Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Certain characteristics of 328 Mozambican male Shangaans with primary hepatocellular cancer (PHC) have been compared with those of 163 Shangaan men with hepatomegaly from causes other than PHC and with those of 122 Black Southern African men with the same tumour but who belonged to tribes other than the Shangaan. Shangaans with PHC were significantly younger than non-Shangaans with the tumour (mean age 33,4 cf. 40,0 years; Pless than 0,001). They also had a significantly higher positivity rate of alpha-fetoprotein by immunodiffusion (71,4%) than the non-Shangaans (16%), although in other respects the tumours appeared to be similar. Cirrhosis of the non-tumorous part of the liver was present at necropsy in 62% of the Shangaans and in 66% of the non-Shangaans. The hepatitis B (surface) antigen (HBsAg) was detected in the serum of 60% of the Shangaans with PHC compared with only 9% of the controls. The antigen was present in 53,4% of the non-Shangaans with PHC (the difference between this fifure and that in the Shangaans was not significant). HBsAg was detected in the serum of 64% of the Shangaans with PHC and cirrhosis, but also in 74% of those with the tumour without associated cirrhosis. The possible role of the hepatitis B verus in the aetiology of PHC is considered in the light both of these findings and of the possibility that the frequency with which the tumour is associated with cirrhosis may be decreasing in Shangaans. Some of the dietary habits of the Shangaans with PHC were compared with those of the controls. Virtually all the patients with PHC, but also almost all the controls, ate groundnuts in large quantities from an early age, as well as cashew nuts in smaller amounts. Cycad pips, mopani leaves and pods, mopani worms and locusts were not eaten by significantly more of the Shangaans with PHC than the controls. The limitations of this type of dietary analysis are discussed.
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PMID:Some characteristics of Mozambican Shangaans with primary hepatocellular cancer. 6 57

The chief causes of liver disease in Ethiopia are reviewed, considering hospital data on admissions for hepatitis, cirrhosis, ascites and hepatoma. Liver diseases account for 11.4% of all medical admissions in 3 medical wards in Addis Ababa. The causes are viral hepatitis, post- hepatic and post necrotic and mixed cirrhosis and hepatocellular carcinoma. Alcoholic cirrhosis is rare. Viral hepatitis with shivering, rigor and fever and elevated direct bilirubin levels are common in Ethiopians, especially in child-bearing women. The hepatitis B surface antigen (HBsAg) is often associated with hepatitis. The disease may be transmitted by several species of mosquitoes, placental transmission, or feces, urine, saliva or semen. Blood products are not screened for hepatitis B. Cirrhosis is common, and causes significant mortality, usually from esophageal varices and hepatic coma. Chronic active hepatitis patients may live for a time, especially if they are near a hospital and are treated with steroids. In Ethiopia presenting symptoms for hepatoma are anorexia, weight loss, persistent, burning, right upper quadrant pain, and a hard, nodular, tender RUQ mass. Over 5% of malignancies seen are primary hepatocellular carcinomas. 50% have HBsAG, compared to 3.8% of controls. 65% have alpha-fetoglobulins. It is suggested that some viral hepatitis cases progress to cirrhosis, of which some go on to hepatocellular carcinoma. Herbal medicines, aflatoxins and other toxins may also contribute to liver disease.
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PMID:Current views on liver diseases in Ethiopia. 20 62

Immunosuppressive treatment with prednisolone and/or azathioprine has been assessed in three chronic liver diseases with immunological features, namely chronic active hepatitis, cryptogenic cirrhosis and primary biliary cirrhosis. In chronic active hepatitis, controlled prospective clinical trials have shown clinical, biochemical and hepatic histological improvement when prednisolone with or without azathioprine is employed. Azathioprine alone has no advantage over placebo tablets. Cirrhosis is probably not prevented. Selection of patients for treatment, the response and therapeutic regimes are discussed. Patients with hepatitis B surface antigen positive chronic active hepatitis have a worse therapeutic response than those patients with chronic active hepatitis who are HBsAg negative. In primary biliary cirrhosis, corticosteroid treatment is contra-indicated on account of bone thinning. Azathioprine has been used in controlled clinical trials and is of only marginal benefit.
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PMID:Immunosuppressive therapy in chronic liver disease. 71 60

