Parathyroid disease and calcium metabolism

Mihai, Radu; Farndon, John

doi:10.1093/bja/85.1.29

Cited by 86 publications

(44 citation statements)

References 68 publications

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“…The majority of hyperparathyroid patients in our study were women, a finding consistent with a higher incidence of parathyroid disease in women than men [14]. This increased incidence is partly due to more frequent measuring of blood calcium levels in women for detection of osteoporosis.…”

Section: Discussionsupporting

confidence: 85%

“…Hyperparathyroidism can be secondary in response to a low serum calcium level initiating a compensatory secretion of PTH [14]. For these reasons, we divided the hyperparathyroid patients into two groups.…”

Section: Discussionmentioning

confidence: 99%

“…The intact peptide hormone is eliminated by the kidneys within a few minutes after its secretion although negligible quantities of small peptide fragments exhibiting PTH activity circulate for many hours [15]. The response of the parathyroid gland to changes in extracellular calcium is profound in individuals with low and normal serum calcium levels, whereas it is subdued in the hypercalcemic patient [14]. Endogenous and exogenous catecholamines can stimulate PTH secretion [8][9][10].…”

Section: Discussionmentioning

confidence: 99%

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Parathyroid Hormone Response to Tracheal Intubation in Hyperparathyroid Patients and Normal Subjects

et al. 2005

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Abstract. The stress of direct laryngoscopy and passing an endotracheal tube through the vocal cords elicits haemodynamic, metabolic and hormonal changes such as raising blood catecholamine levels. Catecholamines are known stimulants of PTH secretion. The effect of tracheal intubation on plasma parathyroid hormone levels has not yet been investigated. We monitored changes in plasma parathyroid hormone levels before and after tracheal intubation in 72 hyperparathyroid patients undergoing elective parathyroidectomy for primary and secondary hyperparathyroidism. These findings were compared to data collected from 20 subjects who underwent elective surgery (thyroidectomy or laparoscopic cholecystectomy) under general anesthesia. In the control group, tracheal intubation significantly increased plasma parathyroid hormone levels from 59 ± 31 pg/ml to 91 ± 40 pg/ml (mean ± SD) (p<0.0003). In primary hyperparathyroid patients, the identical procedure increased plasma parathyroid hormone levels from 206 ± 104 pg/ml to 217 ± 113 pg/ml (p = 0.12) and from 898 ± 495 pg/ml to 1162 ± 613 pg/ml (p = 0.07) in secondary hyperparathyroidism patients. We concluded that tracheal intubation raises plasma parathyroid hormone levels. The mechanism underlying this response requires further investigation. THE physiologic response to tracheal intubation was investigated many years ago and we are now aware of rapid changes in blood levels of adrenalin, noradrenalin, cortisol, adrenocorticotropic hormone, aldosterone and thyroid hormone following this procedure [1][2][3][4]. These responses were attributed to the stress of direct laryngoscopy and passing the tube through the vocal cords [5][6][7]. Catecholamines are known stimulants of parathyroid hormone (PTH) secretion [8][9][10]. The effect of intubation on blood levels of PTH is unknown. Therefore, the purpose of this study was to establish whether there is a change in plasma PTH levels following tracheal intubation in patients with hyperparathyroidism and in individuals with normal parathyroid function. Except for understanding the endocrine physiology, it has a practical aspect, since intraoperative PTH level is essential for confirmation of all hyperfunctioning parathyroid tissue removal.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Parathyroid Hormone Response to Tracheal Intubation in Hyperparathyroid Patients and Normal Subjects

et al. 2005

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“…59 CaxPi product and other anions containing calcium normally account for 5% of serum calcium, whereas free ionized calcium accounts for 45% of serum calcium and the remaining serum calcium is bonded to albumin. 60 Elevated levels of serum phosphorus in hyperphosphatemia-associated with impaired kidney function, dietary phosphorus overload or both-unite with free calcium to form an additional CaxPi product. Accumlated excess CaxPi product is likely to be deposited into soft tissue causing ectopic calcification.…”

Section: Phosphate Toxicity Associated With Ectopic Calcificationmentioning

confidence: 99%

Dysregulation of phosphate metabolism and conditions associated with phosphate toxicity

Brown

2015

BoneKEy Reports

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Phosphate homeostasis is coordinated and regulated by complex cross-organ talk through delicate hormonal networks. Parathyroid hormone (PTH), secreted in response to low serum calcium, has an important role in maintaining phosphate homeostasis by influencing renal synthesis of 1,25-dihydroxyvitamin D, thereby increasing intestinal phosphate absorption. Moreover, PTH can increase phosphate efflux from bone and contribute to renal phosphate homeostasis through phosphaturic effects. In addition, PTH can induce skeletal synthesis of another potent phosphaturic hormone, fibroblast growth factor 23 (FGF23), which is able to inhibit renal tubular phosphate reabsorption, thereby increasing urinary phosphate excretion. FGF23 can also fine-tune vitamin D homeostasis by suppressing renal expression of 1-alpha hydroxylase (1a(OH)ase). This review briefly discusses how FGF23, by forming a bone-kidney axis, regulates phosphate homeostasis, and how its dysregulation can lead to phosphate toxicity that induces widespread tissue injury. We also provide evidence to explain how phosphate toxicity related to dietary phosphorus overload may facilitate incidence of noncommunicable diseases including kidney disease, cardiovascular disease, cancers and skeletal disorders.

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“…Renal involvement was present in 60% to 70% of patients prior to 1970. With earlier detection, renal complications have occurred in <20% of patients in many recent series (4). In occasional patients, repeated episodes of nephrolithiasis may lead to urinary tract obstruction, infection, and loss of renal function (5).…”

Section: Discussionmentioning

confidence: 99%