Heinrich H C, Bender-Götze C, Gabbe E E, Bartels H, Oppitz K H
Klin Wochenschr. 1977 Jun 15;55(12):587-93. doi: 10.1007/BF01490513.
The absorption of 59Fe from a diagnostic 0.56 mg 59Fe2+ dose was measured by 4pi-geometry whole body counting and related to the amount of stainable diffuse cytoplasmatic non heme storage iron in the bone marrow macrophages of children with cystic fibrosis. When the storage iron was within the normal range (+/2+) children with cystic fibrosis absorbed 10-38% (Xa+/-S.D.=21+/-9.3) of the oral 59Fe2+ dose which is identical with the 59Fe-absorption in normal children with normal iron stores (9-45:23+/-8.7%). Depleted iron stores caused an increase of 59Fe-absorption to 43-95% (Xa+/-S.D.=62+/-19) in children with cystic fibrosis and to 45-100% (Xa+/-S.D.=73+/-18) in control children. The interruption or continuation of pancreatin maintenance therapy and the simultaneous administration of 1-1.5 g pancreatin did not influence 59Fe2+ absorption in cystic fibrosis. There is no evidence for a pancreatic factor required for or inhibiting inorganic and food iron absorption in human beings. Iron absorption is controlled also in cystic fibrosis chiefly by the amounts of available storage iron. It is therefore not justified to apprehend the development of hemosiderosis in children with cystic fibrosis who are not or not sufficiently treated with pancreatin.
通过4π几何全身计数法测量了0.56毫克诊断剂量的59Fe2+的吸收情况,并将其与患有囊性纤维化儿童骨髓巨噬细胞中可染色的弥漫性细胞质非血红素储存铁的量相关联。当储存铁处于正常范围(+/2+)时,患有囊性纤维化的儿童吸收了口服59Fe2+剂量的10 - 38%(Xa±标准差 = 21±9.3),这与铁储存正常的正常儿童的59Fe吸收情况相同(9 - 45:23±8.7%)。铁储存耗尽导致患有囊性纤维化的儿童的59Fe吸收增加到43 - 95%(Xa±标准差 = 62±19),而对照儿童增加到45 - 100%(Xa±标准差 = 73±18)。胰酶维持治疗的中断或继续以及同时给予1 - 1.5克胰酶对囊性纤维化患者的59Fe2+吸收没有影响。没有证据表明人体吸收无机铁和食物铁需要或存在抑制性的胰腺因子。在囊性纤维化中,铁的吸收也主要由可用储存铁的量控制。因此,对于未接受或未充分接受胰酶治疗的囊性纤维化儿童,担心其发生血色素沉着症是没有道理的。