Decrease in serum immunoreactive parathyroid hormone in rats and in parathyroid hormone secretion in vitro by 1,25-dihydroxycholecalciferol.

Chertow, Bruce S.; Baylink, David J.; Wergedal, J. E.; Su, Mingming; Norman, Anthony W.

doi:10.1172/jci108137

Cited by 213 publications

(50 citation statements)

References 43 publications

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“…Active vitamin D 3 and its analogues such as calcitriol and alfacalcidol are potent suppressors of PTH synthesis and secretion by parathyroid cells [20,21]. Alfacalcidol also decreased serum PTH levels in the PHP patients in this study, and similar results were observed in previous studies [11,19,22].…”

Section: +supporting

confidence: 91%

The administration of an active vitamin D3 analogue reduced the serum concentrations of 1-84 and truncated parathyroid hormone in pseudohypoparathyroidism type Ib patients

et al. 2010

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Proteolytic modifications of parathyroid hormone (PTH) is one of mechanisms for regulating the secretion of full-length (1-84)PTH from parathyroid glands. Therefore, not only (1-84)PTH but also other PTH fragments, such as carboxy-terminal (C-terminal) PTH fragments [1,2] and N-terminally truncated fragments such as (7-84)PTH can be measured by commercially available two-site total PTH (T-PTH) assays. The development of whole PTH (W-PTH) assays specific for full-length (1-84)PTH has enabled us to distinguish between N-terminally truncated PTH and full-length (1-84)PTH. W-PTH/T-PTH ratios were calculated and used as an index of PTH N-terminal truncations. Both serum W-PTH and T-PTH levels were elevated in untreated PHP Ib patients. The administration of alfacalcidol reduced both the W-PTH and T-PTH levels; however, the W-PTH/T-PTH ratios were stable. Serum calcium levels were significantly and negatively correlated with both the W-PTH and T-PTH levels, but not with the W-PTH/T-PTH ratios. Thus, the administration of an active vitamin D 3 analogue did not seem to have a major effect on the rate of PTH N-terminal truncation, even though it did reduce the secretion of both full-length and truncated PTH. Possibly, active vitamin D 3 attenuates the effect of elevated calcium on PTH N-terminal truncation in PHP Ib patients.

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Section: +supporting

confidence: 91%

The administration of an active vitamin D3 analogue reduced the serum concentrations of 1-84 and truncated parathyroid hormone in pseudohypoparathyroidism type Ib patients

et al. 2010

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“…According to the results shown in Fig. 1 Several studies suggest that 1 ,25(OH)2D3 directly inhibits the secretion of PTHfrom the parathyroid glands (22)(23)(24)(25) and also suppresses the production of PTHmRNA in parathyroid glands, independent of the concentration of ionized Ca (26)(27)(28). In the present study, the weekly administration of 8.0 |Ug of 1,25(OH)2D3 suppressed the PTH level without elevating the serum Ca.…”

Section: Discussionsupporting

confidence: 65%

Suppression of Secondary Hyperparathyroidism in Chronic Dialysis Patients by Single Oral Weekly Dose of 1,25-Dihydroxycholecalciferol.

et al. 1993

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Eleven hemodialysis patients who developed refractory secondary hyperparathyroidism, despite conventional vitamin D therapy, were treated with large oral doses of 1,25-dihydroxycholecalciferol [1,25(OH)2D3]. Therapeutic regimen was a single oral dose of up to 8.0 jug administered once weekly following hemodialysis. A maximum serum level of 1,25(OH)2D occurred four hours after the 8.0 jig dose. A positive correlation (Y=84.3X-22.1: P<0.01) was found between the maximal serum 1,25(OH)2D concentration (Cmax) and the dose of 1,25(OH)2D3 when plotted on a logarithmic scale. Forty-eight hours after the administration of the 8.0 jag dose, the parathyroid hormone (PTH) level and the alkaline phosphatase activity (ALP) were markedly decreased without evidence of hypercalcemia. A significant inverse relationship was found between the Cmax of 1,25(OH)2D and the percent change in the PTH level measured after 48 hours, either with carboxy-terminal (C-PTH) or the highly sensitive mid-portion assay (HS-PTH). From these results, the level of serum 1,25(OH)2D required to blunt the rise in serum PTH was 168 pg/ml and 203 pg/ml, respectively; these serum levels were achieved by the oral administration of doses of 6.0-8.0 |LLg or higher. There were no adverse effects of treatment. Following this study, one patient was continuously treated with 8.0 jig of 1,25(OH)2D3 orally once a week for 18 months. There was a therapeutic effect (as evidenced by PTHsuppression, ALPsuppression and the disappearance of subjective complaints) without the development of severe hypercalcemia or hyperphosphatemia. This treatment may help to prevent or treat secondary hyperparathyroidism in patients receiving long-term dialysis.

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“…Serum immunoreactive parathyroid hormone (iPTH) was measured using an antiserum (chick 12) directed against the carboxy terminus of the PTH molecule (24). Creatinine clearance was calculated using the conventional formula for clearance.…”

Section: Methodsmentioning

confidence: 99%

Short-term aluminum administration in the rat. Effects on bone formation and relationship to renal osteomalacia.

Goodman¹,

Gilligan²,

Horst³

1984

J. Clin. Invest.

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Abstract. Aluminum may be pathogenic in the osteomalacia observed in some patients receiving hemodialysis. To study the early effects ofAl on bone growth, bone formation, mineralization, and resorption were measured during short-term Al exposure in the tibial cortex of pair-fed control (C, n = 10), aluminum-treated (AL, n = 9), subtotally nephrectomized control (NX-C, n = 7), and subtotally nephrectomized aluminum-treated (NX-AL, n = 8) rats using double tetracycline labeling of bone. Animals received 2 mg/d of elemental Al intraperitoneally for 5 d/wk over 4 wk. Total bone and matrix (osteoid) formation, periosteal bone and matrix formation, and periosteal bone and matrix apposition fell by 20% in AL from C, P < 0.05 for all values, and by 40% in NX-AL from NX-C, P < 0.01 for all values. Moreover, each measurement was significantly less in NX-AL than in AL, P < 0.05 for all values. Osteoid width did not increase following aluminum administration in either AL or NX-AL. Resorption surface increased from control values in both AL and NX-AL; also, resorptive activity at the endosteum was greater in NX-AL than in NX-C, P < 0.05. Thus, aluminum impairs new bone and matrix formation but does not cause classic osteomalacia in the cortical bone of rats whether renal function is normal or reduced. These findings may represent either a different response to aluminum administration in cortical bone as contrasted to trabecular bone or an early phase in the development of osteomalacia.

show abstract

Decrease in serum immunoreactive parathyroid hormone in rats and in parathyroid hormone secretion in vitro by 1,25-dihydroxycholecalciferol.

Cited by 213 publications

References 43 publications

The administration of an active vitamin D3 analogue reduced the serum concentrations of 1-84 and truncated parathyroid hormone in pseudohypoparathyroidism type Ib patients

The administration of an active vitamin D3 analogue reduced the serum concentrations of 1-84 and truncated parathyroid hormone in pseudohypoparathyroidism type Ib patients

Suppression of Secondary Hyperparathyroidism in Chronic Dialysis Patients by Single Oral Weekly Dose of 1,25-Dihydroxycholecalciferol.

Short-term aluminum administration in the rat. Effects on bone formation and relationship to renal osteomalacia.

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