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)

We reviewed the records of all patients with a diagnosis of malignancy who were treated at our center and who had not had chemotherapy for at least 18 months, to assess the prevalence of chronic hepatitis B surface antigen (HBsAg)-negative hepatitis, to assess the prevalence of a marker of hepatitis C virus infection, and to determine the severity of chronic liver disease. Of 557 eligible patients, 38 (6.8%) had chronic HBsAg-negative hepatitis. Of these 38 patients, 20 (52.6%) had a marker of hepatitis C virus infection. The prevalence of chronic HBsAg-negative hepatitis was higher in patients previously treated for leukemia than in patients treated for another malignancy (11.8% vs 4.6%; p = 0.004). The liver biopsy revealed chronic active hepatitis or cirrhosis or both in 8 (28%) of 28 patients with clinical chronic HBsAg-negative hepatitis. Four patients without hepatitis C virus infection who underwent liver biopsy had hepatitis B virus antigen in the liver, confirmed by immunohistochemistry studies. One patient uninfected with hepatitis C virus had hemochromatosis. We conclude that infection with hepatitis C virus was the major cause of chronic HBsAg-negative hepatitis in pediatric patients previously treated for malignancy; the cause remained unidentified in 30% of the patients.
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PMID:Chronic hepatitis B surface antigen-negative hepatitis after treatment of malignancy. 132 Jun 73

The prevalence of antibodies to hepatitis C virus (HCV) was investigated in 129 patients with chronic liver disease (85 with chronic active hepatitis and 44 with cirrhosis) and 53 patients with hepatocellular carcinoma. The commercially available second generation anti-HCV enzyme immunoassay kit was used. Antibodies to hepatitis C virus were detected in 16.2% of the patients with chronic liver disease and in 15.1% with hepatocellular carcinoma. Of the HCV positive patients in all groups 51.7% were positive for hepatitis B virus (HBV) markers indicating present or past infection. Prevalence of HBV markers in all the three groups (CAH, cirrhosis and HCC) was higher as compared with anti-HCV prevalence. These results suggest that HCV infection may not be a major cause of chronic liver disease and hepatocellular carcinoma in India and indicate the presence of other aetiological agents.
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PMID:Prevalence of hepatitis C virus antibodies in chronic liver disease and hepatocellular carcinoma patients in India. 132 97

The prevalences of serological markers of hepatitis B virus (HBV) and antibody to hepatitis C virus (anti-HCV) were determined in 168 patients (135 males and 33 females), aged 19-79 years (mean = 50.8) in Thailand. Of these, 33 had chronic persistent hepatitis, 35 chronic active hepatitis, 50 cirrhosis and 50 hepatocellular carcinoma (HCC). Seromarkers for either HBV or anti-HCV or both were detected in 140 (83.3%), 3 (1.8%) and 18 (10.7%) patients, respectively, but 7 (4.2%) were sero-negative for both viruses. The overall prevalence of anti-HCV was 12.5% but was significantly lower in HCC (2%) compared to the other 3 groups of liver disease (12-21.5%, p less than or equal to 0.05) and in HBsAg positive (5%) compared to HBsAg negative (30%) patients (p less than 0.001). After 0.5-9 years follow-up of all anti-HCV positive patients, 2 died and another 6 had progressive liver disease. The prevalence of coexistent HBV seromarkers was similar in patients with a progressive (87.5%) and a stable clinical course (92.3%) (p = 0.62). A higher proportion of the anti-HCV-positive patients with a progressive course had a history of blood transfusion [75.0% vs 46.1% (p = 0.20)]. These findings suggest that HBV is the most important etiologic virus associated with chronic liver disease and HCC in Thailand, but HCV may play a role particularly in HBsAg-negative patients.
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PMID:Prevalence and outcomes of HBV and anti-HCV seropositive patients with chronic liver disease and hepatocellular carcinoma. 132 24

A recent case-control study on 577 lichen planus (LP) patients and 1008 controls confirmed that LP patients may significantly associate with a chronic liver disease (CLD) which is independent from drug or alcohol intake and has some connection with hepatitis B virus (HBV) infection. The study, however, failed to define the nature of CLD. This has been investigated through the clinical and laboratory features of 50 patients with LP and impaired liver function tests. Overall, the laboratory signs of cell necrosis prevailed over those of cholestasis and a good relationship with the HBV and HCV infections was found. Ninety percent of patients with LP and CLD had antibodies to one or another of the major viruses involved in infectious hepatitis. No patient had anti-liver kidney microsomal antibodies type 1. Liver biopsies were done in 12 cases and mostly revealed a chronic active hepatitis evolving into cirrhosis. No evident cases of primary biliary cirrhosis were found. It appears that LP associated CLD is post-viral in nature.
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PMID:Clinical and laboratory presentation of lichen planus patients with chronic liver disease. 132 93

