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Treating prediabetes does not affect progression |
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Clinical Question: Does treatment of postprandial hyperglycemia in patients with early, asymptomatic diabetes delay progression to frank fasting hyperglycemia? Bottom Line: The jury is still out regarding the identification and treatment of patients with prediabetes. According to this study, a similar percentage of patients with early diabetes will develop frank diabetes whether or not they receive therapy to lower postprandial glucose levels. A larger, though shorter, study has shown a difference, but it looks like early benefit is lost over time. Ameliorating postprandial hyperglycemia did not appear to delay progression of early type 2 diabetes. Factors other than postprandial hyperglycemia may be greater determinants of progression of diabetes. Alternatively, once FPG exceeds 126 mg/dl, beta-cell failure may no longer be remediable. Reference: Kirkman MS, Shankar RR, Shankar S. Treating postprandial hyperglycemia does not appear to delay progression of early type 2 diabetes. Diabetes Care 2006;29:2095-2101. Study Design: Randomized controlled trial (nonblinded) Synopsis: Postprandial hyperglycemia characterizes early type 2 diabetes. Researcher investigated whether ameliorating postprandial hyperglycemia with acarbose would prevent or delay progression of diabetes, defined as progression to frank fasting hyperglycemia, in subjects with early diabetes (fasting plasma glucose [FPG] <140 mg/dl and 2-h plasma glucose > or =200 mg/dl). Two hundred nineteen subjects with early diabetes were randomly assigned to 100 mg acarbose t.i.d. or identical placebo and followed for 5 years or until they reached the primary outcome (two consecutive quarterly FPG measurements of > or =140 mg/dl). Secondary outcomes included measures of glycemia (meal tolerance tests, HbA(1c), annual oral glucose tolerance tests [OGTTs]), measures of insulin resistance (homeostasis model assessment [HOMA] of insulin resistance and insulin sensitivity index from hyperglycemic clamps), and secondary measures of beta-cell function (HOMA-beta, early- and late-phase insulin secretion, and proinsulin-to-insulin ratio). Acarbose significantly reduced postprandial hyperglycemia. However, there was no difference in the cumulative rate of frank fasting hyperglycemia (29% with acarbose and 34% with placebo; P = 0.65 for survival analysis). There were no significant differences between groups in OGTT values, measures of insulin resistance, or secondary measures of beta-cell function. In a post hoc analysis of subjects with initial FPG <126 mg/dl, acarbose reduced the rate of development of FPG > or =126 mg/dl (27 vs. 50%; P = 0.04). |
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