الملخص
BACKGROUND/AIMS: The Model for End-Stage Liver Disease (MELD) consists of serum bilirubin and creatinine levels, International Normalized Ratio (INR) for prothrombin time, and etiology of liver disease. The MELD score is a reliable measurement of mortality risk and is suitable for a disease severity index in patients with end-stage liver disease. We examined the validity of the MELD as a disease severity index for patients with end-stage liver disease. METHODS: We investigated the 379 patients with liver cirrhosis hospitalized between January 1995 and May 2001. We retrospectively reviewed the hospital records to verify the diagnosis of cirrhosis and to collect exact patient information about their demographic data, portal hypertensive complications and laboratory data. The ability to classify patients with liver cirrhosis according to their risk of death was examined using the concordance c-statistic. RESULTS: The MELD score performed well in predicting death within 3 months with a c-statistic of 0.73 with etiology and 0.71 without etiology. The significant clinical, laboratory variables on 3 month survival in patients with liver cirrhosis are serum bilirubin, ascites and hepatic encephalopathy. The addition of portal hypertensive complications to the MELD score did not improve the accuracy of the MELD score. CONCLUSIONS: The MELD score is a useful disease severity index for the patients with end-stage liver disease and provides reliable measurement of short term survival over a wide range of liver disease severity and diverse etiology.
الموضوعات
Adult , Female , Humans , Male , Middle Aged , Bilirubin/blood , Creatinine/blood , International Normalized Ratio , Liver Cirrhosis/blood , Risk Factors , Severity of Illness Index , Survival Rateالملخص
BACKGROUND/AIMS: During cryopreservation of hepatocytes, a dramatic loss in cell number, viability and differentiated cell function is usually inevitable because hepatocytes are very sensitive to stress during freezing and thawing. We tried to investigate the optimal cryopreservation conditions of hepatocytes including the constituents of the freezing medium and freezing rate. METHODS: Isolated hepatocytes were cryopreserved in media containing 10% glycerol or dimethyl sulfoxide (DMSO) of variable concentration. Different freezing procedures (stepwise, rapid, and programmed with or without shock cooling) were used and they were stored in a liquid nitrogen tank. After rapid thawing at 39degrees C, followed by dilution and removal of the cryopreservative, the ability of the hepatocytes to exclude trypan blue dye (TB) was evaluated. Hepatocytes were fractionated through a Nycodenz density gradient centrifugation (DGC) to eliminate dead cells. Cells were plated on dishes coated with type I collagen. RESULTS: Cell viability of hepatocytes recovered from cryopreservation was maintained better using 10, 15, and 20% DMSO as a cryopreservative and programmed cell freezer with shock cooling. After Nycodenz DGC a hepatocyte fraction highly enriched in viable cells could be taken between 11% and 30%. In culture, cryopreserved hepatocytes exhibited a morphology with epithelial characteristics. CONCLUSIONS: These results suggest that rate-adjusted programmed freezing with shock cooling and 10, 15 and 20% DMSO increased the viability of cryopreserved hepatocytes. The hepatocyte fraction highly enriched in viable cells could be taken using Nycodenz DGC. In order to establish a bank of hepatocytes for hepatocyte transplantations and artificial livers a more improved method is nevertheless necessary to increase the viability of hepatocytes after cryopreservation.
الموضوعات
Animals , Rats , Cell Count , Cell Culture Techniques , Cell Survival , Centrifugation, Density Gradient , Collagen Type I , Cryopreservation , Dimethyl Sulfoxide , Freezing , Glycerol , Hepatocytes , Iohexol , Liver, Artificial , Nitrogen , Shock , Trypan Blueالملخص
BACKGROUND AND AIMS: The overall age-matched incidence of gastroduodenal ulcers was considerably higher in cirrhotic patients compared to the general population. There are several possible underlying mechanisms which may explain the ulcerogenic factors in cirrhotic patients. Recently, Helicobacter pylori (H. pylori) was proven as the cause of peptic ulcer disease in the general population. But the role of H. pylori infection in the pathogenesis of peptic ulcers of cirrhotic patients has not been clearly elucidated. The purpose of this study was to determine the role of H. pylori infection in cirrhotic patients with peptic ulcers. METHODS: From 1995 to 1997, 105 patients with histologically or radiologically proven liver cirrhosis (LC) who received panendoscopic examination due to presence of any upper gastrointestinal symptoms were studied. During endoscopic examination, a CLO (campylobacter like organism) test or gastric antral mucosal biopsy was performed in all patients. The severity of LC assessed by Child's criteria revealed that 31 patients had Child's A, 26 patients Child's B, and the remain 48 patients, Child's C. Child B or C was classified as decompensated LC. An esophageal varix was present in 73 patients or absent in 32. RESULTS: There was no statistical difference in the H. pylori prevalance between the ulcer group and non-ulcer group (67% vs 52%). In Child A group, the H. pylori prevalence was significantly higher in the ulcer group when compared with the non-ulcer group (87% vs 50%, p<0.05). In contrast, in the Child B or C group, there was no statistical difference between the ulcer group and non-ulcer group. In the abscence of esophageal varix, the ulcer group showed significantly higher prevalence of H. pylori than the non-ulcer group (87% vs 59%, p<0.05). But in the esophageal variceal group, there was no significant difference in the H. pylori prevalence between the ulcer and non-ulcer group (60% vs 40%). CONCLUSIONS: These observations suggest that H. pylori infection may play a role in the pathogenesis of peptic ulcer in compensated cirrhotic patients. However, in cirrhotic patients with decompensation or an esophageal varix, the association between H. pylori infection and peptic ulcers was weak, so other factors (portal hypertension etc.) should be considered as more potent etiology of peptic ulcers in cases of decompensated cirrhosis.
