Hypocalcemia in magnesium-depleted dogs: Evidence for reduced responsiveness to parathyroid hormone and relative failure of parathyroid gland function

Levi, J; Massry, Shaul G.; Coburn, Jack W.; Llach, Francisco; Kleeman, Charles R.

doi:10.1016/0026-0495(74)90050-x

Cited by 84 publications

(39 citation statements)

References 37 publications

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“…This observation suggested that her PTH secretion on admission was not sufficient enough to counteract hypocalcemia. Another mechanism by which hypocalcemia develops in Mg deficiency is through the resistance of PTH actions on target organs such as bone [29] and kidney [29][30][31]. In our case, bone metabolic markers and 1,25(OH) 2 D were not elevated and %TRP was not suppressed despite the high value of intact PTH on admission, suggesting that bone and kidney were refractory to PTH action.…”

Section: Discussionmentioning

confidence: 58%

A Case of Magnesium Deficiency Associated with Insufficient Parathyroid Hormone Action and Severe Osteoporosis

et al. 2007

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Abstract. The relationship between osteoporosis and magnesium (Mg) deficiency is still controversial. Here we report a case of an 82-year-old woman with a giant adenomatous goiter and severe osteoporosis with multiple vertebral fractures, whose clinical course indicated that her osteoporosis was probably due to Mg deficiency. She visited our hospital for treatments of tetany. Laboratory data showed the existence of hypomagnesemia, hypocalcemia, hypokalemia, vitamin D deficiency, and slightly elevated intact PTH. Intravenous administration of Mg not only improved these electrolyte abnormalities but also increased serum levels of intact PTH, bone formation markers, 1,25-dihydroxyvitamin D, as well as bone resorption markers in the urine, and lowered urinary phosphate reabsorption. Hypomagnesemia on admission seemed to arise from long-lasting poor food intake and malnutrition, because it improved after the disappearance of dysphagia with a goiter resection. After the operation, BMD values at the lumbar spine and femoral neck obviously increased during 6 months of Mg supplementation without any specific therapies for osteoporosis. Mg deficiency in this case seemed to cause impaired secretion of PTH from the parathyroid and the refractoriness of bone and kidney to the hormone, which led to the suppression of both bone remodeling and renal vitamin D production. These processes were probably linked to her severe osteoporosis, which was reversed by Mg supplementation. SERUM calcium levels are normally regulated within a relatively narrow range by the parathyroid gland through a negative feedback mechanism: Increased secretion of parathyroid hormone (PTH) by a fall in blood calcium levels enhances the mobilization of calcium, mainly by bone resorption, and then calcium levels are rapidly restored. Chronic magnesium (Mg) deficiency would result in hypocalcemia [1, 2], because of the impairment of PTH secretion [3][4][5][6][7] and/ or resistance of target organ to PTH action [4,6,8].Previous studies have demonstrated that serum PTH concentration was suppressed in patients with hypomagnesemia [4,5], and Mg substitution therapy enhanced PTH secretion and reversed PTH target-organ resistance, and thus serum calcium concentration returned to normal within several days [4,7]. In addition, Mg deficiency could inhibit the synthesis of 1,25-dihydroxy vitamin D (1,25(OH) 2 D) [9][10][11] as well as its action on bone [11]. Accumulating data have shown that a long-term Mg deficiency and resulting hypomagnesemia could cause osteoporosis and bone fractures through these dysfunctions of PTH and vitamin D action [12,[13][14][15][16][17][18][19]. However, other studies have shown no relationship between Mg deficiency and osteoporosis [20][21][22], and it still seems to be controversial whether or not Mg deficiency could cause osteoporosis. Here we report a patient with a giant adenomatous goiter and severe osteoporosis exhibiting hypomagnesemic hypocalcemia, whose osteoporosis was reversed by Mg supplementation with chronological improv...

