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Hepatic Encephalopathy (hepatic + encephalopathy)
Kinds of Hepatic Encephalopathy Selected AbstractsEFFECTS OF A SINGLE, SHORT INTRAVENOUS DOSE OF ACETYL- l -CARNITINE ON PATTERN-REVERSAL VISUAL-EVOKED POTENTIALS IN CIRRHOTIC PATIENTS WITH HEPATIC ENCEPHALOPATHYCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1-2 2006Massimo Siciliano SUMMARY 1In animals and in cultured neurons, l -carnitine and acetyl- l -carnitine (ALCAR) have been shown to counteract some of the toxic effects of ammonia. In order to detect similar properties in humans, we studied neuronal function after ALCAR administration in cirrhotics with hepatic encephalopathy (HE). 2Eighteen cirrhotic patients with persistent HE and hyperammonaemia were investigated in the present study and six subjects with a prior transient ischaemic attack were used as controls. 3The prominent positive component that occurs approximately 100 msec after the pattern reversal (P100) latencies of visual-evoked potentials were used to evaluate neuronal function. At first, the P100 latency was measured in six cirrhotic patients with HE and in the six controls before the administration of 0.5 g ALCAR in 50 mL isotonic saline (infusion rate 10 mL/min) and 15, 30, 60 and 90 min later. 4A significant reduction in P100 latencies was identified 30 min after ALCAR infusion in HE patients, whereas no differences were observed in controls. 5Thereafter, the P100 latency was evaluated in the 12 other cirrhotic patients with HE only before and 30 min after ALCAR infusion. The mean of the P100 latencies measured in these subjects was significantly shorter after ALCAR infusion compared with values obtained before ALCAR administration (mean (SD) 130.78 5.50 vs 136.08 6.45 msec, respectively; P = 0.0013). 6The present study suggests that a single intravenous dose of ALCAR may transiently improve neuronal function in cirrhotic patients with persistent HE and hyperammonaemia. [source] Inhibition of glutamine transport into mitochondria protects astrocytes from ammonia toxicityGLIA, Issue 8 2007V. B. R. Pichili Abstract Hepatic encephalopathy (HE) is a major neurological complication that occurs in the setting of severe liver failure. Ammonia is a key neurotoxin implicated in this condition, and astrocytes are the principal neural cells histopathologically and functionally affected. Although the mechanism by which ammonia causes astrocyte dysfunction is incompletely understood, glutamine, a by-product of ammonia metabolism, has been strongly implicated in many of the deleterious effects of ammonia on astrocytes. Inhibiting mitochondrial glutamine hydrolysis in astrocytes mitigates many of the toxic effects of ammonia, suggesting the involvement of mitochondrial glutamine metabolism in the mechanism of ammonia neurotoxicity. To determine whether mitochondriaare indeed the organelle where glutamine exerts its toxic effects, we examined the effect of L -histidine, an inhibitor of mitochondrial glutamine transport, on ammonia-mediated astrocyte defects. Treatment of cultured astrocytes with L -histidine completely blocked or significantly attenuated ammonia-induced reactive oxygen species production, cell swelling, mitochondrial permeability transition, and loss of ATP. These findings implicate mitochondrial glutamine transport in the mechanism of ammonia neurotoxicity. © 2007 Wiley-Liss, Inc. [source] Minimal hepatic encephalopathy: Consensus statement of a working party of the Indian National Association for Study of the LiverJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 6 2010Radha K Dhiman Abstract Hepatic encephalopathy (HE) is a major complication that develops in some form and at some stage in a majority of patients with liver cirrhosis. Overt HE occurs in approximately 30,45% of cirrhotic patients. Minimal HE (MHE), the mildest form of HE, is characterized by subtle motor and cognitive deficits and impairs health-related quality of life. The Indian National Association for Study of the Liver (INASL) set up a Working Party on MHE in 2008 with a mandate to develop consensus guidelines on various aspects of MHE relevant to clinical practice. Questions related to the definition of MHE, its prevalence, diagnosis, clinical characteristics, pathogenesis, natural history and treatment were addressed by the members of the Working Party. [source] Malnutrition and hypermetabolism are not risk factors for the presence of hepatic encephalopathy: A cross-sectional studyJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 4 2008Peter Sörös Abstract Background and Aim:, Hepatic encephalopathy is a frequent complication of cirrhosis. The present retrospective investigation was conducted to characterize metabolic alterations in cirrhotic patients with and without hepatic encephalopathy. We tested the hypothesis that reduced nutritional status or the degree of tissue catabolism are associated with the presence of hepatic encephalopathy. Methods:, We investigated 223 patients with histologically confirmed nonalcoholic cirrhosis without hepatic encephalopathy and with hepatic encephalopathy (grades 1,3). To assess liver function, nutritional status, and energy metabolism, a variety of biochemical and clinical tests were performed including anthropometric measurements, bioelectrical impedance analysis, and indirect calorimetry. Results:, Nutritional status and tissue catabolism were not significantly different between patients with and without hepatic encephalopathy. Conclusions:, Our data do not support the hypothesis that malnutrition or tissue catabolism are independent risk factors for the presence of hepatic encephalopathy in patients with