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)

Breakthroughs during lamivudine therapy were assessed according to hepatitis flares and mutational polymorphism of hepatitis B virus (HBV) infecting patients. Of 42 patients with chronic hepatitis B and positive for hepatitis B e antigen in serum, 13 (30%) harbored HBV mutants with lamivudine resistance after a mean duration of 29 months on lamivudine. The virological breakthrough occurred 14.5 months after the start of lamivudine treatment, and all the patients with it developed breakthrough hepatitis 3 months later. The clinical course of breakthrough hepatitis was self-limited except in one patient who had already developed cirrhosis at the baseline. One year after breakthrough hepatitis, serum ALT, albumin, prothrombin time and platelet counts were maintained well on conventional treatments without resorting to interferon. Major HBV mutants during breakthrough hepatitis were those with M552I in the YMDD motif of viral DNA polymerase/reverse transcriptase in 7 patients (54%), M552I/L528M in 4 patients (31%) and M552V/L528M in 2 patients (15%). There were no patients in whom mutations at nucleotide 529 occurred including the 2 who later developed hepatocellular carcinoma. There was no clear relationship between distinct mutational patterns and clinical courses. Further studies are needed for making out the effects of lamivudine-resistant mutants on clinical outcomes, taking into considerations genotypes of HBV.
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PMID:Subclones of drug-resistant hepatitis B virus mutants and the outcome of breakthrough hepatitis in patients treated with lamivudine. 1468 51

The liver plays a central role in haemostasis, being the site of synthesis of most of the clotting factors, coagulation inhibitors and fibrinolytic parameters, in addition to its clearance of activated clotting and fibrinolytic factors. Nonetheless, no haemostatic test(s) is included among the routine liver function tests and this study aims to probe this possibility. The liver disease group (n=258) included acute hepatitis (n=25), chronic viral hepatitis (n=128), hepatitis B (HB) carriers (n=25), liver cirrhosis (n=67), and hepatocellular carcinoma (HCC) (n=13). The prothrombin time was significantly prolonged in acute hepatitis, liver cirrhosis and HCC. However, the reptilase time was prolonged in all the groups except in HB carriers, while the thrombin time was prolonged only in the HCC group. Antithrombin III and protein C levels exhibited significant reduction in acute hepatitis, liver cirrhosis and HCC. On the other hand, protein S levels (total and free) were reduced significantly in all the patients groups, including HB carriers when compared with healthy controls. Derangement of haemostatic tests is a common feature in liver disease, being most significant in acute hepatitis, liver cirrhosis and hepatocellular carcinoma. The most sensitive markers of hepatocyte malfunction are protein S (total and free) and the reptilase time as they were abnormal, in the mildest liver affections, when other biochemical tests as well as other haemostatic tests were normal. Further studies are needed to see whether these two tests qualify for inclusion among the routine liver function tests.
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PMID:Haemostatic abnormalities in liver disease: could some haemostatic tests be useful as liver function tests? 1597 Jul 16

Chronic hepatitis B infection (HBV) is a major health problem worldwide. The prognosis is grave for patients with HBV-related decompensated liver cirrhosis (LC). We evaluated the effectiveness and the determinants of early mortality of lamivudine treatment in patients with HBV-related decompensated LC. Thirty patients with HBV-related decompensated LC and active viral replication were treated with lamivudine 100 mg daily for a median duration of 9 months. Among these patients, five patients died within 3 months. Two patients were lost to follow-up at week 8 and 9. One patient was treated for <6 months. Twenty-two patients were treated over 6 months. Univariate analysis revealed that the total bilirubin (P = 0.008), prothrombin time (P = 0.004), Child-Turcotte-Pugh score (P = 0.005), the model of efd-stage liver disease score (P = 0.004) and stage III hepatic encephalopathy (P = 0.001) were predictive factors of early mortality. Multivariate analysis revealed that the independent factor associated with early mortality was stage III encephalopathy. Among 22 patients, liver function improved markedly after lamivudine therapy. Of the nine hepatitis B e antigen (HBeAg)-positive patients, three had HBeAg seroconversion. Two patients had YMDD mutant and virological breakthrough at 41 and 46 weeks. One of the two had hepatocellular carcinoma and died of hepatic failure at week 125; the other received adefovir and is doing well. Lamivudine appeared to have benefits in viral suppression and significant improvement in liver function in patients with HBV-related decompensated LC. As noted in prior studies, poor baseline liver function is associated with a poor prognosis in Asian patients with decompensated HBV cirrhosis treated with lamivudine.
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PMID:Determinants of early mortality and benefits of lamivudine therapy in patients with hepatitis B virus-related decompensated liver cirrhosis. 1598 9

