Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Taiwanese have a high prevalence of HBsAg carrier rate and chronic liver diseases. To evaluate the role of delta (delta) agent infection in our patients, 45 HBsAg-positive patients with chronic active hepatitis, 4 with chronic persistent hepatitis and 11 with HBsAg-positive hepatocellular carcinoma were studied for delta antibody by radioimmunoassay of serum; liver was studied for delta antigen by immunofluorescence in 23 patients. delta Antibody was only found in three patients with chronic active hepatitis (6.7%); the prevalence was 5% in HBsAg-positive chronic liver diseases and hepatocellular carcinoma. None of the liver specimens studied had delta antigen. The study indicates that delta agent infection does not seem to play an important role in chronic liver diseases and hepatocarcinoma in Chinese who live in Taiwan, despite a high prevalence of chronic hepatitis B virus infection.
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PMID:Delta agent infection in patients with chronic liver diseases and hepatocellular carcinoma--an infrequent finding in Taiwan. 632 88

A prospective study of the clinical and pathological sequelae of hepatitis B disease in 22 immunosuppressed renal transplant patients is reported. All patients had allografts that functioned for more than 1 year, and all were hepatitis B surface antigen (HBsAg)-positive following transplantation. None of the 18 patients who had serial HBsAg tests converted to HBsAg negative. Serial liver biopsies were performed in 19 patients and one liver biopsy was available in the remaining three patients. Follow-up ranged from 12 to 93 months. Seven patients ultimately developed cirrhosis, 6 developed chronic active hepatitis, 5 developed chronic persistent hepatitis, and in 4 the presence of HB virus in hepatocytes was the sole morphologic alteration. The initial liver biopsy was not an accurate predictor of ultimate severity of liver disease because 5 of the 12 patients with virus only or chronic persistent hepatitis subsequently developed chronic active hepatitis or cirrhosis. Clinical liver dysfunction occurred in 8 patients, all of whom had chronic active hepatitis or cirrhosis. Three patients died with hepatic failure and 2 with hepatoma. The risk of death from liver disease in HBsAg-positive renal transplant patients was 5% per patient-year. For comparison, 10 HBsAg-positive patients whose renal failure had been treated by hemodialysis were also studied over a comparable period. Biochemical evidence of persistent liver dysfunction recurred in 1 patient only; 4 patients converted to the HBsAg-negative state; and no patient has died from complications of liver disease. We conclude that in the immunosuppressed renal transplant patient HB infection often results in the development of chronic active hepatitis, leading to cirrhosis and death from hepatoma and hepatic failure.
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PMID:The clinical and pathological course of hepatitis B liver disease in renal transplant recipients. 637 1

In a retrospective study a total of 754 sera from 397 hepatitis patients were assayed for delta antigen and antibody by radioimmunoassay. The study included patients of all age groups (3 months up to 85 years) whose first serum sample, taken from 1978 until January 1984, was positive for HBsAg. Clinically the patients could be subdivided into three major groups: 311 sera were from 181 patients with acute hepatitis, 296 from 135 CPH/CAH patients, including a few cases of liver cirrhosis and 3 cases of HCC, and 147 sera were from 81 asymptomatic carriers. Delta markers were found in 30 patients (7.6%). 20 of these were under the age of 30, and 13 presented with acute, often fulminant hepatitis or (in a minority of cases) exacerbations of preexisting HBV infection. Only two symptomless carriers had anti-delta. It seems of particular interest that all 10 cases where delta antigen could be demonstrated in the first serum sample presented with acute, often fulminant hepatic disease and 9 had anti-HBc-IgM antibodies. Where a second sample could be tested (5 cases), seroconversion to anti-delta was always demonstrated. Delta superinfection could be shown in 2 cases where anti-delta antibodies appeared more than a year after HBsAg positivity was first detected.
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PMID:[Delta hepatitis in Switzerland. Determination of delta antigens and delta antibodies in 397 HBsAg-positive patients (1978-1984)]. 647 32

