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The Changing Landscape of Type 2 Diabetes: The Role of Incretin-Based Therapies in Managed Care Outcomes
BACKGROUND: The prevalence of diabetes is growing in the United States and, for many patients, blood glucose continues to be poorly managed. Significantly, more than half of people with type 2 diabetes mellitus (T2DM) have hemoglobin A1Cs greater than 7%. Several factors contribute to the failure to...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Academy of Managed Care Pharmacy
2007
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10438357/ https://www.ncbi.nlm.nih.gov/pubmed/18062735 http://dx.doi.org/10.18553/jmcp.2007.13.9-c.1 |
Sumario: | BACKGROUND: The prevalence of diabetes is growing in the United States and, for many patients, blood glucose continues to be poorly managed. Significantly, more than half of people with type 2 diabetes mellitus (T2DM) have hemoglobin A1Cs greater than 7%. Several factors contribute to the failure to achieve treatment goals, including clinical inertia (the failure to initiate or advance therapy in a patient who is not at the evidence-based therapeutic goal) and failure to address all components of disease pathophysiology. Newer classes of antihyperglycemic agents, the incretin-based therapies, have the potential to improve goal achievement. OBJECTIVES: To review incretin physiology and the latest clinical data on glucagon-like peptide-1 (GLP-1) mimetics and dipeptidyl peptidase-IV (DPP-4) inhibitors and to use this as a foundation to discuss the practical issues of disease management, including clinical inertia, clinical recommendations, and evaluation of the best fit for incretin-based therapies in current treatment paradigms. SUMMARY: Clinical inertia is an important contributing factor to T2DM treatment failure and may be improved through more specific diagnosis, more complete patient education, and an emphasis on earlier and more aggressive therapy in goal-oriented fashion. Based largely on the underlying pathophysiology of T2DM, newer ACE/AACE guidelines have been developed to facilitate this more aggressive approach. The incretin-based therapies can favorably impact some underlying elements in T2DM pathophysiology, including glucagon hypersecretion, rapid gastric emptying, postprandial hyperglycemia, and possibly, chronic -cell dysfunction. When incorporated early into a long-term, treat-to-target management plan, incretin-based therapies have the potential to reduce the prevalence of treatment failure in T2DM and may positively impact disease progression. CONCLUSIONS: Clinicians need to recognize and address the scope and impact of clinical inertia on T2DM patient outcomes. Better use of conventional treatment options and/or consideration of newer incretin-based therapies can contribute to improvements in patient health. |
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