AIM: We investigated the clinical and metabolic parameters in type 2 diabetic patients who were inadequately controlled on sulfonylurea (SU) before initiating insulin therapy to characterise patients who are likely to achieve target glycaemic control with insulin analogues. METHODS: A total of 120 Korean patients aged ≥ 40 years with insulin-naïve, poorly controlled, SU-treated type 2 diabetes were randomised on the basis of SU dose, and obesity with 1 : 1 ratio of insulin detemir (long-acting analogue; LAA) and 70% insulin aspart protamine and 30% insulin aspart (biphasic insulin analogue; BIA). Patients who failed to reach ≤ 20% glycated albumin (GA) at 3 weeks were switched to therapy with a twice-daily BIA for 16 weeks. RESULTS:Mean HbA(1c) , GA, fasting and stimulatedplasma glucose levels were significantly reduced after 16 weeks compared with the baseline in all groups, and 40% of patients reached the target HbA(1c) ( ≤ 7%). Compared with responders, non-responders had significantly longer duration of diabetes and higher dose of glimepiride. However, there was no significant difference in insulin secretory profiles between responders and non-responders. Clinical factors such as diabetes duration, SU dose and BMI were independently associated with inadequate response to insulin analogues in patients with secondary failure. CONCLUSIONS: In type 2 diabetics with secondary SU failure, clinical parameters such as duration of diabetes (< 10 years), SU dose ( ≤ 4 mg) and BMI should be taken into consideration as important factors than laboratory indices related to β-cell function when predicting the response to insulin analogues.
RCT Entities:
AIM: We investigated the clinical and metabolic parameters in type 2 diabeticpatients who were inadequately controlled on sulfonylurea (SU) before initiating insulin therapy to characterise patients who are likely to achieve target glycaemic control with insulin analogues. METHODS: A total of 120 Korean patients aged ≥ 40 years with insulin-naïve, poorly controlled, SU-treated type 2 diabetes were randomised on the basis of SU dose, and obesity with 1 : 1 ratio of insulin detemir (long-acting analogue; LAA) and 70% insulin aspart protamine and 30% insulin aspart (biphasic insulin analogue; BIA). Patients who failed to reach ≤ 20% glycated albumin (GA) at 3 weeks were switched to therapy with a twice-daily BIA for 16 weeks. RESULTS: Mean HbA(1c) , GA, fasting and stimulated plasma glucose levels were significantly reduced after 16 weeks compared with the baseline in all groups, and 40% of patients reached the target HbA(1c) ( ≤ 7%). Compared with responders, non-responders had significantly longer duration of diabetes and higher dose of glimepiride. However, there was no significant difference in insulin secretory profiles between responders and non-responders. Clinical factors such as diabetes duration, SU dose and BMI were independently associated with inadequate response to insulin analogues in patients with secondary failure. CONCLUSIONS: In type 2 diabetics with secondary SU failure, clinical parameters such as duration of diabetes (< 10 years), SU dose ( ≤ 4 mg) and BMI should be taken into consideration as important factors than laboratory indices related to β-cell function when predicting the response to insulin analogues.