globulin in preventing complications and in influencing the severity and the length of time of acute viral hepatitis and in preventing the development of chronic hepatitis and cirrhosis. For controlling the clinical, biochemical and histopathologic course 12 functional parameters were repeatedly measured under stable clinical conditions and 3--12 liver biopsies were performed in an individual patient using the Menghini needle with an intercostal approach. During the 5-year trial an overall of 825 liver biopsis were performed with this 148 patients. We conclude from this study, that in about 80% of patients with acute viral hepatitis recovery is complete, but takes several month's. A protracted course of 4 month's duration until recovery was found in 45 patients (30,4%), persistent hepatitis with recovery after 1--4 years duration occurred in 37 patients (25%), global liver necrosis with hepatic coma in 3 (2,3%), chronic hepatitis in 22 (14,8%), 8 of them as chronic aggressive hepatitis and cirrhosis in 3 (2,3%). The study demonstrated no therapeutic efficacy of gamma globulin in modifying the course or preventing complications of both AuAg+ and AuAg-neg. acute viral hepatitis in man. There was no striking difference in the groups treated with various doses of gamma globulin compared with a control group.
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PMID:[Gamma globulin therapy of acute viral hepatitis. Studies on the therapeutic effect of gamma globulin on the course and late prognosis of manifested acute viral hepatitis in man]. 5 14


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