Whyte M P, McAlister W H, Patton L S, Magill H L, Fallon M D, Lorentz W B, Herrod H G
J Pediatr. 1984 Dec;105(6):926-33. doi: 10.1016/s0022-3476(84)80079-7.
After biochemical and radiographic studies, enzyme replacement therapy in three patients with the infantile form of hypophosphatasia was attempted by weekly intravenous infusions of bone alkaline phosphatase-rich (BAP) plasma from patients with Paget bone disease. Subsequently, circulating BAP activity was substantially increased in each patient, and in one was maintained in the normal range for nearly 2 months. Despite partial or complete correction of the deficiency of circulating BAP activity, we observed no radiographic evidence for arrest of progressive osteopenia or improvement in rachitic defects in any of the patients. Failure of infants with hypophosphatasia to show significant healing of rickets on correction of circulating BAP activity supports the hypothesis that this isoenzyme functions in situ during normal skeletal mineralization.
在进行生化和影像学研究后,对三名患有婴儿型低磷酸酯酶症的患者尝试了酶替代疗法,方法是每周静脉输注来自佩吉特骨病患者的富含骨碱性磷酸酶(BAP)的血浆。随后,每名患者循环中的BAP活性均大幅增加,其中一名患者的活性在正常范围内维持了近2个月。尽管循环中BAP活性的缺乏得到了部分或完全纠正,但我们未观察到任何患者有影像学证据表明进行性骨质减少停止或佝偻病缺陷有所改善。低磷酸酯酶症婴儿在循环BAP活性得到纠正后未显示佝偻病有明显愈合,这一现象支持了以下假说:这种同工酶在正常骨骼矿化过程中在原位发挥作用。