Serious late sequelae including chronic active hepatitis, cirrhosis, massive necrosis, and hepatocellular carcinoma may develop in patients infected with hepatitis B virus. Clinical and epidemiologic risk factors for such complications have not been identified. To examine this question, the clinical and pathologic features of the 60 patients with documented hepatitis B virus infection who underwent postmortem examination at the Johns Hopkins Hospital were reviewed. In 27 patients (45 percent), the outcome of hepatitis B infection was nonlethal, i.e., at autopsy, the liver showed either no histopathologic lesions attributable to hepatitis B infection, acute viral hepatitis, or chronic persistent hepatitis. Lethal outcomes of hepatitis B infection, i.e., chronic active hepatitis, cirrhosis, hepatocellular carcinoma, and/or massive hepatic necrosis, were present in the remaining 33 (55 percent) patients. Chronic active hepatitis was observed more frequently in whites (p less than 0.05) and males (p less than 0.05). Lethal outcomes of hepatitis B infection were correlated with recent or concomitant exposure to known hepatotoxic agents (p less than 0.05), including heavy ethanol abuse, isoniazide, hydrocarbon exposure, methyldopa, and the chemotherapeutic agents busulfan and methotrexate. In addition, a lethal outcome of hepatitis B virus, particularly massive hepatic necrosis, was positively correlated with a history of nephrolithiasis (p less than 0.005). Recent, concomitant treatment with immunosuppressive agents, given in 24 patients (40 percent), was correlated with the absence of lethal sequelae (p less than 0.005). These data suggest that patients with recent exposure to hepatotoxic agents have an increased risk of lethal sequelae following hepatitis B infection. Furthermore, the results suggest that immunosuppressive or antiinflammatory therapy may be beneficial in reducing morbidity and mortality from hepatitis B virus infection.
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PMID:Risk factors for development of lethal sequelae after hepatitis B virus infection in humans. 647 89

We prospectively analysed the liver histology and clinical data of 45 patients with a clinical diagnosis of chronic hepatitis. There was more chronic active hepatitis than chronic persistent hepatitis. In both, there were more men than women except in the subgroup of lupoid hepatitis, where all were women. As a group, chronic persistent hepatitis patients tended to have less severe abnormalities in biochemical liver function tests. Chronic hepatitis B infection accounted for 38% (17/45) of all patients. Of these, 53% (9/17) were Maori or Polynesian, although they only account for approximately 1/5 of the European population in Auckland. This correlated with the known high hepatitis B surface antigen carrier frequency in the Maori and Polynesian and the high incidence of primary hepatocellular carcinoma in this ethnic group. The present study also showed there are relatively few chronic active hepatitis patients, those with immunological abnormalities (lupoid hepatitis, 5/45), who are likely to respond to steroid treatment.
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PMID:A clinical-pathological study on chronic hepatitis in Auckland. 659 Oct 11

Nine HBeAg+ and 24 anti-HBe+ subjects with chronic hepatitis B virus (HBV) infection were studied for HBV DNA in the serum by molecular hybridization, for HBcAg in the liver by immunofluorescence, and for histologic evidence of liver disease. All HBeAg+ patients had underlying chronic liver disease (chronic persistent hepatitis, chronic active hepatitis, or cirrhosis with or without hepatocellular carcinoma), and all were found positive for both HBV DNA in the serum and HBcAg in the nucleus of hepatocytes. Of the 24 anti-HBe+ individuals, 18 had various forms of chronic liver disease. Six HBsAg+/anti-HBe+ patients had normal liver histology except for numerous "ground-glass" hepatocytes with abundant cytoplasmic HBsAg. All six were negative for nuclear HBcAg and serum HBV DNA, but three showed HBV DNA which appeared to be integrated into unique sites in host liver DNA by hybridization analysis. In contrast, 14/18 (78%) of HBsAg+/anti-HBe+ patients with chronic liver disease were positive for nuclear HBcAg, serum HBV DNA, or both of these markers of HBV replication. It is suggested that in long-term HBsAg carriers with serum anti-HBe and normal liver histology, viral replication is suppressed or inactive and HBV potential infectivity is presumably very low or absent. However, when viral replication is present in HBsAg+/anti-HBe+ carriers (as demonstrated by serum HBV DNA and/or nuclear HBcAg), active liver disease is often found. In these individuals, active chronic liver disease appears to be related to continued replication and secretion of HBV and may occur in a much higher proportion of HBsAg+/anti-HBe+ carriers than was previously suspected.
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PMID:Analysis of liver disease, nuclear HBcAg, viral replication, and hepatitis B virus DNA in liver and serum of HBeAg Vs. anti-HBe positive carriers of hepatitis B virus. 661 32

