The relation between parameters from homeostasis model assessment and glycemic control in type 2 diabetes.

OBJECTIVE: To determine the association of insulin sensitivity and pancreatic beta-cell function parameters assessed by the homeostasis model assessment (HOMA) and glycemic control, and their potential utilization in the clinical care of patients with type 2 diabetes mellitus. MATERIAL AND METHOD: The HOMA indices were assessed in 204 (62 males, 142 females) type 2 diabetic outpatients aged 60.7 +/- 10.9 years. All patients were non-insulin treated for their diabetes. The correlation between variables including logarithmically transformed HOMA-%S and HOMA-%B, body mass index (BMI) and duration of diabetes to glycemic control were assessed The value of the disposition index (HOMA-%SxHOMA-%B) that best discriminated patients with good glycemic control (HbA1C < 7%) from those without (HbA1C > or = 7%) was determined. RESULTS: Both log (HOMA-%S) and log (HOMA-%B) were inversely related to HbA1C with comparable degrees of association (beta = -0.62, p < 0.001 and beta = -0.61, p < 0.001, respectively). The log-transformed disposition index of at least 3.57 had a sensitivity of 74.2% and a specificity of 67.6% in classifying patients as having HbA1C < 7%. The result suggested that in order to achieve acceptable glycemic control, oral hypoglycemic agents should be adjusted to maximize the likelihood of the log-transformed disposition index reaching 3.57. CONCLUSIONS: Glycemic control in diabetic patients partially depends on both insulin sensitivity and pancreatic beta-cell function. Assessing both parameters with the HOMA model is likely to result in a more rational approach for achieving better glycemic control in type 2 diabetic patients.

Advancing age and renal impairment as important predisposing factors of gatifloxacin-induced hyperglycemia in non-diabetes patients.

There have been case reports about adverse effects to glucose homeostasis related to gatifloxacin use. The authors report an elderly, non-diabetic patient who developed severe hyperglycemia after receiving oral gatifloxacin 400mg/d. He was a 73-year-old male, patient with a history of hypertension, cured vesical pheochromocytoma, idiopathic dilated cardiomyopathy, chronic renal insufficiency (baseline serum creatinine of 1.7 mg/dL), and gouty arthritis admitted to the hospital with a diagnosis of acute bronchitis. Seven days after initiating gatifloxacin, his symptoms were improved. Subsequently he developed polyuria, polydipsia, and fatigue with an increase in serum creatinine to 2.8 mg/dL, and random plasma glucose levels elevated to 903 mg/dL. Gatifloxacin was stopped. Intravenous regular insulin infusion was administered. Euglycemia was achieved within 8 hours after fluid rehydration and only low dose insulin was required He maintained normal glucose levels without any antidiabetic drugs afterward. Old age and renal impairment were considered significant contributing factors for this hyperglycemic adverse event from gatifloxacin.