Hysteresis in the Relationship Between Serum Ionized Calcium and Intact Parathyroid Hormone during Recovery from Induced Hyper-and Hypocalcemia in Normal Humans*

Conlin, P. R.; Fajtova, V. T.; Mortensen, Richard M.; LeBoff, Meryl S.; Brown, Edward M.

doi:10.1210/jcem-69-3-593

Cited by 77 publications

(54 citation statements)

References 17 publications

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“…In contrast, PTH levels never fell below 20 pg/ml in our patients, which is clearly above the level of 10 pg/ml expected for the continuous tonic secretion of PTH [12,37], which suggests that the continuous tonic PTH secretion might be elevated in diabetic subjects. In adults, PTH levels are expected to rise steeply above 40 pg/ml at 25D levels below 50 nmol/L and above 50 pg/ml at 25 D levels below 25 nmol/L [27].…”

Section: Discussioncontrasting

confidence: 70%

“…Second, hypocalcaemia was too mild to induce a rise in PTH in our patients. Physiologically the set-point in the inverse sigmoidal relationship between ionised calcium and PTH is around 1.22 mmol/L and PTH secretion reaches a plateau at ionised calcium concentrations below 1.15 mmol/L [37]. The concentration of ionised calcium in our patients, however, was mostly above 1.2 mmol/L and only three patients had values below 1.15 mmol/L.…”

Section: Discussioncontrasting

confidence: 48%

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High prevalence of vitamin D deficiency in children and adolescents with type 1 diabetes

Janner

Flueck

Mullis

2009

Bone

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SummaryBackground: Vitamin D is important for bone health. An inadequate supply of vitamin D to the body is associated with a higher fracture risk in the elderly. Young adults with type 1 diabetes are reported to have a lower peak bone mass than healthy individuals, which could possibly lead to an increased fracture risk in the future. The prevalence of vitamin D deficiency in healthy young people is high. Thus, optimal supply of vitamin D may be of particular importance for bone health in children with type 1 diabetes.Methods: In this prospective cross-sectional study we measured serum 25-hydroxy-vitamin D, iPTH, total and ionised calcium, phosphate, and alkaline phosphatase in 129 Swiss children and adolescents with type 1 diabetes.Results: Of the 129 subjects 78 (60.5%) were vitamin D deficient, defined as a 25-hydroxy-vitamin-D level below 50 nmol/L. During the winter this number rose to 84.1%. 25-hydroxy-vitamin-D levels showed marked seasonal fluctuations, whereas there was no correlation with diabetes control. Despite the high prevalence of vitamin D deficiency, we found a low prevalence of secondary hyperparathyroidism in vitamin D deficient diabetic children and adolescents.Conclusions: Prevalence of vitamin D deficiency in diabetic children and adolescents is high. Therefore, screening for vitamin D deficiency and supplementation in children with low vitamin D levels may be considered.

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Section: Discussioncontrasting

confidence: 70%

Section: Discussioncontrasting

confidence: 48%

High prevalence of vitamin D deficiency in children and adolescents with type 1 diabetes

Janner

Flueck

Mullis

2009

Bone

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“…In respiratory acidosis, the failure of ionized calcium values to continue to increase, and perhaps the lesser magnitude of calcium increase compared with metabolic acidosis, would seem to have allowed the stimulatory effect of respiratory acidosis on PTH secretion to prevail. Finally, the dynamic of an increasing ionized calcium concentration followed by a static level may also have contributed to the observed PTH response in the nonclamped group (5).…”

Section: Discussionmentioning

confidence: 97%

Role of acidosis-induced increases in calcium on PTH secretion in acute metabolic and respiratory acidosis in the dog

