Narrative review reveals potential associations between incretin-based therapies and anemia in metabolic disorders, highlighting the need for nutritional monitoring.
Key Points
To evaluate whether incretin-based therapies inadvertently trigger anemia or erythroid suppression through reduced intake, altered gastrointestinal function, and micronutrient deficiencies.
Reviewed available clinical and observational literature covering agents spanning from dipeptidyl peptidase-4 inhibitors (gliptins) to novel multi-agonists including retatrutide.
Assessed underlying pathophysiological mechanisms, including delayed gastric emptying, gastrointestinal intolerance, reduced food consumption, and nutrient malabsorption.
Observational studies indicate potential links between incretin-based therapies and increased risks of anemia, driven primarily by deficiencies in iron, vitamin B12, vitamin D, and other essential micronutrients.
Existing clinical evidence remains heterogeneous and insufficient to confirm a definitive causal relationship or identify a class-wide adverse effect across all incretin agents.