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[Parathyroid function in hyperthyroidism: implications for bone metabolism and effect of the treatment]
R P Furlanetto1, M L Castro, C H de Mesquita
1Disc. de Endocrinologia, EPM, São Paulo.
Purpose:
using bone densitometry, to evaluate bone loss of hyperthyroidism patients, and to study the possible contribution of parathyroid hormone (PTH) in the genesis of this osteopenia. TYPE: prospective study of patients with hyperthyroidism before and after treatment.
Place:
Division of Endocrinology, Escola Paulista de Medicina. São Paulo, SP.
Patients:
14 outpatients with clinical and laboratory diagnosis of toxic diffuse goiter (Basedow-Graves disease). Six of these patients were studied again after treatment, with at least 6 months of clinical and laboratory euthyroidism.
Method:
bone mineral content of the lumbar vertebral bodies was evaluated by dual-photon bone densitometry. Parathyroid hormone secretion was studied with an amino-terminal specific assay after EDTA-induced hypocalcemia; results were compared to those obtained from a group of 10 normal controls.
Results:
there was a significant increase in bone mineral density after treatment (1.300 +/- 0.079 g/cm2) as compared to the pre-treatment condition (1.229 +/- 0.091 g/cm2, p less than 0.001). Decrement rate of serum calcium during EDTA infusion was significantly lower (p less than 0.001) in hyperthyroid (-0.698 x 10(-3) +/- 0.12 x 10(-5)) than in normal control individuals (-1.486 x 10(-3) +/- 9.33 x 10(-5)), and went back to normal after treatment. EDTA-induced calcium lowering was sufficient to induce a PTH plateau of maximum response. Maximum PTH response in hyperthyroidism patients (2.34 +/- 0.45pmol) was significantly lower (p less than 0.001) than that observed in normal controls (7.51 +/- 0.40), PTH response was normal after six months of euthyroidism.
Conclusions:
bone mineral density showed a significant increment in treated patients, suggesting that these patients had suffered some degree of bone loss during the course of thyrotoxicosis. The lower PTH secretory reserve found in untreated hyperthyroid patients suggests that hyperthyroid state-induced bone loss may be a consequence of a direct action of thyroid hormones. This conditions was reverted after 6 months of euthyroidism.