To study the relationship between duck hepatitis B virus (DHBV) infection and duck hepatocellular carcinoma (DHCC), histological examination and DHBV DNA hybridization were performed in 875 ducks from three flocks in Qidong County. Among them, 34 suffered from hepatoma, including 23 hepatocellular carcinoma, 8 cholangiocarcinoma and 3 hepatocellular-cholangiocarcinoma. Of the 34 ducks with hepatoma 27 were positive for DHBV DNA in the liver and/or serum. DHBV DNA was demonstrated in neoplastic nodules of 22 ducks. Southern blot analysis showed that 13 cases were of the integrated pattern of DHBV DNA in neoplastic nodules. The paratumor tissues of 14 ducks with massive tumor were analysed at the same time. Five cases showed integrated pattern, 4 cases free pattern and the other 4 cases both integration and free pattern of DHBV DNA. The hybridization pattern of DHBV DNA in tumor nodule was different from that in paratumor regions in 11 cases and identical in 3 cases. DHBV antigen was positive in 13 tumor nodules and 21 paratumor tissues in the 34 ducks with hepatic tumor by both victoria blue and orcein stain methods. Advanced liver diseases were found in 30 out of the 34 ducks with hepatoma, including 12 cirrhosis and 18 chronic active hepatitis. In southern blot analysis of 122 DHBV DNA positive Qidong ducks without hepatoma, only free pattern of DHBV was seen, while 44 control ducks from Changchun were negative for DHBV DNA. Neither hepatic tumor nor liver diseases were seen in the control ducks. The results suggest that hepatocellular carcinoma in ducks is similar to that in human HCC. They have a high frequency of viral DNA integrated into the host genome and a liver disease background.
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PMID:Duck hepatitis B virus infection and duck hepatocellular carcinoma. 132 68

Anti-c100-3 (Ortho) was determined in the sera of 152 patients with HBs antigen-positive chronic liver diseases to assess coinfection of hepatitis B virus (HBV) and hepatitis C virus (HCV). Eleven patients (7.2%) were positive for anti-c100-3. Anti-CP-9 (Okamoto) and HCV-RNA (RT-PCR) were also examined in these 11 patients. Anti-CP-9 was detected in 7 patients and HCV-RNA was detected in all 11 patients. Four of the 11 anti-c100-3-positive patients were positive for HBe antigen (HBeAg) and others were negative. In 8 of the 11 patients, HCV was suspected to be superinfected by blood transfusion. In HBeAg-positive patients, serum glutamic pyruvic transaminase (SGPT) was elevated in relation to active replication of HBV shown by DNA-polymerase activity. The histological findings showed chronic active hepatitis, with or without cirrhosis. On the other hand, in HBeAg-negative patients, SGPT fluctuated without evidence of active replication of HBV. Active inflammation in the liver was observed in 3 of 5 HBeAg-negative patients by liver biopsy. These findings suggest that HBV might play an important role in chronic active inflammation in HBeAg-positive patients coinfected with HCV, and that HCV might be responsible for continuous inflammation in HBeAg-negative patients coinfected with HCV.
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PMID:Hepatitis type C virus infection in patients with type B chronic liver disease. 133 Jul 96

The natural history of chronic hepatitis B patients who spontaneously cleared serum HBsAg was investigated. A total of 351 patients with chronic hepatitis B were observed in our hospital for at least 3 yr. Seven of these patients became HBsAg negative during the follow-up period. HBsAg disappeared within 6 mo (range = 11 to 169 days, mean = 70 days) after acute elevation of ALT. ALT levels as high as 500 IU were found in three patients, whereas such elevation was not demonstrated in the other four patients. After the disappearance of HBsAg, ALT levels returned to normal in all patients. With one exception, all patients seroconverted to antibody to HBsAg; however, hepatitis B virus DNA remained detectable in serum using the polymerase chain reaction in five patients. The titer of percent inhibition of antibody to HBcAg gradually decreased to less than 70% when a 1:200 dilution of the serum of six patients was used. Four of the patients had active liver disease develop: two had chronic active hepatitis and two had cirrhosis. Three of these four patients subsequently had hepatocellular carcinoma develop. These findings suggest that patients may suffer complications of chronic hepatitis even after normalization of transaminase activities and after the clearance of HBsAg. Thus hepatitis B virus should be considered as a possible factor associated with hepatocellular carcinoma even in the absence of HBsAg, particularly if serum hepatitis B virus DNA persists.
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PMID:Clearance of HBsAg in seven patients with chronic hepatitis B. 133 20

