Heinicke H J, Köstler E, Töppich D, Paul R
Abteilung für Nephrologie, Bezirkskrankenhauses Dresden- Friedrichstadt.
Z Gesamte Inn Med. 1987 Dec 1;42(23):683-5.
In 24 patients undergoing haemodialysis, two of them with pseudoporphyria, the total erythrocytic protoporphyrin and in four patients separately the zinc protoporphyrin were investigated. 20 patients showed an increase of the erythrocytic protoporphyrin of low to moderate degree, which only partly is to be ascribed to the zinc protoporphyrin. Since, as a rule, there is no iron deficit in haemodialysis, a secondary damage of the ferrochelatase, which physiologically by administration of iron leads to haem (ferroprotoporphyrin), is assumed as cause of the increase of erythrocytic protoporphyrin. Apart from the toxic lesion in particular a deficiency of the ferrochelatase coenzyme pyridoxal phosphate can be taken into consideration. Diagnostic and therapeutic investigations carrying on are proposed. The erythrocytic protoporphyrin does not only contribute to the pseudoporphyria in haemodialysis.
在24例接受血液透析的患者中，其中2例患有假性卟啉病，对其全红细胞原卟啉进行了研究，并分别对4例患者的锌原卟啉进行了研究。20例患者的红细胞原卟啉呈低度至中度升高，其中部分升高归因于锌原卟啉。由于通常血液透析患者不存在铁缺乏，推测红细胞原卟啉升高的原因是亚铁螯合酶受到继发性损害，生理情况下补充铁可生成血红素（亚铁原卟啉）。除毒性损害外，尤其要考虑亚铁螯合酶辅酶磷酸吡哆醛缺乏的情况。建议进行诊断和治疗方面的研究。红细胞原卟啉不仅与血液透析中的假性卟啉病有关。
