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. 2019 Sep 29;3(1):e00094.
doi: 10.1002/edm2.94. eCollection 2020 Jan.

Evaluating glycaemic control in patients poorly controlled on oral antidiabetic drugs in real-world setting: Results from assessing the Appropriate Timing of Type 2 diAbetes INtensification (ATTAIN)

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Evaluating glycaemic control in patients poorly controlled on oral antidiabetic drugs in real-world setting: Results from assessing the Appropriate Timing of Type 2 diAbetes INtensification (ATTAIN)

Edward B Jude et al. Endocrinol Diabetes Metab. .

Abstract

Introduction: Many patients with type 2 diabetes mellitus (DM) fail to achieve glycaemic control despite recommended treatment strategies to reduce glycated haemoglobin (HbA1c). This real-world retrospective cohort study compared HbA1c change and treatment patterns between those intensifying and not intensifying therapy with oral antidiabetic drugs (OADs).

Materials and methods: Patients suboptimally controlled on OADs (>58 mmol/mol [>7.5%] or >64 mmol/mol [>8.0%] for high risk, index 1) were included from IQVIA Medical Research Data. Intensifiers within 12 months of index 1 were matched (1:1) to nonintensifiers. Primary outcomes were HbA1c change and proportion of participants achieving HbA1c targets 6 and 12 months post-index 2 (date of intensification [intensifiers] or pseudodate [nonintensifiers]). Therapy adherence was also assessed.

Results: A total of 10 832 participants (5539 intensifiers and 5293 nonintensifiers) were included. Mean HbA1c decrease from baseline to 6 months was -1.13% (intensifiers) vs -0.75% (nonintensifiers), with no substantial further change at 12 months. Cox proportional hazards (PH) analysis suggested a nearly 20% greater chance of target achievement at 6 months for intensifiers vs nonintensifiers (hazard ratio [HR]: 0.79 [95% confidence interval [CI]: 0.73-0.86]), which was similar at 12 months (HR: 0.80 [95% CI: 0.74-0.86]). Intensifiers tended towards greater adherence to baseline therapy (90% [standard deviation (SD): 14.9] vs nonintensifiers 87% [SD: 16.0]), which decreased following intensification.

Conclusions: Significant reductions in HbA1c were evident at 6 months and were greater in intensifiers vs nonintensifiers. Little additional clinical benefit was seen 12 months postintensification. Despite good treatment adherence, many participants failed to achieve target HbA1c; actions beyond improved adherence are needed to improve suboptimal HbA1c.

Keywords: adherence; electronic medical records; glycaemic control; oral antidiabetic drugs; real‐world study; treatment intensification; type 2 diabetes melitus.

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Conflict of interest statement

EBJ has received advisory board honoraria and grant/research support from Sanofi, and has received speaker honoraria from Bayer AG, Boehringer Ingelheim, Eli Lilly, Novo Nordisk and Takeda. CO, MM and MN are employees of IQVIA, UK, which was contracted by Sanofi to conduct the analyses. NG, AS and EL are employees of Sanofi.

Figures

Figure 1
Figure 1
A, Change in HbA1c over time for intensifiers vs nonintensifiers. B, Change in HbA1c over time according to specific regimen subgroup. BI, basal insulin; GLP‐1 RA, glucagon‐like peptide‐1 receptor agonist; HbA1c, glycated haemoglobin; OAD, oral antidiabetic drug
Figure 2
Figure 2
A, Kaplan‐Meier plot for time‐to‐target achievement within 6 mo* of intensification. B, Kaplan‐Meier plot for time‐to‐target achievement within 12 mo* of intensification. *Including a 3‐month window to allow for the real‐world nature of the data. It should be noted that the crossing of the curves at approximately 3 mo is an artefact of the data due to intensifiers being ‘anchored’ by the intensification event, meaning they are unlikely to be retested within the next 3 mo (ie the earliest point that a change is likely to be seen is at 3 mo when they are retested). Nonintensifiers are assigned a ‘pseudo’ date with no anchoring event, which means they may be tested sooner than 3 mo. Consequently, some nonintensifiers seemingly improve faster, but following 3 mo of intensifiers, consistently do better. OAD, oral antidiabetic drug

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