Aluminum Uptake by the Parathyroid Glands

Cann, Christopher E.; Prussin, S.G.; Gordan, Gilbert S.

doi:10.1210/jcem-49-4-543

Cited by 110 publications

(20 citation statements)

References 6 publications

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“…It has been suggested that impaired parathyroid hormone secretion may explain this state of low bone formation. Aluminum may accumulate in parathyroid tissue (26), and Morrissey et al ( 17) have shown that aluminum reduces the secretion of iPTH from dispersed bovine parathyroid cells in vitro. The present results demonstrate that bone formation and apposition decrease early in the course of aluminum administration without concomitant reductions in the serum levels of iPTH.…”

Section: Discussionmentioning

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.

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Section: Discussionmentioning

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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“…In addition, a preliminary study reported that the PTH lev els in osteomalacic patients do not increase in response to hypocalcemia induced by low calcium dialysate [35], Thus, whether the low level of PTH results from parathy roidectomy or as part of the spontaneously occurring osteomalacic syndrome, the parathyroid axis may be defective and may contribute to the evolution of this syn drome. A potentially unifying element between alu minum and low levels of PTH is suggested by the report that aluminum is preferentially deposited in the parathy roid gland [36]. However, confirmation of these data is required and, in addition, proof that high parathyroid gland aluminum impairs production and/or secretion of PTH is essential.…”

Section: Discussionmentioning

confidence: 99%

Osteomalacia in Chronic Renal Failure: a Syndrome Previously Reported Only with Maintenance Dialysis

Felsenfeld

Gutman²,

Llach

et al. 1982

Am J Nephrol

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Osteomalacia without marked elevations of parathyroid hormone (PTH) has been described in maintenance dialysis patients. The proposed etiology has centered upon the transfer of an environmental agent (aluminum) from the dialysis water system. The present report describes an azotemic patient, who, prior to the initiation of dialytic therapy, presented with severe osteomalacia and low PTH concentrations for the severity of renal failure. The osteomalacia was documented by bone histology on two occasions 1 year apart, and aluminum deposits at the osteoid-mineralized bone interface were demonstrated with histologic techniques. PTHconcentrations were within the normal range (less than 0.1 ng/ml) on three widely spaced intervals. No definite statement can be made regarding the etiology of the osteomalacic syndrome in this patient, but maintenance dialysis does not appear to be necessary for its expression.

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“…Indeed, aluminum accumulates in parathyroid glands and is known to inhibit their hormonal secretion. [27][28][29][30] We found no relation between the presence of aluminum deposits in bone biopsy specimens and the function of parathyroid subcutaneous grafts. This is in keeping with the results of Berland et al, 27 who found that the aluminum content of parathyroid glands was similar in patients with or without bone aluminum deposits and was only correlated with serum aluminum levels.…”

mentioning

confidence: 99%