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)

Acquired factor X deficiency has been described in patients with amyloidosis but acquired factor V deficiency is quite rare. We report here a case of life-threatening bleeding and acquired factor V deficiency associated with primary amyloidosis. A 50-year-old man who had no previous hemorrhagic diathesis was referred to our hospital because of recurrent epistaxis, gingival bleeding and hemospermia. The laboratory examination revealed that both the prothrombin time (PT) and the activated partial thromboplastin time (aPTT) were significantly prolonged, and factor V activities were markedly decreased to 14-39% of the normal value. Other coagulation factors such as fibrinogen, prothrombin, factor VII, factor VIII, factor IX and factor X were subnormal and normal. Transaminases were slightly elevated but serological tests of hepatitis B and hepatitis C were negative. Mild hepatosplenomegaly was noted without sign of liver cirrhosis. The PT and aPTT obtained 8 years ago when he received a cholecystectomy due to cholecystitis were both normal. Specific assays for the detection of factor V inhibitor were repeatedly performed but no factor V inhibitor was found. Furthermore, a significant recovery of the infused factor V was noted shortly after an intravenous administration of 5-10 U fresh frozen plasma, but it did not last more than 6 h. Melena, bleedings into the left shoulder and buttock, and finally mortal retroperitoneal hemorrhage developed despite repeated infusions of large amounts of fresh frozen plasma. Acquired factor V deficiency associated with primary amyloidosis was suspected but histological diagnosis was not obtained because of the severe bleeding tendency. Autopsy revealed hepatosplenomegaly and massive deposits of AL amyloid in the liver, spleen, heart and other parenchymal organs. Perivascular amyloid deposition and factor V deficiency are both thought to be the cause of the severe hemorrhagic tendency seen in this patient.
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PMID:Life-threatening bleeding and acquired factor V deficiency associated with primary systemic amyloidosis. 1219 8

Forty-seven patients with severe hepatitis B exacerbation were compared with patients who had mild exacerbation (n=96) or no exacerbation (n=96). Seventeen patients (36.2%) died or underwent liver transplantation. Preexisting cirrhosis and a prothrombin time (PT) of >30 s were associated with adverse outcome in 60.9% and 87.5% of patients, respectively. The rate of adverse outcome increased to 92.3% when albumin levels of < or =35 g/L and bilirubin levels of >200 microM were present. Other factors associated with adverse outcomes included peak bilirubin level, peak PT, time to reach peak PT, and the presence of encephalopathy and/or ascites. There was no difference in the frequency of precore mutations in patients with severe or mild exacerbation or without exacerbation. A significantly lower prevalence of core promoter mutants was found in patients with severe exacerbation (50%), compared with those who had mild exacerbation (81.3%; P=.004). Patients with severe exacerbation of hepatitis B with poor prognostic factors should be considered for early liver transplantation.
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PMID:Prognostic factors in severe exacerbation of chronic hepatitis B. 1268 9

The early prognostic indicators for acute liver failure in endemic zones for hepatitis E virus have not been determined. All consecutive patients with acute liver failure from a geographically defined region endemic for hepatitis E virus were studied over the period April 1989-April 1996. Demographic, clinical and biochemical parameters were recorded at presentation and serum samples were analysed for known viral hepatitis (A-E) markers. Multiple parameters were compared in survivors and non-survivors in a univariate analysis. All significant factors on univariate analysis were entered into a stepwise logistic regression analysis to identify independent variables of prognosis. The sensitivity and specificity of significant prognostic factors was then assessed. A total of 180 [69 males and 111 females: age (mean +/- SD) 31.1 +/- 14.7 years] with acute liver failure were studied. Of these, 131 (72.8%) patients died. Hepatitis E virus was the aetiological cause in 79 (43.9%) patients, while hepatitis A virus, hepatitis B virus, hepatitis C virus and non-A, non-E agent/'s could be incriminated in four (2.1%), 25 (13.9%), 13 (7.2%) and 56 (31.1%) patients respectively. Of 83 women in childbearing age, 49 (59.0%) were pregnant, 33 (67.3%) of these were in the third trimester. Forty-seven (95.8%) pregnant women had HEV infection. Nine variables differed significantly between survivors and non-survivors on univariate analysis. Of these, four variables which predicted the adverse outcome on multivariate analysis were non-hepatitis-E aetiology, prothrombin time >30 s, grade of coma >2 and age >40 years in that order of significance. Pregnancy per se or duration of gestation did not adversely affect the prognosis. In endemic areas, hepatitis E virus is the commonest cause of acute liver failure. Acute liver failure occurs in a high proportion of pregnant women, mostly in third trimester. Early predictors of a poor outcome are non-E aetiology, prothrombin time >30 s, grade of coma >2 and age >40 years.
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PMID:Aetiology and prognostic factors in acute liver failure in India. 1275 42

