Cap-assisted colonoscopy and detection of Adenomatous Polyps (CAP) study: a randomized trial.

BACKGROUND AND STUDY AIM: Cap-assisted colonoscopy has improved adenoma detection in some but not other studies. Most previous studies have been limited by small sample sizes and few participating endoscopists. The aim of the current study was to evaluate whether cap-assisted colonoscopy improves adenoma detection in a two-center, multi-endoscopist, randomized trial. PATIENTS AND METHODS: Consecutive patients who presented for an elective colonoscopy were randomized to cap-assisted colonoscopy (4-mm cap) or standard colonoscopy performed by one of 10 experienced endoscopists. Primary outcome measures were mean number of adenomas per patient and adenoma detection rate (ADR). Secondary outcomes included procedural measures and endoscopist variation; a logistic regression model was employed to examine predictors of increased detection with cap use. RESULTS: A total of 1113 patients (64 % male, mean age 62 years) were randomized to cap-assisted (n = 561) or standard (n = 552) colonoscopy. The mean number of adenomas detected per patient in the cap-assisted and standard groups was similar (0.89 vs. 0.82; P = 0.432), as was the ADR (42 % vs. 40 %; P = 0.452). Cap-assisted colonoscopy achieved a faster cecal intubation time (4.9 vs. 5.8 minutes; P < 0.001), a similar cecal intubation rate (99 % vs. 98 %; P = 0.326), and a higher terminal ileum intubation rate (93 % vs. 89 %; P < 0.028). Cap-assisted colonoscopy resulted in a 20 % increase in ADR for some endoscopists and in a 15 % decrease for others. Individual preference for the cap was an independent predictor of increased adenoma detection in adjusted analysis (P < 0.001), whereas baseline low adenoma detection was not. CONCLUSION: Although the efficiency of cecal and terminal ileum intubation was slightly improved by cap-assisted colonoscopy, adenoma detection was not. Cap-assisted colonoscopy may be beneficial for selected endoscopists. TRIAL REGISTRATION: clinicalTrials.gov (NCT01935180).

Total body weight loss of ≥ 10 % is associated with improved hepatic fibrosis in patients with nonalcoholic steatohepatitis.

BACKGROUND: Given the rising epidemics of obesity and metabolic syndrome, nonalcoholic steatohepatitis (NASH) is now the most common cause of liver disease in the developed world. Effective treatment for NASH, either to reverse or prevent the progression of hepatic fibrosis, is currently lacking. AIM: To define the predictors associated with improved hepatic fibrosis in NASH patients undergoing serial liver biopsies at prolonged biopsy interval. METHODS: This is a cohort study of 45 NASH patients undergoing serial liver biopsies for clinical monitoring in a tertiary care setting. Biopsies were scored using the NASH Clinical Research Network guidelines. Fibrosis regression was defined as improvement in fibrosis score ≥1 stage. Univariate analysis utilized Fisher's exact or Student's t test. Multivariate regression models determined independent predictors for regression of fibrosis. RESULTS: Forty-five NASH patients with biopsies collected at a mean interval of 4.6 years (±1.4) were included. The mean initial fibrosis stage was 1.96, two patients had cirrhosis and 12 patients (26.7 %) underwent bariatric surgery. There was a significantly higher rate of fibrosis regression among patients who lost ≥10 % total body weight (TBW) (63.2 vs. 9.1 %; p = 0.001) and who underwent bariatric surgery (47.4 vs. 4.5 %; p = 0.003). Factors such as age, gender, glucose intolerance, elevated ferritin, and A1AT heterozygosity did not influence fibrosis regression. On multivariate analysis, only weight loss of ≥10 % TBW predicted fibrosis regression [OR 8.14 (CI 1.08-61.17)]. CONCLUSION: Results indicate that regression of fibrosis in NASH is possible, even in advanced stages. Weight loss of ≥10 % TBW predicts fibrosis regression.

MELD and prediction of post-liver transplantation survival.

The model for end-stage liver disease (MELD) was developed to predict short-term mortality in patients with cirrhosis. It has since become the standard tool to prioritize patients for liver transplantation. We assessed the value of pretransplant MELD in the prediction of posttransplant survival. We identified adult patients who underwent liver transplantation at our institution during 1991-2002. Among 2,009 recipients, 1,472 met the inclusion criteria. Based on pretransplant MELD scores, recipients were stratified as low risk (< or = 15), medium risk (16-25), and high risk (>25). The primary endpoints were patient and graft survival. Mean posttransplant follow-up was 5.5 years. One-, 5- and 10-year patient survival was 83%, 72%, and 58%, respectively, and graft survival was 76%, 65%, and 53%, respectively. In univariable analysis, patient and donor age, patient sex, MELD score, disease etiology, and retransplantation were associated with posttransplantation patient and graft survival. In multivariable analysis adjusted for year of transplantation, patient age >65 years, donor age >50 years, male sex, and retransplantation and pretransplant MELD scores >25 were associated with poor patient and graft survival. The impact of MELD score >25 was maximal during the first year posttransplant. In conclusion, older patient and donor age, male sex of recipient, retransplantation, and high pretransplant MELD score are associated with poor posttransplant outcome. Pretransplant MELD scores correlate inversely with posttransplant survival. However, better prognostic models are needed that would provide an overall assessment of transplant benefit relative to the severity of hepatic dysfunction.