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1例克罗恩病患者在硫唑嘌呤诱发全血细胞减少后病情改善。

A case of Crohn's disease with improvement after azathioprine-induced pancytopenia.

作者信息

Choi Yong Sung, Suh Jung Pil, Song Kee Ho, Lee Jae Bum, Lee Doo Seok, Lee In Taek, Kim Do Sun, Lee Doo Han

机构信息

Department of Gastroenterology, Daehang Hospital, Seoul, Korea.

出版信息

Case Rep Gastroenterol. 2011;5(2):344-9. doi: 10.1159/000329707. Epub 2011 Jul 5.

DOI:10.1159/000329707
PMID:21769285
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3134056/
Abstract

The immunosuppressant azathioprine (AZA) is widely used in the treatment of inflammatory bowel disease (IBD) for both inducing and maintaining remission. However, the adverse effects of AZA can often necessitate a dose reduction or discontinuation. Bone marrow suppression is one of the most serious complications with AZA treatment. On the other hand, some reports have suggested that neutropenia during AZA therapy reduced the relapse rates of IBD patients, and there have been some cases where eradication of the sensitized leukocytes by leukapheresis or bone marrow transplantation improved the IBD, which may explain the relevant role of neutropenia in controlling disease activity. This report describes the case of a 22-year-old male patient who had Crohn's colitis and complicated perianal fistulas that required immunosuppression; he achieved endoscopically determined remission and showed accelerated mucosal healing as well as clinical remission following the AZA-induced pancytopenia.

摘要

免疫抑制剂硫唑嘌呤(AZA)广泛用于诱导和维持炎症性肠病(IBD)的缓解。然而,AZA的不良反应常常需要减少剂量或停药。骨髓抑制是AZA治疗最严重的并发症之一。另一方面,一些报告表明,AZA治疗期间的中性粒细胞减少降低了IBD患者的复发率,并且有一些病例通过白细胞分离术或骨髓移植清除致敏白细胞改善了IBD,这可能解释了中性粒细胞减少在控制疾病活动中的相关作用。本报告描述了一名22岁男性患者的病例,该患者患有克罗恩结肠炎并伴有复杂的肛周瘘管,需要进行免疫抑制治疗;在AZA诱导的全血细胞减少后,他通过内镜检查确定达到缓解,并显示黏膜愈合加速以及临床缓解。

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Am J Gastroenterol. 2006 Dec;101(12):2769-76. doi: 10.1111/j.1572-0241.2006.00843.x. Epub 2006 Oct 6.
2
Inosine triphosphate pyrophosphatase and thiopurine s-methyltransferase genotypes relationship to azathioprine-induced myelosuppression.三磷酸肌苷焦磷酸酶和硫嘌呤S-甲基转移酶基因型与硫唑嘌呤诱导的骨髓抑制的关系。
Clin Gastroenterol Hepatol. 2006 Jan;4(1):44-9. doi: 10.1016/j.cgh.2005.10.019.
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