Our knowledge of the cellular changes that lead to liver cell carcinoma in humans is limited by proper and necessary ethical restriction on clinical research. We know rather more about risk factors, the most important of which is cirrhosis, it seems that both the causative agent and the time of duration of the cirrhotic process are relevent to the magnitude of this risk. According to present knowledge, alpha1-antitrypsin deficiency, alcoholism, naturally occurring carcinogens, drugs, and the hepatitis B virus seem to carry the greatest risk of cancer developing in a cirrhotic patient. Cirrhosis, however, is not an essential prerequisite, and some or possibly all of these agents can also induce cancer without cirrhosis. Bile duct carcinoma commonly follows infestation with liver flukes. Cirrhosis is usually absent but duct epithelial hyperplasia is present prior to the development of cancer. Many cellular changes have been observed in patients and among populations considered to be at risk from liver cancer. Of these, liver cell dysplasia is the most striking and studies of its prevalence, natural history, and association with cirrhosis suggest that it is a precancerous change.
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PMID:Precursor lesions for liver cancer in humans. 77 94

This study was designed to compare the clinical and immunological characteristics of the hepatitis B surface antigen (HBsAg)-positive and HBsAg-negative (cryptogenic) forms of chronic active hepatitis. The data of 48 patients with chronic active hepatitis, 24 with persistent HBs antigenemia and 24 without HBsAg, were analysed. HBsAg was detected by counter-immunoelectrophoresis and radioimmunoassay. The clinical features, biochemical liver function tests, immunoglobulins, complement C3, antoantibodies, and cell-mediated immunoreactivity of the two forms of the disease were compared. Cirrhosis was found to occur more frequently at the time of diagnosis in the HBsAg-negative group, and the serum alkaline phosphatase level was raised significantly compared to the HBsAg-positive form. The elevation of the IgG level was greater in the cryptogenic form, but the difference was not statistically significant compared to the HBsAg-positive patients. There was a marked difference in the frequency of the mitochondrial antibodies, but not of the antinuclear factor and other autoantibody-like serum factors. Lymphoblastic transformation revealed a similar diminution in response to phytohaemagglutinin stimulation in both groups of patients compared to the normal controls. An increase of the 3H-thymidine incorporation was seen after stimulation with human liver mitochondrial antigen, and leukocyte migration inhibition could be observed with this antigen in both forms of chronic active hepatitis.
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PMID:Chronic active hepatitis in patients with and without hepatitis B surface antigenemia. 91 64

Male sex, age, cirrhosis, and HBsAg are the major risk factors for hepatocellular carcinoma (HCC). The geographic distribution of HCC is highly uneven, such that three distinct incidence areas are recognized. To clarify the reason(s) for this geographic variability of HCC, the risk factors in each incidence area were assessed. In parallel with the geographic distribution of HCC, HBsAg prevalence was highest in both HCC patients and in general population in Africa and Asia, where mothers of HCC patients are frequently HBsAg-positive, suggesting that hepatitis B virus hyperendemicity and perinatal infection account for the high HCC incidence in these areas. Cirrhosis, which is found on autopsy in 80% of the cases of HCC patients worldwide, is the most prevalent risk factor for HCC in areas where hepatitis B virus infection is less common. However, HBsAg carriage adds to the HCC risk carried by cirrhosis and explains the higher incidence of HCC in cirrhotics from Africa and Asia as well as elsewhere. Available data suggest that chronic HCV infection is a risk factor for cirrhosis and HCC. HBV vaccination should decrease HCC incidence rates worldwide; however, HCC prevention in regions where HBsAg carriage is infrequent may also require prevention of the other causes of cirrhosis in order for HCC rates to decline.
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PMID:Hepatocellular carcinoma. A worldwide problem and the major risk factors. 164 41

The preceding discussions outline the various forms of cirrhosis that may be encountered in the elderly population. Cirrhosis is not uncommon in older patients. Although it has been stated that most cirrhosis in the elderly is due to alcohol, these assumptions are perhaps overestimations. In the authors' experience, many older patients are inappropriately labeled with alcoholic liver disease--presumed guilty until proven otherwise--and have subsequently been shown to have nonalcoholic liver disease. Careful investigation is required. Hepatotoxic drug exposure (e.g., to alpha methyldopa, nitrofurantoin, or isoniazid) should be ruled out, and hepatitis B and hepatitis C serology obtained. Primary biliary cirrhosis may occur in both sexes, and thus antimitochondrial antibody should be assayed. Severe heart disease may result in cardiac cirrhosis in the elderly, with ascites and hepatomegaly. Alpha 1-antitrypsin deficiency, primary sclerosing cholangitis, idiopathic hemochromatosis, and chronic autoimmune hepatitis may result in advanced cirrhosis in the elderly; appropriate serum studies should be obtained. If questions remain and if therapy may be changed, liver biopsy can be performed. A recent study suggested, however, that the risk of hemorrhage from liver biopsy in the elderly may be increased, especially if malignancy is present. The era of treatment for liver diseases has arrived. Colchicine, methotrexate, ursodeoxycholic acid, and others have shown promise in the treatment of PBC, primary sclerosing cholangitis, and alcoholic liver disease. Corticosteroids may be lifesaving in autoimmune liver disease. Phlebotomy remains the treatment of choice for hemochromatosis in any age group. Interferons and other antiviral agents are being used in chronic type B and type C hepatitis. Treatment of the complications of cirrhosis in the elderly may be safely accomplished. Advanced age is not a contraindication to variceal sclerotherapy. Vasopressin, however, may be contraindicated in the elderly patient if there is an underlying history of atherosclerotic coronary or peripheral vascular disease. Large-volume paracentesis and peritoneal venous shunting can afford symptomatic relief of ascites, even in the geriatric population. Finally, as noted previously, advanced age is no longer to be considered an absolute contraindication for liver transplantation. The evaluation of liver disease in the elderly may be diagnostically challenging, and its treatment rewarding.
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PMID:Liver diseases in the elderly. 185 64

