Regression of intestinal diffuse large B cell lymphoma after treatment with vedolizumab in a patient with Crohn's disease
Regression of intestinal diffuse large B cell lymphoma after treatment with vedolizumab in a patient with Crohn's disease
复制标题
克罗恩病患者接受维多珠单抗治疗后肠道弥漫性大 B 细胞淋巴瘤的消退
DOI：
10.1016/j.ejca.2022.09.015
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发表时间：
2022
影响因子：
8.4
通讯作者：
Seno Hiroshi
中科院分区：
文献类型：
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作者：
Yamamoto Shuji;Shindo Takero;Kitamoto Hiroki;Kuwada Takeshi;Seno Hiroshi
Vedolizumab是一种人源化免疫球蛋白G1单克隆抗体，可结合肠道归巢受体a4 b7整联蛋白，并抑制其结合粘膜地址素细胞粘附分子-1的能力，后者在肠道相关淋巴组织和肠系膜淋巴结（MLN）内的内皮上表达[1]。因此，Vedolizumab可防止淋巴细胞外渗至胃肠道粘膜组织和局部淋巴结，从而减轻肠道炎症[1]。在溃疡性结肠炎[2]和克罗恩病（CD）[3]患者中证实了Vedolizumab治疗炎症性肠病的疗效。我们描述了1例原发性胃肠道弥漫性大B细胞淋巴瘤（DLBCL），其中Vedolizumab诱导了完全代谢缓解。一名59岁男性，有13年回肠CD病史，主诉腹痛。患者接受每日剂量4 mg他克莫司和25 mg硫唑嘌呤治疗CD，并维持临床缓解4年。经口双气囊小肠镜检查显示空肠有一个大的溃疡性病变。活检钳活检标本的组织学检查显示聚集的大，非典型淋巴细胞。这些细胞在免疫组织化学分析中对CD 79 a、BCL 2和MUM 1呈弥漫阳性，对CD 20和BCL 6呈部分阳性，对CD 10、CD 138和CD 30呈阴性，在原位杂交中对EBER-1呈阴性（图1A）。流式细胞术显示κ轻链限制。腹部计算机断层扫描显示空肠壁肿胀（图1 B上图，箭头）和局部MLN（图1 B上图，箭头）。正电子发射计算机断层扫描显示空肠病变（图1 B，下图，箭头）和MLN（图1 B，下图，箭头）中有较强的氟脱氧葡萄糖摄取，无其他播散性病变。骨髓活检正常。基于这些发现，根据Lugano分类，患者被诊断为DLBCL（未另行说明）和非生发中心B细胞样II 1期。停用他克莫司和硫唑嘌呤治疗CD，并开始治疗DLBCL。他接受了6个疗程的ReCHOP一线化疗，但没有达到缓解。自体造血干细胞移植与抗CD 19嵌合抗原
Vedolizumab is a humanized immunoglobin G1 monoclonal antibody that binds the gut homing receptor a4b7 integrin and inhibits its ability to bind mucosal addressin cell adhesion molecule-1, which is expressed on the endothelium within the gut-associated lymphoid tissues and mesenteric lymph nodes (MLN)[1]. Therefore, vedolizumab prevents lymphocytes from extravasating into gastrointestinal mucosal tissues and regional lymph nodes, thus attenuating intestinal inflammation [1]. The efficacy of vedolizumab for inflammatory bowel disease was demonstrated in patients with ulcerative colitis [2] and Crohn’s disease (CD)[3]. We describe a case of primary gastrointestinal diffuse large B cell lymphoma (DLBCL) in which vedolizumab induced complete metabolic remission. A 59-year-old man with a 13-year history of ileal CD complained of abdominal pain. He had been treated with daily doses of 4 mg tacrolimus and 25 mg azathioprine for CD and maintained clinical remission for 4 years. Peroral double balloon enteroscopy demonstrated a large ulcerative lesion in the jejunum. Histopathological examination of forceps biopsy specimens revealed aggregation of large, atypical lymphocytes. These cells were diffusely positive for CD79a, BCL2, and MUM1, partially positive for CD20 and BCL6, and negative for CD10, CD138, and CD30 in immunohistochemical analysis, and negative for EBER-1 in in situ hybridization (Fig. 1 A). Flow cytometry indicated kappa light chain restriction. Abdominal computed tomography revealed swelling of the jejunal wall (Fig. 1 B upper panel, arrowheads) and regional MLN (Fig. 1 B upper panel, arrows). Positron emission tomographycomputed tomography showed strong fluorodeoxyglucose uptake in the jejunal lesion (Fig. 1 B lower panel, arrow heads) and MLN (Fig. 1 B lower panel, arrow) without other disseminated lesions. Bone marrow biopsy was normal. Based on these findings, the patient was diagnosed with DLBCL, not otherwise specified, and non-germinal center B-cell-like, stage II1, according to the Lugano classification. Tacrolimus and azathioprine for CD were discontinued, and treatment for DLBCL was started. He underwent first-line chemotherapy with six courses of ReCHOP, but did not achieve remission. Autologous hematopoietic stem cell transplantation and anti-CD19 chimeric antigen