Hypercalcemia and Familial Pheochromocytoma

Swinton, Neil W.; Clerkin, Eugene P.; Flint, Lloyd D.

doi:10.7326/0003-4819-76-3-455

Cited by 48 publications

(10 citation statements)

References 8 publications

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“…Only in the distal tubule, where the final adjustments in calcium excretion occur, does this concordance between calcium and sodium excretion break down. 17 …”

Section: Discussionmentioning

confidence: 99%

Enhanced parathyroid function in essential hypertension: a homeostatic response to a urinary calcium leak.

McCarron¹,

Pingree²,

Rubin³

et al. 1980

Hypertension

327

123

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SUMMARY Disorders of calcium metabolism are not generally considered important either clinically or patbophysiologkally in essential hypertension. Recent reports, though, suggest that increased parathyroid gland function may be one of the more common endocrine disturbances associated with hypertension. We measured serum parathyroid hormone (PTH) concentrations as well as routine blood and arine chemistries in 34 hypertensives. Their mean PTH, 79.1 ± 3.1 filter Eq/ziUter, was rignlflcaatiy higher {p < 0.025) than the mean PTH, 66.9 ± 33, of an age-and sex-matched nonnotenshe control population. The mean serum calcium, 9.5 ± 0.1 mg%, was identical in the two populations. Compared to a second age-aad sex-matched normotensive population, the hypertensives demonstrated a significant (p < 0.005) relatiTe hypercalduria. For any lerd of urinary sodium, hypertenshes excreted more calcium. These preliminary data suggest that parathyroid gland function may be enhanced in essential hypertension. This increased gland actirity appears, in part, to be an appropriate, physiologic response to a previously unrecognized relative hypercalduria, or renal caldum leak, associated with essential hypertension. We condude that the increased prevalence of hypertension in subjects with byperparathyroidfam probably represents the final event In a continuum that begins with obligatory urinary caldum losses in hypertensives, but whose pathological presentation is hyperparathyroidism. The results of this pilot study indicate a need for derivative experiments directed at defining the importance of our preliminary findings In the patbogenesis of human and experimental hypertension. 1 "' Conversely, the prevalence of hyperparathyroidism may be two to eight times greater in hypertensive than in normotensive subjects. 4-• In addition, thiazide diuretics cause overt hypercalcemia in certain hyper-

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“…Only in the distal tubule, where the final adjustments in calcium excretion occur, does this concordance between calcium and sodium excretion break down. 17 …”

Section: Discussionmentioning

confidence: 99%

Enhanced parathyroid function in essential hypertension: a homeostatic response to a urinary calcium leak.

McCarron¹,

Pingree²,

Rubin³

et al. 1980

Hypertension

327

123

View full text Add to dashboard Cite

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“…The possibility that the pheochromocytoma of this patient secreted a substance with PTH-like activity cannot, of course, be ruled out (27 …”

Section: Resultsmentioning

confidence: 99%

Acute Parathyroid Hormone Response to Epinephrine In Vivo

Fischer¹,

Blum²,

Binswanger³

1973

J. Clin. Invest.

153

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A B S T R A C T The acute effects of epinephrine, norepinephrine, and isoproterenol on the plasma immunoreactive parathyroid hormone (iPTH) response were studied in 13 550-600 kg cows. Catecholamines were infused for 7.0 min. During epinephrine infusions at 0.08 Amol/min iPTH increased from 0.48±0.12 (mean+SE, ng/ml) to 1.09±0.18 ng/ml (P < 0.02). Small increases in plasma free fatty acids and glucose could be detected with 0.08 Amol/min epinephrine; the iPTH response to epinephrine was as sensitive as the free fatty acid and glucose responses and possibly of physiological importance. Plasma calcium (total and ionized) and magnesium did not change.The responses were more pronounced at 0.8 /mol/min epinephrine with a mean iPTH increase from 0.49±0.16 ng/ml to 1.74±0.35 ng/ml (P < 0.01). Small decreases in plasma calcium occurred at 0.8 Amol/min epinephrine, but the plasma magnesium remained unchanged. However, when the plasma calcium was lowered with ethylene glycol bis (3-aminoethyl ether) -N, N'-tetraacetic acid (EGTA), a much more pronounced lowering of the plasma calcium was required to produce comparable increases of the plasma iPTH concentrations than when epinephrine was infused. It appears that epinephrine has a direct effect on the release of iPTH from the parathyroid glands.Simultaneous infusions of calcium and epinephrine suppressed the stimulation by epinephrine. This points towards a common mechanism of the regulation of parathyroid hormone secretion caused by decreases in the extracellular calcium concentration and/or alterations in

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“…Interestingly, pheochromocytomas are rarely associated with hyperparathyroidism (45)(46)(47)(48), unless the patients suffer from genetically determined familial polyendocrine adenomatosis type 2 (49).…”

Section: Discussionmentioning

confidence: 99%