The prevalence of cholelithiasis (gallstones or previous cholecystectomy) was evaluated in a series of 500 cirrhotic patients from Northern Italy (329 males and 171 females, mean age 58 +/- 11 (SD) yr and 61 +/- 10 yr, respectively). Cirrhosis was related to chronic alcohol abuse in 180 cases, non-A non-B (NANB) hepatitis in 160, hepatitis B virus (HBV) in 94 (including 38 with concomitant alcohol abuse), idiopathic hemochromatosis in 44, and miscellaneous causes in the remaining 22 (including 15 with primary biliary cirrhosis). One hundred and sixteen patients (23.2%) had gallstones, and 31 others (6.2%) had previously undergone cholecystectomy, with an overall prevalence of cholelithiasis of 29.4%. The frequency was similar in both sexes (91/329 males, 27.7% vs. 56/171 females, 32.7%; p = NS), showed a slight increase with age, and differed significantly according to etiology (p less than 0.05), with the highest prevalence in the miscellaneous group and the alcoholics (36.4% and 33.3%, respectively). No significant difference was found in the prevalence of cholelithiasis according to Child's A, B, or C class.
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PMID:Cholelithiasis in cirrhosis: analysis of 500 cases. 842 Feb 66

Cirrhosis mortality death rates in Ontario for ages 20 and over declined from a high of 9.3 per 100,000 in 1911 to a low of 5.6 per 100,000 in 1919 (p less than 0.001) and after a 17-year period of relative stability, rose steadily to a high of 19.7 per 100,000 in 1975 (p less than 0.0001) and then declined to 13.3 per 100,000 in 1986 (p less than 0.001). Rates were consistently higher for men than for women and the male to female ratio of the rates increased from a low of 1.3 in 1933 to a high of 2.5 in 1986. The rate of increase in the rates for both men and women, and the rate of decline after the mid 1970s was most noted in the younger ages. Differences in trend could not be related to changes in disease classification, method of recording deaths, changes in diagnostic habits such as introduction of needle liver biopsy or to method of standardizing the rates. There was a positive and significant correlation between per capita alcohol consumption and rates of cirrhosis in Ontario from 1932 to 1975. However, while cirrhosis rates declined markedly from 1976 to 1986, alcohol consumption remained stable from 1976 to 1980 and declined only slightly from 1981 to 1986. A possible explanation for lack of correlation between alcohol consumption and the cirrhosis rates from 1976 to 1986 could be that the balance of force favoured recovery i.e. those people who already had cirrhosis who decreased (or stopped) their consumption of alcohol, did not die. Correlations with lagged alcohol consumption could not explain all the changes in the cirrhosis rates. Although cirrhosis rates consistently increased with increasing age from 35 to 85, our results showed that succeeding generations were developing cirrhosis at successively younger ages after the age of 35. Possible explanations for this cohort effect are increased survival from infectious diseases in infancy and childhood, increase in hepatitis B infection, excessive drinking habits being established at younger ages or a change in the pathogenesis of the disease.
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PMID:Changing trends of cirrhosis mortality in Ontario, Canada, 1911-1986. 206 20

Antibodies against hepatitis C virus (anti-HCV) were detected in 60.8% of 78 patients with hepatocellular carcinoma (HCC). Cirrhosis, present in most of the patients, as well as alcohol abuse, age, sex, and alpha-fetoprotein were equally distributed in the anti-HCV-positive and -negative groups. HBsAg positivity was significatively higher in negative anti-HCV group. By contrast, hepatitis B virus (HBV) antibodies were detected more frequently in positive anti-HCV patients than in the negative anti-HCV group. These data must be considered with caution because of the small number of HBsAg-positive patients. It is concluded that the high prevalence of anti-HCV in patients with HCC may suggest an etiological role of the hepatitis C virus, although in relationship to age, alcohol abuse and cirrhosis, the similarity in the two groups questions this hypothesis.
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PMID:Serum antibodies to hepatitis C virus in Italian patients with hepatocellular carcinoma. 216 May 17


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