UMLS:C0019163 - FACTA Search

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)

The outcome of liver transplantation for HBV-related liver disease has been dramatically improved by the introduction of hepatitis B immune globulin and antiviral drug such as lamivudine. On the other hand, prophylaxis against HCV recurrence has not been established. As for hepatocellular carcinoma, Milan criteria predict acceptable posttransplant outcome. MELD scores, calculated from serum creatinine, bilirubin, and PT-INR, have been shown to be effective in predicting patient survival 1) on the waiting list and 2) following transplantation. ABO-incompatible liver transplantation has been associated with poor patient survival, especially when the recipients are adults. Intraportal infusion of methylprednisolone, prostaglandin E1, and gabexate mesilate, however, has been reported to be effective. It has been reported that 12.4% of the living liver donor experienced postoperative complication, and therefore, more effort should be made to increase brain-dead donor.
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PMID:[Liver transplantation--present and future]. 1627 59

Foscarnet (PFA), a viral DNA polymerase inhibitor, is a clinical agent for herpes viruses. The goal of the study was to evaluate the therapeutic efficacy of PFA in hepatitis B virus (HBV) infection. Intravenous infusion of PFA (1 g/day) for 4 weeks significantly reduced serum HBeAg (p<0.01) and HBV DNA copies (p<0.05) in 31 patients who were diagnosed with active chronic HBV infection (CHB) and had not received antiviral treatment previously. Alanine aminotransaminase (ALT), aspartate aminotransaminase (AST) and gamma glutamyl transpeptidase (gamma-GT) of the patients declined (p<0.001, 0.001 and 0.01, respectively). Kidney function (blood creatinine and urea nitrogen) remained unchanged. Another 21 lamivudine-resistant CHB patients with mutations at the tyrosine-methionine-aspartate-aspartate motif (YMDD) displayed a response to PFA similar to that mentioned above, with reductions in HBeAg (p<0.05), HBV DNA (p<0.01) and liver enzymes (ALT and AST, p<0.001; gamma-GT, p<0.05). Moreover, PFA reduced serum HBeAg (p<0.01), HBV DNA (P<0.05), AST (p<0.05) and ALT (p<0.02) in a cohort of 13 severe CHB patients with advanced liver damage. PFA was also evaluated in vitro and in vivo. PFA inhibited HBV DNA replication in HBV-transfected human HepG2 cells (2.2.15 cells) with reduced amount of HBV RC-DNA and DS-DNA. In the duck HBV-infected ducklings, PFA reduced viral DNA and duck HBsAg in the serum (p<0.01 for both).
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PMID:Antiviral therapeutic efficacy of foscarnet in hepatitis B virus infection. 1628 Jan 77

Model for end-stage liver disease (MELD) score is a good parameter to establish the patient survival before liver transplantation and give priority to the sickest patients. The aim of this study was to evaluate the variability and potential regression of MELD score during the months before liver transplant. From the 350 patients waitlisted for transplantation, we evaluated the 124 patients who had enough blood tests during 12 months before the final event (transplantation, death, removal from list due to improvement or worsening). We considered month 12 as the final event and blood tests from 0, 3, 6, and 12 months were analyzed. MELD score was calculated and compared using ANOVA for repeated measures test. To determine variability of MELD and its components, intraclass correlation coefficient (ICC) was calculated for 0, 3, and 6 months. The degree of constancy was defined by proximity of ICC to 1. Two groups by initial MELD (< or =17 or >17) were considered. Patient data are: mean age, 53 +/- 9 years; sex: 70% men, etiology, 28% hepatitis C, 11% alcohol and hepatitis C, 16% alcohol, 28% hepatocellular carcinoma, 6% hepatitis B, 11% others; Initial Child-score, 8.5 +/- 2.0; Initial MELD score, 15.2 +/- 4.9; mean time on waiting list, 8.1 +/- 5.7 months. MELD score from 6 and 12 months was significantly higher than the initial one. The most constant parameter was creatinine (ICC:0.89); bilirubin (ICC:0.58) and INR (ICC:0.59) were the most variable ones. MELD score ICC was 0.79. In only one patient did MELD score decrease 5 points below the initial one. For initial MELD < or = 17 and >17, variability was lower in the former. In conclusion, MELD became significantly higher 6 months after the basal determination. This score is reliable as it does not tend to decrease in time. In high MELD scores (>17), 3-month survival was lower and variability greater so that more careful follow-up and prioritizing are needed.
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PMID:Variability of MELD score during the year before liver transplantation. 1638 73

