We would like to thank Esposito et al. (1) for their interest in and comment on our article (2), in particular their recognition of the importance of the study and the significance of our results. Regarding their concern surrounding the definition of clinical inertia, there are several points that we would like to expand upon. First, we acknowledge that individualizing HbA1c targets may be needed for certain patients (e.g., the elderly) for whom balancing good glycemic control against the risk of hypoglycemia is even more important (3). HbA1c targets in treatment guidelines are only a recommendation. However, these clinical guidelines are used by physicians in practice, and as the basis of our analyses, we used the most appropriate cutoff points available for examining a large population. Information regarding personalized treatment is not available in the Clinical Practice Research Datalink (CPRD) database and thus could not be factored into the analyses. However, in considering individualization of glycemic targets, we specifically conducted analyses for HbA1c targets of <7%, <7.5%, and <8% to reflect the impact of a number of factors, such as disease trajectory, on the goals set. For example, those people treated with one oral antidiabetes drug would, in many cases, be earlier in their disease progression and therefore may need stricter targets, while those treated with three oral antidiabetes drugs may have more flexible targets. Several studies have indicated that extremes of blood glucose concentration (both low and high) should be avoided (4) to minimize the risk of all-cause mortality. The clinical guidelines are, on average, a valuable yardstick for treating patients. In our study, the baseline HbA1c levels were >8.4%, well above what would be considered good glycemic control. Individualized targets may not be sufficient in explaining this discrepancy (5).
Our results reflect the current situation in the U.K., and the large and nationally representative cohort used in our analysis provides a robust assessment of clinical inertia despite any limitations surrounding its definition.
Article Information
Acknowledgments. The authors would like to thank Paul Tisdale and Daria Renshaw, Watermeadow Medical, U.K., for writing and editorial assistance, respectively.
Funding. K.K. is the recipient of the Anglo-Danish-Dutch study of Intensive Treatment In peOple with screeN detected diabetes in primary care (ADDITION) Study grant from National Health Service Research and Development for the commented-on article.
Duality of Interest. K.K., M.L.W., B.L.T., M.A., and M.J.D. have received editorial support for the submitted work from Watermeadow Medical, U.K., which was funded by Novo Nordisk A/S. K.K. has been an advisory board member, received research funding, and has been a paid speaker on behalf of Novo Nordisk in the previous 3 years. M.L.W. and B.L.T. are employees and shareholders of Novo Nordisk A/S. M.A. is a partner in StatGroup ApS, and, as such, has received consulting fees from Novo Nordisk in the previous 3 years. M.J.D. has been an advisory board member, received research funding, has been a paid speaker, and has been paid to develop educational programs and compensated for travel/accommodation/meeting expenses on behalf of Novo Nordisk in the previous 3 years. No other potential conflicts of interest relevant to this article were reported.
