Fowler P B, McIvor J, Sykes L, Macrae K D
Charing Cross Hospital, London.
J R Coll Physicians Lond. 1996 Nov-Dec;30(6):527-32.
The effect of thyrotrophin suppression on bone mineral density (BMD) and serum cholesterol concentration was assessed in 31 treated hypothyroid women. Measurements of the BMD of the lumbar spine and femoral neck were repeated in seven of those with the lowest value after an average period of 22.7 months. Final cholesterol concentrations were compared with values before thyroxine was started. The dose of thyroxine was based on clinical assessment, serum triiodothyronine concentrations kept within the normal range, and thyrotrophin values within the normal range or suppressed. The patients had taken thyroxine replacement for a mean of 12.7 years. Two-thirds (21 subjects) had suppressed thyrotrophin concentrations, and it was normal in one-third (10). Fifteen subjects had a past history of thyrotoxicosis. BMD and cholesterol concentrations were compared between those with suppressed and normal thyrotrophin concentrations and between those with and without a past history of thyrotoxicosis. No patient had a pathological fracture. One had a Z value for the femoral neck of -1.6, denoting early but definite osteoporosis, and five had borderline osteoporosis with Z values for one or other site between -1.1 and -1.5. None of the seven with the lowest BMDs had any significant change when measurements were repeated. The difference in Z values between subjects with suppressed and normal thyrotrophin concentrations was not significant for either the lumbar spine (p = 0.68) or the femoral neck (p = 0.28). A past history of thyrotoxicosis had a greater effect on BMD for both sites than thyrotrophin suppression, but again the difference between those with and without a past history of thyrotoxicosis was significant neither for the lumbar spine (p = 0.18) nor for the femoral neck (p = 0.34). The combination of thyrotrophin suppression and a past history of thyrotoxicosis also failed significantly to reduce the BMD of the lumbar spine (p = 0.38) or femoral neck (p = 0.30) in comparison with those who had neither thyrotrophin suppression nor a past history of thyrotoxicosis. The mean fall in serum cholesterol concentration was 2.1 mmol/l (SD 1.78) (p = 0.001) in those with a suppressed thyrotrophin concentration taking a mean daily dose of thyroxine of 171 micrograms (SD: 34.7), compared with a fall of 0.89 mmol/l (SD: 1.04) (p = 0.065) in those whose thyrotrophin concentration was not suppressed on a mean daily thyroxine dose of 140 micrograms (SD: 50). No patient had atrial fibrillation or cardiographic evidence of coronary artery disease (CAD). The serum cholesterol concentration should play at least as important a part in influencing the dose of thyroxine as a fear of osteoporosis. Fractures are not a feature in the natural history of treated hypothyroidism, whereas CAD is a common cause of death in these patients.
在31例接受治疗的甲状腺功能减退女性中，评估了促甲状腺激素抑制对骨矿物质密度（BMD）和血清胆固醇浓度的影响。对其中7例BMD值最低者在平均22.7个月的时间段后重复测量腰椎和股骨颈的BMD。将最终胆固醇浓度与开始使用甲状腺素前的值进行比较。甲状腺素剂量基于临床评估，血清三碘甲状腺原氨酸浓度保持在正常范围内，促甲状腺激素值在正常范围内或被抑制。患者平均接受甲状腺素替代治疗12.7年。三分之二（21例受试者）的促甲状腺激素浓度被抑制，三分之一（10例）正常。15例受试者有甲状腺毒症病史。比较了促甲状腺激素浓度被抑制和正常者之间以及有和无甲状腺毒症病史者之间的BMD和胆固醇浓度。没有患者发生病理性骨折。1例股骨颈的Z值为-1.6，表明早期但明确的骨质疏松，5例有临界骨质疏松，一个或另一个部位的Z值在-1.1至-1.5之间。7例BMD最低者重复测量时均无显著变化。促甲状腺激素浓度被抑制和正常的受试者之间腰椎（p = 0.68）或股骨颈（p = 0.28）的Z值差异均无统计学意义。有甲状腺毒症病史对两个部位BMD的影响均大于促甲状腺激素抑制，但有和无甲状腺毒症病史者之间腰椎（p = 0.18）或股骨颈（p = 0.34）的差异同样无统计学意义。与既无促甲状腺激素抑制也无甲状腺毒症病史者相比，促甲状腺激素抑制和有甲状腺毒症病史的组合也未显著降低腰椎（p = 0.38）或股骨颈（p = 0.30）的BMD。促甲状腺激素浓度被抑制且平均每日服用171微克（标准差：34.7）甲状腺素的患者血清胆固醇浓度平均下降2.1 mmol/L（标准差1.78）（p = 0.001），而促甲状腺激素浓度未被抑制且平均每日服用140微克（标准差：50）甲状腺素的患者血清胆固醇浓度下降0.89 mmol/L（标准差：1.04）（p = 0.065）。没有患者发生心房颤动或有冠状动脉疾病（CAD）的心电图证据。血清胆固醇浓度在影响甲状腺素剂量方面应至少与对骨质疏松的担忧起到同样重要的作用。骨折并非治疗的甲状腺功能减退自然病程中的特征，而CAD是这些患者常见的死亡原因。