nonalcoholic cirrhosis. [source] Detrimental effects of nitric oxide inhibition on hepatic encephalopathy in rats with thioacetamide-induced fulminant hepatic failure: Role of nitric oxide synthase isoformsJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 7 2006Chi-Jen Chu Abstract Background:, Hepatic encephalopathy is a complex neuropsychiatric syndrome. A previous study showed that chronic nitric oxide (NO) inhibition aggravated the severity of encephalopathy in thioacetamide (TAA)-treated rats. The present study investigated the relative contribution of NO synthase (NOS) isoforms on the severity of hepatic encephalopathy in TAA-treated rats. Method:, Fulminant hepatic failure was induced in male Sprague-Dawley rats by intraperitoneal injection of TAA (350 mg/kg/day) for 3 days. Rats were divided into three groups to receive N, -nitro-L-arginine methyl ester (L-NAME, a non-selective NOS inhibitor, 25 mg/kg/day in tap water), L-canavanine (an inducible NOS inhibitor, 100 mg/kg/day via intraperitoneal injection) or normal saline (N/S) from 2 days prior to TAA administration and lasting for 5 days. Severity of encephalopathy was assessed by the counts of motor activity. Plasma levels of tumor necrosis factor-, (TNF- ,) were determined by enzyme-linked immunosorbent assay (ELISA), and total bilirubin, alanine aminotransferase (ALT) and creatinine were determined by colorimetric assay. Results:, Compared with L-canavanine or N/S-treated rats (0% and 4%, respectively), the mortality rate was significantly higher in rats receiving L-NAME administration (29%, P < 0.005). Inhibition of NO created detrimental effects on the counts of motor activities (P < 0.05). Rats treated with L-NAME had significantly higher plasma levels of total bilirubin, ALT, creatinine and TNF- , as compared with rats treated with L-canavanine or N/S (P < 0.01). Conclusion:, Chronic L-NAME administration, but not L-canavanine, had detrimental effects on the severity of hepatic damage and motor activities in TAA-treated rats. These results suggest that constitutive NOS activities play a major protective role in rats with fulminant hepatic failure. [source] Hepatic encephalopathy and mild lack of awarenessALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2 2010A. Braillon No abstract is available for this article. [source] Review article: the modern management of hepatic encephalopathyALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 5 2010J. S. BAJAJ Aliment Pharmacol Ther,31, 537,547 Summary Background, Hepatic encephalopathy, both overt and minimal, forms a continuum of cognitive change in cirrhosis. Strategies to diagnose and treat hepatic encephalopathy have evolved considerably. Aim To examine the updated diagnostic and treatment strategies for hepatic encephalopathy. Methods, Techniques for the clinical, psychometric and neurophysiological evaluation of hepatic encephalopathy are reviewed. The methods reviewed include pure clinical scales (West-Haven), psychometric tests (PSE-syndrome test), neurophysiological tests (EEG, Critical flicker frequency, CFF) and computerized tests (Inhibitory control test, ICT). Results, Clinical scales are limited, whereas psychometric tests (specifically PSE-syndrome test), CFF and ICT can be used to diagnose minimal hepatic encephalopathy. However, there is no single test that can capture the entire spectrum of cognitive impairment. Treatment options and goals depend on the acuity of hepatic encephalopathy. In-patient management should concentrate on supportive care, precipitating factor reversal and lactulose and/or rifaximin therapy. Out-patient therapy should aim to prevent recurrences, and both lactulose and rifaximin have evidence to support their use. Conclusions, Diagnostic techniques for hepatic encephalopathy range from simple scales to sophisticated tools. Treatment options depend on the stage of hepatic encephalopathy. The future challenge is to evaluate cognitive function as a continuum with clinically relevant outcomes and to develop well-tolerated and inexpensive treatments for hepatic encephalopathy. [source] Cerebral blood flow velocity increases during a single treatment with the molecular adsorbents recirculating system in patients with acute on chronic liver failureLIVER TRANSPLANTATION, Issue 8 2001Lars E. Schmidt The aim of this uncontrolled pilot study is to determine the effect of treatment with the molecular adsorbents recirculating system (MARS) on cerebral perfusion in patients with acute on chronic liver failure (AOCLF). In 8 patients (median age, 44 years; range, 35 to 52 years) admitted with AOCLF, a single 10-hour MARS treatment was performed. Hepatic encephalopathy (HE) was graded according to the Fogarty criteria. Changes in cerebral perfusion were determined by transcranial Doppler as mean flow velocity (Vmean) in the middle cerebral artery. Arterial ammonia and bilirubin levels were monitored as a measure of the capability of the MARS to remove water-soluble and protein-bound toxins. During MARS treatment, HE grade improved in 3 patients and remained unchanged in 5 patients (P = .11). Vmean increased from 42 cm/sec (range, 26 to 59 cm/sec) to 72 cm/sec (range, 52 to 106 cm/sec; P < .05), whereas arterial ammonia level decreased from 88 ,mol/L (range, 45 to 117 ,mol/L) to 71 ,mol/L (range, 26 to 98 ,mol/L; P < .05) and bilirubin level from 537 ,mol/L (range, 324 to 877 ,mol/L) to 351 ,mol/L (range, 228 to 512 ,mol/L; P < .05). In conclusion, cerebral perfusion is increased and levels of ammonia and bilirubin are reduced during MARS treatment in patients with AOCLF. [source] The bile acid receptor TGR5 (Gpbar-1) acts as a neurosteroid receptor in brainGLIA, Issue 