Lead poisoning from mobilization of bone stores during thyrotoxicosis.
We describe a case of thyrotoxicosis accompanied by markedly elevated blood lead levels (initially 53 micrograms/dl) in a 37-year-old woman. No current source of lead exposure was found; the woman gave a history indicative of lead exposure as a child and as an adult 7 years previously, however. In addition, she was found to have markedly elevated bone lead levels, as measured by K-x-ray fluorescence (154 +/- 5 in the mid-tibia and 253 +/- 6 micrograms/g bone mineral in the patella), and an increased serum osteocalcin level (2.76 nmol/l), reflecting the increased bone turnover that often accompanies hyperthyroidism. During treatment with propylthiouracil, serial observations demonstrated a decline in serum osteocalcin that paralleled a decline in blood lead levels. Bone lead levels did not change appreciably. The patient also continued to have lingering neuropsychological symptoms consistent with chronic lead effects. We suggest that increased bone turnover accompanying thyrotoxicosis led to clinically significant lead poisoning in this patient, due to mobilization of accumulated bone lead stores acquired many years earlier. This phenomenon raises the general issue of more subtle forms of lead exposure from increased bone turnover states (e.g., osteoporosis).
Goldman
R H
RH
Department of Medicine, Cambridge Hospital, Harvard Medical School, MA.
White
R
R
Kales
S N
SN
Hu
H
H
D000328:Adult; D001842:Bone and Bones / Q000737:chemistry* / Q000378:metabolism; D005260:Female; D006801:Humans; D007854:Lead / Q000032:analysis / Q000378:metabolism*; D007855:Lead Poisoning / Q000209:etiology*; D013052:Spectrometry, X-Ray Emission; D013971:Thyrotoxicosis / Q000150:complications* / Q000378:metabolism
D007854:Lead