We studied the safety of right-lobe donor hepatectomy in living donors with a positive serological test result for antibody against hepatitis B core antigen (anti-HBc). Of 54 right-lobe living liver donors, serum anti-HBc was positive in 29 donors (54%) and negative in 25 donors (46%). None had a history of hepatitis and all had normal liver biochemistry test results before surgery. Surgical data, postoperative liver function, and outcome of donors were compared according to anti-HBc status. Donors positive for anti-HBc were significantly older (median age, 42 v 31 years; P <.001), but there was no difference in other demographics and liver size. Median blood loss was greater in anti-HBc-positive donors (600 v 350 mL; P =.007). Histological examination showed no difference in degree of portal fibrosis or fatty change in liver grafts. There was no significant difference in postoperative serum transaminase levels or prothrombin times; however, anti-HBc-positive donors had greater serum bilirubin levels day 6 (26 v 21 micromol/L; P =.01) and day 7 (22 v 15 micromol/L; P =.004) after surgery. Postoperative complications developed in 10 anti-HBc-positive and 6 anti-HBc-negative donors (P =.4). All donors who developed cholestasis were positive for anti-HBc, aged 45 years or older, and had mild fatty changes of the liver. Hospital stays were similar. All donors had completely normal liver function at a median follow-up of 31 months (range, 21 to 76 months). A positive serological test result for anti-HBc should not be regarded as a contraindication for right-lobe liver donation.
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PMID:Safety and outcome of hepatitis B core antibody-positive donors in right-lobe living donor liver transplantation. 1288 96

BACKGROUND/AIMS: Flare-up of hepatitis due to the reactivation of hepatitis B virus (HBV) is a well-known complication in patients with malignant disease who receive chemotherapy. Despite the widespread use of chemotherapy for patients with HBV-related hepatocellular carcinoma (HCC), there is little corresponding data on exacerbation of liver damage in these patients. In the present study, we investigated the associating factors in exacerbation of liver damage in patients with HBV-related HCC who were undergoing trans-hepatic arterial infusion chemotherapy (THAIC). PATIENTS AND METHODS: Thirty-three patients who received THAIC for HCC were investigated. All patients were hepatitis B surface antigen positive. Hepatitis e antigen and antibody were generally tested at baseline and within 1 month of final chemotherapy. Serum alanine aminotransferase, asparate aminotransferase, albumin, total bilirubin, and prothrombin time were estimated once a week or every 2 weeks. HBV-DNA levels were measured at baseline and once a month. Mutation in the regions of precore and core promoter in HBV DNA was generally estimated at baseline and within 1 month of final chemotherapy. RESULTS: Eight patients with hepatitis Be antigen positive and hepatitis Be antibody negative at baseline were found to have exacerbation of liver damage during or after chemotherapy. Of these, three patients died of progressive liver failure. There was no association between exacerbation of liver damage and age, sex, hepatic reserve function, HBV-DNA levels, precore and core promoter sequencing, therapeutic regimen, or tumor stage. The only associating factor was HBeAg positivity. CONCLUSIONS: These results suggest that hepatitis B e antigen positivity is a significant associating factor in exacerbation of liver damage during or after chemotherapy in patients with HBV-related HCC.
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PMID:Investigation of associating factors in exacerbation of liver damage after chemotherapy in patients with HBV-related HCC. 1296 29

