Hypomagnesemic hypocalcemia. Early serum calcium and late parathyroid hormone increase with magnesium therapy

A case of functional hypoparathyoidism due to hypomagnesaemia leading to hypocalcaemic seizures

“…It is known that magnesium is crucial in formation of cyclic AMP (adenosine monophosphate) both in the parathyroid glands as well as in their end-organs, such that both synthesis and secretion of PTH would be impaired [7], whilst it's activity at end organs would be blunted, in the face of a low magnesium [7,9,10,11]. We surmise that failure of the parathyroid mechanism to reabsorb calcium from the bone, intestines and nephron (via activation of a specific calcium pump) dangerously lowered the serum calcium level which was producing seizure activity.…”

Hypomagnesemia masking the appearance of elevated parathyroid hormone concentrations in familial pseudohypoparathyroidism

“…This is due, in part, to a state of relative hypoparathyroidism resulting from impaired PTH secretion [Rude et al, 1978;Wiegmann and Kaye, 1977;Duran et al, 1984;Anast et al, 19761. Although hypomagnesemia has been associated with undetectable, normal, and elevated PTH concentrations [Rude et al, 19781, intravenous magnesium supplementation to magnesium-deficient, hypocalcemic patients (even those with elevated PTH levels) has been shown to increase the serum concentrations of PTH [Rude et al, 1978;Wiegmann and Kaye, 1977;Duran et al, 1984;Anast et al, 19761. While this PTH response may occasionally be delayed [Wiegmann and Kaye, 19771, the usual rapidity of this phenomenon supports in vitro evidence for effect of magnesium on release of stored PTH rather than on PTH biosynthesis [Targovnik et al, 19711. However, suppression of parathyroid hormone secretion may not be totally responsible for hypocalcemia in hypomagnesemic patients.…”

“…The finding of normal or elevated PTH concentrations in some hypomagnesemic, hypocalcemic patients [Rude et al, 19781 would appear to support the concept of end-organ resistance. However, studies of hypomagnesemic children and adults [Wiegmann and Kaye, 1977;Duran et al, 1984;Anast et al, 19761 have shown a normal response to parathyroid extract as judged by changes in serum pseudohypoparathyroidism; I , 3-extreme short stature (by history); 2--short stature, history of "seizures." calcium levels and urinary phosphate and cyclic AMP excretion.…”

“…Magnesium deficiency is often associated with reduced serum calcium concentrations. This is due, in part, to a state of relative hypoparathyroidism resulting from impaired PTH secretion [Rude et al, 1978;Wiegmann and Kaye, 1977;Duran et al, 1984;Anast et al, 19761. Although hypomagnesemia has been associated with undetectable, normal, and elevated PTH concentrations [Rude et al, 19781, intravenous magnesium supplementation to magnesium-deficient, hypocalcemic patients (even those with elevated PTH levels) has been shown to increase the serum concentrations of PTH [Rude et al, 1978;Wiegmann and Kaye, 1977;Duran et al, 1984;Anast et al, 19761.…”

“…Disorders of magnesium metabolism a r e known to have important effects on calcium homeostasis. Hypomagnesemia appears to contribute to the development of hypocalcemia by impeding parathyroid hormone release [Rude et al, 1978;Wiegmann and Kaye, 1977;Duran et al, 1984;Anast et al, 19761 and, in some cases, by altering endorgan responsiveness to this homone [Estep et al, 1969;MacManus et al, 1971;Rude et al, 19761. Familial pseudohypoparathyroidism, a syndrome of renal and/or skeletal unresponsiveness to parathyroid hormone (PTH), is characterized by the typical manifestations of Albright syndrome, hypocalcemia, hyperphosphatemia, and elevated serum PTH concentrations [Daneman et al, 19821.…”