Jose Lopez

Estimation of the Glycation Gap in Diabetic Patients With Stable Glycemic Control

OBJECTIVE The glycation gap (the difference between measured A1C and the value predicted by regression on fructosamine) is stable and is associated with microvascular complications of diabetes but has not hitherto been estimated within a clinically useful time frame. We investigated whether two determinations 30 days apart suffice for a reasonably reliable estimate if both A1C and fructosamine exhibit stability. RESEARCH DESIGN AND METHODS We studied 311 patients with type 1 or type 2 diabetes for whom simultaneous measurements of A1C and serum fructosamine had been made on at least two occasions separated by 1 month (t0 and t1). Glycemia was deemed stable if A1C(t1) – A1C(t0) and fructosamine(t1) − fructosamine(t0) were both less than their reference change values (RCVs). Instantaneous glycation gaps [gg(t0) and gg(t1)] and their mean (GG), were calculated using the data from all stable patients for the required regression. RESULTS Stable glycemia was shown by 144 patients. In 90% of unstable case subjects, a change in medication was identified as the cause of instability. Among 129 stable patients with an average of eight gg determinations prior to t0, GG correlated closely with the mean of these prior determinations (r2 = 0.902, slope 1.025, intercept −0.038). CONCLUSIONS The glycation gap can be calculated reliably from pairs of A1C and fructosamine measurements taken 1 month apart if these measurements satisfy the RCV criteria for glycemic control.

Long-Term Efficacy of Glibenclamide and Sitagliptin Therapy in Adult Patients With KCNJ11 Permanent Diabetes

Permanent neonatal diabetes (PND) is a rare disease characterized by hyperglycemia diagnosed within the first 6 months of life (1). Activating mutation of the KCNJ11 gene encoding Kir6.2 subunit of the ATP-potassium (KATP) channel has been described as the most frequent cause of PND. Under physiologic circumstances, KATP channel closure plays a central role in glucose-stimulated insulin secretion from pancreatic β-cells. Sulfonylureas (SUs) stimulate insulin secretion by closing KATP channels via an ATP-independent mechanism. Since 2004, SUs are best choice of treatment in PND with such mutations and allow better glycemic control in children and adults than insulin (2). Some authors report that adult patients are unable to switch successfully from insulin to SU and that the doses required to get the insulin independence are higher (3,4). We present our …