Kojima N, Sakata S, Nakamura S, Nagai K, Takuno H, Ogawa T, Matsui I, Sarui H, Miura K
Third Department of Internal Medicine, Gifu University School of Medicine, Japan.
J Endocrinol Invest. 1992 Jul-Aug;15(7):491-6. doi: 10.1007/BF03348786.
Serum concentration of osteocalcin (OC) was measured in sera from untreated patients with Graves' disease, hypothyroidism due to Hashimoto's thyroiditis, and subacute thyroiditis. Serum concentration of OC in Graves' disease and hypothyroidism were 14.1 +/- 5.6 micrograms/L and 3.8 +/- 2.7 micrograms/L, respectively which were significantly different from that of healthy subjects (Graves' disease, p less than 0.001, hypothyroidism, p less than 0.01). Serum concentration of OC in patients with subacute thyroiditis was 8.0 +/- 3.5 micrograms/L which was not statistically different from age-matched normal controls. Serial measurement of serum OC for 24 mo in 15 patients with Graves' disease after initiation of antithyroid drugs disclosed that the decline of serum OC was obtained only 24 mo after antithyroid drug therapy. On the other hand, in hypothyroid patients, increased serum OC was observed after 1-2 months treatment of L-T4. Correlation coefficients between serum concentrations of OC and T3, T4, FT3 or FT4 in all the patients with thyroid disorders were 0.66, 0.51, 0.50 and 0.54, respectively, which were statistically significant (all, p less than 0.001). These results suggest that osteoblastic activity is enhanced in hyperthyroidism and suppressed in hypothyroidism. In hyperthyroid patients, despite of normalization of FT4 concentration in relatively short period (within 3-4 mo), it took 24 mo after initiation of antithyroid drugs for OC to normalize, suggesting not only thyroid hormone per se but also some unknown factor(s) participates in serum OC secretion. In contrast to thyrotoxic patients, rapid increase in serum OC after initiation of supplemental L-T4 treatment in hypothyroidism was observed, suggesting a direct effect of thyroid hormone on the osteoblasts in patients with hypothyroidism.
检测了未经治疗的格雷夫斯病患者、桥本甲状腺炎所致甲状腺功能减退患者以及亚急性甲状腺炎患者血清中的骨钙素(OC)浓度。格雷夫斯病和甲状腺功能减退患者血清中OC浓度分别为14.1±5.6μg/L和3.8±2.7μg/L,与健康受试者相比差异有统计学意义(格雷夫斯病,p<0.001;甲状腺功能减退,p<0.01)。亚急性甲状腺炎患者血清中OC浓度为8.0±3.5μg/L,与年龄匹配的正常对照组相比无统计学差异。对15例格雷夫斯病患者在开始抗甲状腺药物治疗后连续24个月检测血清OC,发现抗甲状腺药物治疗24个月后血清OC才下降。另一方面,甲状腺功能减退患者在接受左甲状腺素(L-T4)治疗1-2个月后,血清OC升高。所有甲状腺疾病患者血清OC浓度与T3、T4、FT3或FT4之间的相关系数分别为0.66、0.51、0.50和0.54,均有统计学意义(均为p<0.001)。这些结果表明,成骨细胞活性在甲状腺功能亢进时增强,在甲状腺功能减退时受到抑制。在甲状腺功能亢进患者中,尽管FT4浓度在相对较短的时间内(3-4个月内)恢复正常,但开始抗甲状腺药物治疗24个月后OC才恢复正常,这表明不仅甲状腺激素本身,而且一些未知因素也参与血清OC的分泌。与甲状腺毒症患者相反,甲状腺功能减退患者开始补充L-T4治疗后血清OC迅速升高,提示甲状腺激素对甲状腺功能减退患者的成骨细胞有直接作用。