Mild hyperparathyroidism

Maniero, Carmela; Fassina, Ambrogio; Seccia, Teresa Maria; Toniato, Antonio; Iacobone, Maurizio; Plebani, Mario; De, Raffaele; Calò, Lorenzo A.; Pessina, Achille C.; Rossi, Gian Paolo

doi:10.1097/hjh.0b013e32834f0451

Cited by 71 publications

(32 citation statements)

References 22 publications

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“…However, only recently the calcium metabolism alterations and hyperaldosteronism have been systematically recognized [11]. In particular, studies aimed to verify the hypothesis postulating the effect of aldosterone on the secretion of PTH are also worth mentioning [10]. In this study we examined the calcium mineral metabolism and BMD in PA patients, (both APA and IHA), compared to EH patients.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, in a relative cohort of patients with unequivocally confirmed PA due to APA, Maniero et al [10] showed a highly significant 31% increase in the number of cases of hyperparathyroidism, thus suggesting that there is a bidirectional functional link between the adrenocortical zona glomerulosa and the parathyroid gland. Moreover, these researchers demonstrated the expression of the mineral corticoid receptors (MR) in both PTH secreting adenoma and in parathyroid tissue [11], and the MR was predominantly located in the nucleus of the parathyroid cells, indicating that aldosterone participate in a “tonic” regulation of PTH synthesis and secretion.…”

Section: Introductionmentioning

confidence: 99%

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Bone and Mineral Metabolism in Patients with Primary Aldosteronism

Petramala

Zinnamosca

Settevendemmie

et al. 2014

International Journal of Endocrinology

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Primary aldosteronism represents major cause of secondary hypertension, strongly associated with high cardiovascular morbidity and mortality. Aldosterone excess may influence mineral homeostasis, through higher urinary calcium excretion inducing secondary increase of parathyroid hormone. Recently, in a cohort of PA patients a significant increase of primary hyperparathyroidism was found, suggesting a bidirectional functional link between the adrenal and parathyroid glands. The aim of this study was to evaluate the impact of aldosterone excess on mineral metabolism and bone mass density. In 73 PA patients we evaluated anthropometric and biochemical parameters, renin-angiotensin-aldosterone system, calcium-phosphorus metabolism, and bone mineral density; control groups were 73 essential hypertension (EH) subjects and 40 healthy subjects. Compared to HS and EH, PA subjects had significantly lower serum calcium levels and higher urinary calcium excretion. Moreover, PA patients showed higher plasma PTH, lower serum 25(OH)-vitamin D levels, higher prevalence of vitamin D deficiency (65% versus 25% and 25%; P < 0.001), and higher prevalence of osteopenia/osteoporosis (38.5 and 10.5%) than EH (28% and 4%) and NS (25% and 5%), respectively. This study supports the hypothesis that bone loss and fracture risk in PA patients are potentially the result of aldosterone mediated hypercalciuria and the consecutive secondary hyperparathyroidism.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Bone and Mineral Metabolism in Patients with Primary Aldosteronism

Petramala

Zinnamosca

Settevendemmie

et al. 2014

International Journal of Endocrinology

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“…Calcium 1,2 , vitamin D 3–9 , and parathyroid hormone (PTH) 10–12 have been implicated in regulating the renin-angiotensin-aldosterone system (RAAS), and the RAAS, in turn, has been implicated in regulating these calcium-regulatory hormones 13–16 . In particular, recent observational studies in individuals with primary hyperaldosteronism (PA) suggest that excess aldosterone may result in hyperparathyroidism 15–17 . A better understanding of the normal physiologic relationship between the RAAS and PTH is of clinical relevance since inappropriate activity of both PTH and the RAAS may negatively impact cardiovascular 18–26 and skeletal health 27,28 .…”

Section: Introductionmentioning

confidence: 99%

“…Human evidence characterizing the positive relationship between RAAS activity and PTH has largely originated from observational studies in disease states such as hyperaldosteronism 15,16 and chronic kidney disease (CKD) 29 . Spironolactone therapy is associated with lower fracture risk in heart failure 27 ; patients with PA have reduced bone mineral density and a higher rate of osteoporosis 30 ; and PA is associated with elevated PTH levels that are lowered following clinically indicated surgical or medical therapy for PA 14–16 .…”