Chronic delta infection occurs in Greece in about 10 to 15% of HBsAg+ subjects, being largely unrelated to parenteral transmission and/or to drug addiction. The observed cases exhibited histological changes ranging from chronic persistent hepatitis to chronic active hepatitis, cirrhosis, and even hepatocellular carcinoma on cirrhosis. The male/female ratio of patients with delta Ag + CLD was 3.8:1 and their mean age 40 years. They were younger compared to delta Ag-/HBsAg+ CLD and they presented with a wide spectrum of symptoms and signs. About 25% of the patients were oligosymptomatic or asymptomatic and about 40% manifested their disease as an episode of acute hepatitis with protracted or relapsing course followed by chronicity. Biochemical changes appeared to be more severe than in delta Ag-/HBsAg + CLD. The natural history was frequently characterised by a progressive course, terminating, in about 15 years, to death from cirrhosis and liver failure, although remissions occasionally occurred. HCC also developed but probably less frequently than in HBsAg positive, delta Ag negative CLD. Whether the natural course of delta Ag+ CLD can be modified by any form of treatment remains to be proved.
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PMID:Delta antigen positive chronic liver disease in Greece: clinical aspects and natural course. 666 75

Follow-up studies were conducted on chronic liver disease patients treated 10 years previously with corticosteroid (CS), Hbs antigen (HbsAg) was measured in previously collected paraffin embedded liver sections by enzyme-labelled antibody technique. Of 57 cases examined, 38 cases were treated with CS or immunosuppressive agents and 19 cases were not treated with CS (control group). -- Two deaths occurred in the CS-treated group and 4 in the non-CS treated group. These patients were diagnosed as either the 2B type (severe activity) of chronic aggressive hepatitis (CAH) or as having liver cirrhosis. One death was found in the 10th year due to hepatocellular carcinoma in a chronic persistent hepatitis (CPH) patient with HBsAg diffusely distributed in liver tissue. No significant difference was found in the rehabilitation rate in HBsAg negative cases of the CS group versus the control group. In positive cases, the rehabilitation rate was found to be 66.7% in the CS group compared with 0% in the non-CS group.
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PMID:Follow-up ten years after corticosteroid therapy for chronic active hepatitis type B. 701 30

HBeAg or anti HBe were detected using radioimmunoassay in 93 out of 100 British patients who were chronic HBsAg carriers. HBeAg was found more commonly than anti HBe in younger patients and those with higher titres of HbsAg and abnormal liver function tests. HBeAg was present particularly in patients with chronic active hepatitis (26 out of 29) and chronic persistent hepatitis (16 out of 21). Anti HBe was found particularly in healthy carriers (19 out of 27), and patients with cirrhosis (4 out of 8) and hepatocellular carcinoma (7 out of 8). However, the system was of little help in predicting the liver biopsy appearances in the individual patient. During a mean follow-up period of 44 months, 6 of the 62 (9.7%) HBeAg positive carriers converted to anti HBe, a spontaneous seroconversion rate of 2.68% per year.
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PMID:The HBe antigen-antibody system and its relationship to clinical and laboratory findings in 100 chronic HBsAg carriers in Great Britain. 732 22

146 patients (62 female, 84 male) with chronic hepatitis B and 80 patients (34 female, 46 male) with chronic hepatitis C were regularly examined in 1 to 2 year intervals with an average follow-up period of 12 years (mean). Each time patients were evaluated by physical examination, routine laboratory data, immunological and serological testing, ultrasonography, and laparoscopy and/or percutaneous liver biopsy. No patient of the study underwent immunosuppressive or antiviral treatment at any time.-The average time data in years are given as the median value (mean). Chronic hepatitis B: Histologic diagnoses and their long-term prognosis: Chronic persistent hepatitis (CPH) on first biopsy: 10% of cases complete recovery after 15 years, 70% progression to chronic active hepatitis (CAH) after 5 years; CAH: 30% advanced remission/complete recovery 8 years after the first diagnosis of CAH, 40% progression to liver cirrhosis after 5 years; liver cirrhosis: 50% advanced remission/recovery 4 years after the first diagnosis of cirrhosis, 5% developed a hepatocellular carcinoma (HCC) 11 years after the first diagnosis of cirrhosis. Natural history: In the 11 years following initial diagnosis of HBV-infection spontaneous recovery was observed in 49% of cases. In 3% of the patients the disease eventually caused death (1 x hemorrhage of oesophageal varices, 3x HCC after 14 to 20 years). Chronic hepatitis C: All patients were anti-HCV- and HCV-RNA-positive.-There was no spontaneous elimination of virus in any patient (maximal follow-up 27 years).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Long-term prognosis of chronic B and C viral hepatitis]. 750 Aug 7


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