Hepatitis B virus (HBV) recurrence and de novo HBV infection are frequent events in liver transplantation recipients. Treatment with lamivudine is initially efficient in both infections but the incidence of lamivudine-resistant HBV emergence increases over time. Adefovir appears to be promising in post-liver transplantation patients with recurrent HBV infection and lamivudine-resistant HBV. This study analyzed adefovir treatment in 42 post-liver transplantation patients who developed recurrent HBV or de novo HBV infection with lamivudine-resistant HBV (54.8% HCV-coinfected). Patients received 10 mg of oral adefovir once daily for a mean period of time of 21.5 months (range from 12 to 31 months). In 62.9% of patients, ALT levels decreased significantly. Serum HBV-DNA was undetectable in 64% of the cases. Twenty percent of patients lost HBeAg marker and 13.3% of them developed anti-HBe. In 9.5% of recipients, HBsAg became negative. There was no significant change in serum creatinine levels. In only one patient was worsening of the renal function detected, making dose adjustment necessary. No other side effects were reported. Our results confirm the efficacy and safety of adefovir treatment in post-liver transplantation patients with lamivudine-resistant HBV, neither were adefovir-resistant mutations identified in patients after 21 months of therapy, nor were there adverse events, especially renal toxicity.
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PMID:Study on the efficacy and safety of adefovir dipivoxil treatment in post-liver transplant patients with hepatitis B virus infection and lamivudine-resistant hepatitis B virus. 1638 96

The number of patients on the kidney waiting list is increasing, creating a shortage of donor organs. To solve this problem, there is an interest in transplanting organs formerly considered marginal or undesirable. We performed seven (four living related, three cadaveric) kidney transplants from hepatitis B surface antigen (HBsAg)-positive donors. Hepatitis B e antigen (HBeAg) and hepatitis B virus (HBV) DNA were negative in the living donors and were unknown in cadaveric donors. Liver function tests were in the normal range in all of the donors. All of the recipients were HBsAg-negative and hepatitis B surface antibody (anti-HBs)-positive. Recipients receiving kidneys from cadaveric donors were given prophylactic lamivudine treatment postoperatively. Anti-HBs remained positive throughout the follow-up period in all but one patient with a cadaveric graft. None of the patients receiving a kidney from an HBsAg-positive donor developed clinical HBV infection in a mean follow-up period of 42.6 +/- 36.8 months (range: 16 to 121 months, median 30 months). Liver function tests remained in the normal ranges in all patients. All the grafts are still functioning with a mean serum creatinine level of 1.6 +/- 0.85 mg/dL. In conclusion, transplants from HBsAg-positive and HBeAg-/HBV DNA-negative donors seem to carry no risk to the recipients who are immune to HBV. Even cadaveric donors with HBsAg-positivity and unknown HBeAg/HBV DNA status can be used with caution in selected recipients without significantly affecting graft and patient outcome.
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PMID:The effect of HBsAg-positivity of kidney donors on long-term patient and graft outcome. 1638 70

A 39-yr-old male with hepatorenal syndrome type 1 and refractory ascites was treated with continuous renal replacement therapy (CRRT) resulting in clinical improvement. He was positive for antibodies to hepatitis B, C, and human immunodeficiency viruses, and had a history of chronic alcohol and iv drug abuse. The patient had 4 hospital admissions during a 12-wk period. He first presented with advanced liver disease including pedal edema and a serum ammonia level of 56 micromol/L (reference range: 11 - 35 micromol/L). In subsequent admissions, he had asterixis, nausea, vomiting, jaundice, and worsening pedal edema. On his 4th admission, there was lethargy, tense ascites, decreased urinary output, bilateral edema of the lower extremities and scrotum, serum creatinine of 6.2 mg/dl (reference range: 0.6 - 1.5 mg/dl), and weight gain of 16 kg during the prior 8 wk. During the first 3 hospitalizations, he was treated with lactulose with slight improvement. On the 4th admission, he was started on low-dose dopamine (3 microg/kg/min) and 25% salt-poor albumin without clinical improvement. A pulmonary artery catheter was placed and hemofiltration by CRRT was performed for 5 days, with removal of 26.7 L of fluid and a net reduction of 11 kg of body weight. Serum creatinine decreased to 4.2 mg/dl during CRRT and was 2.2 mg/dl at hospital discharge 2 weeks later. His PaO(2) improved from 66 to 78 mmHg and his systemic vascular resistance increased from 571 to 799 dyne.sec/cm(5). CRRT was effective in relieving severe fluid retention and producing marked clinical improvement. We suggest that CRRT should be considered for the treatment of refractory ascites including that caused by hepatorenal syndrome.
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PMID:Hepatorenal syndrome: resolution of ascites by continuous renal replacement therapy in an alcoholic coinfected with hepatitis B, C, and human immunodeficiency viruses. 1650 Dec 43

