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Baseline A1C Can Be a Predictor of Response to GLP-1 Treatments

Nov 16, 2012

Are patients with a higher baseline A1C more likely to have a better glycemic response to GLP-1 treatments?…

The retrospective observational cohort study was done to determine predictors of glycemic response to exenatide and to assess change in glycosylated hemoglobin (A1C) and whether a correlation exists between weight loss and glycemic response.

One hundred adult patients with type 2 diabetes were given exenatide then a retrospective chart review of patients was done to collect demographic data, weight, serum creatinine, diabetes education, and concurrent diabetes medications.

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Patients were categorized as responders or nonresponders based on change in A1C. Responders had an A1C decrease of 0.5% or more and nonresponders had an A1C decrease of less than 0.5% from baseline to post–exenatide initiation. Demographic data for each cohort were analyzed.

The results from the 100 patients who met inclusion criteria (61 responders and 39 nonresponders) were analyzed. Responders had a mean A1C decrease of 1.6%, whereas nonresponders had a mean A1C increase of 0.23% (P < 0.001). Post hoc linear regression analysis revealed that baseline A1C was a predictor of response to exenatide (P < 0.001).

Binary logistic regression analysis demonstrated that no other variables were predictors of response to exenatide (P > 0.05 for all). No correlation was found between weight loss and exenatide and glycemic response (P = 0.99).

The initial analysis of the primary outcome failed to reveal any predictors of response. However, post hoc analysis determined baseline A1C to be a predictor of response to exenatide. Patients with a lower baseline A1C (<7.3%) were not likely to respond to exenatide, whereas those with a higher baseline A1C (≥7.3%) were likely to respond to exenatide. This trend toward lower baseline A1C correlating with reduced medication response has been demonstrated previously with oral antihyperglycemic medications and with GLP-1 agonists, including exenatide and liraglutide. In a study by Klonoff et al., 47 patients with a baseline A1C of 9% or higher had an A1C lowering of 2.1 ± 0.2% on exenatide therapy, while 170 patients with a baseline A1C less than 9% had an A1C lowering of only 0.6 ± 0.1% (P value not reported). Another study also found, as a secondary outcome, that higher baseline A1C (9.3 vs. 8.3%, P < 0.001) was a statistically significant predictor of clinical response to exenatide. Similar to our findings, the authors of the current work noted a linear relationship between baseline A1C and decrease in A1C at 6 months. Buse et al. observed greater decreases in A1C in patients on either exenatide (–1.2% [SE 0.37%]) or liraglutide (–2.4% [SE 0.21%]) when their baseline A1C was 10% or more compared with patients with a baseline A1C less than 10% (P value not reported), demonstrating the same trend in two different GLP-1 agonists.

From the results it was concluded that the data indicates that patients with a higher baseline A1C are more likely to have an increased glycemic response to exenatide than patients with a lower baseline A1C. However, given the observational nature of the study, elevated baseline A1C levels — not necessarily the presence of exenatide — may be driving the treatment.

J Am Pharm Assoc (2003). 2012 Jul-Aug;52(4):466-71.