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1 (P<0.01 for each canagliflozin group versus glimepiride).
2 ; 95% CI, 31.9% to 62.2%; P<0.001) than with glimepiride.
3 as not released from cells by treatment with glimepiride.
4 e comparison of each canagliflozin dose with glimepiride.
5 and after administration of the sulfonylurea glimepiride.
6 polipoprotein A-I (r = -0.20, p = 0.01) with glimepiride.
7 4 inhibitor linagliptin and the sulfonylurea glimepiride.
8 on of coronary atherosclerosis compared with glimepiride.
9 hypoglycaemia, and blood pressure than does glimepiride.
10 all thickness compared with the sulfonylurea glimepiride.
11 one slowed progression of CIMT compared with glimepiride.
12 abetic effect (% potency = 218%) compared to glimepiride.
13 ed progression of maximum CIMT compared with glimepiride (0.002 mm vs 0.026 mm, respectively, at 72 w
14 n of mean CIMT was less with pioglitazone vs glimepiride (-0.001 mm vs +0.012 mm, respectively; diffe
16 emic clamps with coadministration of: 1) SU (glimepiride 1 mg) or placebo, combined with 2) infusions
18 th 50 mg to -0.65% [0.114] with 6.25 mg) and glimepiride (-1.05% [SE 0.111]) groups versus placebo (-
19 trasonography and were randomized to receive glimepiride, 1 to 4 mg, or pioglitazone, 15 to 45 mg, fo
20 per year for patients receiving sitagliptin; glimepiride, -1.92 (95% CI, -2.08 to -1.75) mL/min/1.73
21 135 (10.6%) patients receiving sitagliptin; glimepiride, 155 (12.4%); liraglutide, 152 (12.0%); and
22 ]), 18 147 started glipizide, 14 282 started glimepiride, 1887 started glyburide, and 13 849 started
25 bo and, on a separate occasion, ingestion of glimepiride (4.0 mg) at 0 min (with glucose infused to p
26 95% confidence interval 394 to 480 days) for glimepiride, 764 (741 to not calculable) days for liragl
28 ucose tolerance after a mixed meal and after glimepiride administration in the absence of a differenc
30 ite sides of and could not exclude the null (glimepiride: aHR(Medicaid) 1.17, 95% CI 0.96-1.42; aHR(O
31 in PAV of 0.64% (95% CI, 0.23% to 1.05%) for glimepiride and a decrease of 0.06% (-0.47% to 0.35%) fo
32 ncreased 0.73% (95% CI, 0.33% to 1.12%) with glimepiride and decreased 0.16% (95% CI, -0.57% to 0.25%
34 for glipizide, 1.07 (95% CI, 0.96-1.16) for glimepiride, and 1.04 (95% CI, 0.83-1.24) for glyburide.
35 for glyburide, 8.6% (95% CI, 7.9%-9.2%) for glimepiride, and 9.1% (95% CI, 8.7%-9.7%) for glipizide.
36 n provides greater HbA1c reduction than does glimepiride, and is well tolerated in patients with type
37 abetes compounds tolbutamide, glibenclamide, glimepiride, and nateglinide and identified glibenclamid
42 , HbA(1c) decreased by 0.51% (SD 1.20%) with glimepiride, compared with 0.84% (1.23%) with liraglutid
43 o establish noninferiority of linagliptin vs glimepiride, defined by the upper limit of the 2-sided 9
45 ry disease were treated with pioglitazone or glimepiride for 18 months in the PERISCOPE (Pioglitazone
48 pproach is demonstrated by the extraction of glimepiride from a water sample, followed by LC-MS analy
50 Initiation of treatment with a sulfonylurea (glimepiride, glipizide, or glyburide) or a DPP4i (refere
52 nificantly higher rates were reported in the glimepiride group (19% [n=12]; p value range 0.010-0.002
55 gliptin group and 362 of 3010 (12.0%) in the glimepiride group (HR, 0.98 [95.47% CI, 0.84-1.14]; P <
58 ) patients had serious adverse events in the glimepiride group versus 24 (5%) in the canagliflozin 10
59 in the linagliptin group vs 16 (0.5%) in the glimepiride group with adjudicated-confirmed acute pancr
60 rgine group, 1.1 (95% CI, 0.9 to 1.4) in the glimepiride group, 0.7 (95% CI, 0.6 to 0.9) in the lirag
61 liflozin 100 mg and 300 mg groups versus the glimepiride group, we recorded a greater number of genit
62 he linagliptin group and 2856 (94.9%) in the glimepiride group, with 15 participants (0.5%) in the li
63 isk of reaching HbA(1c) >=7.0% compared with glimepiride (hazard ratio 0.57, 95% confidence interval
64 In the pioglitazone group, compared with glimepiride, high-density lipoprotein levels increased 5
66 y of canagliflozin, an SGLT2 inhibitor, with glimepiride in patients with type 2 diabetes inadequatel
69 as rare but significantly more frequent with glimepiride (in 2.2% of the participants) than with glar
70 albiglutide, placebo, or active comparators (glimepiride, insulin glargine, insulin lispro, liragluti
71 ks, canagliflozin 100 mg was non-inferior to glimepiride (least-squares mean difference -0.01% [95% C
72 with 1.9, 1.9, 1.4, and 2.0 in the glargine, glimepiride, liraglutide, and sitagliptin groups, respec
75 pants randomly assigned to insulin glargine, glimepiride, liraglutide, or sitagliptin, added to basel
76 mised patients received at least one dose of glimepiride (n=482), canagliflozin 100 mg (n=483), or ca
80 liptin once daily (n = 3023) or 1 to 4 mg of glimepiride once daily (n = 3010) in addition to usual c
81 fective at maintaining glycemic control than glimepiride or sitagliptin when added to metformin monot
82 r risk, the use of linagliptin compared with glimepiride over a median 6.3 years resulted in a noninf
85 in type 2 diabetic and normal mice, whereas glimepiride proved efficacious against stroke in normal
86 6 events occurred in the groups treated with glimepiride (rate ratio, 1.61 [95% CI, 1.13-2.29]) or si
89 smooth muscle types), whereas glibenclamide, glimepiride, repaglinide, and meglitinide block both typ
90 canagliflozin 100 or 300 mg/d, compared with glimepiride, slowed the progression of renal disease ove
91 ed cardiovascular outcomes of linagliptin vs glimepiride (sulfonylurea) in patients with relatively e
94 -100 (hereafter, glargine), the sulfonylurea glimepiride, the glucagon-like peptide-1 receptor agonis
96 o receive canagliflozin 100 mg or 300 mg, or glimepiride (up-titrated to 6 mg or 8 mg per day) orally
100 4 inhibitor linagliptin and the sulfonylurea glimepiride, which restore T2D-induced brain vascular pa