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. 2018 Jun 11;1(3):e00019.
doi: 10.1002/edm2.19. eCollection 2018 Jul.

Glycaemic impact of treatment intensification in patients with type 2 diabetes uncontrolled with oral antidiabetes drugs or basal insulin

Erin K Buysman  1 , Tao Fan  2 , Cori Blauer-Peterson  1 , Lesley-Ann Miller-Wilson  2
Affiliations

Glycaemic impact of treatment intensification in patients with type 2 diabetes uncontrolled with oral antidiabetes drugs or basal insulin

Erin K Buysman et al. Endocrinol Diabetes Metab. .

Abstract

Aims: To investigate the impact of treatment intensification (TI) on glycaemic outcomes in patients with type 2 diabetes with glycated haemoglobin A1c (A1C) ≥7% after ≥6 months of treatment with 2 oral antidiabetes drugs (OADs) or basal insulin (BI).

Materials and methods: Data were extracted from the Optum administrative claims database from 1 January 2009 to 31 August 2015. Patients with TI ≤6 months after the first A1C ≥7% (index date) were compared with patients with no TI (NTI). TI included addition of OAD, GLP-1 receptor agonist or premixed insulin in OAD and BI cohorts, addition of BI and/or bolus insulin in the OAD cohort and addition of bolus insulin or increasing BI dose in the BI cohort. Change from the index A1C value and hypoglycaemia events was compared at 12 months after TI after adjusting for confounders.

Results: A total of 3990/28 123 (14.2%) and 10 425/16 140 (65%) of eligible adults in the OAD and BI cohorts, respectively, underwent TI. These patients showed greater adjusted A1C change vs NTI patients (OAD cohort: -0.59% vs -0.25%; BI cohort: -0.30% vs -0.16%; P < .001 for both comparisons), but with higher hypoglycaemia rates (OAD cohort: odds ratio [OR] 1.68; P < .001; BI cohort: OR: 1.23; P = .004) at follow-up.

Conclusions: Clinical inertia appears to be a significant issue in this population. Although associated with more frequent hypoglycaemia, these results demonstrate that timely TI improves A1C levels, highlighting the need for new and improved agents to effectively manage glycaemia while reducing hypoglycaemia risk.

Keywords: database study; glycaemic control; hypoglycaemia; type 2 diabetes.

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Figures

Figure 1
Figure 1
Study design. aFor patients who did not undergo treatment intensification, a random date to begin follow‐up was defined
Figure 2
Figure 2
Study population attrition for the OAD and the BI cohorts. A1C, glycated haemoglobin A1c; BI, basal insulin; DPP‐4, dipeptidyl peptidase‐4; GLP‐1 RA, glucagon‐like peptide‐1 receptor agonist; OAD, oral antidiabetes drug; SGLT‐2, sodium glucose cotransporter 2; T2D, type 2 diabetes
Figure 3
Figure 3
Adjusted change in A1C from index date to 12 mo after TI in patients with T2D with TI (A) following dual OAD therapy vs NTI (N = 17 334) and (B) following BI therapy vs NTI (N = 9937). A1C, glycated haemoglobin A1c; BI, basal insulin; NTI, no treatment intensification; T2D, type 2 diabetes; TI, treatment intensification. *P < .001. P value refers to intensification ≤6 mo after index date vs no intensification
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