|
| ||
|
|
||
Abnormal Liver Tests (abnormal + liver_test)
Selected AbstractsSmall-for-size liver syndrome after auxiliary and split liver transplantation: Donor selectionLIVER TRANSPLANTATION, Issue 9 2003Nigel Heaton Small-for-size liver grafts can be defined by a recognizable clinical syndrome that results from the transplantation of too small a functional mass of liver for a designated recipient. A graft to recipient body weight ratio less than 0.8, impaired venous inflow, and enhanced metabolic demands in patients with poor clinical conditions must be considered as main factors leading to the small-for-size syndrome (SFSS) when using living and cadaveric partial grafts such as split and auxiliary liver grafts. Increased risk of graft dysfunction is currently observed in fatty infiltration of more than 30%, abnormal liver test results (especially bilirubin and gamma glutaryl transferase), and other donor risk factors such as high inotrope administration and donor stay in the intensive care unit (>5 days). Older donors are especially vulnerable to prolonged cold ischemia and high inotrope levels, giving rise to early graft dysfunction and prolonged cholestasis. Increased metabolic need on a functionally small-for-size graft predisposes to surgical and septic complications and poorer survival. Splitting livers into right and left lobe grafts increases the potential risk of small-for-size grafts for both recipients. Several techniques of venous outflow reconstruction/implantation have been proposed to reduce the risk of obstruction postoperatively. Prevention and management of SFSS will improve in parallel with the increased experience, allowing us optimum usage of available organs and reducing overall morbidity and mortality. (Liver Transpl 2003;9:S26-S28.) [source] Exercise-induced cholangitis and pancreatitisHPB, Issue 2 2005JOHN G. TOUZIOS Abstract Background. Cholangitis requires bactibilia and increased biliary pressure. Pancreatitis may be initiated by elevated intraductal pressure. The sphincter of Oddi regulates pancreatobiliary pressures and prevents reflux of duodenal contents. However, following biliary bypass or pancreatoduodenectomy, increased intra-abdominal pressure may be transmitted into the bile ducts and/or pancreas. The aim of this analysis is to document that cholangitis or pancreatitis may be exercise-induced. Methods. The records of patients with one or more episodes of cholangitis or pancreatitis precipitated by exercise and documented to have patent hepatico- or pancreatojejunostomies were reviewed. Cholangitis was defined as fever with or without abdominal pain and transiently abnormal liver tests. Pancreatitis was defined as abdominal pain, with transient elevation of serum amylase and documented by peripancreatic inflammation on computerized tomography. Results. Twelve episodes of cholangitis occurred in six patients who had undergone hepaticojejunostomy for biliary stricture (N=3), Type I choledochal cyst (N=2), or pancreatoduodenectomy for renal cell carcinoma metastatic to the pancreas (N=1). Four episodes of pancreatitis occurred in two patients who had undergone pancreatoduodenectomy for ampullary carcinoma or chronic pancreatitis. Workup and subsequent follow-up for a median of 21 months have not documented anastomotic stricture. Each episode of cholangitis and pancreatitis was brought on by heavy exercise and avoidance of this level of exercise has prevented future episodes. Conclusion. Following biliary bypass or pancreatoduodenectomy, significant exercise may increase intra-abdominal pressure and cause cholangitis or pancreatitis. Awareness of this entity and behavior modification will avoid unnecessary procedures in these patients. [source] Effect of a lifestyle intervention in patients with abnormal liver enzymes and metabolic risk factorsJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 3 2009Alexis St. George Abstract Background and Aim:, Non-alcoholic fatty liver disease associated with insulin resistance is the most common cause of abnormal liver tests in clinical practice. To date, practical and effective strategies to improve the metabolic profile of this large group of patients have not been well characterised. We sought to assess the effect at 3 months of a behavior change-based lifestyle intervention on the metabolic profile of patients characterised by elevated liver enzymes. Methods:, A total of 152 patients with elevated liver enzymes, central obesity and a range of metabolic risk factors were randomised to either a moderate- (6 sessions/10 weeks) or low-intensity (3 sessions/4 weeks) lifestyle counselling intervention or control group. Results:, There was improvement in all metabolic risk factors in the moderate-intensity group, versus a smaller number of changes in the low-intensity intervention group and no change in any metabolic risk factors in control subjects. Reduction in liver enzymes was greatest in the moderate-intensity intervention group and least in the control group. The likelihood of elevated alanine aminotransferase (ALT) levels in both the moderate and low-intensity groups was reduced by over 70% compared to controls. The proportion of subjects achieving weight loss (, 2%) was significantly higher in the moderate-intensity intervention group (66%) versus the