Optimizing Glycemic Regulation Through Combination Therapy
Focus on the Safety, Convenience, HA1c Control, Reducing Risk of Hypoglycemia, and Efficacy of Combination Basal Insulin-GLP-1 RA Regimens in T2D
Focus on the Safety, Convenience, HA1c Control, Reducing Risk of Hypoglycemia, and Efficacy of Combination Basal Insulin-GLP-1 RA Regimens in T2D
Course Videos
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What is the underlying physiology that explains the role of incretins in the disease processes leading to T2D?
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How do we define PPG? How do we confirm its presence as an actionable metabolic derangement in need of intervention? And where does iGlarLixi fit into this treatment algorithm for PPG?
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Are there head-to-head comparisons looking at the effects of different GLP-1 RAs on PPG control? What are the results and implications of those studies?
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What specific strategies are currently in the T2D pharmacologic toolkit that have been shown effective for reducing PPG? Where do GLP-1 RAs fit into this scheme?
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What do we know about the relationship between PPG and cardiovascular risk?
What do we know about the relationship between PPG and cardiovascular risk?
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What was the physiological, safety, and compliance-focused rationale for combining basal insulin plus GLP-1 RA into a fixed ratio formulation?
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From a practical perspective, how do we assess to what degree PPG is playing a role in failing to achieve goal-directed HA1c levels? How do we use FPG and PPG levels to determine the need for agents useful for PPG control?
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What is the importance of postprandial hyperglycemia (PPG) and glucose excursions as a management metric and what are the implications for selecting a specific GLP-1 RA with a specific PK/PD profile?
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How would deploy the fixed ratio combination agents in a 58-year old obese male patient who was not meeting HA1c target goals on metformin alone, or a second oral agent?
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Where might the fixed ratio, combination regimens consisting of a long-acting insulin and GLP-1 RA fit into the ADA and AACE guidelines and how do your see their use in the sequencing algorithm for T2D?
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Are there clinically relevant differences between the fixed ratio, combination regimens— iGlarLixi or iDegLira— consisting of a long-acting insulin and GLP-1 RA?
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Why are the risks of hypoglycemia very low when using the fixed ratio, combination regimens? Does this have to do with slow titration or mechanistic complementarity? By what mechanism do they mitigate hypoglycemic risk?