The Annals of pharmacotherapy · 2001
Transient hypoparathyroidism due to amphotericin B-induced hypomagnesemia in a patient with beta-thalassemia.
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Marcus N, Garty B Z
Аннотация
OBJECTIVE: To report a case of transient hypoparathyroidism that developed in a beta-thalassemic patient due to amphotericin B-induced hypomagnesemia. CASE SIJMMARY: A 21-year-old man with beta-thalassemia was treated with amphotericin B for Candida albicans intravenous line sepsis. After five days of treatment (cumulative dose 160 mg), he developed hypomagnesemia, which caused hypoparathyroidism and hypocalcemia; all three abnormalities resolved after the drug was withdrawn.
DISCUSSION: Patients with beta-thalassemia may develop endocrinologic abnormalities due to excessive iron deposition. Some may have subclinical hypoparathyroidism that clinically emerges after even a mild homeostasis disturbance. 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 hypoparathyroidism in our patient after discontinuation of amphotericin B treatment suggests that the endocrine dysfunction was due to a drug-related adverse effect and not to parathyroid dysfunction caused by iron deposition.
CONCLUSIONS: This case demonstrates a known but rarely reported adverse effect of amphotericin B, namely hypomagnesemia, that may occur even at a low cumulative dose. It also emphasizes that patients with an underlying disease, such as thalassemia, may be more susceptible to hypoparathyroidism and hypocalcemia during treatment with amphotericin B.
DISCUSSION: Patients with beta-thalassemia may develop endocrinologic abnormalities due to excessive iron deposition. Some may have subclinical hypoparathyroidism that clinically emerges after even a mild homeostasis disturbance. 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 hypoparathyroidism in our patient after discontinuation of amphotericin B treatment suggests that the endocrine dysfunction was due to a drug-related adverse effect and not to parathyroid dysfunction caused by iron deposition.
CONCLUSIONS: This case demonstrates a known but rarely reported adverse effect of amphotericin B, namely hypomagnesemia, that may occur even at a low cumulative dose. It also emphasizes that patients with an underlying disease, such as thalassemia, may be more susceptible to hypoparathyroidism and hypocalcemia during treatment with amphotericin B.