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)

Chronic liver disease results in more than 1 million physician visits and more than 300,000 hospitalizations per year in the United States. More than 27,000 patients annually progress to end-stage liver disease (ESLD), liver failure, or death. Patients with ESLD experience such complications as encephalopathy, malnutrition, muscle wasting, ascites, esophagogastric variceal hemorrhage, spontaneous bacterial peritonitis, fatigue, and depression. Despite significant improvements in palliation, patients' quality of life diminishes and their disease will often inexorably progress. Liver transplantation, a valid treatment option, increases life and reduces many symptoms. With the current shortage of organs, up to 10% to 15% of these patients die without receiving an organ. Many patients also are not candidates for transplantation due to comorbid illness. In addition, some patients receive a transplant but succumb to complications of the transplant itself. Such patients and families face the conundrum of a potentially treatable yet often fatal illness. Through the case of a 55-year-old woman with a life-long history of hepatitis B virus infection who is awaiting transplant, we discuss the transplant eligibility process and the struggle with maintaining hope for a cure in the face a life-threatening illness. In all of these circumstances, the health care team must combine elements of palliative care with life-sustaining therapy to maximize the patient's quality and quantity of life.
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PMID:Integrating palliative care for liver transplant candidates: "too well for transplant, too sick for life". 1677 29

Vogt-Koyanagi-Harada (VKH) syndrome is a rare entity characterized by depigmentation of the skin and eye lashes, chronic granulomatous iridocyclitis and exudative retinal detachment, as well as aseptic meningitis and encephalopathy. We describe a 22-year-old male intravenous drug addict, infected with hepatitis B and C virus, suffering from this syndrome, associated with progressive renal sclerosis, malignant hypertension, heart failure and chronic myeloproliferative disorder. The association with these various diseases is discussed and relevant cases are reviewed.
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PMID:Vogt-Koyanagi-Harada syndrome associated with renal failure: a case report. 1673 27

In spite of a decrease of the prevalence of hepato-splenic schistosomiasis thanks to mass-treatment with Praziquentel from December 1994 till now (CNM - MSF - WHO - Health Provincial Director) of target-populations in Kratie Province, severe cases of portal hypertension are not exceptional (digestive bleedings, after rupture of oesophageal varices). Out of 106 cases of portal hypertension: alI patients have had clinical survey biological tests (liver function, haematology and serology). Most of them had ultrasonography (Aloka 55,500 Sound 3.5 MHz). Nearly half of the group of 153 patients has never had bleedings. More than 45 were not eligible for surgery for different reasons: severe anaemia (few possibilities for massive transfusion in Cambodia), serology (S. mekongi) + but also hepatitis B or C +, hepatic biological exams (hepatic insufficiency). So we decided for eleven of them to use a surgical decompression procedure in order to decrease portal hypertension and the porto-systemic gradient. After defining portal hypertension, specific clinical features of portal hypertension (secondary to Schistosomiasis) the authors report eleven cases who were operated on (2000-2002): 4 mesenterico-cave shunt with interposition of a graft (Drapanas' procedure), 1 operation of HASSAB (after splenectomy), 6 proximal spleno-renal diversion (after splenectomy). After studying the results of the eleven patients, discussion with other surgical procedures, particularly endoscopic procedures is developed. The follow-up of these patients during at least five years is mandatory to give guidelines for post-systemic shunts to prevent rebleeding (near other methods). Treated too late, schistosomiasis has no benefit from drugs (Praziquentel). After a mean period of forty two months, the following results are: mortality: one case (10 days after operation): hepatic insufficiency (group Child B/C). morbidity: one occlusion of the small intestine, after 4 months (debridment), operated at the Provincial hospital of Kratie (case no1). Ten patients resume work, family and social life between Kratie and Sambor in 2002. No rebleeding. No encephalopathy.
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PMID:[Place of surgery in the prevention of recurrences of digestive haemorrhages at the patients presenting a portal hypertension due to Schistosoma mekongi]. 1725 55

