Could Plasma Glucose (PG) Increment (PG%) Expand the Clinical Weight of OGTT? Preliminary Findings in 19 TDT Patients (β-TDT) with Normal Glucose Tolerance.

Background: Worldwide, glucose dysregulation (GD) and diabetes mellitus are common complications in transfusion-dependent β-thalassemia (β-TDT) patients. Impaired insulin sensitivity and insulin secretion are both involved in the deterioration of glucose tolerance from a normal to a glucose-intolerant state. Objective: The main aim of the present study was to evaluate the plasma glucose (PG) increment (PG %) retrospectively at two h during oral glucose tolerance test (OGTT) over fasting plasma (FPG) concentration as a simple parameter to recognize early β-cell dysfunction in normoglycemic β-TDT patients with NGT and different severities of iron overload (IOL). Patients and Methods: A total of 19 β-TDT young adult patients with normal OGTT were re-evaluated according to the American Diabetes Association (ADA) guidelines. Venous blood samples were collected at baseline and at 30, 60, and 120 minutes to determine PG (mg/dL) and insulin concentrations (μIU/mL). The time required for the PG concentration to return to the fasting level was calculated by computing the percentage increment of 2-h PG with respect to FPG (PG%), using the formula [(2-h PG-FPG)/FPG]x 100. The early phase of insulin secretion (IGI) and sensitivity were assessed by validated surrogate indices calculated from parameters obtained during the four-point OGTT. Results: The mean age of patients was 30.3 ± 5.7 (range: 23.10-44.3). The mean ± SD, median, and range of PG% increment between 2 h-PG and FPG were 35.5 ± 20.2, 38.7, and 0 - 68.2 mg/dL, respectively. The PG% increment was negatively correlated to the patient's age, FPG, and IGI, and positively correlated with 2-h PG post-glucose load. IGI was negatively correlated with 1-h and 2-h PG after post-glucose load and positively correlated with oral disposition index (oDI). Conclusions: The PG% increment is a simple, useful screening parameter that can expand the clinical weight of OGTT and can provide valuable metabolic information on β-cell dysfunction.