p;
95% CI for Difference (-1.01, -0.57) (-1.11, -0.67) (-0.99, -0.56)
p-value for pairwise comparison < 0.001 < 0.001 < 0.001
Fasting Plasma Glucose (mg/dL)
n 143 141 145 144
Baseline 163.4 ± 4.6 163.2 ± 4.7 158.8 ± 4.7 164.0 ± 4.7
Mean Change ± SE at Final Visit -13.7 ± 3.7 -15.7 ± 3.7 -9.4 ± 3.7 15.5 ± 3.7
Mean Difference ± SE from Glyburide Alone -29.2 ± 4.9 -31.2 ± 40.9 -24.9 ± 4.9 N/A
95% CI for Difference (-38.8, -19.6) (-40.9, -21.6) (-34.5, -15.4)
p-value for pairwise comparison < 0.001 < 0.001 < 0.001
Body Weight (kg)
n 143 141 146 144
Baseline 89.38 ± 11.21 103.70 ± 11.21 102.90 ± 11.21 95.56 ± 7.96
Mean Change ± SE at Final Visit 0.28 ± 1.05 0.08 ± 1.05 -0.03 ± 1.05 0.71 ± 1.04
Mean Difference ± SE from Glyburide Alone -0.43 ± 0.52 -0.63 ± 0.53 -0.74 ± 0.52 N/A
95% CI for Difference (-1.46, 0.60) (-1.67, 0.40) (-1.77, 0.28)
p-value for pairwise comparison 0.410 0.230 0.156
GLUMETZA is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus.
GLUMETZA is contraindicated in patients with:
GLUMETZA should be temporarily discontinued in patients undergoing radiologic studies involving intravascular administration of iodinated contrast materials, because use of such products may result in acute alteration of renal function. (See also PRECAUTIONS )
Lactic acidosis is a rare, but serious, metabolic complication that can occur due to metformin accumulation during treatment with GLUMETZA; when it occurs, it is fatal in approximately 50% of cases. Lactic acidosis may also occur in association with a number of pathophysiologic conditions, including diabetes mellitus, and whenever there is significant tissue hypoperfusion and hypoxemia. Lactic acidosis is characterized by elevated blood lactate levels (>5 mmol/L), decreased blood pH, electrolyte disturbances with an increased anion gap, and an increased lactate/pyruvate ratio. When metformin is implicated as the cause of lactic acidosis, metformin plasma levels >5 μg/mL are generally found. The reported incidence of lactic acidosis in patients receiving metformin hydrochloride is very low (approximately 0.03 cases/1000 patient-years, with approximately 0.015 fatal cases/1000 patient-years). In more than 20,000 patient-years exposure to metformin in clinical trials, there were no reports of lactic acidosis. Reported cases have occurred primarily in diabetic patients with significant renal insufficiency, including both intrinsic renal disease and renal hypoperfusion, often in the setting of multiple concomitant medical/surgical problems and multiple concomitant medications. Patients with congestive heart failure requiring pharmacologic man