The association of hepatitis B virus (HBV) infection and liver cancer is well documented in epidemiological study. Patients with chronic hepatitis B have increased risk of hepatocelluar carcinoma (HCC), in particular those with active liver disease and cirrhosis. The incidence of HCC increases with age and is more common among male patients. The introduction of universal HBV vaccination program for the newborn in endemic regions has started to show beneficial impact. Taiwan introduced this program two decades ago and the incidence of liver cancer among infants and young children have declined significantly. The carcinogenic events leading to HCC are under intense research. A number of hypotheses have been proposed. HBV is not directly hepatotoxic but its interaction with the host immune system creates opportunity for HBV DNA integration into the host genome. One of the main foci of research is the HBX-encoded X protein. Its integration and protein expression impose alteration in cell proliferation cycle and apoptosis process. Many other factors may be involved including viral-induced alterations in p53 and telemerase, HBV genotypes, co-infection with HCV or delta agents, patient's lifestyle such as smoking, alcohol excesses, and genetic factors of the host patient. The processes of necroinflammation, cell proliferation and fibrosis facilitate the initial carcinogenic development. HCC surveillance with tumor markers such as alpha-foetal protein, decarboxylated prothrombin, in conjunction with imaging techniques has identified early small HCC that is amenable to curative therapy. Viral load has been correlated with increase risk of HCC. The available anti-viral agents have demonstrated clinical benefit among those with maintained and sustained response. Interferon and lamivudine therapy have demonstrated reduction of HCC among responders. However, they only constitute a minority proportion of treated patients. The mainstay of prevention should lie in prevention of HBV infection and early effective therapy of chronic hepatitis B infection.
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PMID:HBV and liver cancer. 1610 76

Hepatocellular carcinoma (HCC) is common throughout the world. The incidence of HCC is higher in cirrhotic patients and, among these patients, the incidence rate is 3% in Europe. The overall survival rate of HCC ranges between 20 and 30 months, and is influenced by the local stage of the neoplasm and by the liver function. The literature reports several serological, urinary and radiological markers used for the early detection of HCC. Currently, it is highly recommended to periodically screen cirrhotic patients and hepatitis B virus carriers older than 35 by serum alpha-fetoprotein (AFP) and liver ultrasound (US) every 6 months. The concomitant determination of des-g-carboxy prothrombin and AFP allows a 23% increase in sensibility of the diagnosis for HCC avoiding the need for invasive diagnostic procedures.
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PMID:[Screening for hepatocellular carcinoma]. 1617 79

The patient was a 57-year-old woman presenting with jaundice as the chief complaint. She began vomiting on July 10, 2003. Jaundice was noted and admitted to our hospital for thorough testing. Tests on admission indicated severe hepatitis, based on: aspartate aminotransferase (AST), 1 076 IU/L; alanine aminotransferase (ALT), 1 400 IU/L; total bilirubin (TB), 20.9 mg/dL; and prothrombin time rate (PT%), 46.9%. Acute hepatitis A (HA) was diagnosed based on negative hepatitis B surface antigen and hepatitis C virus RNA and positive immunoglobulin (Ig) M HA antibody, but elevation of anti-nuclear antigen (X320) and IgG (3 112 mg/dL) led to suspicion of autoimmune hepatitis (AIH). Plasma exchange was performed for 3 d from July 17, and steroid pulse therapy was performed for 3 d starting on July 18, followed by oral steroid therapy. Liver biopsy was performed on August 5, and the results confirmed acute hepatitis and mild chronic inflammation. Levels of AST and ALT normalized, so dose of oral steroid was markedly reduced. Steroid therapy was terminated after 4 mo, as the patient had glaucoma. Starting 3 mo after cessation of steroid therapy, levels of AST and ALT began to increase again. Another liver biopsy was performed and AIH was diagnosed based on serum data and biopsy specimen. Oral steroid therapy was reinitiated. Levels of AST and ALT again normalized. The present case was thus considered to represent AIH triggered by acute HA.
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PMID:Autoimmune hepatitis triggered by acute hepatitis A. 1627 28

The prognosis of decompensated cirrhosis of liver resulting from chronic Hepatitis B Virus (HBV) infection is poor and liver transplantation is the only established mode of treatment. The benefits of treatment with interferon are outweighed by serious side effects and risks of fatal exacerbation of disease activity. Lamivudine rapidly reduces hepatitis B viral DNA in serum to undetectable levels. The purpose of this study was to evaluate effectiveness and safety of Lamivudine treatment in patients with advanced and end stage liver disease caused by Hepatitis B. This was a prospective observational study in which a total of 45 patients, 39 (87.0%) male and 6 (13.0%) female who had viral activity and child pugh score e" 8 were given Lamivudine 100 mg orally once daily. Among them 30 patients completed at least 6 months of therapy, majority (27 patients) showed improvement in liver function with decrease in serum ALT from mean (+/- SD) 118.8 +/- 106.5 to 50.2 +/- 57.1 U/L (p < 0.001), decrease in serum bilirubin from 73.9 +/- 80.5 to 44.7 +/- 62.9 micromol/l (p = 0.129), increase in serum albumin from 26.2 +/- 4.2 to 33.2 +/- 3.4 g/l (p < 0.05), decrease in prothrombin time from 8.3 +/- 4.0 to 3.9 +/- 2.9 seconds prolonged (p < 0.05) and reduction in child pugh score from 11.0 +/- 1.7 to 7.0 +/- 1.3 (p < 0.001). Seroconversion was found in 5 (11.1%) patients on Intention to treat analysis. Among the seroconverted group, 1 (2.2%) patient also lost HBsAg. Six (13.0%) patient had procore mutant virus, 2 (4.4%) of them showed virological response. Therefore, total 7 (15.5%) patients showed virological response by intention to treat analysis. We conclude that inhibition of viral replication with Lamivudine results in a significant improvement of liver function in patients with decompensated cirrhosis of liver due to HBV infection.
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PMID:A study on efficacy of lamivudine therapy in decompensated cirrhosis of liver due to chronic hepatitis B virus infection. 1629 39

