Hormone, calcium and blood pressure relationships in primary hyperparathyroidism

Richards, A. Mark; Espiner, Eric A.; Nicholls, M. Gary; Ikram, Hamid; Hamilton, E J; Maslowski, A H

doi:10.1097/00004872-198809000-00009

Cited by 33 publications

(20 citation statements)

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“…So far, the high incidence of hypertension in pHPT patients have complicated the decision making about the any pathogenetic role of high PTH levels on cardiovascular abnormalities observed in these patients. High prevalence of hypertension in our pHPT patients is in agreement with previous studies which point to the association between pHPT and systemic hypertension [18]. We subdivided pHPT patients into 2 groups based on the presence of hypertension to examine the confounding effect of this common risk factor for development and progression of coronary atherosclerosis in these patients.…”

Section: Discussionsupporting

confidence: 89%

“…All subjects in study population underwent tomographic coronary calcification scoring by using 16-multidetector computed tomography . Results Median tomographic coronary calcification score was comparable between the whole group of pHPT patients [0.0 (Interquartile Range, IQR: 18.70] and the controls [0.0 (IQR: 0.90). Median tomographic coronary calcification scores of pHPT patients with hypertension was 0.90 (IQR: 75.0) HU, whereas no calcification was noted in coronary arteries of normotensive pHPT patients.…”

mentioning

confidence: 96%

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Evaluation of subclinical coronary atherosclerosis in mild asymptomatic primary hyperparathyroidism patients

Kepez

Harmancı

Hazırolan

et al. 2008

Int J Cardiovasc Imaging

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Section: Discussionsupporting

confidence: 89%

mentioning

confidence: 96%

Evaluation of subclinical coronary atherosclerosis in mild asymptomatic primary hyperparathyroidism patients

Kepez

Harmancı

Hazırolan

et al. 2008

Int J Cardiovasc Imaging

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“…13 It remains to be determined whether parathyroidectomy (PTX) might result in BP reduction, recovery of large-artery properties and improvement of cardiovascular morbidity and mortality. 12,[14][15][16] Our study sought to investigate the arterial stiffness assessed by carotid-femoral PWV in the presence of PH. Specifically, we investigated the hypothesis that PWV is increased in patients with PH with or without concomitant hypertension when compared with patients with essential hypertension (EH) and healthy controls; that is, independently of prevailing arterial BP.…”

Section: Introductionmentioning

confidence: 99%

Pulse wave velocity in primary hyperparathyroidism and effect of surgical therapy

et al. 2010

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The study was aimed at investigating the arterial stiffness assessed by aortic pulse wave velocity (PWV) in the presence of primary hyperparathyroidism (PH), with and without concomitant hypertension. Subsequently, we examined the effect of parathyroidectomy (PTX) on arterial stiffness. A total of 28 patients with PH and concomitant hypertension, and 16 with PH without hypertension were investigated in comparison with 28 essential hypertensive patients and 18 healthy controls, respectively. Patients were matched for age, blood pressure (BP), body mass index, lipid profile and fasting glucose. Six months after PTX, 15 patients were examined again (hypertensive as well as normotensive). PWV was obtained using the SphygmoCor applanation tonometer (AtCor Medical, West Ryde, Australia). PWV was significantly higher in patients with PH and hypertension when compared with patients with essential hypertension (10.1 vs. 8.5 m s À1 , P¼0.013). PWV remained significant even after adjustment for age and BP (P¼0.02). Similarly, PWV was significantly higher in PH patients without hypertension in comparison with healthy controls (7.6 vs. 5.8 m s À1 , Po0.001). Six months after surgery, in addition to a normalization of calcium metabolism, a significant decrease in systolic BP (131 vs. 123 mm Hg, P¼0.004) and PWV (9.1 vs. 8.5 m s À1 , P¼0.024) was observed. After adjusting for BP reduction, the decrease in PWV appeared non-significant. Our data indicate that PH increases PWV as a marker of arterial stiffness, in both hypertensive and non-hypertensive patients. However, neither the calcium serum level nor the parathyroid hormone level has been associated with PWV. Specific treatment by PTX significantly decreases PWV, which may be determined primarily by improved BP control after surgery.

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“…Systemic hypertension accompanying hypercalcémie pHPT is hemodynamically characterized by an increase in total peripheral vascular resistance, but the mechanisms through which pHPT affects blood pressure regulation are not known [4], Theoretically hypercalcemia may exert its effects through a primary change in peripheral vascular smooth muscle function, through the altered release and/or action of pressor substances such as renin or catechola mines or may indirectly cause high blood pressure by lead ing to progressive renal failure. It is also possible that excess iPTH enhances the cellular uptake of the raised serum calci um in hypercalcemia and that such an event augments the hypertensive response to the rise in scrum calcium [5][6][7][8]. Finally, the secretion of a parathyroid hypertensive factor represents another possible mechanism which may precip itate hypertension [9], However, no single disorder in the regulation of arterial blood pressure provides an adequate and consistent explanation for the majority of cases o f hy pertension of parathyroid origin encountered in man.…”

Section: Introductionmentioning

confidence: 99%

Noradrenergic Blood Pressure Dysregulation and Cytosolic Calcium in Primary Hyperparathyroidism

Schiffl¹,

Sitter²,

Lang³

1997

Kidney Blood Press Res

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The purpose of this study was to characterize the changes in noradrenergic blood pressure regulation and the causes of this dysregulation in patients with histologically proven primary hyperparathyroidism before and after parathyroidectomy. In untreated hypertensive patients with primary hyperparathyroidism slightly higher plasma levels of norepinephrine, enhanced cardiovascular reactivity to norepinephrine (p < 0.05) and increased cytosolic free calcium concentration in platelets (p < 0.05) were found. Parathyroidectomy resulted in the correction of noradrenergic blood pressure dysregulation and in the reduction of cytosolic free calcium and led to normotension. In vitro incubation of platelets from normal subjects with heterologous plasma ultrafiltrates from either hypertensive patients with primary hyperparathyroidism or normotensive uremic patients with secondary hyperparathyroidism led to raised platelet calcium in primary hyperparathyroidism but not in secondary hyperparathyroidism, although in both conditions intact parathormone levels were elevated equally. Furthermore, when platelets of normotensive subjects were preincubated with commercially available parathormone, no effect on resting platelet cytosolic calcium was observed. Our results suggest that hypertension in primary hyperparathyroidism may be caused in part by noradrenergic blood pressure dysregulation and seems to be causally linked to the secretion of a parathyroid hypertensive factor, which increases cytosolic calcium and alters vascular tone and reactivity.

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Hormone, calcium and blood pressure relationships in primary hyperparathyroidism

Cited by 33 publications

References 0 publications

Evaluation of subclinical coronary atherosclerosis in mild asymptomatic primary hyperparathyroidism patients

Evaluation of subclinical coronary atherosclerosis in mild asymptomatic primary hyperparathyroidism patients

Pulse wave velocity in primary hyperparathyroidism and effect of surgical therapy

Noradrenergic Blood Pressure Dysregulation and Cytosolic Calcium in Primary Hyperparathyroidism

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