Hypercalcemia in Thyrotoxicosis

Rose, Edward; Boles, Russell S.

doi:10.1016/s0025-7125(16)34935-5

Cited by 45 publications

(4 citation statements)

References 7 publications

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“…More difficult to explain is the rare association of hypercalcemia and thyrotoxicosis, as demonstrated by the present case and a few previously reported (7)(8)(9)(10). The presence of hypercalcemia may greatly confuse the clinical picture of thyrotoxicosis.…”

contrasting

confidence: 49%

“…4). It is interest that when thyrotoxicosis recurred in 2 of the cases previously reported, hypercalcemia did not recur (10). The fundamental homeostatic factors controlling the level of ionized calcium in the body fluids are the steady state of equilibrium between the extracellular calcium ion and the surface of the bone crystals (31) and the renal clearance of filtrable calcium.…”

Section: Serum Calcium and Phosphorus Levelsmentioning

confidence: 98%

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Metabolic Observations in a Case of Thyrotoxicosis With Hypercalcemia*

Kleeman¹,

Tuttle²,

Bassett³

1958

The Journal of Clinical Endocrinology & Metabolism

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Hyperthyroidism characteristically causes excessive urinary and fecal excretion of calcium and, rarely, hypercalcemia. These abnormalities were studied in a 58-ycar-old thyrotoxic male. The investigation consisted of a 125-day balance study as the patient became euthyroid and a similar 50-day balance study during a recurrence of the thyrotoxicosis. The excessive urinary and fecal loss of calcium bore little relationship to the calcium or caloric content of the diet or to the level of nitrogen balance. A high phosphate diet ameliorated the metabolic abnormality and corrected the hypercalcemia. Successful treatment of the thyrotoxicosis produced similar changes in calcium metabolism. Hypercalcemia was not present during recurrence of the thyrotoxicosis.The metabolic observations in this case and those previously reported strongly suggest that the excessive urinary and fecal excretion of calcium in thyrotoxicosis is due to a direct effect of thyroid hormone on osseous metabolism. The hypercalcemia is probably secondary to a disorder in the homeostatic mechanism(s) regulating the content of ionized calcium in the extracellular fluid.

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contrasting

confidence: 49%

Section: Serum Calcium and Phosphorus Levelsmentioning

confidence: 98%

Metabolic Observations in a Case of Thyrotoxicosis With Hypercalcemia*

Kleeman¹,

Tuttle²,

Bassett³

1958

The Journal of Clinical Endocrinology & Metabolism

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“…Usually, calcium and phosphorus blood levels are found within normal limits in hyperthyroidism. However, other studies (Aub, Bauer, Heath & Ropes, 1929;Stanley & Fazekas, 1949;Rose & Boles, 1953;Pribek & Meade, 1957 ;Koenig, Scholz & Salassa, 1957 ;Sallin, 1958;Bortz, Eisenberg, Bowers & Pont, 1961 ;Adams, Jowsey, Kelly, Riggs, Kinney & Jones, 1967) have shown that the concentration of blood calcium is sometimes increased in hyperthyroidism, but that it is unlikely that thyroxine has any action on the parathyroids. The ionized portion of plasma calcium may be more frequently increased in hyperthyroidism, even in normocalcaemic cases.…”

Section: Introductionmentioning

confidence: 99%

The Renal Handling of Phosphate in Thyroid Disease

Malamos¹,

Sfikakis²,

Pandos³

1969

Journal of Endocrinology

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The fasting serum phosphate level, the tubular maximal (Tm) phosphate reabsorption and the mean renal phosphate threshold were measured in 18 hyper-and six hypothyroid patients in comparison with 11 euthyroid control subjects. A significant increase of serum inorganic phosphate, phosphate Tm and of the mean renal phosphate threshold were found in hyperthyroidism. These findings suggest an increased tubular reabsorption of phosphate in hyperthyroidism. Four main possible mechanisms of such a renal handling of phosphate in thyroid disease are briefly mentioned although their acceptance needs more direct proof.

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“…The height of plasma (or serum) calcium can be extremely variable, and bears no relation to the severity of the thyrotoxicosis (Bortz et al, 1961;Baxter & Bondy, 1966). In the second case of Rose & Boles (1953), the serum calcium ranged from 11-2 to 19-9 mg/100 ml, and gradually fell following subtotal thyroidectomy. An interesting feature of that case is that recurrence of thyrotoxicosis did not then provoke a rise in the serum calcium.…”

mentioning

confidence: 99%