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尽管一些激素和营养因素可致骨质疏松,常常发现在骨质疏松病例中是有选择的钙吸收不良,原因不明。某些著者归因于血中1,25-二羟基维生素 D(简称1,25D)浓度减少,但另一些著者认为是肠粘膜受体水平功能异常,他们发现这些患者1,25D 水平正常。若肠道钙吸收减少到一定程度,就会动员骨钙来维持血浆浓度,这可能由甲状旁腺激素(PTH)分泌相对增加来调节,表现在尿中羟脯氨酸排出增多。已知口服1,25D 可纠正骨质疏松者的钙吸收不良,但这在治疗学上的价值尚未确立,它在钙吸收上的好处会被其骨吸收作用抵消,这可能限制其应用。
Although some hormones and nutritional factors can cause osteoporosis, it is often found that there is a selective calcium deficiency in osteoporosis cases for unknown reasons. Some authors attributed to a decrease in 1,25-dihydroxyvitamin D concentrations (1,25D) in the blood, but others considered dysfunction of intestinal mucosal receptor levels and found that these patients had normal levels of 1,25D. If intestinal calcium absorption reduced to a certain extent, it will mobilize bone calcium to maintain plasma concentrations, which may be relatively increased by the secretion of parathyroid hormone (PTH) to regulate the performance of urinary hydroxyproline increased. Oral 1,25D is known to correct poor malabsorption in osteoporosis, but its therapeutic value has not been established and its benefit in calcium absorption is counteracted by its bone resorption which may limit its use.