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用于治疗华氏巨球蛋白血症的克拉屈滨治疗后发生的早发性自身免疫性溶血性贫血。

Early-onset autoimmune hemolytic anemia after cladribine therapy for Waldenström's macroglobulinemia.

作者信息

Aslan Deniz L, Peterson Bruce A, Long-Tsai Michaela, Eastlund Ted

机构信息

Division of Transfusion Medicine, Department of Laboratory Medicine and Pathology, Oncology and Transplantation, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA.

出版信息

Transfusion. 2006 Jan;46(1):90-4. doi: 10.1111/j.1537-2995.2006.00678.x.

DOI:10.1111/j.1537-2995.2006.00678.x
PMID:16398735
Abstract

BACKGROUND

Purine nucleoside analogs are a class of antineoplastic drugs with potent lymphotoxicity against T and B lymphocytes, causing prolonged lymphopenia and linked to delayed immune complications such as opportunistic infections and more recently autoimmune hemolytic anemia (AIHA), seen mostly in patients with chronic lymphocytic leukemia (CLL). A characteristic temporal relation between fludarabine therapy and the appearance of a warm-reactive immunoglobulin G (IgG)-mediated AIHA in patients with CLL has been observed and, in some, the AIHA has been fatal. Whether both fludarabine and cladribine cause AIHA is uncertain because AIHA is commonly seen in patients with CLL without the use of these drugs. In contrast, AIHA is encountered in Waldenström's macroglobulinemia (WM) much less frequently, and the autoantibody is usually cold-reactive and IgM-mediated. In a few reported cases of AIHA arising in patients with WM after cladribine therapy, there was a latency of 24 to 60 months between therapy and the onset of AIHA, three of which were warm-reactive and IgG-mediated.

CASE REPORT

A warm-reacting IgG red cell autoantibody and evidence of hemolysis detected 1 month after completing cladribine therapy for WM, with warm antibody AIHA developing 4 months later, are described.

CONCLUSIONS

Cladribine, like fludarabine, is possibly able to produce this complication during or early after therapy. Because the use of purine analogs is becoming increasingly common, it is important to have an awareness of the complications that can arise during and after treatment. Further observations of warm AIHA during cladribine therapy are needed to establish it as a distinct complication.

摘要

背景

嘌呤核苷类似物是一类抗肿瘤药物,对T和B淋巴细胞具有强大的淋巴毒性,可导致长期淋巴细胞减少,并与机会性感染等延迟性免疫并发症相关,最近还与自身免疫性溶血性贫血(AIHA)有关,多见于慢性淋巴细胞白血病(CLL)患者。已观察到氟达拉滨治疗与CLL患者中出现的温反应性免疫球蛋白G(IgG)介导的AIHA之间存在特征性的时间关系,在某些情况下,AIHA是致命的。氟达拉滨和克拉屈滨是否都会导致AIHA尚不确定,因为在未使用这些药物的CLL患者中也常见AIHA。相比之下,在华氏巨球蛋白血症(WM)中AIHA的发生率要低得多,自身抗体通常是冷反应性且由IgM介导。在少数报道的克拉屈滨治疗后WM患者发生AIHA的病例中,治疗与AIHA发作之间的潜伏期为24至60个月,其中三例为温反应性且由IgG介导。

病例报告

描述了一例在完成WM的克拉屈滨治疗1个月后检测到温反应性IgG红细胞自身抗体和溶血证据,4个月后发生温抗体AIHA的病例。

结论

与氟达拉滨一样,克拉屈滨可能在治疗期间或治疗后早期引发这种并发症。由于嘌呤类似物的使用越来越普遍,了解治疗期间及之后可能出现的并发症很重要。需要对克拉屈滨治疗期间的温抗体AIHA进行进一步观察,以确定其为一种独特的并发症。

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