HYPOPARATHYROIDISM SECONDARY TO HYPOMAGNESEMIA IN A PATIENT TAKING POLYMYXIN B: A CASE REPORT
DOI:
https://doi.org/10.56238/levv13n31-056Keywords:
Functional Hypoparathyroidism, Hypomagnesemia, Polymyxin B, NephrotoxicityAbstract
This study presents the case of a young, previously healthy patient who developed functional hypoparathyroidism secondary to hypomagnesemia induced by prolonged use of Polymyxin B. After severe polytrauma and multiple surgeries, the patient was treated with Polymyxin B for a bone infection caused by Pseudomonas aeruginosa. During the antibiotic therapy, he developed persistent hypomagnesemia, hypocalcemia and inadequately low PTH levels, indicating functional parathyroid dysfunction. Hypomagnesemia, caused by proximal tubular damage induced by Polymyxin B, impaired the secretion and action of PTH, generating electrolyte disturbances with systemic repercussions. The patient presented neuromuscular symptoms compatible with symptomatic hypocalcemia, such as myoclonus and irritability. Intravenous calcium and magnesium replacement, vitamin D supplementation and a phosphorus-restricted diet resulted in laboratory and clinical improvement. The case highlights the subclinical nephrotoxicity of Polymyxin B, which can occur even with normal creatinine levels, reinforcing the need for strict monitoring of electrolytes in patients using it. In addition, it highlights how isolated ion disturbances can reflect major hormonal alterations, such as functional hypoparathyroidism, and that early diagnosis and treatment are crucial to avoid chronic complications.
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