甲状腺功能亢进患者治疗前后骨矿代谢的变化与机制

Changes of bone and mineral metabolism in patients with hyperthyroidism before and after treatment

目的了解甲状腺功能亢进（甲亢）患者治疗前后骨矿物质代谢的变化与机制。方法选择４５例甲亢治疗前和治疗后患者，采用酶联免疫法测定了血清骨特异性碱性磷酸酶（ＢＡＰ）、尿脱氧吡啶啉（ＤＰＤ）；用放射免疫法测定了血清降钙素（ＣＴ）、甲状旁腺素（ＰＴＨＭ）、骨钙素（ＢＧＰ）及相关生化指标，双能Ｘ线吸收法测定腰椎（Ｌ２４）和股骨颈（Ｎｅｃｋ）、大转子（Ｔｒｏｃｈ）、Ｗａｒｄ′ｓ三角（Ｗａｒｄ′ｓ）骨密度（ＢＭＤ），并与５８例健康对照者进行比较。结果甲亢治疗前尿ＤＰＤ较对照组升高５２７％，血清碱性磷酸酶（ＡＬＰ）、ＢＡＰ、ＢＧＰ分别升高６２％、１４６％、８７％（Ｐ均＜０００１），ＢＭＤ有不同程度降低，以女性Ｌ２～４、Ｗａｒｄ′ｓ点为显著（Ｐ＜０．０５）。治疗后与治疗前比较尿ＤＰＤ下降７９％，血清ＡＬＰ、ＢＡＢ、ＢＧＰ分别下降１９．５％、２４．７％、２７．５％（Ｐ分别＜０．００１、０．０５、０．０５、＞０．０５），各部位ＢＭＤ均有增加，以女性Ｔｒｏｃｈ点最显著（Ｐ＜００５）。相关分析显示，尿ＤＰＤ与血ＢＧＰ正相关（ｒ＝０３４９Ｐ＜０．０５），血ＦＴ４与ＢＡＰ、ＡＬＰ、ＤＰＤ正相关（分别为ｒ＝０３５３，Ｐ＜００５?

Objective To investigate the changes of bone and mineral metabolism in patients with hyperthyroidism before and after treatment. Methods Enzyme linked immunosorbent assay was used to measure bonespecific alkaline phosphatase (BAP) and deoxypyridinoline (DPD); radioimmunoassay to measure serum calcitonin (CT), parathyroid hormone (PTHM), bone GLA protein (BGP) and other markers related to bone metabolism ; dual energy Xray absorptiometry to measure bone mineral density (BMD) of spine(L2～4) and femur(Neck,Troch,Ward′s) in 45 patients with hyperthyroidism before and after treatment and 58 healthy volunteers. Results The urinary DPD level was elevated by 527% in patients with hyperthyroidism before treatmentCompared to controls the serum ALP, BAP, BGP elevated by 62%, 146%, 87% (P<0.001), BMD decreased to various extent, and women L24,Ward′s were marked (P<0.05). The results after treatment and before treatment showed that urinary DPD decreased by 79%; serum ALP, BAP, BGP decreased by 19.5%,247%, 27.5% respectively (P<0.001,0.05,0.05,>0.05) All sites BMD increased, and women Troch sites were marked (P<0.05). The correlation analysis showed that the urinary DPD was positively correlated with serum BGP(r=0.349 P<0.05). FT4 was positively correlated with BAP, ALP and DPD respectively) (r=0353,P<0.05,r=0.294 P=0.05,r=0.426 P<0.01). Conclusion Hyperthyroidism bone disease is caused by excessive serum thyroid hormone that speeds up bone turnover and marked bone absorption compared to bone formation.