Hepatocellular carcinoma (HCC) ranks fifth in frequency of cancers worldwide. The main aetiological factor is hepatitis B virus (HBV) although the importance of hepatitis C virus (HCV) is growing. The most important tumour marker for HCC is alpha-fetoprotein (AFP). The common method of screening high risk patients by AFP and ultrasonography has been shown to result in earlier detection and consequently more easily treatable tumours and longer survival. Proposed screening interval varies from once every 3 months to annually to "as indicated' but, most commonly, is once every 6 months. AFP is a fairly specific but insensitive marker for HCC. Sensitivity of HCC detection by blood markers is improved by combining various other markers with AFP. Of the other markers, the newer high sensitivity des-gamma-carboxy-prothrombin (DCP) has been found to be useful. In addition the AFP fractions L3, P4/5 and the +II band are highly specific for HCC. Among routinely assayed tumour markers in the laboratory, CA 125 is more sensitive for HCC than AFP but far less specific. Various other enzymes, isoenzymes, growth factors, adhesion molecules, other proteins such as interleukin-2 receptor (IL-2R), human cervical cancer oncogene protein (HCCR) and glypican-3 (GPC3), p15 and p16 hypermethylation and nitrite/nitrate ratio have been tested; some of these show promise but none is presently in routine use. The value of other newer markers such as the HBx protein that is produced by HBV, and what are thought to be specific proteins and signatures identified by proteomics remain to be determined.
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PMID:Recent developments in the first detection of hepatocellular carcinoma. 1645 14

Patients with chronic liver disease (CLD) respond poorly to standard hepatitis B (HBV) vaccine given as sequential 20 microg IM shots because of an overall impaired immune response. Many of these patients go on to liver transplantation and are at risk of acquiring recurrent or de novo HBV infection. To evaluate the efficacy and safety of high-dose (80 microg) IM HBV vaccination in patients with CLD who had previously failed to respond to a standard three-dose schedule of 40 microg IM vaccine given monthly. A retrospective review was undertaken at our institution of 79 patients with CLD who were treated with high-dose (80 microg) HBV vaccinations. All had previously failed a three-dose course of 40 microg HBV vaccine. An HBV vaccine response was defined as an anti-HBs titer greater than 100 mIU/ml. Liver enzymes, creatinine, age, prothrombin time, total vaccine dose, and MELD score were recorded. No adverse events were reported. Seventy-two per cent (57/79) of the subjects had an adequate response after receiving a mean total dose of 220 mug vaccine (range 80-800 microg). Twenty-eight per cent (22/79) of the subjects did not respond after receiving a mean total dose of 420 microg vaccine (range 240-720 microg). Non-responders had more severe hepatic disease defined as a higher mean total bilirubin level (p = 0.003) and a lower mean albumin level (p < 0.05). Age, prothrombin time, MELD score, and creatinine were not statistically significant between the responders and non-responders. Repeated high-dose (80 microg) HBV vaccination, in patients who do not respond to standard HBV vaccine doses, is safe and effective in the majority of patients with CLD.
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PMID:Efficacy of repeated high-dose hepatitis B vaccine (80 microg) in patients with chronic liver disease. 1661 Nov 86

Switching to adefovir (ADV) monotherapy is effective in patients with lamivudine (LAM)-resistant hepatitis B virus (HBV) mutations (rtM204 I/V). However, it was recommended to continue LAM therapy for months after starting ADV therapy for safety concern. The safety and efficacy of switching to ADV monotherapy was examined in compensated and decompensated patients with liver cirrhosis. The clinical, biochemical and virological responses were compared between ADV monotherapy in 18 cirrhotic patients and ADV add-on LAM therapy in 10 comparable cirrhotic patients with LAM-resistant rtM204 I/V. After switching to ADV monotherapy, Child-Pugh's score, serum alanine aminotransferase (ALT), bilirubin, albumin and HBV DNA levels improved significantly (P < 0.01). Serum HBV DNA response, defined as HBV DNA decreased to below 10(5) copies/mL or > or =2 log(10) reduction form baseline, was achieved in all patients. A transient ALT flare without concurrent changes in serum bilirubin or prothrombin time was observed in only two patients (11%). The efficacy and safety profile was similar to those with ADV add-on LAM therapy. In conclusion, switching to ADV monotherapy after emergence of LAM-resistant rtM204 I/V is effective and safe in cirrhotic patients, even in those with hepatic decompensation. To stop LAM and switch to ADV in patients with breakthrough is a reasonably safe and cost-effective approach.
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PMID:Switching to adefovir monotherapy after emergence of lamivudine-resistant mutations in patients with liver cirrhosis. 1661 Nov 91


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