15 2010Verena Keitel Abstract TGR5 (Gpbar-1) is a membrane-bound bile acid receptor in the gastrointestinal tract and immune cells with pleiotropic actions. As shown in the present study, TGR5 is also expressed in astrocytes and neurons. Here, TGR5 may act as a neurosteroid receptor, which is activated by nanomolar concentrations of 5,-pregnan-3,-ol-20-one and micromolar concentrations of 5,-pregnan-3,-17,-21-triol-20-one and 5,-pregnan-3,-ol-20-one (allopregnanolone). TGR5 stimulation in astrocytes and neurons is coupled to adenylate cyclase activation, elevation of intracellular Ca2+ and the generation of reactive oxygen species. In cultured rat astrocytes, TGR5 mRNA is downregulated in the presence of neurosteroids and ammonia already at concentrations of 0.5 mmol L,1. Furthermore, TGR5 protein levels are significantly reduced in isolated rat astrocytes after incubation with ammonia. A marked downregulation of TGR5 mRNA is also found in cerebral cortex from cirrhotic patients dying with hepatic encephalopathy (HE) when compared with brains from noncirrhotic control subjects. It is concluded that TGR5 is a novel neurosteroid receptor in brain with implications for the pathogenesis of HE. © 2010 Wiley-Liss, Inc. [source] Pharmacology and safety of glycerol phenylbutyrate in healthy adults and adults with cirrhosis,,HEPATOLOGY, Issue 6 2010Brendan M. McGuire Phenylbutyric acid (PBA), which is approved for treatment of urea cycle disorders (UCDs) as sodium phenylbutyrate (NaPBA), mediates waste nitrogen excretion via combination of PBA-derived phenylacetic acid with glutamine to form phenylactylglutamine (PAGN) that is excreted in urine. Glycerol phenylbutyrate (GPB), a liquid triglyceride pro-drug of PBA, containing no sodium and having favorable palatability, is being studied for treatment of hepatic encephalopathy (HE). In vitro and clinical studies have been performed to assess GPB digestion, safety, and pharmacology in healthy adults and individuals with cirrhosis. GPB hydrolysis was measured in vitro by way of pH titration. Twenty-four healthy adults underwent single-dose administration of GPB and NaPBA and eight healthy adults and 24 cirrhotic subjects underwent single-day and multiple-day dosing of GPB, with metabolites measured in blood and urine. Simulations were performed to assess GPB dosing at higher levels. GPB was hydrolyzed by human pancreatic triglyceride lipase, pancreatic lipase-related protein 2, and carboxyl-ester lipase. Clinical safety was satisfactory. Compared with NaPBA, peak metabolite blood levels with GPB occurred later and were lower; urinary PAGN excretion was similar but took longer. Steady state was achieved within 4 days for both NaPBA and GPB; intact GPB was not detected in blood or urine. Cirrhotic subjects converted GPB to PAGN similarly to healthy adults. Simulations suggest that GPB can be administered safely to cirrhotic subjects at levels equivalent to the highest approved NaPBA dose for UCDs. Conclusion: GPB exhibits delayed release characteristics, presumably reflecting gradual PBA release by pancreatic lipases, and is well tolerated in adults with cirrhosis, suggesting that further clinical testing for HE is warranted. (HEPATOLOGY 2010;) [source] Can we ignore minimal hepatic encephalopathy any longer?,,HEPATOLOGY, Issue 3 2007Asif M. Qadri No abstract is available for this article. [source] Quantitative T1 mapping of hepatic encephalopathy using magnetic resonance imagingHEPATOLOGY, Issue 5 2003Nadim Joni Shah M.D. Changes are shown in the spin-lattice (T1) relaxation time caused by the putative deposition of manganese in various brain regions of hepatic encephalopathy (HE) patients using a novel and fast magnetic resonance imaging (MRI) method for quantitative relaxation time mapping. A new method, T1 mapping with partial inversion recovery (TAPIR), was used to obtain a series of T1 -weighted images to produce T1 maps. Imaging of 15 control subjects and 11 patients was performed on a 1.5T MRI scanner. The measurement time per patient with this technique, including adjustments, was ,5 minutes. Regions of interest in the globus pallidus, the caudate nucleus, the posterior and anterior limbs of the internal capsule, the putamen, the frontal and occipital white matter, the white matter of the corona radiata, the occipital visual and frontal cortices, and the thalamus were interactively defined in the left hemisphere and analyzed with respect to their T1 values. T1 changes in the brains of HE patients can be determined quantitatively with TAPIR in short, clinically relevant measurement times. Significant correlations between the change in T1 and HE severity have been shown in the globus pallidus, the caudate nucleus, and the posterior limb of the internal capsule. No significant correlation of T1 with grade of HE was found in the putamen, frontal white matter, white matter of the corona radiata, white matter in the occipital lobe, the anterior limb of the internal capsule, visual cortex, thalamus, or frontal cortex. In conclusion, these measurements show that T1 mapping is feasible in short, clinically relevant acquisition times. [source] Interorgan ammonia and amino acid metabolism in metabolically stable patients with cirrhosis and a TIPSSHEPATOLOGY, Issue 5 2002Steven W. M. Olde Damink Ammonia is central to the pathogenesis of hepatic encephalopathy. This study was designed to determine the quantitative dynamics of ammonia metabolism in patients with cirrhosis and previous treatment with a transjugular intrahepatic portosystemic stent shunt (TIPSS). We studied 24 patients with cirrhosis who underwent TIPSS portography. Blood was sampled and blood flows were measured across