机构地区:[1]复旦大学附属华东医院骨质疏松科,老年医学研究所骨代谢研究室,上海200040
出 处:《中华内分泌代谢杂志》2013年第4期302-306,共5页Chinese Journal of Endocrinology and Metabolism
摘 要:目的 探讨维生素D缺乏对骨转换和骨量的影响,比较维生素D缺乏伴有继发性甲状旁腺功能亢进或无甲状旁腺功能亢进的患者其骨代谢与骨量的差异。方法 542名绝经后妇女[平均年龄(64.0 ± 10.8)岁]纳入研究,检测血钙、磷、碱性磷酸酶、血25-羟维生素D(25-OHD)、甲状旁腺激素(PTH)、骨钙素、Ⅰ型胶原羧基端肽(CTX)和Ⅰ型前胶原氨基端前肽(PINP),以及腰椎、股骨颈和全髋骨密度。结果(1)研究人群中维生素D缺乏的患病率为24%,血清25-OHD水平随季节不同存在明显差异(P=0.023),秋季来访的研究对象高于春季和冬季(P=0.012和P=0.039)。(2)将研究对象分为4组,组1:25-OHD<10 ng/ml及PTH≥65 pg/ml(7.0%);组2:25-OHD<10 ng/ml及PTH<65 pg/ml(17.0%);组3:25-OHD≥10 ng/ml及PTH<65 pg/ml(73.6%);组4:25-OHD≥10 ng/ml及PTH≥65 pg/ml(2.4%)。与组1相比,组2血钙水平低,骨转换低,骨密度高。(3)多元逐步线性回归显示腰椎骨密度的主要影响因子为体重指数(r^2=0.370,P<0.01),年龄(r^2=-0.158,P<0.01),PTH(r^2=-0.121,P<0.05),以及CTX(r^2=-0.118,P<0.05);股骨颈骨密度的主要影响因子为绝经年限(r^2=-0.201,P<0.01)和体重指数(r^2=0.139,P<0.05);髋部骨密度的主要影响因子为年龄(r^2=-0.239,P<0.01)和体重指数(r^2=0.239,P<0.01)。而血清25-OHD与腰椎、股骨颈、髋部骨密度均无显著相关性。结论 绝经后妇女维生素D缺乏的发病率高,在维生素D缺乏伴甲状旁腺反应降低的人群中钙平衡受损,但PTH升高介导的骨丢失减轻。与髋部相比,腰椎对血PTH升高和骨转换加速引起的骨丢失更为敏感。Objective To investigate the effects of vitamin D deficiency on bone turnover and bone mineral density in patients with a blunted PTH response as compared to patients with vitamin D deficiency and secondary hyperparathyroidism. Method A total of 542 postmenopausal women [mean age(64.0 ± 10.8)years] were evaluated by assessing serum calcium, phosphate, alkaline phosphatase, 25-hydroxy vitamin D(25-OHD), PTH, bone turnover markers such as osteocalcin, C-terminal telopeptide of type Ⅰ collagen(CTX) and procollagen type Ⅰ amino-terminal propeptide(PINP), and bone mineral density of lumber spine, total hip and femur neck etc. Result (1)The prevalence of vitamin D deficiency in this cohort was 24%. Mean 25-OHD varied across seasons(P=0.023); women who paid visits during winter and spring yielded significantly lower levels of 25-OHD than those who had their visit during the fall(P=0.012 and P=0.039). Serum PTH and bone turnover markers did not vary by season.(2)All subjects could be divided into four groups occording to their serum 25-OHD and PTH levels. Group 1: 25-OHD〈10 ng/ml and PTH≥65 pg/ml(7.0%), group 2: 25-OHD〈10 ng/ml and PTH〈65 pg/ml(17.0%), group 3: 25-OHD≥10 ng/ml and PTH〈65 pg/ml(73.6%), group 4: 25-OHD≥10 ng/ml and PTH≥65 pg/ml(2.4%). Blunted PTH response was found in 70.8% of patients with vitamin D deficiency. Patients with vitamin D deficiency and a blunted PTH response were characterized by a lowered serum calcium, a reduction in bone turnover(serum CTX and serum osteocalcin), but protection in bone density as compared to those with vitamin D deficiency and secondary hyperparathyroidism.(3) As for spine bone mineral density, the significant independent predictors were body mass index(r^2=0.370,P〈0.01), age(r^2=-0.158,P〈0.01), PTH(r^2=-0.121,P〈0.05), and serum CTX(r^2=-0.118,P〈0.05). For femoral neck bone mineral density, the significant independent predictors were years since menopause(r^2=-0.
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