Randomized Noninferiority Trial Comparing Diagnostic Yield of Cytopathologist-guided versus 7 passes for EUS-FNA of Pancreatic Masses.

BACKGROUND AND AIM: To improve diagnostic yield of endoscopic ultrasound-guided fine needle aspiration (EUS-FNA) in solid pancreatic lesions, on-site cytology review has been recommended. Because this is not widely available throughout the world, the aim of this study was to compare the diagnostic yield of EUS-FNA performed with rapid on-site evaluation (ROSE) versus 7 FNA passes without ROSE in pancreatic masses. METHODS: In this multicenter randomized noninferiority trial, patients were randomized to ROSE versus 7 passes into a solid pancreatic mass. On the basis of the absolute difference in diagnostic yield with 7 passes versus cytopathologist-guidance, the noninferiority margin for the difference in diagnostic yield was defined as -15%. Definite diagnosis was defined to include positive for malignancy, neoplastic cells present, and negative for malignancy. RESULTS: A total of 142 patients were randomized with 73 in the cytopathologist arm and 69 in the 7 passes arm. Diagnostic yield for definite diagnosis was 78.3% with 7 passes and 78.1% with cytopathology guidance. With an absolute difference 0.2%, 95% CI -14.4 to 14.6, performing 7 passes was noninferior to cytopathologist-guided EUS-FNA. There was no significant difference in complications or time to perform FNA. A median of 5 passes were performed with ROSE. The median charge with onsite cytopathology was significantly greater than performing 7 passes [$1058 (958, 1445) versus $375 (275, 460), p<0.001]. CONCLUSIONS: The diagnostic yield for performing 7 passes during EUS-FNA into solid pancreatic masses is noninferior with lower charge compared to cytopathologist-guidance. This article is protected by copyright. All rights reserved.

Metformin and survival in pancreatic cancer: a retrospective cohort study.

OBJECTIVES: Our aim was to determine the effect of metformin exposure on survival in patients with advanced pancreatic adenocarcinoma (PAC). METHODS: A retrospective cohort study was conducted using The Health Improvement Network, a primary care electronic medical record database from the United Kingdom (2003-2010). The study cohort included all subjects with a diagnostic code for incident PAC and a preexisting diagnosis of type 2 diabetes mellitus. Subjects were classified as exposed if they were prescribed metformin around the time of PAC diagnosis (between 6 months prior and 1 month after). A secondary analysis was performed only on exposed subjects without prior (ie, 6 months before PAC diagnosis) exposure to metformin. The primary outcome was overall survival. The analysis was performed using univariate and multivariable Cox proportional hazards models. RESULTS: The study included 516 subjects with preexisting type 2 diabetes mellitus and PAC, 247 of which were exposed to metformin. In univariate and multivariable analysis, there was no difference in survival between those exposed and those unexposed to metformin in the primary analysis (hazards ratio, 1.11 [0.89-1.38], P = 0.367) or the secondary analysis (hazards ratio, 1.09 [0.80-1.47], P = 0.585). CONCLUSIONS: Metformin use is not associated with improved survival in subjects with advanced PAC.

Exaggeration of postprandial hyperglycemia in patients with type 2 diabetes by administration of caffeine in coffee.

OBJECTIVE: To test whether caffeine administered in coffee increases postprandial hyperglycemia in patients with type 2 diabetes who are habitual coffee drinkers. METHODS: The study used a within-subject, double-blind, placebo-controlled experimental design. Twenty adult coffee drinkers (11 women and 9 men) with type 2 diabetes treated with diet, exercise, orally administered antidiabetic agents, or some combination of these factors completed two mixed-meal tolerance tests (MMTT) after an overnight fast. Before the MMTT, each study participant received 250 mg of caffeine in 16 oz (475 mL) of decaffeinated coffee or decaffeinated coffee alone, with the treatment order counterbalanced in the group. Fasting and 1-hour and 2-hour postprandial blood samples were collected for measurement of plasma glucose and insulin concentrations. RESULTS: Glucose and insulin responses to the MMTT were quantified by the incremental areas under the 2-hour concentration-time curves (AUC2h). Administration of caffeine in decaffeinated coffee increased postprandial glucose and insulin responses (both P = 0.02). The mean plasma glucose AUC2h was 28% larger and the mean plasma insulin AUC2h was 19% larger after administration of caffeine than after administration of placebo. CONCLUSION: Other constituents in coffee did not prevent the exaggeration of postprandial hyperglycemia by caffeine in these patients with type 2 diabetes, who were habitual coffee drinkers. Repeated on a daily basis, such effects could impair long-term glucose control in those patients with type 2 diabetes who habitually drink coffee or other caffeinated beverages.