A study was conducted among 67 patients presenting with hepatic encephalopathy to establish the aetiological diagnosis and record the incidence of acute and chronic liver diseases. They all had undergone thorough clinical and laboratory evaluation. The factor precipitating encephalopathy was also identified. Among 67 patients 19 (28.4%) had acute liver disease and 48 (71.6%) had chronic liver disease. Majority of patients had grade 2 encephalopathy at presentation. Among the acute cases most common aetiology was acute viral hepatitis due to hepatitis B and E viruses whereas alcoholic liver disease was the most frequent cause of chronic liver disease. The most common precipitating factor was gastro-intestinal haemorrhage.
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PMID:Observations of hepatic encephalopathy profile in a tertiary care centre. 1738 10

This is prospective cross-sectional study on 37 patients presenting to different hospitals in Khartoum state, Sudan, sought to determine the etiology, clinical course, and predictors of mortality in patients presenting with fulminant hepatic failure (FHF). Patients were subclassified into hyperacute, acute, and subacute FHF; all sera were tested for hepatitis A, B, C, and E; negative samples were tested for antinuclear antibodies and anti-smooth muscle antibodies. The commonest etiologic factors included seronegative hepatitis (38%), hepatitis B virus (22%), severe Plasmodium falciparum malaria (8%), autoimmune hepatitis (8%), hepatitis E virus (5%), anti-tuberculous drugs (5%), and lymphomatous infiltration of the liver (5%). The mortality rate was high at 84%. Poor prognostic factors included presentation with grade III/IV encephalopathy, evidence of bacterial infection, and a prolonged prothrombin time of >25 seconds over the controls.
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PMID:Fulminant hepatic failure in an African setting: etiology, clinical course, and predictors of mortality. 1743 91

Liver disease is frequently seen in HIV+ patients as a result of coinfection with hepatitis B (HBV) or C (HCV) viruses, alcohol abuse and/or exposure to hepatotoxic drugs. The aim of this study was to assess the prevalence of liver cirrhosis, its main causes and clinical presentation in HIV+ patients. Observational, cross-sectional, retrospective study of all HIV+ individuals followed at one reference HIV outpatient clinic in Madrid. Liver fibrosis was measured in all cases using transient elastometry (FibroScan). All 2168 HIV+ patients on regular follow-up (76% males, 46% injecting drug users) were successfully examined by FibroScan) between October 2004 and August 2006. Liver cirrhosis was recognized in 181 (overall prevalence, 8.3%), and the main aetiologies were HCV, 82.3%; HBV, 1.6%; dual HBV/HCV, 2.8%; and triple HBV/HCV/ hepatitis delta virus (HDV) infection, 6.6%. The prevalence of cirrhosis differed among patients with distinct chronic viral hepatitis: HCV, 19.2%; HBV, 6.1%; HBV/HCV, 41.7%; and HBV/HCV/HDV, 66.7%. In 12 patients with cirrhosis (6.7%), no definite aetiology was recognized. Overall, cirrhotics had lower mean CD4 counts than noncirrhotics (408 vs 528 cells/microL respectively; P = 0.02), despite similar proportion of subjects with undetectable viraemia on highly active antiretroviral therapy. Clinical manifestations of liver cirrhosis were: splenomegaly, 61.5%; oesophageal varices, 59.8%; ascites, 22.6%; encephalopathy, 12.1%; and variceal bleeding, 6.1%. Liver cirrhosis and hepatic decompensation events are relatively frequent in HIV+ individuals. Chronic HCV and alcohol abuse, but not chronic HBV, play a major role. Transient elastometry may allow the identification of a significant number of HIV+ individuals with asymptomatic liver cirrhosis.
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PMID:Liver cirrhosis in HIV-infected patients: prevalence, aetiology and clinical outcome. 1823 89

The annual incidence of fulminant hepatitis (FH) in Japan has decreased from 3700 patients in 1972 to 1000 patients in 1989, 1050 patients in 1995 and 426 in 2004. The most frequent cause of FH in Japan is hepatitis B virus (HBV)-related hepatitis, which accounts for around 40%, with hepatitis A accounting for around 10%; drug reaction accounts for around 10%; other hepatitis, including an unknown cause, accounts for around 40%. The acute type FH, which has a disease duration as 10 days or shorter before the development of encephalopathy (onset-coma days [OCD]), mainly consists of hepatitis A and B and has relatively better prognosis, with an approximately 40% survival rate without transplantation. The subacute type FH, which has 11 to 56 days OCD, mainly consists of unknown hepatitis including acute-onset autoimmune hepatitis and has poorer prognosis of about 20% survival. Approximately 25% of FH patients underwent liver transplantation and about 80% of them survived. High volume plasma exchange (PE) and hemodialysis filtration (HDF) have been the most common and principal therapies and they are administered to about 90% and 70% of patients, respectively. The progress of artificial liver support such as combination treatment of PE with HDF is considered to play a role in the slight improvement of the survival proportion of patients with acute type FH in recent years.
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PMID:Clinical epidemiology of fulminant hepatitis in Japan. 1912 45

