CAC did not significantly different from SC in term of cecal intubation time and polyp detection rate.

Long-term lamivudine monotherapy was effective in preventing development of HBV infection in HBsAg-negative liver transplant recipients from HBcAb-positive donors.

The aim of this study was to examine the importance of the serum hepatitis C viral load within the first year post-liver transplant in determining posttransplant survival. A retrospective analysis of 118 consecutive hepatitis C virus-positive liver transplant recipients who received an allograft from January 1997 to September 2005 was undertaken with a median duration of follow-up of 32.4 months. Univariate and multivariate analyses were used to examine the effects of recipient, donor, surgical, and viral factors on posttransplant outcomes. A total of 620 viral load estimations were undertaken in the first 12 months following transplantation. Patient and graft survival rates at 1, 3, and 5 years were 87.8%, 79.9%, and 70.1% and 87.0%, 79.2%, and 68.2%, respectively. According to multivariate analysis, a peak viral load Ն 10 7 IU/mL (P ϭ 0.004; hazard ratio, 8.68; 95% confidence interval, 2.04-37.02) and exposure to antirejection therapy (P ϭ 0.05; hazard ratio, 2.26; 95% confidence interval, 1.01-5.38) were both independent predictors of diminished patient and graft survival and hepatitis C-related allograft failure. The only other independent predictor of hepatitis C virus-related outcome after transplant was azathioprine use, which was associated with improved outcomes (P ϭ 0.04; hazard ratio, 0.25; 95% confidence interval, 0.07-0.91). A peak viral load in the first year after transplant of Ͼ10 8 , 10 7 to 10 8 , and Ͻ10 7 IU/mL was associated with a mean survival of 11.8, 70.6, and 89.1 months respectively (P Յ 0. Cirrhosis related to chronic infection with hepatitis C virus (HCV) has emerged as the most frequent indication for orthotopic liver transplantation. Presently, approximately 50% of transplants performed in the United States and Europe are for patients infected with HCV.1 The health burden due to HCV is expected to increase to such a degree that by the year 2020, the proportion of untreated HCV patients developing cirrhosis will have increased by 30%.1 Furthermore, it is projected that the number of HCV patients with cirrhosis will double and the number of HCV patients with cirrhosis developing hepatocellular carcinoma (HCC) will increase by 80%.

Background: Intrahepatic expression of dipeptidyl peptidase-4 (DPP4), and circulating DPP4 (cDPP4) levels and its enzymatic activity, are increased in non-alcoholic fatty liver disease (NAFLD) and in type 2 diabetes mellitus and/or obesity. DPP4 has been implicated as a causative factor in NAFLD progression but few studies have examined associations between cDPP4 activity and NAFLD severity in humans. This study aimed to examine the relationship of cDPP4 activity with measures of liver disease severity in NAFLD in subjects with diabetes and/or obesity. Methods: cDPP4 was measured in 106 individuals with type 2 diabetes who had transient elastography (Cohort 1) and 145 individuals with morbid obesity who had liver biopsy (Cohort 2). Both cohorts had caspase-cleaved keratin-18 (ccK18) measured as a marker of apoptosis. Results: Natural log increases in cDPP4 activity were associated with increasing quartiles of ccK18 (Cohorts 1 and 2) and with median liver stiffness ≥10.3 kPa (Cohort 1) and significant fibrosis (F ≥ 2) on liver biopsy (Cohort 2). Conclusions: In diabetes and/or obesity, cDPP4 activity is associated with current apoptosis and liver fibrosis. Given the pathogenic mechanisms by which DPP4 may progress NAFLD, measurement of cDPP4 activity may have utility to predict disease progression and DPP4 inhibition may improve liver histology over time.

CE may detect the presence and extent of SB metastases in patients with melanoma more reliably than conventional investigations. It should be considered in the workup of melanoma patients with suspected SB disease.

Currently, CE is not reliable to visualize the AoV and by inference the proximal duodenum. This is most likely related to the speed at which the capsule passes through the fixed second part of the duodenum. Faster frame rates plus a wider field of view do not overcome this limitation, which could account for missed lesions elsewhere in the small bowel.

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