Transient hypoparathyroidism due to amphotericin B-induced hypomagnesemia in a patient with beta-thalassemia

OBJECTIVE: To report a case of transient hypoparathyroidism that developed in a beta -thalassemic patient due to amphotericin B-induced hypomagnesemia . CASE SUMMARY: A 21-year-old man with beta -thalassemia was treated with amp hotericin B for Candida albicans intravenous line sepsis. After five days o f treatment (cumulative dose 160 mg), he developed hypomagnesemia, which ca used hypoparathyroidism and hypocalcemia; all three abnormalities resolved after the drug was withdrawn. DISCUSSION: Patients with beta -thalassemia may develop endocrinologic abno rmalities due to excessive iron deposition. Some may have subclinical hypop arathyroidism that clinically emerges after even a mild homeostasis disturb ance. Amphotericin B is associated with variable adverse effects including renal tubular insult, which may induce hypomagnesemia following relatively short treatment. The resolution of hypomagnesemia, hypocalcemia, and hypopa rathyroidism in our patient after discontinuation of amphotericin B treatme nt suggests that the endocrine dysfunction was due to a drug-related advers e effect and not to parathyroid dysfunction caused by iron deposition. CONCLUSIONS: This case demonstrates a known but rarely reported adverse eff ect of amphotericin B, namely hypomagnesemia, that may occur even at a low cumulative dose, It also emphasizes that patients with an underlying diseas e, such as thalassemia, may be more susceptible to hypoparathyroidism and h ypocalcemia during treatment with amphotericin B.