Beta-cell function evaluated by HOMA as a predictor of secondary sulphonylurea failure in Type 2 diabetes

Background and aims Secondary failure to oral hypoglycaemic agents, a commo n evolution of long-standing Type 2 diabetes, is usually assessed by non-st andardized indices requiring fine clinical assessment, including hyperglyca emia resistant to maximum doses of sulphonylureas despite appropriate diet and follow-up. The goal of this study was to evaluate if HOMA, a modelized plasma insulin/glucose ratio allowing simple evaluation of residual insulin secretion and sensitivity, is a better predictor of the insulin requiring stage than clinical indices. Materials and methods HOMA was measured in 84 Type 2 diabetic patients aged 58 +/- SD 6 years, with diabetes duration 11 +/-4 years, hospitalized beca use of hyperglycaemia resistant to maximal doses of sulphonylureas (e.g. gl ibenclamide greater than or equal to 15 mg/day), with no apparent external reason for hyperglycaemia. Despite reinforced appropriate diet recommendati ons, 62 of these patients remained hyperglycaemic (insulin-requiring group) . Results Age, duration of diabetes, body mass index (BMI) and HOMA value for insulin sensitivity (71 +/-6% vs. 76 +/-7%, normal values 59 +/- 161%) wer e comparable in the two groups. HbA(1c) was higher (10.0 +/-0.2% vs. 8.3 +/ -0.3%, P<0.001) and HOMA insulin secretion values lower (25<plus/minus>2% v s. 43 +/-6%, normal values 70-150%, P<0.01) in the insulin-requiring group. Of the following potential predictors: HbA(1c) >8%, duration of diabetes g reater than or equal to 10years, HbA(1c) combined with diabetes duration, i nsulin sensitivity less than or equal to 40%, insulin secretion less than o r equal to 20%, the latter showed the best positive predictivity (86% patie nts with low insulin secretion were insulin-requiring). Conclusions (i) HOMA is a simple and good predictor of the insulin-requirin g stage in Type 2 diabetes mellitus; (ii) this stage of diabetes is charact erized by a further decline of insulin secretion rather than of insulin sen sitivity.