Liver transplantation is the only curative treatment in patients with end-stage liver disease. Neurological complications (NC) are increasingly reported to occur in patients after cadaveric liver transplantation. This retrospective cohort study aims to evaluate the incidence and causes of NC in living donor liver transplant (LDLT) patients in our transplant center. Between August 1998 and December 2005, 121 adult LDLT patients were recruited into our study. 17% of patients experienced NC, and it occurred significantly more frequently in patients with alcoholic cirrhosis (42%) and autoimmune hepatitis (43%) as compared with patients with hepatitis B or C (9/10%, P = 0.013). The most common NC was encephalopathy (47.6%) followed by seizures (9.5%). The choice of immunosuppression by calcineurin inhibitor (Tacrolimus or Cyclosporin A) showed no significant difference in the incidence of NC (19 vs. 17%). The occurrence of NC did not influence the clinical outcome, since mortality rate, median ICU stay and length of hospital stay were similar between the two groups. Most patients who survived showed a nearly complete recovery of their NC. NCs occur in approximately 1 in 6 patients after LDLT and seem to be predominantly transient in nature, without major impact on clinical outcome.
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PMID:Neurologic complications in adult living donor liver transplant patients: an underestimated factor? 1972 99

Cancer chemotherapy in chronic hepatitis B virus (HBV) carriers occasionally leads to acute hepatic failure (AHF) from viral reactivation resulting in an high mortality rate. In this situation, living donor liver transplantation (LDLT) can be life saving. Herein we have reported 2 cases of successful LDLT performed for AHF caused by reactivation of HBV infection during chemotherapy for hematologic malignancies. In case 1, a 38-year-old male HBV carrier with a neck mass was hisopathologically diagnosed as Hodgkin's lymphoma. During 4 cycles of chemotherapy he developed right upper quadrant pain and jaundice. Laboratory data (alanine amino transferase, 701 U/L, total bilirubin: 7.92 mg/dL, positive hepatitis B e antigen showed that he had experienced an acute exacerbation of chronic hepatitis. Soon, he developed grade IV hepatic encephalopathy with a total bilirubin level of 50.56 mg/dL and a model for End-Stage Liver Disease score of 40. After LDLT, he has been free of relapse for 52 months so far. In case 2, a 49-year-old male HBV carrier was diagnosed in the chronic phase of chronic myeloid leukemia. The patient had been under Imatinib treatment for 1 year until he was admitted for AHF. He developed grade II encephalopathy with a total bilirubin of 50.8 mg/dL. We performed LDLT; the patient has been free of relapse for 17 months. LDLT was a life-saving procedure for AHF caused by reactivation of HBV during chemotherapy for hematologic malignancy. It can provide long-term survival if the coexistent hematologic malignancy has been controlled.
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PMID:Living donor liver transplantation for acute hepatic failure caused by reactivation of hepatitis B virus infection after chemotherapy for hematologic malignancy: case reports. 2043 Jan 87

In a patient with cirrhosis of the liver, associated with hepatitis B virus, who was admitted for confusion and acute elevation of liver enzymes, a diagnosis of hepatic encephalopathy was made. A serum ammonia level of 54 (normal less than 33) microgram/liter, supported the diagnosis, but puzzled the medical staff regarding the possibility that ammonia may directly induce the confusion. While it is widely accepted that the ammonia level is a marker that usually parallels the amount of toxins and metabolites that bypasses the liver, its role in causing brain dysfunction is debated. However, since ammonia may directly hinder the metabolism of neuro-transmitters, and drugs and treatments specifically aimed at reducing ammonia levels may minimize the time interval for recovery from the acute brain insult, it is assumed that ammonia by itself had a role in bringing about the encephalopathy manifestations in our patients and other patients with cirrhosis of the liver.
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PMID:[Ammonia as a cause for hepatic encephalopathy]. 2054 31


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