الموضوعات
Child , Humans , Biopsy , Esophageal and Gastric Varices , Fibrosis , Helicobacter pylori , Helicobacter , Hypertension , Incidence , Liver Cirrhosis , Peptic Ulcer , Prevalence , Ulcerالملخص
BACKGROUND: The anticoagulant efficacy of low molecular weight heparin (LMWH) as an alternative substitute for standard heparin (SH) was evaluated by measuring thrombin-antithrombin complex (TAT) and tissue factor pathway inhibitor (TFPI). METHODS: Twenty-two patients with coronary artery disease (CAD) were divided into three groups and plasma heparin concentration, platelet count, aPTT, TAT and TFPI before and after injection of SH and LMWH were measured. RESULTS: Plasma heparin concentrations were well correlated after the injection of heparin in group B (LMWH 200 U/kg) and C (LMWH 240 U/kg), but not in group A (SH). Platelet counts were not decreased in most patients and life-threatened bleeding was not observed in any patients. APTT prolongations were observed in all patients of SH group, but not in any patients of B and C. TAT levels were not significantly different between groups. TFPI levels were not significantly different between groups. Heparin levels were well correlated with TFPI levels, but not with TAT levels. CONCLUSION: The anticoagulant effect of LMWH up to 240 U/kg/D was not superior over SH in CAD patients, although it has several merits such as no requirement of aPTT monitoring or better predictability.
الموضوعات
Humans , Coronary Artery Disease , Coronary Vessels , Hemorrhage , Heparin , Heparin, Low-Molecular-Weight , Plasma , Platelet Count , Thromboplastinالملخص
BACKGROUND/AIMS: The aim of this study was to evaluate the effect of alpha-interferon (IFN) on liver histology as well as on activation of hepatic stellate cell ( HSC) and trans for ming growth fact or beta-1 (TGF beta-1) expression. We had also investigated the clinical usefulness of TGFbeta-1 and alpha-smooth muscle actin (alpha-SMA) expression in liver tissue for predicting a response to alpha-IFN therapy in chronic hepat it is B. METHODS: We studied the expression of TGFbeta-1 and alpha-SMA in liver biopsys pecimens from 51 chronic hepatitis B pat ients. Using immunohistochemical staining and a semiquant it ative scoring met hod, we also evaluated TGF-beta1 and alpha-SMA expression in liver stellate cells before and after alpha-IFN therapy in liver tissue from rebiopsys pecimen of the 12 chronic hepatitis B pat ients. Recombinant IFN alpha-2b (Intron A) in doses of 6 MU/ d was given to patients intramus cularly three times per week for 6 months (total doses , 432 MU). The patients were divided into two groups according to serum alanine aminotransferase levels as well as HBV- DNA and HBeAg s eroconversion stat e. Histological grading and staging scores were according to modified Histological Activity Index (HAI) grading systems of Ishak (1995). RESULTS: The index of portal inflammation and total scores of HAI grading significantly decreased in biopsies after alpha-IFN treatment, but the scores of fibrosis staging showed no significant change in biopsies after IFN treatment. A significant decrease in alpha-SMA expression, especially in periportal area, was found, but the change of TGFbeta-1 expression was not significant. The immunoreactivity of alpha-SMA was significantly lower in responders than in non-responders, whereas the diffference of immunoreactivity of TGF-beta1 between these two groups was not found. CONCLUSIONS: These findings suggest that alpha-IFN therapy may reduce the necroinflammatory activity in liver tissues of chronic B viral hepatitis and that the degree of alpha-SMA expression before treatment may be employed as a pottent predicting indicator for the therapeutic efficacy of IFN-alpha.