portal drained viscera, leg, kidney, and liver, and arteriovenous differences across the spleen and the inferior and superior mesenteric veins. The highest amount of ammonia was produced by the portal drained viscera. The kidneys also produced ammonia in amounts that equaled total hepatosplanchnic area production. Skeletal muscle removed more ammonia than the cirrhotic liver. The amount of nitrogen that was taken up by muscle in the form of ammonia was less than the glutamine that was released. The portal drained viscera consumed glutamine and produced ammonia, alanine, and citrulline. Urea was released in the splenic and superior mesenteric vein, contributing to whole-body ureagenesis in these cirrhotic patients. In conclusion, hyperammonemia in metabolically stable, overnight-fasted patients with cirrhosis of the liver and a TIPSS results from portosystemic shunting and renal ammonia production. Skeletal muscle removes more ammonia from the circulation than the cirrhotic liver. Muscle releases excessive amounts of the nontoxic nitrogen carrier glutamine, which can lead to ammonia production in the portal drained viscera (PDV) and kidneys. Urinary ammonia excretion and urea synthesis appear to be the only way to remove ammonia from the body. [source] Oxidative stress and hippocampus in a low-grade hepatic encephalopathy model: protective effects of curcuminHEPATOLOGY RESEARCH, Issue 11 2008Diego Martín Roselló Aim:, The present study was performed on prehepatic portal hypertensive rats, a model of low-grade hepatic encephalopathy, designed to evaluate whether oxidative stress was a possible pathway implicated in hippocampal damage and if so, the effect of an anti-oxidant to prevent it. Methods:, Prehepatic portal hypertension was induced by a regulated portal vein stricture. Oxidative stress was investigated by assessing related biochemical parameters in rat hippocampus. The effect of the anti-oxidant curcumin, administered in a single i.p. dose of 100 mg/kg on the seventh, ninth and eleventh days after surgery, was evaluated. Results:, Oxidative stress in the rat hippocampal area was documented. Curcumin significantly decreased tissue malondialdehyde levels and significantly increased glutathione peroxidase, catalase and superoxide dismutase activities in the hippocampal tissue of portal hypertensive rats. Conclusion:, Oxidative stress was found to be implicated in the hippocampal damage and curcumin protected against this oxidative stress in low-grade hepatic encephalopathic rats. These protective effects may be attributed to its anti-oxidant properties. [source] Acute liver failure and living donor liver transplantationHEPATOLOGY RESEARCH, Issue 2008Nobuhisa Akamatsu Acute liver failure (ALF) is defined by the presence of hepatic encephalopathy due to severe liver damage in patients without pre-existing liver disease. Although the mortality of ALF without liver transplantation is over 80%, the survival rates of ALF patients have improved considerably with the advent of liver transplantation, up to 60,80% in the last decade. Living donor liver transplantation (LDLT), which has mainly evolved in Asian countries where organ availability from deceased donors is extremely scarce, has also improved the survival rate of ALF patients. According to recent reports, the overall survival rate of adult ALF patients who underwent LDLT is 60% to 90%. Although there is still controversy regarding the graft type, the optimal graft volume, and ethical issues of defining the indications for LDLT in ALF patients with respect to donor risk, LDLT has become an established treatment option for ALF in areas where the use of deceased donors organs is severely restricted. [source] Cocirculation of and coinfections with hepatitis A virus subgenotypes IIIA and IB in patients from Pune, western IndiaHEPATOLOGY RESEARCH, Issue 2 2007Shobha Chitambar Aim:, During the 1990s, a changing pattern of epidemiology of hepatitis A was reported in different populations of India. The present study was undertaken to investigate the molecular epidemiology of hepatitis A virus (HAV) strains over a period of 10 years. Methods:, Stool/serum samples were collected from hepatitis A patients clinically presenting acute viral hepatitis and hepatic encephalopathy. Reverse transcriptase polymerase chain reaction (RT-PCR) was performed to detect HAV-RNA. HAV genomes were examined by sequencing PCR products of VP1/2A junction (168 bp) and RNA polymerase (116 bp) regions. Results:, Subgenotype IIIA and IB were detected in 74.2% and 9.7% of specimens, respectively, while 16.1% of patients had mixed infections. Sewage samples also showed presence of both IIIA (9/10) and IB (1/10) subgenotypes. RNA polymerase region showed two clusters constituting 51.6% and 19.4% strains closer to Nor21 and HM175 strains, respectively, in clinical specimens. Three isolates appeared as discordant subgenotypes in VP1/2A and RNA polymerase regions. Conclusion:, The data revealed cocirculation of and coinfection with subgenotypes IIIA and IB, with predominance of IIIA and genetic heterogeneity of HAV strains in western India. [source] Discontinuation of penicillamine in the absence of alternative orphan drugs (trientine,zinc): a case of decompensated liver cirrhosis in Wilson's diseaseJOURNAL OF CLINICAL PHARMACY & THERAPEUTICS, Issue 1 2007C. C. Ping MPharm Summary Objectives:, To report a case of early-decompensated liver cirrhosis secondary to discontinuation of penicillamine therapy in a patient with Wilson's disease. Case summary:, A 33-year-old Chinese female patient was diagnosed with Wilson's disease, for which penicillamine 250 mg p.o. once daily was prescribed. However, the