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. 2011 Dec;34(12):2508-14.
doi: 10.2337/dc11-0632. Epub 2011 Oct 25.

Contributions of basal and postprandial hyperglycemia over a wide range of A1C levels before and after treatment intensification in type 2 diabetes

Matthew Riddle  1 , Guillermo Umpierrez, Andres DiGenio, Rong Zhou, Julio Rosenstock
Affiliations

Contributions of basal and postprandial hyperglycemia over a wide range of A1C levels before and after treatment intensification in type 2 diabetes

Matthew Riddle et al. Diabetes Care. 2011 Dec.

Abstract

Objective: To determine the relative contributions of basal hyperglycemia (BHG) versus postprandial hyperglycemia (PPHG) before and after treatment intensification in patients with glycated hemoglobin A(1c) (A1C) >7.0% while on prior oral therapy.

Research design and methods: Self-measured, plasma-referenced glucose profiles and A1C values were evaluated from participants in six studies comparing systematically titrated insulin glargine with an alternative regimen (adding basal, premixed, or prandial insulin, or increasing oral agents). Hyperglycemic exposure (>100 mg/dL [5.6 mmol/L]) as a result of BHG versus PPHG was calculated.

Results: On prior oral therapy, 1,699 participants (mean age 59 years, diabetes duration 9 years) had mean fasting plasma glucose (FPG) of 194 mg/dL (10.8 mmol/L), and mean A1C was 8.7%. BHG contributed an average of 76-80% to hyperglycemia over the observed range of baseline A1C levels. Adding basal insulin for 24 or 28 weeks lowered mean FPG to 117 mg/dL (6.5 mmol/L), A1C to 7.0%, and BHG contribution to 32-41%. Alternative regimens reduced FPG to 146 mg/dL (8.1 mmol/L), A1C to 7.1%, and the contribution of BHG to 64-71%. BHG contributions for patients with A1C averaging 7.6-7.7% were 76% at baseline and 34 and 68% after adding basal insulin or other therapies, respectively.

Conclusions: When A1C is >7.0% despite oral therapy, BHG routinely dominates exposure. Intensified therapy reduces A1C and changes this relationship, but BHG amenable to further intervention still accounts for one-third of total hyperglycemia after basal insulin treatment and two-thirds after alternative methods.

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Figures

Figure 1
Figure 1
A: Baseline seven-point glucose profiles by A1C category. B: Relative contributions of BHG and PPHG to overall hyperglycemia by A1C category at baseline. C: The seven-point glucose profiles by A1C category at week 24 or 28. D: Relative contributions of BHG and PPHG to overall hyperglycemia by A1C category at week 24 or 28.
Figure 2
Figure 2
A: The seven-point glucose profiles for patients on basal insulin versus other treatments at week 24 or 28. B: Relative contributions of BHG and PPHG to overall hypoglycemia by A1C category after 24 or 28 weeks of basal insulin treatment. C: Relative contributions of BHG and PPHG to overall hyperglycemia by A1C category after 24 or 28 weeks of treatment with insulin lispro, premixed insulin, or OAD intensification.
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