Plasma Magnesium Concentration in Primary Hyperparathyroidism

Sutton, R. A. L.

doi:10.1136/bmj.1.5695.529

Cited by 30 publications

(12 citation statements)

References 18 publications

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“…Fur thermore, a tendency towards hypermagnesaemia is seen in hyperparathyroid patients with a modest degree of hypercalcaemia (King and , 1970;Sutton, 1970). The findings of Nielsen et al (1977) that iPTH also increases as evaluated by an N-terminal immunoassay lends further support to the view that the rise in iPTH reflects increased secretion rather than an altered degradation of the hormone.…”

Section: Discussionsupporting

confidence: 55%

Development of ‘Primary’ Hyperparathyroidism during Lithium Therapy: Longitudinal Study

Christiansen

Baastrup

Transbøl³

1980

Neuropsychobiology

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The bone mineral content and the serum levels of immunoreactive parathyroid hormone (iPTH), and protein-corrected calcium and magnesium were measured in 13 manic depressive patients before and duringtreatment with lithium. Initially all four parameters were normal. During the treatment the bone mineral decreased and the serum levels of iPTH, calcium, and magnesium increased. Although altered metabolism of parathyroid hormone cannot be ruled out, these data, together with other observations, suggest that a mild ‘primary’ hyperparathyroidism sets in quite early after institution of lithium therapy.

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Section: Discussionsupporting

confidence: 55%

Development of ‘Primary’ Hyperparathyroidism during Lithium Therapy: Longitudinal Study

Christiansen

Baastrup

Transbøl³

1980

Neuropsychobiology

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“…However, our findings concerning the relation between PTH and different indices do not suggest that increased bioactivity of PTH accounts for the changes observed (Table 4). Furthermore the hypermagnesaemia observed in our FHH patients and previously reported by other research groups (Marx et al, 1978a;Davies et al, 1981;Menko el al., 1983) is in distinct contrast to the variable depression of serum magnesium, which characterizes typical primary hyperparathyroidism (Sutton, 1970;King & Stanbury, 1970). Finally the poor response of hypercalcaemia to subtotal parathyroidectomy, and the persistence of increased tubular calcium reabsorption even after total parathyroidectomy (Attie et al, 1983) suggest a complex pathogenesis in FHH.…”

Section: Role Of Pth In Fhhmentioning

confidence: 99%

Familial Hypocalciuric Hypercalcaemia I: Renal Handling of Calcium, Magnesium and Phosphate

Kristiansen

Mortensen

Pedersen

1985

Clinical Endocrinology

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Ten hypercalcaemic members from three generations of a family with familial hypocalciuric hypercalcaemia (FHH) were compared with age and sex matched healthy subjects. Two of the former had undergone unsuccessful subtotal parathyroidectomy. Our results showed that the hypercalcaemia was mainly attributable to an increased capacity for tubular reabsorption of calcium, but in part also to an increased release of calcium from bone. The relative hypermagnesaemia had a similar dual origin. The serum phosphate concentration was low and this could be accounted for in full by a decrease in renal tubular reabsorption of phosphate, as assessed by the renal threshold phosphate concentration (TmPO4/GFR). The results of PHT measurements with two radioimmunoassays were equivocal. Most patients had normal serum PTH values, but with one assay mean serum PTH was significantly higher in the hypercalcaemic group. We conclude that the abnormalities of the divalent cation and phosphate metabolism cannot be accounted for in full by increased circulating PTH activity, and are predominantly due to an intrinsic renal abnormality.

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“…Previous studies have shown low-normal or low serum magnesium concentrations in patients with primary hyperparathyroidism and an inverse cor¬ relation between serum calcium and serum mag¬ nesium (27)(28)(29). However, at serum total calcium values about 3 mmol/1, like in our patients, most patients have normal serum magnesium concen¬ tration (27,29,30).…”

Section: Discussionmentioning

confidence: 45%

“…However, at serum total calcium values about 3 mmol/1, like in our patients, most patients have normal serum magnesium concen¬ tration (27,29,30).…”

Section: Discussionmentioning

confidence: 88%

Renal tubular reabsorption of calcium and sodium in primary hyperparathyroidism

Kristiansen

Brøchner‐Mortensen²,

Pedersen³

et al. 1990

Acta Endocrinologica

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Nine patients with primary hyperparathyroidism were studied to investigate the renal tubular reabsorption of calcium and sodium. Fasting serum and urine samples were analysed, and the glomerular filtration rate and the renal plasma clearance of lithium were determined simultaneously. Comparison was made with 9 ageand sex-matched normocalcemic controls. In the proximal tubule, there was a significantly higher absolute reabsorption of calcium in patients than in controls, whereas the fractional reabsorption rate of calcium did not differ between the two groups. In the distal tubule, the absolute calcium reabsorption rate was significantly higher in the patients, whereas the fractional reabsorption rate of calcium was significantly lower than in controls. In the patient group there was a significantly positive linear correlation between the increased tubular capacity for calsium reabsorption and the absolute proximal calcium reabsorption rate, but not between the increased capacity and the absolute distal calcium reabsorption rate. No significant differences were found in the renal tubular handling of sodium between patients and controls. Our results suggest that the increased capacity for tubular calcium reabsorption in primary hyperparathyroidism mainly is localized in the proximal tubule, and that the renal tubular handling of calcium and sodium in this disease differs from that in familial hypocalciuric hypercalcemia.Primary hyperparathyroidism is a disease charac¬ terized biochemically by hypercalcemia, hypophosphatemia, and elevated level of immunoreactive parathyroid hormone (PTH). The hypercalcemia in primary hyperparathyroidism can be accounted for by the enhancing effect of PTH on flux of cal¬ cium from gut and bone and an increased capacity for renal tubular reabsorption of calcium (1), the latter apparently playing the major role (1,2).Another hypercalcémie disorder which biochem¬ ically have much in common with primary hyper¬ parathyroidism is familial hypocalciuric hypercal¬ cemia (3). However, several studies have estab¬ lished that aspects of the pathophysiology of famil¬ ial hypocalcimic hypercalcemia differ from those of typical primary hyperparathyroidism (4-9).Recently we investigated the nephron site of the enhanced tubular calcium reabsorption in familial hypocalcimic hypercalcemia by means of combined determination of the glomerular filtration rate (GFR) and lithium clearance (10). Compared with normal healthy controls, the results suggested that the increased tubular calcium reabsorption in fa¬ milial hypocalcimic hypercalcemia took place ex¬ clusively in the proximal tubule. Furthermore, the same study revealed a difference in renal handling of sodium between familial hypocalcimic hypercal¬ cemia and controls (11).As an extension of that study we have attempted to elucidate the renal tubular function in primary hyperparathyroidism with special reference to:1. Estimation of the increased capacity for renal tubular reabsorption of calcium.2. Determination of fractional and absolute reabsorptio...

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Plasma Magnesium Concentration in Primary Hyperparathyroidism

Cited by 30 publications

References 18 publications

Development of ‘Primary’ Hyperparathyroidism during Lithium Therapy: Longitudinal Study

Development of ‘Primary’ Hyperparathyroidism during Lithium Therapy: Longitudinal Study

Familial Hypocalciuric Hypercalcaemia I: Renal Handling of Calcium, Magnesium and Phosphate

Renal tubular reabsorption of calcium and sodium in primary hyperparathyroidism

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