The aim of this study was to evaluate the efficacy of and tolerance for radiofrequency thermoablation (RFTA) in patients with hepatocellular carcinoma (HCC). From March 1999 to September 2001, a total of 56 patients (46 men and 10 women) whose mean age was 67.8 years (range 51 to 76 years) underwent RFTA for 71 HCCs at our institution. RFTA was carried out in 45 patients with one lesion less than 6 cm in diameter, in seven patients with two lesions less than 4 cm in diameter each, and in four patients with three lesions less than 3 cm in diameter each. The mean diameter of the lesions was 4.1 cm (range 0.8 to 6.0 cm). The etiology of the cirrhosis was alcoholism in 31 patients, post-hepatitis C in 19 patients, post-hepatitis B in four patients, and hemochromatosis in two patients. Forty-five patients were classified as Child stage A and 11 were Child stage B. No ascites, prothrombin time >60%, and platelet count <60,000/mm(3) were needed. Two types of cooled needles were used depending on the size of the lesion (a needle 15 cm in length was used for 2 or 3 cm tumors, and a cluster of needles was used for tumors larger than 4 cm). Helical computed tomography was performed 8 weeks after treatment. The main criterion for a complete response was the presence of a hypodense lesion without contrast enhancement. Mean follow-up was 14 months. Complete tumor destruction was achieved in 50 (89.2%) of 56 patients after one session and in 52 (92.8%) of 56 after two sessions. Twelve months later, a complete response was confirmed in 45 patients (80.3%), four patients had a local recurrence and new liver nodules, and three patients had died (one of bone metastasis, one of acute alcoholic hepatitis, and one of bronchial carcinoma). Thirty-nine patients (69.6%) were still in complete remission 36 months later, and a new HCC had developed in six patients. At 36 months 49 of 56 patients were alive and 39 of 56 were free of disease. Patients with HCCs that developed following viral cirrhosis had a worse prognosis than those with HCCs that occurred after alcoholic cirrhosis (2-year survival, 57.7% vs. 77.7%; P=0.0241). It was concluded that radiofrequency ablation is an effective treatment for HCC, although the prognosis is better in patients who develop HCC after alcoholic cirrhosis compared to those in whom HCC occurs after viral cirrhosis.
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PMID:Treatment of hepatocellular carcinoma using percutaneous radiofrequency thermoablation: results and outcomes in 56 patients. 1312 58

This study was carried out to find the etiological spectrum and clinical profile of acute viral hepatitis in Ludhiana. Hepatitis E was encountered most frequently (44.56%) followed by hepatitis B (29.7%), whereas hepatitis D occurred least frequently (0.99%). The age group most commonly affected was 20-30 years(32,67%) followed by 30-40 years (23.76%). Males showed higher incidence as compared to females in the ratio of 62.4:37.6. The most frequent clinical features were anorexia and jaundice. The disease was found to be more common in urban set up(78.2%) than in rural regions (21.8%). Mortality was mainly because of fulminant hepatitic failure. In 1.98% of cases, etiology remained undecided. Total bilirubin and prothrombin time were found to be useful prognostic indicators.
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PMID:Spectrum of acute viral hepatitis and its clinical outcome--a study from Ludhiana, Punjab. 1451 73

A recombinant enzyme-linked immunosorbent assay (ELISA) followed by a neutralization test (NT) and recombinant immunoblot assay (RIBA) were used for the detection of antibody to hepatitis C virus (anti-HCV) in 71 patients receiving 84 orthotopic liver grafts between 1984 and 1990. Before the liver transplantation (LTX) anti-HCV was present in six of the 71 recipients (8.5%) who were accepted for LTX because of acute or chronic liver failure. After LTX anti-HCV could not be detected in one of the patients, but it was continuously present in the others for more than 12 months. Detectable HCV antibodies were not present in the three patients who underwent LTX because of clinical evidence of fulminant NANB hepatitis. Two of 48 (4.2%) previously HCV seronegative recipients, who survived more than 3 months, seroconverted 9 and 16 months, respectively, after transplantation. The postoperative seroconversion was probably due to the transfer of virus via perioperative blood transfusions. Thus, these liver recipients may be able to respond by producing anti-HCV despite immunosuppressive therapy. None of the seven post-transplant HCV-seropositive patients developed symptoms such as icterus or fatigue, which would suggest the presence of liver insufficiency due to HCV infection. However, two of them had increased transaminase levels and histological signs of mild hepatitis. No significant difference was found in 1-year survival, prothrombin complex, albumin levels or the risk for retransplantation in post-transplant anti-HCV-seropositive patients, compared with those without detectable HCV antibodies (71% vs 69%, respectively). Thus, during the study period of 1-5 years, the clinical course of HCV infection was milder than that reported for hepatitis B infection in liver recipients.
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PMID:Seroprevalence and outcome of hepatitis C in liver transplantation. 1462 69