patient developed intolerance and penicillamine was discontinued without alternative treatment. Five months later, she developed decompensated liver cirrhosis with hepatic encephalopathy. Eventually, the patient died because of the complications of sepsis and decompensated liver failure. Discussion:, Chelating agent is the mainstay of treatment in Wilson's disease, which is an inherited disorder of hepatic copper metabolism. Therapy must be instituted and continued for life once diagnosis is confirmed. Interruption of therapy can be fatal or cause irreversible relapse. Penicillamine given orally is the chelating agent of first choice. However, its unfavourable side-effects profile leads to discontinuation of therapy in 20,30% of patients. In most case reports, cessation of penicillamine without replacement treatment causes rapid progression to fulminant hepatitis, which is fatal unless liver transplantation is performed. Conclusion:, In this, we highlight a case of discontinuation of penicillamine in a patient with Wilson's disease without substitution with alternative regimen. This was caused by unavailability of the alternative agents such as trientine in our country. Consequently, the patient progressed to decompensated liver cirrhosis with encephalopathy and eventually passed-away within 5 months. One recent study supports a combination of trientine and zinc in treating patient with decompensated liver cirrhosis. This combination is capable of reversing liver failure and prevents the need of liver transplantation. Both trientine and zinc are not registered in Malaysia. Therefore, liver transplantation was probably the only treatment option for this patient. Hence, non-availability of orphan drugs in clinical practice is certainly a subject of serious concern. Systems for better management of patients with rare diseases need to be instituted by all the institutions concerned. [source] Minimal hepatic encephalopathy: Consensus statement of a working party of the Indian National Association for Study of the LiverJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 6 2010Radha K Dhiman Abstract Hepatic encephalopathy (HE) is a major complication that develops in some form and at some stage in a majority of patients with liver cirrhosis. Overt HE occurs in approximately 30,45% of cirrhotic patients. Minimal HE (MHE), the mildest form of HE, is characterized by subtle motor and cognitive deficits and impairs health-related quality of life. The Indian National Association for Study of the Liver (INASL) set up a Working Party on MHE in 2008 with a mandate to develop consensus guidelines on various aspects of MHE relevant to clinical practice. Questions related to the definition of MHE, its prevalence, diagnosis, clinical characteristics, pathogenesis, natural history and treatment were addressed by the members of the Working Party. [source] Major adverse events, pretransplant assessment and outcome predictionJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 11 2009Hui-Chun Huang Abstract Liver cirrhosis and portal hypertension pose enormous loss of lives and resources throughout the world, especially in endemic areas of chronic viral hepatitis. Although the pathophysiology of cirrhosis is not completely understood, the accumulating evidence has paved the way for better control of the complications, including gastroesophageal variceal bleeding, hepatic encephalopathy, ascites, hepatorenal syndrome, hepatopulmonary syndrome and portopulmonary hypertension. Modern pharmacological and interventional therapies have been designed to treat these complications. However, liver transplantation (LT) is the only definite treatment for patients with preterminal end-stage liver disease. To pursue successful LT, the meticulous evaluation of potential recipients and donors is pivotal, especially for living donor transplantation. The critical shortage of cadaveric donor livers is another concern. In many Asian countries, cultural and religious concerns further limit the number of the donors, which lags far behind that of the recipients. The model for end-stage liver disease (MELD) scoring system has recently become the prevailing criterion for organ allocation. Initial results showed clear benefits of moving from the Child,Turcotte,Pugh-based system toward the MELD-based organ allocation system. In addition to the MELD, serum sodium is another important prognostic predictor in patients with advanced cirrhosis. The incorporation of serum sodium into the MELD could enhance the performance of the MELD and could become an indispensable strategy in refining the priority for LT. However, the feasibility of the MELD in combination with sodium in predicting the outcome for patients on transplant waiting list awaits actual outcome data before this becomes standard practice in the Asia,Pacific region. [source] Development and evaluation of the quality of life instrument in chronic liver disease patients with minimal hepatic encephalopathyJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 3 2009Ying-qun Zhou Abstract Objectives:, The objective was to develop a valid and reliable health-related quality of life (HRQOL) assessment tool to measure the functional and health status of patients with minimal hepatic encephalopathy (mHE). Methods:, Items potentially affecting the HRQOL of these patients were identified, based on the responses from 53 patients with minimal hepatic encephalopathy, from seven liver experts, four epidemiologists and from a PubMed search of the literature. Results were explored using factor analysis and redundant questions were eliminated. The final stated questionnaire was used in 178 patients with mHE to evaluate its