Increased Lead Excretion Correlates with Desoxypyridinoline Crosslinks in Hyperthyroid Patients

Abstract

Lead is a widespread toxic metal that accumulates predominantly in human bone. Altered bone metabolism in hyperthyroidism is characterized mainly by bone resorption. Thus, we speculated that lead excretion could be increased in hyperthyroid patients. In 12 hyperthyroid patients (43.3 +/- 16.1 years) who were not previously occupationally exposed to lead, lead concentrations in blood (PbB), spot urine samples corrected by urine creatinine (PbUs), and in 24-hour urine samples (PbU24) were determined in the hyperthyroid state and after euthyroidism had been induced by therapy. Serum osteocalcin (OC) and desoxypyridinoline crosslinks (Pyr) served as specific markers for bone metabolism. After induction of euthyroidism (duration of antithyroid therapy: mean 17.3 +/- 6.9 weeks) PbB was reduced (3.7 +/- 2.6 vs. 5.7 +/- 4.7 microg/dL, p = 0.041) as was PbUs (0.39 +/-0.27 vs. 0.61 +/- 0.32 microg/mg Cr, p = 0.005). A fourfold decrease of PbU24 was associated with a 3.3-fold decrease of Pyr, and moreover there was a significant correlation between Pyr and PbUs (r = 0.58, p = 0.047). Concentration of total triiodothyronine correlated with Pyr (r = 0.66, p = 0.018), but not with PbB or PbUs. OC showed only a tendency to be increased before antithyroid medication, and did not correlate with either thyroid hormone or Pyr. Our results indicate that in hyperthyroid patients, even when not previously exposed to lead, lead excretion is increased due to bone resorption.

Lead accumulation in tidemark of articular cartilage

“…The half life of Pb in the blood is one month, but it accumulates in the skeleton, where approximately 95% of the total body burden of Pb is present (4) with an estimated half life up to 20 years (5). Diseases or states with increased bone turnover, such as osteoporosis, pregnancy, hyperthyroidism and hyperparathyroidism are associated with increased mobilization of Pb from the skeleton (6)(7)(8). Aging-associated release of bone lead into the circulation is a potentially important source of soft-tissue lead exposure and toxicity (9) Moreover, reports in humans and animals support a role of Pb in osteopenia (9,10) and…”