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

Many Koreans, in addition to Japanese, were killed or injured by the atomic bombs detonated over Hiroshima and Nagasaki, Japan, in 1945. Our study examined noncancer diseases of Korean A-bomb survivors in residence at Hapcheon, Republic of Korea and evaluated whether they had significantly higher prevalence of noncancer diseases than non-exposed people. We evaluated a number of tests, including anthropometric measurements, blood pressure, blood chemistry, hepatitis B surface antigen, and urinalysis, of survivors (n=223) and controls (n=372). Univariate analysis revealed significantly lower fasting glucose and creatinine, and higher diastolic blood pressure, aspartate aminotransferase, alanine aminotransferase, and blood urea nitrogen levels in the survivors than in the controls. The calculation of crude prevalence ratios (PRs) revealed that A-bomb survivors had a significantly higher prevalence of hypertension (PR, 1.16; 95% CI, 1.00-1.35) and chronic liver disease (2.20; 1.59-3.06) than controls. After adjusting for covariates (age, sex, body mass index, marital status, education, alcohol consumption, and smoking), A-bomb survivors had a significantly higher prevalence of hypertension (1.24; 1.06-1.44), chronic liver disease (2.07; 1.51-2.84), and hypercholesterolemia (1.79; 1.11-2.90) than controls. This study suggests that A-bomb exposure is associated with a higher prevalence of non-cancer diseases in Korean survivors.
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PMID:Non-cancer diseases of Korean atomic bomb survivors in residence at Hapcheon, Republic of Korea. 1677 77

Truvada is the coformulation of tenofovir disoproxil fumarate (TDF; 300 mg) and emtricitabine (FTC; 200 mg) in a single tablet, providing the nucleotide backbone for once-daily dosing, as a component of highly active antiretroviral therapy (HAART). TDF (the bioavailable prodrug of tenofovir) is hydrolyzed to tenofovir intracellularly and phosphorylated to the active metabolite, tenofovir diphosphate. Tenofovir is a nucleotide analog of deoxyadenosine monophosphate, with activity against HIV-1, -2 and hepatitis B virus. FTC, the fluorinated derivative of lamivudine, is an analog of deoxycitidine, active against HIV-1, -2 and hepatitis B virus. Their long half-lives in plasma and in peripheral blood mononuclear cells allow once-daily dosing. Both are eliminated renally. Resistance mutation K65R is selected for by tenofovir and confers a two- to fourfold reduced susceptibility to this drug. The incidence of K65R is low (3%) and has not been observed in clinical trials with the concomitant use of tenofovir and FTC. FTC selects for M184V mutation less frequently than lamivudine. Tenofovir drug interactions include increased exposure to didanosine and inferior immune recovery that preclude their concomitant use. Boosted protease inhibitors increase exposure to tenofovir without dose adjustment required. FTC has no significant drug interactions. They are not metabolized by cytochrome P450, which confers little potential for interactions with drugs metabolized by these enzymes. As tenofovir and FTC are renally eliminated, drugs eliminated by tubular secretion must be avoided. Both antiretrovirals, as individual agents and in coadministration have evidenced antiviral potency in clinical trials. Pivotal study 934 evidenced superior efficacy of the combination TDF/FTC/efavirenz (EFV) versus zidovudine/FTC/EFV. The toxicity profile of tenofovir and FTC has been extensively studied. Lipid profile is more favorable with tenofovir than thymidine analog. Tenofovir requires surveillance of glomerular filtration rate and dosing interval adjustment when creatinine clearance is less than 50 ml/min and avoidance less than 30 ml/min. Fat loss is less likely with tenofovir than with thymidine analog. Clinical trials have assessed the performance of the coformulation of TDF and FTC.
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PMID:Tenofovir disoproxil fumarate-emtricitabine coformulation for once-daily dual NRTI backbone. 1700 33

Small-vessel vasculitis is a convenient descriptor for a wide range of diseases characterized by vascular inflammation of the venules, capillaries, and/or arterioles with pleomorphic clinical manifestations. The classical clinical phenotype is leukocytoclastic vasculitis with palpable purpura, but manifestations vary widely depending upon the organs involved. Histopathologic examination in leukocytoclastic vasculitis reveals angiocentric segmental inflammation, fibrinoid necrosis, and a neutrophilic infiltrate around the blood vessel walls with erythrocyte extravasation. The etiology of small-vessel vasculitis is unknown in many cases, but in others, drugs, post viral syndromes, malignancy, primary vasculitis such as microscopic polyarteritis, and connective tissue disorders are associated. The diagnosis of small-vessel vasculitis relies on a thorough history and physical examination, as well as relevant antibody testing including antinuclear antibody and antineutrophil cytoplasmic antibody, hepatitis B and C serologies, assessment of complement, immunoglobulins, blood count, serum creatinine, liver function tests, urinalysis, radiographic imaging, and biopsy.
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PMID:Small-vessel vasculitis. 1768 40

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