Abstract

BackgroundThe occurrence of hypomagnesemia in patients with primary hyperparathyroidism (PHPT) has been noted previously; however, the association of hypomagnesemia and severity of primary hyperparathyroidism remains unknown. The present study aimed to evaluate the association of hypomagnesemia with biochemical and clinical manifestations in patients with PHPT.MethodsThis was a retrospective study conducted at a tertiary hospital. We obtained data from 307 patients with PHPT from January 2010 through August 2020. Data on demographics, history, laboratory findings, bone densitometry findings, and clinical presentation and complications were collected and were compared in normal magnesium group vs hypomagnesemia group.ResultsAmong the 307 patients with PHPT included in our study, 77 patients (33/102 [32.4%] males and 44/205 [21.5%] females) had hypomagnesemia. Mean hemoglobin levels in the hypomagnesemia group were significantly lower than those in the normal magnesium group in both males and females. In contrast, patients with hypomagnesemia had a higher mean serum calcium and parathyroid hormone than individuals with normal magnesium. The typical symptoms of PHPT, such as nephrolithiasis, bone pain/fractures, polyuria, or polydipsia, were more common in the hypomagnesemia group. In addition, patients with hypomagnesemia had a higher prevalence of osteoporosis, anemia, and hypercalcemic crisis. Even after adjusting for potential confounders, including age, sex, body mass index, estimated glomerular filtration rate, and parathyroid hormone levels, these associations remained essentially unchanged.ConclusionBiochemical and clinical evidence indicates that patients with PHPT with hypomagnesemia have more severe hyperparathyroidism than those without hypomagnesemia. In addition, PHPT patients with hypomagnesemia had a higher prevalence of osteoporosis, anemia, and hypercalcemic crisis.

Highlights

  • Primary hyperparathyroidism (PHPT) is a generalized endocrine disorder characterized by hypercalcemia and high or inappropriately normal concentrations of parathyroid hormone (PTH) [1,2,3]

  • In the present study, using a retrospective review of 307 consecutive primary hyperparathyroidism (PHPT) patients who were continuously hospitalized, we investigated the association of hypomagnesemia with biochemical and clinical manifestations in patients with PHPT

  • The average hemoglobin in the hypomagnesemia group was significantly lower than that in the normal magnesium group in both males and females; patients with hypomagnesemia had a higher prevalence of anemia (53.8% versus 27.3%, P < 0.001; Fig. 1)

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Summary

Introduction

Primary hyperparathyroidism (PHPT) is a generalized endocrine disorder characterized by hypercalcemia and high or inappropriately normal concentrations of parathyroid hormone (PTH) [1,2,3]. Parathyroid hormone activates the parathyroid hormone receptor, increasing bone and distal tubular calcium resorption [4]. Hypermagnesemia may cause hypocalcemia, through activation of calcium-sensing receptors in the parathyroid glands, thereby suppressing PTH secretion [5,6,7,8]. Magnesium deficiency may lead to the production of defective cyclic adenosine monophosphate in the parathyroid glands and in PTH target organs. This may be the principal mechanism underlying both impaired PTH secretion and endorgan resistance to PTH, which together contribute to the development of hypocalcemia [9,10,11].

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