Tsourdi E, Lademann F, Siggelkow H
Bereich Endokrinologie, Diabetes und Knochenerkrankungen, Medizinische Klinik III, Universitätsklinikum Carl Gustav Carus, Technische Universität Dresden, Dresden, Deutschland.
Zentrum für Gesundes Altern, Medizinische Fakultät, Technische Universität Dresden, Dresden, Deutschland.
Internist (Berl). 2018 Jul;59(7):661-667. doi: 10.1007/s00108-018-0436-z.
Thyroid hormones are key regulators of skeletal development in childhood and bone homeostasis in adulthood, and thyroid diseases have been associated with increased osteoporotic fractures. Hypothyroidism in children leads to an impaired skeletal maturation and mineralization, but an adequate and timely substitution with thyroid hormones stimulates bone growth. Conversely, hyperthyroidism at a young age accelerates skeletal development, but may also cause short stature because of a premature fusion of the growth plates. Hypothyroidism in adults causes an increase in the duration of the remodeling cycle and, thus, leads to low bone turnover and enhanced mineralization, but an association with a higher fracture risk is less well established. In adults, a surplus of thyroid hormones enhances bone turnover, mostly due to an increased bone resorption driven by osteoclasts. Thus, hyperthyroidism is a well-recognized cause of high-bone turnover secondary osteoporosis, resulting in an increased susceptibility to fragility fractures. Subclinical hyperthyroidism, especially resulting from endogenous disease, also has an adverse effect on bone mineral density and is associated with fractures. In most patients with overt or subclinical hyperthyroidism restoration of the euthyroid status reverses bone loss. In postmenopausal women who receive thyroid-stimulating hormone suppression therapy because of thyroid cancer, antiresorptive treatments may be indicated. Overall, extensive data support the importance of a euthyroid status for bone mineral accrual and growth in childhood as well as maintenance of bone health in adulthood.
甲状腺激素是儿童骨骼发育和成人骨稳态的关键调节因子，甲状腺疾病与骨质疏松性骨折风险增加有关。儿童甲状腺功能减退会导致骨骼成熟和矿化受损，但及时给予足够的甲状腺激素替代治疗可刺激骨骼生长。相反，幼年时甲状腺功能亢进会加速骨骼发育，但也可能因生长板过早融合而导致身材矮小。成人甲状腺功能减退会导致重塑周期延长，从而导致骨转换率降低和矿化增强，但与较高骨折风险的关联尚不明确。在成人中，甲状腺激素过多会增强骨转换，主要是由于破骨细胞驱动的骨吸收增加。因此，甲状腺功能亢进是高骨转换继发性骨质疏松的一个公认原因，导致脆性骨折易感性增加。亚临床甲状腺功能亢进，尤其是由内源性疾病引起的，也会对骨密度产生不利影响并与骨折相关。在大多数显性或亚临床甲状腺功能亢进患者中，恢复甲状腺功能正常状态可逆转骨质流失。对于因甲状腺癌接受促甲状腺激素抑制治疗的绝经后女性，可能需要采用抗吸收治疗。总体而言，大量数据支持甲状腺功能正常状态对儿童骨矿物质积累和生长以及成人骨骼健康维持的重要性。