low-intensity intervention group (39%; P < 0.05) and controls (29%; P < 0.001). Conclusions:, Moderate and even low-intensity lifestyle counselling interventions targeting improvement in physical activity and nutritional behaviors and modest weight loss are a practical and effective method for improving the health of patients with elevated liver enzymes and a range of metabolic risk factors. [source] Predictive Factors for Pure Steatosis in Alcoholic PatientsALCOHOLISM, Issue 6 2009Sylvie Naveau Background:, Bearing in mind the mechanisms involved in nonalcoholic fatty liver disease, this study aims to verify whether metabolic syndrome or its various individual components are independent predictive factors for steatosis ,10% in alcoholic patients. Methods:, This study included 281 consecutive alcoholic patients with abnormal liver tests and either normal liver histology or steatosis <10% (n = 119) or steatosis ,10% (n = 162). Logistic regression analysis was used to study the relationship between metabolic syndrome components and various risk factors and the presence of steatosis ,10%. We assessed apolipoprotein A1 (ApoA-1) levels, a major protein component of plasma high-density lipoprotein (HDL), rather than HDL-cholesterol levels. Results:, Plasma ApoA-1 levels (p < 0.01), body mass index (BMI) (p < 0.01), and waist circumference (p < 0.05) were significantly higher in patients with steatosis ,10% than in patients with normal liver histology or steatosis <10%. A higher percentage of patients with steatosis ,10% had high blood pressure (p = 0.003) than patients with normal liver histology or steatosis <10%. In the logistic regression, ApoA-1 [odds ratio (OR) = 1.57 (1.10,2.22)], BMI [OR = 1.10 (1.01,1.23)], and high blood pressure [OR = 1.84 (1.10,3.06)] were positively and independently correlated with the presence of steatosis ,10%. In the multivariate regression high blood pressure was independently and positively correlated with steatosis score (r = 0.55 ± 0.26; p < 0.05). On the other hand, when the presence of high blood pressure was the dependent variable, the presence of steatosis ,10% positively and independently correlated with it [OR = 1.82 (1.05,3.15)]. Conclusion:, In alcoholic patients without fibrosis, ApoA-1, BMI, and high blood pressure on the next morning after the admission were predictive of steatosis ,10%. High blood pressure was the only metabolic syndrome component associated with the presence of alcoholic steatosis ,10% and was not correlated with other metabolic syndrome components. These findings suggest that steatosis mechanisms are different in alcoholic and nonalcoholic fatty liver. [source] Liver pathology in compound heterozygous patients for hemochromatosis mutationsLIVER INTERNATIONAL, Issue 4 2002Maximilian Schöniger-Hekele Abstract: Background: While hepatic pathology of homozygous carriers of the C282Y mutation of the HFE haemochromatosis gene is well defined, the impact of the C282Y/H63D compound heterozygous carrier state is unknown. Aims: To evaluate the range of hepatic pathology in C282Y/H63D compound heterozygous patients. Patients: 25 C282Y/H63D compound heterozygous patients with and without known underlying liver disease underwent liver biopsies for evaluation or abnormal liver tests. Eleven cadaveric liver donors with HFE wild type served as controls. Methods: Mutations in the HFE gene were detected by polyacrylamide gel electrophoresis (PAGE) separation of digested polymerase chain reaction (PCR)-amplificates. The extent of light microscopic changes of liver architecture were studied on haematoxylin, eosin (H. E.) stains. In addition, the extent and the distribution of iron deposition was graded on Prussian blue-stained sections and hepatic iron was quantified by atom absorption spectroscopy. Serum ferritin concentration and the transferrin saturation index were measured using routine laboratory methods. Results: Patients without underlying liver disease (n = 15): Hepatic inflammation was seen in only 8% but fibrosis was found in 36% of compound heterozygous patients. Eighty six percent of those patients had stainable iron predominantly found in Rappaport's zone 1 and 2, but all had a liver iron-index < 1.9. Transferrin saturation was found elevated in 36% of compound heterozygous patients. Patients with liver fibrosis showed significantly higher ferritin levels than patients without liver fibrosis (1110 ng/mL versus 307 ng/mL, p < 0.05). Patients with underlying disease (n = 10): In compound heterozygous patients, 77% had hepatic inflammation and 88% fibrosis. Stainable iron (44%) was less frequently found than in patients without underlying liver disease. Hepatic iron-index in patients with underlying liver disease was always below 1.17; transferrin saturation was elevated in only 22% of the compound heterozygous patients. Histologic hepatic iron-index was significantly lower in patients with underlying disease (median 0.047) as compared to patients without underlying liver disease (median 0.274, P < 0.05). Conclusions: The underlying liver disease determines the extent of hepatic pathology seen in livers of compound heterozygous patients. However, considerable histologic fibrosis can also be found in compound heterozygous patients without underlying liver disease. [source] | ||||||||||