Slow Titration and Delayed Intensification of Basal Insulin Among Patients with Type 2 Diabetes

Abstract

This study was funded by Novo Nordisk. Mocarski, Guerrero, Langer, and Thorsted are employees and shareholders of Novo Nordisk. Yeaw, Divino, and DeKoven are employed by QuintilesIMS, which received remuneration from Novo Nordisk for work on this study. Study concept and design were contributed by Mocarski, DeKoven, Langer, and Thorsted. Yeaw took the lead in data collection, along with Divino and DeKoven. Data interpretation was performed by Yeaw, Divino, DeKoven, and Guerrero. The manuscript was written by Mocarski and Divino and revised by Guerrero, Langer, and Thorsted, along with Yeaw and DeKoven. Some of the data from this study were presented via poster at the AMCP Annual Meeting in March 2017 and at the 53rd EASD Annual Meeting in September 2017.

Double‐blind, randomized clinical trial comparing the efficacy and safety of continuing or discontinuing the dipeptidyl peptidase‐4 inhibitor sitagliptin when initiating insulin glargine therapy in patients with type 2 diabetes: The CompoSIT‐I Study

“…In a recently published database analysis, it was observed that titration of basal insulin was characterized by substantial treatment inertia in the real world . This may be attributable to the reluctance of patients and physicians to titrate insulin for many reasons, including fear of hypoglycaemia.…”

“…32 In a recently published database analysis, it was observed that titration of basal insulin was characterized by substantial treatment inertia in the real world. 33 This may be attributable to the reluctance of patients and physicians to titrate insulin for many reasons, including fear of hypoglycaemia. In the present study, continuation of sitagliptin when initiating and intensively titrating insulin glargine led to participants achieving greater glycaemic control and no evidence of an increased hypoglycaemic burden typically associated with intensifying insulin glargine.…”

When basal insulin is not enough: A dose–response relationship between insulin glargine 100 units/mL and glycaemic control

“…2,14 An insulin dose of >0.4 IU/kg/d should be a signal to clinicians to start considering antidiabetic agents that better address PPG excursions, including prandial insulin, or oral or injectable incretin therapies, so that treatment intensification can be initiated before basal insulin doses exceed 0.5 IU/kg/d. 2,18 The limitations of the present study primarily relate to the fact that it is a post hoc analysis of pooled data from three studies not specifically designed to determine if there is a diminishing response to increasing basal insulin dose. Furthermore, specifying that participants required a background therapy of metformin and a sulphonylurea limited the number studies that could be included in the analysis.…”

“…18 Moreover, a significant proportion of people with diabetes are concerned about the risks of hypoglycaemia and potential weight gain associated with higher basal insulin doses. Early intensive glucose control is essential to prevent long-term micro-and macrovascular complications of type 2 diabetes, 17 but many people with type 2 diabetes do not achieve their HbA1c targets on basal insulin.…”

“…Early intensive glucose control is essential to prevent long-term micro-and macrovascular complications of type 2 diabetes, 17 but many people with type 2 diabetes do not achieve their HbA1c targets on basal insulin. 18 Moreover, a significant proportion of people with diabetes are concerned about the risks of hypoglycaemia and potential weight gain associated with higher basal insulin doses. 19,20 There is an unmet need for better appreciation of the balance between improved glycaemic control and the potential risks of a higher basal insulin dose as well as the dose at which intensification beyond basal insulin is required.…”