Infection with the hepatitis B virus (HBV) can have many different outcomes. Transient infection may result in acute hepatitis or may remain subclinical. Persistent infection may also be subclinical, or may involve chronic active hepatitis, and can finally lead to the development of primary hepatocellular carcinoma. A mathematical model is given to account for the many different outcomes of HBV pathogenesis. The model is based on the assumption that the liver contains two cell populations with differing abilities to support active HBV replication and/or viral integration into the genome. The model helps account for the relationship of the different clinical courses of HBV infection to the age when the disease is acquired, together with the state of the immune system of the patient.
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PMID:Analysis of a cellular model to account for the natural history of infection by the hepatitis B virus and its role in the development of primary hepatocellular carcinoma. 133 19

The viral hepatitis is a serious public health problem worldwide. Some problem is hepatitis B, particularly superinfection HBV-HDV and least hepatitis C (HCV), because they are transmitted via parenteral routes. About 20% of patients becomes a chronic carrier. Some chronic carriers are healthy: and they have no functional deficiencies. Others however, chronic active hepatitis develops and can lead to cirrhosis of the liver and finally to hepatocellular carcinoma, that is one of the major cancers of the world today. The immunocomplexes play a role in pathogenesis of several syndromes, such as: polyarthritis nodosa, glomerulonephritis, acrodermatitis. In the study based on questionnaires mailed 645 persons after acute viral hepatitis they were observed: cholecystitis--13.9%, stomach and/or duodenum ulcer--11.5%, and cholelithiasis--8.1%. An important results of the investigation is the conclusion that hepatitis caused distinct decrease of the health condition and change of the lifestyle. After the viral hepatitis 9% of patients shifted to a lighter job for a time, 3.8% for good and 5.6% patients after hepatitis B were receiving disability payment. In the light of the problems discussed here the vaccination would prevent not only the acute liver illness but also the sequelae of the disease.
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PMID:[Viral hepatitis sequelae]. 133 49

Reports of an increase in a serum epoxide hydrolase (sEH), immunochemically related to microsomal EH in humans and rats with hepatocellular carcinoma (HCC), suggested its use as a serum marker for this disease. We have now measured sEH levels (as either immunochemically determined content or enzyme activity) in a number of human and experimental models of liver disease. sEH was elevated above the normal range in at least 50% of individuals with HCC, including: 3 of 6 northern Californians; 4 of 7 Koreans with hepatitis B-associated HCC; hepatitis B-associated HCC in woodchucks; and male rats receiving chronic treatment with aflatoxin B1 or ciprofibrate. sEH was rarely elevated in other forms of chronic liver disease. Only 2 of 9 Koreans with hepatitis B-associated cirrhosis, 1 of 8 carriers, but none with chronic active hepatitis or infection with no apparent liver disease had elevated sEH. In addition, no elevations were found in woodchucks with noncancerous viral hepatitis. In aflatoxin B1- and M1-treated rats sEH was not elevated in those with only hyperplastic foci or hepatocellular adenomas, and in two rat initiation-promotion protocols sEH was elevated only in those rats which received the entire set of treatments. sEH was also increased during acute hepatotoxicity in rats treated with CCl4 or 1,2-dibromo-3-chloropropane. The mechanism of increase in sEH during hepatocarcinogenesis appears to be different from that of other markers of HCC, for in the Korean patients, there was no correlation between sEH concentrations and those of alpha-fetoprotein or ferritin, nor was there a correlation with alpha-fetoprotein concentrations in the aflatoxin-treated rats. Furthermore, the increase in sEH does not correlate with induction of microsomal EH in the liver of experimental animals. Studies to date indicate that sEH is selective for HCC and severe hepatonecrotic injury, and may be of some use in the diagnosis of HCC, particularly as a complement to other serum markers.
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PMID:Serum epoxide hydrolase (preneoplastic antigen) in human and experimental liver injury. 133 49


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