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许多药物长期应用可使骨质脱钙,小儿可发生软骨病(佝偻病),成人可导致骨软化症,下统称为骨软化(Osteomalacia)。现简述药物引起骨软化的若干问题。一、诱发骨软化的药物及发病机理1.抗惊药物:苯妥因钠、苯巴比妥、氨甲安定和醋唑磺胺等药均可引起骨软化。长期大剂量用抗惊药治疗的病人,在未见明显骨软化临床表现之前,可有骨质疏松、硷性磷酸酶增高及25-(OH)D_3浓度降低。抗惊药所致临床明显骨软化,儿童青少年占5%,成人占1~5%。其机理:(1)能诱导肝药物代谢酶活性,促进维生素D代谢,使维生素D减少而发生骨软化;(2)抑制肝脏25-羟化酶活性,使维生素D不能转化为25-(OH)D_3,有活性的维生素D减
Long-term use of many drugs can decalcification of bone, children can occur rickets (rickets), adults can lead to osteomalacia, generally referred to as osteomalacia (Osteomalacia). A brief account of some of the problems caused by drug-induced osteomalacia. First, induced osteomalacia drugs and pathogenesis 1. Anti-shock drugs: phenytoin sodium, phenobarbital, methotadine and acetochlor sulfa drugs can cause osteomalacia. Long-term high-dose anti-shock drug treatment in patients without obvious clinical manifestations of osteomalacia, may have osteoporosis, increased alkaline phosphatase and 25- (OH) D 3 concentration decreased. Clinical manifestations caused by anti-shock drug obvious osteomalacia, children and adolescents accounted for 5%, adults accounted for 1 to 5%. The mechanism: (1) can induce hepatic drug metabolism enzyme activity, promote vitamin D metabolism, reduce vitamin D and osteomalacia; (2) inhibit hepatic 25-hydroxylase activity, so that vitamin D can not be converted to 25- (OH ) D_3, active vitamin D minus