Effects of parathyroidectomy on lead mobilization from bone in patients with primary hyperparathyroidism |
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Authors: | Osterode W Winker R Bieglmayer C Vierhapper H |
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Affiliation: | Universit?tsklinik für Innere Medizin IV, Klinische Abteilung für Arbeitsmedizin, A-1090 Wien, Austria. wolf.osterode@akh-wien.ac.at |
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Abstract: | Since lead (Pb) accrued from environmental exposure accumulates in bone with a half life time between 6 and 10 years, a release of bone Pb into the circulation and/or urine (PbU) should be expected in diseases with increased bone metabolism such as hyperparathyroidism. We studied 60 patients with primary hyperparathyroidism (pHPT, 50 women, 10 men, aged 61.4 +/- 10.6 and 64.1 +/- 9.9 years, respectively) (a) before, (b) 1-6 months, and (c) 6-12 months after parathyroidectomy. Besides lead in blood (PbB) and lead in 24-h urine samples (PbU), parathyroid hormone (PTH), serum Ca2+, osteocalcin (OC), phosphate (PO4), and serum pyridinoline cross-linked telopeptide (cTP) were determined. Control data were determined in 20 healthy age-matched subjects. As expected, Ca2+ decreased after parathyroidectomy. Mean PbB in patients with pHPT was in the same range as in controls. A decrease of PbB after parathyroidectomy was found in the interval beyond 6 months. In contrast, mean PbU initially increased after surgery (3.05 +/- 1.94 vs. 4.25 +/- 2.65 microg/l, P = 0.004) and was not different beyond 6 months in comparison with preoperative values at (c). Investigating only patients with PTH < 150 ng/l, no significant PbB or PbU alterations were detected before and after parathyroidectomy. In patients with PTH > 150 ng/l, the decrease of PbB at (c) was more pronounced as was the increase of PbU at (b). In these patients, PbB and OC as well as PbB and cTP were correlated preoperatively. In conclusion, our data show that in environmentally lead-exposed (by food or by pollution) hyperparathyroid individuals, there is no hazardous PbB release from bone. The preoperative correlation between PbB and OC in pHPT patients with PTH > 150 ng/l provides evidence that in fact there is a Pb release from bone into the blood-pool by bone remodeling. The increase of PbU after parathyroidectomy is suspected to be caused by PTH-dependent Pb accumulation in the kidney, which seems to be restored with decreasing PTH. Moreover, our data confirm prior findings that bone remodeling seems to be normalized 6 months after parathyroidectomy. |
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