reliability and validity. Results:, Thirty-five items proved to be important for 32 respondents in the item reduction sample. The final instrument included five domains (30 items) which were shown as follows: physical functioning (8 items), psychological well-being (7 items), symptoms/side effects (7 items), social functioning (4 items) and general-health (4 items). An inter-item correlation for each of the five domains ranged from 0.220 to 0.776, with a mean of 0.280. Cronbach's alpha for above five domains was 0.8775, 0.8446, 0.8360, 0.7087 and 0.7016 respectively. The test-retest coefficients for the five domains were 0.94, 0.93, 0.96, 0.82 and 0.83 respectively. Factor analysis showed preservation of five components structure. Cumulative variance of principal components was 63.12%. Patients with more advanced disease seemed to have more impairment of their well-being, especially in the symptoms/side effects domain. Conclusions:, The instrument is short, easy to administer and is of good validity and reliability in patients with mHE. [source] Malnutrition and hypermetabolism are not risk factors for the presence of hepatic encephalopathy: A cross-sectional studyJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 4 2008Peter Sörös Abstract Background and Aim:, Hepatic encephalopathy is a frequent complication of cirrhosis. The present retrospective investigation was conducted to characterize metabolic alterations in cirrhotic patients with and without hepatic encephalopathy. We tested the hypothesis that reduced nutritional status or the degree of tissue catabolism are associated with the presence of hepatic encephalopathy. Methods:, We investigated 223 patients with histologically confirmed nonalcoholic cirrhosis without hepatic encephalopathy and with hepatic encephalopathy (grades 1,3). To assess liver function, nutritional status, and energy metabolism, a variety of biochemical and clinical tests were performed including anthropometric measurements, bioelectrical impedance analysis, and indirect calorimetry. Results:, Nutritional status and tissue catabolism were not significantly different between patients with and without hepatic encephalopathy. Conclusions:, Our data do not support the hypothesis that malnutrition or tissue catabolism are independent risk factors for the presence of hepatic encephalopathy in patients with nonalcoholic cirrhosis. [source] Spontaneous bacterial peritonitis and bacterascites prevalence in asymptomatic cirrhotic outpatients undergoing large-volume paracentesisJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2 2008José Castellote Abstract Background and Aim:, Spontaneous bacterial peritonitis and bacterascites prevalence in asymptomatic cirrhotic patients on large-volume paracentesis is unknown. The aim of this study was to investigate spontaneous bacterial peritonitis and bacterascites prevalence in a prospective cohort of cirrhotic outpatients following large-volume paracentesis with low risk of infection. Methods:, We prospectively studied all large-volume paracenteses performed in cirrhotic outpatients for 1 year. Patients with fever, abdominal pain, peritonism or hepatic encephalopathy were excluded from the study. The ascitic fluid was analyzed by means of a reagent strip with a colorimetric scale from 0 to 4. A strip test of 0 or 1 was considered negative. In those cases with a reagent strip ,2, conventional polymorphonuclear count was performed. Ascitic fluid culture was done into blood culture bottles in all cases. Results:, We performed 204 paracenteses in 40 patients. Nine cases were excluded. Culture-negative neutrocytic ascites was diagnosed in one case (0.5%), while bacterascites was diagnosed in six out of 195 cases (3%), mainly by gram-positive cocci. Conclusion:, The spontaneous bacterial peritonitis prevalence in outpatient cirrhotics with low risk of infection undergoing large-volume paracentesis is very low. Moreover, the prevalence of bacterascites is low and without clinical consequences. The routine analysis of ascitic fluid may be unnecessary in this clinical setting. Nevertheless, the use of reagent strips is a reasonable alternative due to its accessibility and low cost. [source] Detrimental effects of nitric oxide inhibition on hepatic encephalopathy in rats with thioacetamide-induced fulminant hepatic failure: Role of nitric oxide synthase isoformsJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 7 2006Chi-Jen Chu Abstract Background:, Hepatic encephalopathy is a complex neuropsychiatric syndrome. A previous study showed that chronic nitric oxide (NO) inhibition aggravated the severity of encephalopathy in thioacetamide (TAA)-treated rats. The present study investigated the relative contribution of NO synthase (NOS) isoforms on the severity of hepatic encephalopathy in TAA-treated rats. Method:, Fulminant hepatic failure was induced in male Sprague-Dawley rats by intraperitoneal injection of TAA (350 mg/kg/day) for 3 days. Rats were divided into three groups to receive N, -nitro-L-arginine methyl ester (L-NAME, a non-selective NOS inhibitor, 25 mg/kg/day in tap water), L-canavanine (an inducible NOS inhibitor, 100 mg/kg/day via intraperitoneal injection) or normal saline (N/S) from 2 days prior to TAA administration and lasting for 5 days. Severity of encephalopathy was assessed by the counts of motor activity. Plasma levels of tumor necrosis factor-, (TNF- ,) were determined by enzyme-linked immunosorbent assay (ELISA), and total bilirubin, alanine aminotransferase (ALT) and creatinine were determined by colorimetric assay. Results:, Compared with L-canavanine or N/S-treated rats (0% and 4%, respectively), the mortality rate was