Positive Outcomes in Type 2 Diabetes Treatment Intensification

HealthDay News — For patients with type 2 diabetes, not delaying intensification of oral antidiabetic drugs is associated with greater reductions in hemoglobin A1c (HbA1c), and with reduced risks of cardiovascular events and amputations, according to a study published in Diabetes, Obesity and Metabolism.

Henry J. Folse, PhD., from Evidera in San Francisco, and colleagues utilized the Archimedes Model to examine the consequences of delays in oral antidiabetic drug treatment intensification in a cohort of hypothetical patients with HbA1c ≥8% on metformin, with no history of insulin use. The intensification sequence included addition of a sulfonylurea, dipeptidyl peptidase-4 (DPP-4) inhibitor, and thiazolidinedione.

The researchers found that HbA1c was 6.8% at 1 year for patients intensifying without delay, compared with 8.2% for those delaying intensification. There were reductions of 18%, 25%, 13.7%, and 20.4% in the risks of major adverse cardiac events, myocardial infarction, heart failure, and amputations, respectively, at 5 years for no delay vs delay. The risk of severe hypoglycemia increased to 19% for no delay, compared with 12.5% for delay. Similar trends were seen in the results at 20 years.

“Timing of intensification of oral antidiabetic drug therapy per guideline recommendations led to greater reductions in HbA1c and lower risks of complications, but higher risks of hypoglycemia, than delaying intensification,” the authors write. “These results highlight the potential impact of timely treatment intensification on long-term outcomes.”

Several authors disclosed financial ties to the pharmaceutical and health technology industries.

Related Articles

Reference

Folse HJ, Mukherjee J, SHeehan JJ, et al. Delays in treatment intensification with oral antidiabetic drugs and risk of microvascular and macrovascular events in patients with poor glycemic control: An individual patient simulation study [published online February 17, 2017]. Diabetes Obes Metab. doi: 10.1111/dom.12913