Delayed therapy intensification may lead to suboptimal glucose control in T2D
In type 2 diabetes (T2D) patients initiating second-line therapy, a delay in glucose-lowering treatment intensification appears to reduce the likelihood of reaching recommended treatment goals, a study has found.
The study used data from DISCOVER and included 9,575 T2D patients who intensified treatment (add-on or insulin initiation) upon initiation of second-line therapy (baseline). Outcomes were evaluated according to baseline HbA1c: ≤7.5 percent (early intensification) or >7.5 percent (late intensification).
Treatment intensification occurred early in 3,275 (34.2 percent) patients and late in 6,300 (65.8 percent). Mean HbA1c during follow-up was lower for patients in the early-intensification group than for those in the late-intensification group; the respective values were 6.9 percent vs 7.5 percent at 36 months.
Furthermore, significantly more patients in the early- than in the late-intensification group had suboptimal HbA1c levels (<7.0 percent) at 36 months (61.8 percent vs 37.9 percent; p<0.001).
Multivariate logistic regression analysis showed that the risk of further intensification was 88-percent higher in the late-intensification group than in the early-intensification group (hazard ratio, 1.88, 95 percent confidence interval, 1.68–2.09).
In terms of safety, the incidence of hypoglycaemia was similar in both groups.
Guidelines for the management of T2D recommend the achievement and maintenance of HbA1c levels below the threshold of 7.0 percent for most patients, with timely intensification of glucose-lowering therapy in case the target is exceeded. However, many patients initiate second-line therapy only when their HbA1c levels have risen above the target. Failure to intensify therapy in a timely manner puts patients in an elevated risk of long-term microvascular and macrovascular complications of T2D. [https://www.idf.org/e-library/guidelines/79-globalguideline-for-type-2-diabetes; Diabetes Obes Metab 2020;22:66-78; Diabetes Metab 2017;43:501-511]