Logan E C, Williamson L M, Ryrie D R
Gut. 1986 Jul;27(7):868-72. doi: 10.1136/gut.27.7.868.
Agranulocytosis and aplastic anaemia associated with sulphasalazine are well recognised, but pancytopenia caused by acute megaloblastic arrest of haemopoiesis while taking sulphasalazine has not previously been described. We report three patients who, after taking sulphasalazine for over two years, suddenly developed severe pancytopenia with gross megaloblastic changes in the marrow. In two patients there was a good response to high dose oral folic acid but the third required folinic acid. The mechanism appears to be acute folate deficiency, and the requirement for folinic acid in one case suggests that the known inhibition of folate metabolism by sulphasalazine also contributes. The syndrome appears to be associated with high dosage and slow acetylator status. The drug has been successfully restarted at reduced dosage with folate supplements in two patients both of whom were slow acetylators. In the third case, whose acetylator status is not known, progression of her disease led to colectomy.
柳氮磺胺吡啶相关的粒细胞缺乏症和再生障碍性贫血已广为人知,但服用柳氮磺胺吡啶时因急性巨幼细胞性造血停滞导致的全血细胞减少症此前尚未见报道。我们报告了3例患者,他们在服用柳氮磺胺吡啶两年多后,突然出现严重全血细胞减少症,骨髓有明显的巨幼细胞改变。2例患者对高剂量口服叶酸反应良好,但第3例需要亚叶酸。其机制似乎是急性叶酸缺乏,而1例患者需要亚叶酸提示柳氮磺胺吡啶对叶酸代谢的已知抑制作用也有影响。该综合征似乎与高剂量和慢乙酰化状态有关。2例慢乙酰化患者在补充叶酸的情况下已成功以减量重新开始使用该药物。在第3例患者中,其乙酰化状态未知,疾病进展导致了结肠切除术。