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The effect on metabolic control of second-generation sulfonylurea drugs in patients with NIDDM after secondary failure to first-generation agents.

作者信息

Sami T, Kabadi U M, Moshiri S

机构信息

VA Medical Center, Phoenix, AZ 85012, USA.

出版信息

J Fam Pract. 1996 Oct;43(4):370-4.

PMID:8874372
Abstract

BACKGROUND

The literature contains few data examining the results of therapy with second-generation sulfonylurea drugs in subjects with non-insulin-dependent diabetes mellitus (NIDDM) after the onset of secondary failure to first-generation agents. The present study was undertaken to assess the efficacy of therapy with second-generation sulfonylurea in subjects with NIDDM following secondary failure to first-generation agents.

METHODS

The study included 55 subjects with NIDDM who manifested secondary failure to first-generation sulfonylurea therapy. Of these, 29 subjects underwent therapy with the second-generation sulfonylurea glipizide, and 26 subjects were treated with glyburide, both drugs administered in the maximum daily dosage. Before initiation of the second-generation sulfonylurea agents and again at the end of 6 months, metabolic control was assessed by determination of fasting plasma glucose, glycosylated hemoglobin (HbA1c), and the lipid profile.

RESULTS

Fasting plasma glucose and HbA1c levels were 209 +/- 31 mg/dL and 12.3 +/- 2.1%, respectively, before initiation of glipizide, and did not significantly change following therapy (fasting plasma glucose, 211 +/- 34 mg/dL; HbA1c, 11.7 +/- 1.8%). Similarly, no significant alteration was noted in these metabolic values in the glyburide group (before glyburide therapy, fasting plasma glucose, 180 +/- 16 mg/dL; HbA1c, 11.2 +/- 1.6%; after glyburide therapy, fasting plasma glucose, 184 +/- 20 mg/dL; HbA1c, 11.0 +/- 1.5%). Lipids also were not significantly altered following therapy with either glipizide or glyburide. Finally, for all subjects, fasting plasma glucose and HbA1c were 200 +/- 27 mg/dL and 11.9 +/- 2.0%, respectively, during treatment with first-generation drugs and did not change significantly following therapy with the second-generation agents (fasting plasma glucose, 205 +/- 20 mg/dL; HbA1c, 11.2 +/- 1.2%). P values were > .60 for all comparisons.

CONCLUSIONS

Treatment with second-generation sulfonylurea agents for patients with NIDDM following onset of secondary failure to first-generation sulfonylurea drugs achieves no better metabolic control than treatment with first-generation agents.

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