557-P: Impact of Extensive HbA1c Control on Major Microvascular Complications in Type 2 Diabetes Mellitus with Short Duration of Disease

The aim of this study was to investigate the impact of extensive HbA1c control on major microvascular complications including neuropathy, retinopathy and nephropathy in T2DM patients with short duration. Detailed Clinical (e.g., full Lipid profile test, BMI, Blood Pressure, eGFR), ophthalmic (e.g., Fundus Photography, Optical Coherence Topography (OCT), Corneal Confocal Microscopy (CCM)) and neurological examinations (e.g., symptoms, electrophysiology, quantitative sensory testing, Cardiac Autonomic Neuropathy tests) were performed in 76 patients with T2DM at baseline and after glycemic control (GC) with or without Extensive HbA1C control (EHC) over 4 years along with 48 controls with normal glucose tolerance (NGT) and 34 subjects with impaired glucose tolerance (IGT). The mean HbA1c levels during whole follow-up period were closely related with the improvement in neurological markers. The multiple regression analysis indicates that the changes in all Corneal Nerve markers (CNF) and neurophysiological measures were closely associated with the mean HbA1c level over whole follow-up period. Higher SD and CV of HbA1c levels were negatively associated with some CNF and neurophysiological measures. The high baseline HbA1c levels deteriorated many neurological markers. In this study patients with poorly controlled type 2 diabetes returned to IGT by normalizing HbA1c level for 2 years without hypoglycemia. Nephropathy reduced from 34.2% to 18.4%. However, the prevalence of retinopathy progressed from 7.9% at baseline to 13.2%. Prevalence of neuropathy reduced from 13.2% to 2.6%. Although improvement of neurological markers in this study was significant, but the changes were small. The intensive GC in T2DM with short duration is associated with a reduction in microvascular complications (mostly albuminuria). The normalized HbA1c levels are more effective than standard care for preventing the development of neuropathy, but not retinopathy. Disclosure M. Tavakoli: None. F. Ishibashi: None.