Journal of hepatology
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Journal of hepatology · Dec 2010
Randomized Controlled Trial Multicenter StudyEnteral nutrition with or without N-acetylcysteine in the treatment of severe acute alcoholic hepatitis: a randomized multicenter controlled trial.
Severe acute alcoholic hepatitis is associated with a high mortality rate. Oxidative stress is involved in the pathogenesis of acute alcoholic hepatitis. Previous findings had also suggested that enteral nutritional support might increase survival in patients with severe acute alcoholic hepatitis. Therefore, the aim of the present study was to evaluate the efficacy of N-acetylcysteine in combination with adequate nutritional support in patients with severe acute alcoholic hepatitis. ⋯ In this study, high doses of intravenous N-acetylcysteine therapy for 14 days conferred neither survival benefits nor early biological improvement in severe acute alcoholic hepatitis patients with adequate nutritional support. However, these results must be viewed with caution, since the study suffered from a lack of power.
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Journal of hepatology · Dec 2010
Brain hypoxanthine concentration correlates to lactate/pyruvate ratio but not intracranial pressure in patients with acute liver failure.
The pathogenesis of cerebral edema in acute liver failure is suggested, in in vitro and animal studies, to involve a compromised oxidative metabolism with a decrease in cerebral ATP levels and an increase in purine concentrations. In this study we hypothesize that the cerebral concentrations of hypoxanthine, inosine, and lactate/pyruvate (LP) ratio are increased and correlated in patients with acute liver failure. Furthermore, we expect the purines and L/P ratio to correlate with intracranial pressure (ICP) (positively), and cerebral perfusion pressure (CPP) (negatively). ⋯ This study shows that the high cerebral LP ratio correlates to the hypoxanthine level in patients with acute liver failure. However, these metabolic alterations were not related to the development of intracranial hypertension.
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Journal of hepatology · Nov 2010
Characterising adrenal function using directly measured plasma free cortisol in stable severe liver disease.
Adrenal insufficiency (AI) has been reported in patients with advanced liver disease. Diagnosing AI is problematic owing to controversies in using total serum cortisol as a measure of adrenal function. No published data exist on directly measured plasma free cortisol (PFC) in patients with liver disease. ⋯ In patients with stable severe liver disease, a significant discrepancy exists between the rates of diagnosis of AI using the total and free cortisol criteria. We would advise caution in the interpretation of adrenal function testing using total cortisol measurements in this group.
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Journal of hepatology · Sep 2010
Meta AnalysisMeta-analysis of performance of Kings's College Hospital Criteria in prediction of outcome in non-paracetamol-induced acute liver failure.
Current techniques for predicting outcome and requirement for emergency liver transplantation (ELT) in acute liver failure (ALF) are imperfect, though The Kings College Criteria (KCC) are the most commonly applied tools for this purpose. Their performance in identification of patients with non-paracetamol-induced ALF (non-POD ALF), who would not survive without ELT, has recently been questioned. Using quantitative techniques, we therefore performed a meta-analysis of outcome data of the KCC for prediction of survival in non-POD ALF. ⋯ KCC for outcome in non-POD ALF have good specificity and more limited sensitivity. There is significant heterogeneity in the published data partially related to methodological quality. KCC perform best in groups with high grade encephalopathy and in historically earlier studies suggesting modern medical management of ALF may modify performance of KCC.
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Journal of hepatology · Aug 2010
Clinical, biochemical, and pathological characteristics of clevudine-associated myopathy.
The aim of this study was to define the clinical, biochemical, and pathological characteristics of myopathy developed during clevudine therapy. ⋯ Myopathy associated with clevudine is characterized by a weakness in proximal muscles of the lower extremities with elevated muscle enzymes and presumably caused by mitochondrial toxicities. Careful medical and serologic examinations are essential for the early detection and management of this potential adverse reaction in CHB patients under clevudine therapy.