López¹,

Aguilera–Tejero²,

Estepa³

et al. 2004

American Journal of Physiology-Endocrinology and Metabolism

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of acidosis-induced increases in calcium on PTH secretion in acute metabolic and respiratory acidosis in the dog. Am J Physiol Endocrinol Metab 286: E780 -E785, 2004. First published January 13, 2004 10.1152/ajpendo.00473.2003.-Recently, we showed that both acute metabolic acidosis and respiratory acidosis stimulate parathyroid hormone (PTH) secretion in the dog. To evaluate the specific effect of acidosis, ionized calcium (iCa) was clamped at a normal value. Because iCa values normally increase during acute acidosis, we now have studied the PTH response to acute metabolic and respiratory acidosis in dogs in which the iCa concentration was allowed to increase (nonclamped) compared with dogs with a normal iCa concentration (clamped). Five groups of dogs were studied: control, metabolic (clamped and nonclamped), and respiratory (clamped and nonclamped) acidosis. Metabolic (HCl infusion) and respiratory (hypoventilation) acidosis was progressively induced during 60 min. In the two clamped groups, iCa was maintained at a normal value with an EDTA infusion. Both metabolic and respiratory acidosis increased (P Ͻ 0.05) iCa values in nonclamped groups. In metabolic acidosis, the increase in iCa was progressive and greater (P Ͻ 0.05) than in respiratory acidosis, in which iCa increased by 0.04 mM and then remained constant despite further pH reductions. The increase in PTH values was greater (P Ͻ 0.05) in clamped than in nonclamped groups (metabolic and respiratory acidosis). In the nonclamped metabolic acidosis group, PTH values first increased and then decreased from peak values when iCa increased by Ͼ0.1 mM. In the nonclamped respiratory acidosis group, PTH values exceeded (P Ͻ 0.05) baseline values only after iCa values stopped increasing at a pH of 7.30. For the same increase in iCa in the nonclamped groups, PTH values increased more in metabolic acidosis. In conclusion, 1) both metabolic acidosis and respiratory acidosis stimulate PTH secretion; 2) the physiological increase in the iCa concentration during the induction of metabolic and respiratory acidosis reduces the magnitude of the PTH increase; 3) in metabolic acidosis, the increase in the iCa concentration can be of sufficient magnitude to reverse the increase in PTH values; and 4) for the same degree of acidosis-induced hypercalcemia, the increase in PTH values is greater in metabolic than in respiratory acidosis.hypercalcemia; metabolic acidosis; parathyroid hormone; respiratory acidosis BESIDES ITS WELL-KNOWN EFFECT on calcium homeostasis, parathyroid hormone (PTH) has also been associated with changes in the acid-base status. In 1970, Wills (26) suggested that PTH-induced bone resorption mobilized phosphate to act as a buffer to neutralize acidosis. In subsequent studies, PTH administration has been shown to increase net acid excretion (14, 24) and induce metabolic alkalosis in dogs and humans by both renal and extrarenal mechanisms (15-17). Because PTH appears to have a role in acid-base homeostasis, it would seem reasonable that acid-base disorders may...

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“…This fact could be explained by the hysteresis of the PTH -Ca 2+ curve. With respect to the PTH -Ca 2+ relationship, the term hysteresis indicates that for the same plasma Ca 2+ , the plasma PTH is lower during the acute induction of hypercalcemia than the acute recovery from hypercalcemia (27). Thus, in Group II rabbits, which have normal baseline Ca 2+ (1.70 mM) and are recovering from an acute hypercalcemia, the hysteresis of the PTH -Ca 2+ curve would increase PTH levels.…”

Section: Discussionmentioning

confidence: 99%

The influence of acute and chronic hypercalcemia on the parathyroid hormone response to hypocalcemia in rabbits

Bas

Aguilera–Tejero

Estepa

et al. 2002

European Journal of Endocrinology

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Objective: To investigate the influence of acute and chronic hypercalcemia on the parathyroid hormone (PTH) response to hypocalcemia. Design: The PTH response to hypocalcemia has been evaluated in three groups of rabbits: Group I, normal rabbits, Group II, normal rabbits subjected to an acute hypercalcemic clamp (induced by CaCl 2 infusion) and Group III, rabbits with chronic hypercalcemia (due to surgical reduction of renal mass). Results: In Group I (baseline Ca 2þ ¼ 1:69^0:02 mM), hypocalcemia resulted in stimulation of PTH secretion which reached a maximum (PTHmax) of 91:7^6:4 pg=ml: In rabbits from Group II, which also had normal baseline Ca 2+ ð1:70^0:02 mMÞ; plasma Ca 2+ was maintained at an elevated level for 2 h, at around 2.05 mM. The PTH response to hypocalcemia in Group II was attenuated and the PTHmax in these rabbits was 45:6^7:4 pg=ml: In rabbits from Group III, baseline Ca 2+ was elevated ð2:06^0:06 mMÞ for 1 month. The PTH response to hypocalcemia in Group III was esentially the same as in Group I and PTHmax reached levels of 94:8^9:9 pg=ml: Conclusions: A difference in PTH response to hypocalcemia has been found in rabbits after exposure to either acute or chronic hypercalcemia. After acute hypercalcemia, an attenuated PTH response to hypocalcemia has been identified. Chronic hypercalcemia, however, did not influence the PTH response to hypocalcemia.

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Hysteresis in the Relationship Between Serum Ionized Calcium and Intact Parathyroid Hormone during Recovery from Induced Hyper-and Hypocalcemia in Normal Humans*

Cited by 77 publications

References 17 publications

High prevalence of vitamin D deficiency in children and adolescents with type 1 diabetes

High prevalence of vitamin D deficiency in children and adolescents with type 1 diabetes

Role of acidosis-induced increases in calcium on PTH secretion in acute metabolic and respiratory acidosis in the dog

The influence of acute and chronic hypercalcemia on the parathyroid hormone response to hypocalcemia in rabbits

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