The Clinical Definition of Overbasalization.

Abstract

This commentary will discuss the issue of overbasalization. To focus the discussion clinically, let us consider two similar patients whose glycemia has not been well managed on noninsulin drugs and who are both started on basal insulin but have different responses. This is an obese man who has had diabetes for 15 years, with a BMI of 36 kg/m2. His diabetes has not been controlled with maximal doses of metformin, a dipeptidyl dipeptidase 4 (DPP-4) inhibitor, and pioglitazone, and his A1C is 9.2%. He is kept on these oral agents, and a basal insulin is initiated and titrated upward. Six months later, the majority of his fasting plasma glucose (FPG) readings are in the range of 140–180 mg/dL, and he is taking 0.7 units/kg of basal insulin. His before-dinner glucose readings range from 160 to 220 mg/dL, and his A1C is 8.1%. Preprandial bolus doses of insulin are started to control his daytime hyperglycemia. This is an obese man who has had diabetes for 9 years with a BMI of 36 kg/m2. His diabetes has not been controlled with maximal doses of metformin, a DPP-4 inhibitor, and pioglitazone, and his A1C is 9.2%. He is kept on these oral agents, and a basal insulin is initiated and titrated upward. Six months later, the majority of his FPG readings are in the range of 100–130 mg/dL, and he is taking 0.7 units/kg of basal insulin. His before-dinner glucose readings range from 160 to 220 mg/dL, and his A1C is 8.1%. His basal insulin dose is titrated upward to 0.9 units/kg to control his daytime hyperglycemia, but he begins to complain of hypoglycemia, occurring mostly overnight but sometimes during the day when he misses or delays a meal. Cowart (1) defined “overbasalization” in an article about clinical inertia …