significantly higher in rats receiving L-NAME administration (29%, P < 0.005). Inhibition of NO created detrimental effects on the counts of motor activities (P < 0.05). Rats treated with L-NAME had significantly higher plasma levels of total bilirubin, ALT, creatinine and TNF- , as compared with rats treated with L-canavanine or N/S (P < 0.01). Conclusion:, Chronic L-NAME administration, but not L-canavanine, had detrimental effects on the severity of hepatic damage and motor activities in TAA-treated rats. These results suggest that constitutive NOS activities play a major protective role in rats with fulminant hepatic failure. [source] Magnetic resonance images of the globus pallidus in patients with idiopathic portal hypertension: A quantitative analysis of the relationship between signal intensity and the grade of portosystemic shuntJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 5 2006Takeshi Fukuzawa Abstract Background and Aim:, To elucidate a quantitative relationship between hyperintensity of the globus pallidus on T1-weighted magnetic resonance images (MRI) and portosystemic shunt (PSS) in portal hypertension. Methods:, Fifteen patients with idiopathic portal hypertension (IPH) and 44 patients with liver cirrhosis (LC) underwent brain MRI to asses signal intensity at the globus pallidus and Doppler sonography to examine the blood flow volume of PSS. Blood manganese (Mn) levels were examined in 36 patients and neuropsychological tests were performed in 15 patients without overt hepatic encephalopathy. Results:, Pallidal hyperintensity on MRI was more prominent in patients with IPH than in patients with LC. There was no correlation between MRI pallidal hyperintensity and the severity of liver dysfunction or hepatic encephalopathy. The grade of hyperintensity correlated well with the grade of PSS. The correlation was stronger in patients with IPH than in patients with LC. The plasma ammonia level and whole blood Mn level significantly correlated with MRI pallidal hyperintensity, but blood Mn level showed a stronger correlation than plasma ammonia. Conclusion:, Hyperintensity of the globus pallidus on T1-weighted MRI correlated with the development of PSS independent of liver cell function. This brain image should be an index of the grade of PSS rather than a landmark of chronic liver failure. [source] Subclinical hepatic encephalopathy: Elusive ,gold standard'JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 1 2004PARAMPREET S KHARBANDA No abstract is available for this article. [source] Value of regional cerebral blood flow in the evaluation of chronic liver disease and subclinical hepatic encephalopathyJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 10 2003YUSUF YAZGAN Abstract Aims:, Regional changes in cerebral blood flow in patients with chronic hepatitis, cirrhosis and subclinical hepatic encephalopathy were investigated in the present study using single photon emission computed tomography (SPECT). Methods:, Twenty patients with cirrhosis, 11 patients with chronic hepatitis, and nine healthy controls were included in the study. Cerebral SPECT were obtained for all patients. The percentages of cerebral blood flow of 14 regions to the cerebellar blood flow were determined. Only the patients with cirrhosis underwent psychometric evaluation: visual evoked potentials (VEP) measurements and electroencephalogram (EEG) recordings along with blood levels of albumin, bilirubin, and ammonia were measured and prothrombin time was determined in cirrhotic patients. These patients were classified according to the Child,Pugh classification. Results:, Among cirrhotic patients, six had abnormal results in VEP studies, 11 in psychometric tests and with six in EEG evaluation. Any abnormality in psychometric tests and/or VEP studies is taken as the main criterion; subclinical hepatic encephalopathy was detected in 12 of 20 patients. According to SPECT results in patients with subclinical encephalopathy, a statistically significant decrease in cerebral blood flow in right thalamus and nearly significant decrease in left thalamus were observed. Regional blood flow was significantly higher in the frontal lobes of patients with cirrhosis when compared with healthy controls. Similarly, cerebral blood flow in frontal and cingulate regions was significantly higher in patients with chronic hepatitis than in healthy controls. There was no relationship between cerebral blood flow and blood levels of ammonia or Child,Pugh score, in cirrhotic patients. Conclusion:, Significant changes in cerebral blood flow may be present in chronic liver diseases and the authors suggest that the measurement of changes in cerebral blood flow might be useful in detecting subclinical hepatic encephalopathy. [source] Spontaneous regression of hepatocellular carcinoma and review of literatureJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 9 2000Yoshio Takeda Abstract A 68-year-old man presented with multiple hepatocellular carcinoma, which was considered to be unresectable at the first admission in January 1994. Pathological diagnosis was made by biopsy of the one lesion among them. From January 1994 to December 1997, 10 transarterial chemoembolizations and six percutaneous ethanol injection therapies were performed on the tumours in the cirrhotic liver. In February 1998 the tumour situated in the right lobe began to increase in size. The maximum tumour diameter was 6.3 cm measured by computed tomography (CT). In the beginning of May 1998 moderate ascites was present and mild hepatic encephalopathy was noticed. The patient was in the terminal stage of hepatocellular carcinoma and no further treatment was possible at that time. However, serum ,-fetoprotein and protein induced by vitamin K absence or antagonist II dramatically decreased in June 1998. The CT scan also showed that the tumour had completely regressed without specific treatment. In February 1999 a new biopsy-proven hepatocellular carcinoma, 2 cm in diameter, developed in the lateral segment of the liver. It was well treated by percutaneous ethanol injection therapy. The patient was alive in good condition without any symptoms or tumour recurrence in June 1999. It was concluded that a rare case of spontaneous regression of hepatocellular carcinoma had occurred. [source] Adding another spectral dimension to 1H magnetic resonance spectroscopy of hepatic encephalopathy,JOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 4 2005Nader Binesh PhD Abstract Purpose To evaluate a localized two-dimensional correlated magnetic resonance spectroscopic (L-COSY) technique in patients with hepatic encephalopathy (HE) and healthy subjects, and to correlate the cerebral metabolite changes with neuropsychological (NP) test scores. Materials and Methods Eighteen minimal hepatic encephalopathy (MHE) patients and 21 healthy controls have been investigated. A GE 1.5-T magnetic resonance (MR) scanner was used in combination with a body MR coil for transmission and a 3-inch surface coil for reception. A 27-mL voxel was localized by three slice-selective radio frequency (RF) pulses (90°-180°-90°) in the anterior cingulate region. The total duration of each two-dimensional L-COSY spectrum was approximately 25 minutes. The NP battery included a total of 15 tests, which were grouped into six domains. Results MR spectroscopic results showed a statistically significant decrease in myo-inositol (mI) and choline (Ch) and an increase in glutamate/glutamine (Glx) in patients when compared to healthy controls. There was also an increase in taurine (Tau) in patients. The NP results indicated a significant correlation between motor function assessed by NP tests and mI ratios recorded using two-dimensional L-COSY. Conclusion The study demonstrated the feasibility of evaluating the two-dimensional L-COSY sequence in a clinical environment. The results showed additional cerebral metabolites that can be measured with the technique in comparison to one-dimensional study. J. Magn. Reson. Imaging 2005;21:398,405. © 2005 Wiley-Liss, Inc. [source] Lamivudine monoprophylaxis and adefovir salvage for liver transplantation in chronic hepatitis B: A seven-year follow-up study,,JOURNAL OF MEDICAL VIROLOGY, Issue 2 2009Jenny L. Limquiaco Abstract In Asia Pacific countries, lamivudine is used frequently as the sole prophylaxis for hepatitis B virus (HBV) recurrence after liver transplantation due to financial consideration. The aim was to evaluate the long-term outcome of lamivudine monoprophylaxis with adefovir salvage for liver transplantation in chronic hepatitis B. Consecutive chronic hepatitis B patients who received liver transplantation from 1999 to 2003 and with at least 12 months follow up were studied. Lamivudine monotherapy was used for antiviral prophylaxis and adefovir was added as salvage treatment for recurrence of HBV. Twenty-four patients were followed up for 272 (76,372) weeks post-liver transplantation. HBV recurrence developed in seven patients with cumulative probabilities of 8%, 13%, 28%, 35%, 35%, and 49% in 1, 2, 3, 4, 5, and 6 years. At the time of recurrence of HBV, the HBV DNA level was 910,244 (363 to 9,×,108) copies/ml. On direct sequencing, four patients had rtM204I mutation and three patients HBV DNA levels were too low for sequencing. Six patients had elevated ALT (two patients had ALT >1,000 IU/L and jaundice) but none had hepatic encephalopathy. After adefovir treatment for 150 (91,193) weeks, six (86%) patients had normal ALT. HBV DNA was undetectable in two (29%) patients, 100,1,000 copies/ml in two (29%) patients and 10,000,100,000 copies/ml in three (43%) patients on last visit. No genotypic resistance to adefovir was detected. Lamivudine followed by adefovir salvage is effective for prophylaxis of recurrence of HBV after liver transplantation up to 7 years. J. Med. Virol. 81:224,229, 2009. © 2008 Wiley-Liss, Inc. [source] Protein kinase G is involved in ammonia-induced swelling of astrocytesJOURNAL OF NEUROCHEMISTRY, Issue 2009Agnieszka Konopacka Abstract Ammonia-induced swelling of astrocytes is a primary cause of brain edema associated with acute hepatic encephalopathy. Previous studies have shown that ammonia transiently increases cGMP in brain in vivo and in cultured astrocytes in vitro. We hypothesized that protein kinase G (PKG), an enzyme activated by cGMP and implicated in regulation of cell shape, size, and/or volume in peripheral and CNS cells, may play a role in the ammonia-induced astrocytic volume increase. Treatment of cultured rat cortical astrocytes with 1 or 5 mM NH4Cl (ammonia) for 24 h increased their cell volume by 50% and 80% above control, respectively, as measured by confocal imaging followed by 3D computational analysis. A cGMP analog, 8-(4-chlorophenylthio)-cGMP, increased the cell volume in control cells and potentiated the increase in 1 mM ammonia-treated cells. A soluble guanylate cyclase inhibitor (1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one) abrogated, and a PKG inhibitor [8-(4-chlorophenylthio)-cGMP-thioate, Rp-isomer] dose-dependently reduced the cell volume-increasing effect of 5 mM ammonia. The results suggest that (i) PKG may play a permissive role in ammonia-induced astrocytic swelling and (ii) elevation of brain cGMP associated with acute exposure to ammonia in vivo may aggravate the ensuing brain edema. [source] | |||||||||||||||||||||||||||||||