Section: Introductionmentioning

confidence: 99%

Human Interventions to Characterize Novel Relationships Between the Renin–Angiotensin–Aldosterone System and Parathyroid Hormone

et al. 2014

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Observational studies in primary hyperaldosteronism (PA) suggest a positive relationship between aldosterone and parathyroid hormone (PTH); however, interventions to better characterize the physiologic relationship between the renin-angiotensin-aldosterone system (RAAS) and PTH are needed. We evaluated the effect of individual RAAS components on PTH using 4 interventions in humans without PA. PTH was measured before and after: Study 1) low-dose angiotensin II [AngII] infusion (1 ng/kg/min) and captopril administration (25 mg × 1); Study 2) high-dose AngII infusion (3 ng/kg/min); Study 3) blinded crossover randomization to aldosterone infusion (0.7 µg/kg/hr) and vehicle; and Study 4) blinded randomization to spironolactone (50mg/daily) or placebo for 6 weeks. Infusion of AngII at 1 ng/kg/min acutely increased aldosterone (+148%) and PTH (+10.3%), while AngII at 3 ng/kg/min induced larger incremental changes in aldosterone (+241%) and PTH (+36%) (P<0.01). Captopril acutely decreased aldosterone (−12%) and PTH (−9.7%) (P<0.01). In contrast, aldosterone infusion robustly raised serum aldosterone (+892%) without modifying PTH. However, spironolactone therapy over 6 weeks modestly lowered PTH when compared to placebo (P<0.05). In vitro studies revealed the presence of AngII type I and mineralocorticoid receptor mRNA and protein expression in normal and adenomatous human parathyroid tissues. We observed novel pleiotropic relationships between RAAS components and the regulation of PTH in individuals without PA: the acute modulation of PTH by the RAAS appears to be mediated by AngII, whereas the long-term influence of the RAAS on PTH may involve aldosterone. Future studies to evaluate the impact of RAAS inhibitors in treating PTH-mediated disorders are warranted.

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“…Indeed, calcium sensing receptors are expressed in juxtaglomerular cells in mice [23] and rats [18]. Recent findings in humans indicate that there is a tight link between the RAAS and the parathyroid glands, suggesting that the RAAS may mediate the furosemide effect on PTH secretion [4,15,16,19,20,22,29]. In a previous experimental study, we demonstrated that administration of the calcimimetic RS568 inhibited renin secretion in rats and blunted the renin response induced by furosemide [18].…”

Section: Several Hypotheses Have Been Proposed To Explain Furosemide-mentioning

confidence: 95%

Furosemide stimulation of parathormone in humans: role of the calcium-sensing receptor and the renin-angiotensin system

Muller

Ogna

Stoudmann

et al. 2015

Pflugers Arch - Eur J Physiol

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Interactions between sodium and calcium regulating systems are poorly characterized but clinically important. Parathyroid hormone (PTH) levels are increased shortly after furosemide treatment by an unknown mechanism and this effect is blunted by the previous administration of a calcimimetic in animal studies. Here, we explored further the possible underlying mechanisms of this observation in a randomized cross-over placebo-controlled study performed in 18 human males. Volunteers took either cinacalcet (60mg) or placebo and received a 20mg furosemide injection 3 hours later. Plasma samples were collected at 15 minutes intervals and analyzed for intact PTH, calcium, sodium, potassium, magnesium, phosphate, plasma renin activity (PRA) and aldosterone up to 6h after furosemide injection. Urinary electrolytes excretion was also monitored. Subjects under placebo presented a sharp increase in PTH levels after furosemide injection. In presence of cinacalcet, PTH levels were suppressed and marginal increase of PTH was observed. No significant changes in electrolytes and urinary excretion were identified that could explain the furosemide-induced increase in PTH levels. PRA and aldosterone were stimulated by furosemide injection, but were not affected by previous cinacalcet ingestion.Expression of NKCC1, but not NKCC2 was found in parathyroid tissue. In conclusion, our results indicate that furosemide acutely stimulates PTH secretion in absence of any detectable electrolyte changes in healthy adults. A possible direct effect of furosemide on parathyroid gland needs further studies. Mechanisms of furosemide-induced PTH secretion3

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Mild hyperparathyroidism

Abstract: Hence, in primary aldosteronism an increased sensitivity of parathyroid cells to Ca lowering leads to an increase of PTH. This subtle hyperparathyroidism by acting on PTHR-1 in APA might contribute to maintaining hyperaldosteronism despite suppression of angiotensin II formation.

Cited by 71 publications

References 22 publications

Bone and Mineral Metabolism in Patients with Primary Aldosteronism

Bone and Mineral Metabolism in Patients with Primary Aldosteronism

Human Interventions to Characterize Novel Relationships Between the Renin–Angiotensin–Aldosterone System and Parathyroid Hormone

Furosemide stimulation of parathormone in humans: role of the calcium-sensing receptor and the renin-angiotensin system

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