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Section: Discussionmentioning

confidence: 58%

A Case of Magnesium Deficiency Associated with Insufficient Parathyroid Hormone Action and Severe Osteoporosis

et al. 2007

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“…There have been discrepancies in renal responsiveness to PTHin magnesiumdeficiency. Renal hyporesponsiveness to the phosphaturic action of PTHhas been reported in some patients with magnesium deficiency (5,13,16). No data on urinary CAMP is available in these patients.…”

Section: Discussionmentioning

confidence: 99%

“…The secretion of parathyroid hormone (PTH) is suppressed in chronic hypomagnesemia(2-1 2). The refractoriness of target organs, kidney and bone, to PTHactions has also been reported in some hypomagnesemic subjects (5,7,9,(12)(13)(14)(15)(16)(17)(18)(19). In the kidney, PTHreduces phosphate reabsorption at the proximal tubules via a CAMP-dependent process (20)(21)(22).…”

Section: Introductionmentioning

confidence: 87%

Renal Refractoriness to Phosphaturic Action of Parathyroid Hormone in a Patient with Hypomagnesemia.

et al. 1995

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A 50-year-old tetanic womanwith hypomagnesemiais described. She had partial resection of the stomach and thejejunum at the age of20 years. Lack of parathyroid hormone (PTH) function was indicated by hypocalcemia, hyperphosphatemia and high tubular reabsorption of phosphate. However, both plasma concentration of PTHand nephrogenous CAMP were normal. Administration of magnesiumsulfate completely normalized serum phosphate and tubular transport of phosphate with only a modest increase in nephrogenous CAMP. The present findings suggest that phosphaturic action of PTHis impaired in magnesiumdeficiency and that steps distal to CAMP production may be responsible for the renal refractoriness to the hormonal action. (Internal Medicine 34: 666-669, 1995)

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“…Hypocalcemia as a direct consequence of magnesium depletion has been well described (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12). The various possible pathogenetic mechanisms that may be responsible for the hypocalcemia associated with hypomagnesemia include: increased urinary calcium excretion, decreased gastrointestinal calcium absorption, and decreased calcium mobilization from bone (13).…”

Section: Introductionmentioning

confidence: 99%

Evidence for Skeletal Resistance to Parathyroid Hormone in Magnesium Deficiency

Freitag¹,

Martin²,

Conrades³

et al. 1979

J. Clin. Invest.

123

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AB S T R A C T Hypocalcemia during magnesium (Mg) depletion has been well described, but the precise mechanism(s) responsible for its occurrence is not yet fully understood. The hypocalcemia has been ascribed to decreased parathyroid hormone (PTH) secretion as well as skeletal resistance to PTH. Whereas the former is well established, controversy exists as to whether or not Mg depletion results in skeletal resistance to PTH. These studies examine the skeletal response to PTH in normal dogs and dogs fed a Mg-free diet for 4-6 mo. Isolated tibia from normal (serum Mg 1.83±0.1 mg/100 ml) and experimental dogs (serum Mg 1.34+0.15 mg/100 ml) were perfused with Krebs-Henseleit buffer during a constant infusion of 3 ng/ml of synthetic bovine PTH 1-34 (syn b-PTH 1-34). The arteriovenous (A-V) difference for immunoreactive PTH (iPTH) across seven normal bones was 37.5+3%. In contrast, the A-V difference for iPTH was markedly depressed to 10.1±1% across seven bones from Mg-depleted dogs. These findings correlated well with a biological effect (cyclic AMP [cAMP] production) of syn b-PTH 1-34 on bone. In control bones, cAMP production rose from a basal level of 5.8±0.2 to 17.5±0.7 pmol/min after syn b-PTH 1-34 infusion. In experimental bones, basal cAMP production was significantly lower than in controls, 4.5±0.1 pmol/min, and increased to only 7.1±0.4 pmol/ min after syn b-PTH 1-34 infusion. Even when PTH concentrations were increased to 20 ng/ml, cAMP pro-

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Hypocalcemia in magnesium-depleted dogs: Evidence for reduced responsiveness to parathyroid hormone and relative failure of parathyroid gland function

Cited by 84 publications

References 37 publications

A Case of Magnesium Deficiency Associated with Insufficient Parathyroid Hormone Action and Severe Osteoporosis

A Case of Magnesium Deficiency Associated with Insufficient Parathyroid Hormone Action and Severe Osteoporosis

Renal Refractoriness to Phosphaturic Action of Parathyroid Hormone in a Patient with Hypomagnesemia.

Evidence for Skeletal Resistance to Parathyroid Hormone in Magnesium Deficiency

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