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Calcium and magnesium ions in the gastrointestinal lumen are divalent cations that serve as essential dietary components and significant pharmacological targets. These ions are the primary targets for non-absorbed binding agents such as cellulose sodium phosphate, which is used to sequester luminal calcium and magnesium to prevent their absorption, thereby managing conditions like absorptive hypercalciuria and recurrent calcium nephrolithiasis [1, 2]. Beyond their role as therapeutic targets, these ions are critical in clinical pharmacology due to their ability to chelate and form insoluble complexes with various medications, including tetracyclines, fluoroquinolones, and bisphosphonates, which significantly reduces the systemic absorption and efficacy of these drugs [3, 4]. Furthermore, while these ions are sensed by the calcium-sensing receptor (CaSR) to modulate gastrointestinal motility and secretion, their presence in the lumen must be carefully balanced; for instance, potassium binders like patiromer can inadvertently bind luminal magnesium, leading to hypomagnesemia [5]. Consequently, therapeutic interventions targeting these ions require diligent monitoring of electrolyte levels and potential drug-drug interactions to prevent complications such as secondary hyperoxaluria or mineral deficiencies [2, 3].
Drugs interact with luminal calcium and magnesium ions through ion exchange, chelation, or complexation to prevent their absorption or the absorption of co-administered medications.
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