Hepatocellular carcinoma (HCC) is linked to environmental, dietary and lifestyle factors. Patients with cirrhosis and chronic carriage of hepatitis B virus (HBV) are at risk for HCC at annual rates of 3%. HCC risk is particularly high in patients with evidence of cirrhosis and histological markers of increased liver cell proliferation. In addition, thrombocytopenia, prolonged prothrombin time and over 55 years of age also predict the development of HCC. Treatment options are defined according to the presence or absence of cirrhosis, number and size of tumors, and degree of hepatic decompensation. Hepatic resection is the primary intervention for these few patients with tumor but surrounding normal liver tissue and well preserved hepatic function. Under such circumstances, the cumulative 5-year survival is approximately 45%. Liver transplantation (OLT) provides long term survivals (90% at 5 years) in patients with a HCC discovered by chance as a minute nodule and of 75% in patients with viral cirrhosis and a single <5 cm tumor or fewer than three <3 cm nodes. Since liver transplantation cannot be offered to most patients with HCC, hepatic resection remains the primary therapeutic option; 5-year survival of 50% is anticipated in patients with compensated cirrhosis and <5 cm of tumor and 75% for those with moderate portal hypertension and normal serum bilirubin values. Ultrasound-guided tumor injection with absolute ethanol or tumor thermoablation with radiofrequency provide similar survival rates but with fewer complications. Whether arterial chemoembolization benefits patients with HCC remains controversial.
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PMID:Etiology, natural history and treatment of hepatocellular carcinoma. 1463 11

Three-hundred and twenty-four patients were enrolled in an open-label, multicenter, international study in which pre- and post-liver transplantation (LT) patients with recurrent chronic hepatitis B (CHB) and evidence of lamivudine-resistant HBV were treated with adefovir dipivoxil 10 mg once daily. In the pre- and post-LT cohorts, 128 and 196 patients were treated for a median duration of 18.7 and 56.1 weeks, respectively. In patients who received 48 weeks of treatment, 81% of the pre-LT and 34% of the post-LT cohort achieved undetectable serum hepatitis B virus (HBV) DNA (Roche Amplicor Monitor polymerase chain reaction [PCR] assay lower limit of quantification [LLQ] < 400 copies/mL) with a median change in serum HBV DNA from baseline of -4.1 log(10) and -4.3 log(10) copies/mL, respectively. Serum alanine aminotransferase (ALT), albumin, bilirubin, and prothrombin time normalized in 76%, 81%, 50%, and 83% of pre-LT patients and 49%, 76%, 75%, and 20% of post-LT patients. The Child-Pugh-Turcotte (CPT) score improved in over 90% of patients in both cohorts. Genotypic analysis of 122 HBV baseline samples revealed that 98% of these patients had lamivudine-resistant mutant HBV. No adefovir resistance mutations were identified in patients after 48 weeks of therapy. One-year survival was 84% for pre-LT and 93% for post-LT patients (Kaplan-Meier analysis). Treatment-related adverse effects associated with adefovir dipivoxil in this setting were primarily mild to moderate in severity. In conclusion, 48 weeks of adefovir dipivoxil resulted in significant improvements in virologic, biochemical, and clinical parameters in CHB patients pre- and post-LT with lamivudine-resistant HBV.
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PMID:Adefovir dipivoxil therapy for lamivudine-resistant hepatitis B in pre- and post-liver transplantation patients. 1464 43


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