P682 对慢性胃袋炎症患者不同治疗方式的回顾性比较

Y. Uchitel, N. A. Cohen, A. Hirsch, H. Tulchinsky, M. Zemel, N. Maharshak
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引用次数: 0

摘要

在接受全结肠切除术和回肠袋肛门吻合术(IPAA)手术的患者中,约有 30% 患有慢性肠袋炎。抗肿瘤坏死因子(anti-TNF)、抗整合素α4β7、抗IL-12/23或克罗恩病排除饮食(CDED)等治疗方法在不同的研究中均显示出良好的疗效。我们的目的是在现实世界中比较这些治疗方法的疗效,并发现有助于选择治疗方法的因素。 这是一项回顾性队列研究,涵盖了特拉维夫医疗中心接受生物制剂或 CDED 治疗的 IPAA 手术后伴有慢性肠袋炎的成年溃疡性结肠炎(UC)患者的人口统计学、临床、内窥镜、组织学和实验室数值。数据收集时间为基线、治疗 12 周、26 周和 52 周。mPDAI反应定义为比基线降低≥2分,而mPDAI缓解定义为除mPDAI反应外,mPDAI评分≤4分。 51例患者的治疗干预包括CDED(10例)、维妥珠单抗(21例)、乌斯特库单抗(7例)和阿达木单抗(13例)[表1]。12周和26周时,mPDAI总应答率分别为52%和48%,组间无显著差异。52周时,乌司替库单抗和维多珠单抗的mPDAI应答率(分别为60%和55%)明显高于阿达木单抗和CDED(分别为27.3%和0%),P=0.043。第26周时,乌司替尼(93%)的粪便钙蛋白减少率最高,其次是维多珠单抗(73%)、阿达木单抗(55%)和CDED(-13%),P=0.003。与阿达木单抗(46%)、维多利珠单抗(33%)和CDED(20%)相比,乌司替尼(100%)的治疗持续时间明显高于阿达木单抗(46%)、维多利珠单抗(33%)和CDED(20%),P<0.001[图1]。终止治疗的主要原因是继发性反应消失(50%),其次是原发性无应答和手术并发症(各占 14.7%)、依从性差(11.8%)、副作用(5.9%)和出现抗体(2.9%)。既往未接受过生物制剂或免疫调节剂治疗的胃袋炎患者在12周时的mPDAI应答率明显更高(分别为90%,p=0.016和73.3%,p=0.03)。有手术小袋并发症的患者在12周时的mPDAI定义应答率呈下降趋势(25% vs. 64.7%; p=0.064)。 与阿达木单抗和CDED相比,优妥单抗和维多珠单抗维持长期临床和内镜反应的可能性更高,粪便钙蛋白的降低幅度也更大。生物制剂和免疫调节剂疗法无效的患者获得的诱导应答率更高。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
P682 A Retrospective Comparison of Different Treatment Modalities in Patients with Chronic Pouchitis
Chronic pouchitis affects ~30% of patients post total colectomy with ileal pouch anal anastomosis (IPAA) surgery. Treatment with anti-TNF, anti-integrin α4β7, anti-IL-12/23, or Crohn's disease exclusion diet (CDED), have shown promise in different studies. We aimed to compare the efficacy of these treatments in a real-world context and to detect factors that can aid in treatment choices. A retrospective cohort study encompassing demographic, clinic, endoscopic, histologic and lab values of adult ulcerative colitis (UC) patients post-IPAA surgery with chronic pouchitis, treated with biologics or CDED at the Tel Aviv Medical Center. Data were collected at baseline, 12, 26, and 52 weeks of treatment. Primary outcomes were assessed using the modified Pouchitis Disease Activity Index (mPDAI). mPDAI response was defined as a reduction from baseline of ≥2 points, while mPDAI remission was defined as mPDAI response in addition to mPDAI score ≤4. Therapeutic interventions among 51 patients included CDED (n=10), vedolizumab (n=21), ustekinumab (n=7) and adalimumab (n=13) [Table 1]. At 12 and 26 weeks, overall mPDAI response rates were 52% and 48%, respectively, with no significant difference between groups. At 52 weeks, mPDAI response rates were significantly higher for ustekinumab and vedolizumab (60% and 55%, respectively) compared with adalimumab and CDED (27.3% and 0%, respectively), p=0.043. Fecal calprotectin reduction at week-26 was greatest for ustekinumab (93%), followed by vedolizumab (73%), adalimumab (55%), and CDED (-13%), p=0.003. Treatment persistence over 150 weeks was significantly higher for ustekinumab (100%) compared with adalimumab (46%), vedolizumab (33%), and CDED (20%), p<0.001 [Figure 1]. The predominant cause for treatment discontinuation was secondary loss of response (50%), followed by primary non-response and surgical complications (14.7% each), poor compliance (11.8%), side-effects (5.9%), and development of antibodies (2.9%). Patients without prior biologic or immunomodulator treatment for pouchitis had significantly higher mPDAI response rates at 12 weeks (90%, p=0.016 and 73.3%, p=0.03, respectively). Patients with surgical pouch complications showed a trend towards lower mPDAI-defined response rates at 12 weeks (25% vs. 64.7%; p = 0.064). Ustekinumab and vedolizumab demonstrate higher likelihood of maintaining long-term clinical and endoscopic response, along with greater reduction in fecal calprotectin compared with adalimumab and CDED. Biologic and immunomodulator therapy-naïve patients achieved higher induction response rates.
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