Control of 24-hour intragastric acidity with morning dosing of immediate-release and delayed-release proton pump inhibitors in patients with GERD.

GOALS: To compare the effects of immediate-release omeprazole and 2 different delayed-release proton pump inhibitors on 24-hour intragastric acidity in gastroesophageal reflux disease patients. BACKGROUND: Because of its unique pharmacokinetic properties, immediate-release omeprazole does not need to be dosed before a meal to control intragastric acidity. Previous studies showed effectiveness of immediate-release omeprazole in controlling nocturnal intragastric acidity with bedtime dosing. This is the first study to compare the effects of prebreakfast dosing of immediate-release omeprazole and delayed-release lansoprazole and pantoprazole on 24-hour intragastric acidity. AIM: To compare the effects of prebreakfast dosing of immediate-release omeprazole 40 mg capsules, lansoprazole 30 mg capsules, and pantoprazole 40 mg tablets on 24-hour intragastric acidity. METHODS: Fifty-five patients with gastroesophageal reflux disease received 7 consecutive once-daily morning doses of each drug in this open-label, randomized, 3-period crossover study. On day 7, intragastric pH was recorded for 24 hours. RESULTS: After 7 days, the percentage of time with intragastric pH >4 over 24 hours was 59.7% (14.3 hours) with immediate-release omeprazole, 48.8% (11.7 hours) with lansoprazole (P=0.005), and 41.8% (10.0 hours) with pantoprazole (P<0.001). Median intragastric pH was significantly higher with immediate-release omeprazole than with lansoprazole (P=0.003) or pantoprazole (P<0.001). All drugs were well tolerated. CONCLUSIONS: When dosed in the morning, immediate-release omeprazole provided significantly better control of 24-hour intragastric acidity than lansoprazole and pantoprazole.

Circulating 1,5-anhydroglucitol levels in adult patients with diabetes reflect longitudinal changes of glycemia: a U.S. trial of the GlycoMark assay.

OBJECTIVE: 1,5-Anhydroglucitol (1,5AG) is a major circulating polyol arising primarily from ingestion and excreted competitively with glucose. Japanese studies have demonstrated reduced concentrations of 1,5AG in serum in hyperglycemic patients in comparison with euglycemic subjects and a gradual normalization of 1,5AG values for patients responding to antihyperglycemic therapies. In this first U.S. study, we assessed the ability of 1,5AG measurements to monitor glycemic control in a cohort of 77 patients with diabetes (22 with type 1 diabetes, 55 with type 2 diabetes) who presented with suboptimal glycemic control at baseline (defined as HbA(1c) >or=7%). RESEARCH DESIGN AND METHODS: Each patient received therapies consisting of combinations of diabetes education, nutritional counseling, and addition or dose adjustment of various insulins or oral antihyperglycemic medications. Therapy was targeted to reduce mean HbA(1c) by >or=1.0% over the monitoring period. 1,5AG, HbA(1c), fructosamine, and random glucose measurements were performed at baseline and at 2, 4, and 8 weeks after the initiation of therapy. RESULTS: 1,5AG, fructosamine, and glucose values progressed significantly toward euglycemia by week 2 of monitoring (Wilcoxon's signed-rank test, P < 0.05), with median changes of 93, -7, and -13% for 1,5AG, fructosamine, and glucose, respectively. In contrast, HbA(1c) values did not respond significantly to therapy until week 4. On an individual patient basis, 89.6% of patients displayed longitudinal changes of 1,5AG from baseline to week 8 in concordance with HbA(1c). 1,5AG was also highly correlated with HbA(1c) and fructosamine (Spearman rho = -0.6459 and -0.6751, respectively; both P < 0.0001). CONCLUSIONS: We conclude that 1,5AG responds sensitively and rapidly to changes in glycemia and monitors glycemic control in accordance with established markers.