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克罗恩狭窄经抗分枝杆菌抗生素治疗后开放:一项回顾性研究。

Crohn's strictures open with anti-mycobacterial antibiotic therapy: A retrospective review.

作者信息

Collyer Rhys, Clancy Annabel, Agrawal Gaurav, Borody Thomas J

机构信息

Centre for Digestive Diseases, Five Dock 2046, NSW, Australia.

出版信息

World J Gastrointest Endosc. 2020 Dec 16;12(12):542-554. doi: 10.4253/wjge.v12.i12.542.

DOI:10.4253/wjge.v12.i12.542
PMID:33362907
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7739142/
Abstract

BACKGROUND

Medical therapy for strictures is limited and first-line treatment consists of endoscopic balloon dilatation, strictureplasty or surgical resection. , and can all cause stenosis, for which antibiotic treatment achieves stricture resolution. is a suspected causative agent in Crohn's disease (CD). Thus, specialized antimicrobial treatment, in particular, anti-mycobacterial antibiotic therapy (AMAT) has been proposed as a potential treatment option. To our knowledge, the opening of CD strictures has not been recorded using any form of antibiotic therapy. We hypothesized that AMAT would resolve strictures in patients with CD.

AIM

To investigate the effect and outcomes of AMAT in a cohort of CD patients with an ileal stricture.

METHODS

A single center, retrospective, medical record case review was conducted on an observational cohort of patients with CD who had an ileal stricture on colonoscopy and were treated with AMAT. Forty patients meeting the inclusion criteria were identified from the internal medical database. Thirty (75%) patients had follow-up colonoscopy and clinical data available. The AMAT regimen was prescribed after the initial colonoscopy for a duration of at least six months until follow-up colonoscopy with the attending gastroenterologist. Patient demographics, symptoms, colonoscopy reports, inflammatory serum markers and concurrent medications were recorded at pre-treatment and follow-up between January 1995 and June 2018.

RESULTS

Of the patients that returned for follow-up after > 24 mo of AMAT, twenty (67%) had complete resolution (CR) of their ileal strictures, three (10%) had partial resolution and seven (23%) had no resolution. Irrespective of stricture outcome, 21 patients (70%) demonstrated clinical response to AMAT and there was a statistically significant reduction in inflammatory serum markers C-reactive protein ( < 0.0001) and erythrocyte sedimentation rate ( = 0.04) from pre-treatment to follow-up. It was observed that 11 (37%) patients experienced side effects, but no serious adverse effects were attributable to AMAT. At follow-up there were 26 (87%) patients on concomitant medication for CD and a statistically significant association between CR and AMAT with a concomitant immunomodulator ( = 0.02).

CONCLUSION

This study demonstrated a high rate of stricture resolution (67%) similar to that seen in tuberculosis strictures (70%), suggesting a shared mycobacterial origin of strictures, and perhaps disease.

摘要

背景

针对狭窄的药物治疗有限,一线治疗包括内镜下球囊扩张、狭窄成形术或手术切除。[具体疾病1]、[具体疾病2]和[具体疾病3]均可导致狭窄,抗生素治疗可使狭窄消退。[具体病原体]被怀疑是克罗恩病(CD)的致病因素。因此,有人提出专门的抗菌治疗,特别是抗分枝杆菌抗生素疗法(AMAT)作为一种潜在的治疗选择。据我们所知,尚未有使用任何形式的抗生素疗法使CD狭窄开放的记录。我们假设AMAT可使CD患者的狭窄消退。

目的

研究AMAT对一组患有回肠狭窄的CD患者的疗效和结果。

方法

对一组经结肠镜检查发现回肠狭窄并接受AMAT治疗的CD患者进行了一项单中心、回顾性病历病例审查。从内科数据库中确定了40名符合纳入标准的患者。30名(75%)患者有随访结肠镜检查和临床数据。在初次结肠镜检查后开出处方AMAT方案,持续至少6个月,直至与主治胃肠病学家进行随访结肠镜检查。记录了1995年1月至2018年6月治疗前和随访时患者的人口统计学特征、症状、结肠镜检查报告、炎症血清标志物和同时服用的药物。

结果

在接受AMAT治疗超过24个月后返回进行随访的患者中,20名(67%)患者的回肠狭窄完全消退(CR),3名(10%)部分消退,7名(23%)未消退。无论狭窄结果如何,21名(70%)患者对AMAT有临床反应,从治疗前到随访,炎症血清标志物C反应蛋白(<0.0001)和红细胞沉降率(=0.04)有统计学意义的降低。观察到11名(37%)患者出现副作用,但无严重不良反应归因于AMAT。随访时有26名(87%)患者同时服用CD治疗药物,并发现CR与AMAT联合使用免疫调节剂之间存在统计学意义的关联(=0.02)。

结论

本研究显示狭窄消退率较高(67%),与结核病狭窄的消退率(70%)相似,提示狭窄可能有共同的分枝杆菌起源,也许疾病也是如此。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b06f/7739142/171c8f721516/WJGE-12-542-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b06f/7739142/6d7ded765e54/WJGE-12-542-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b06f/7739142/40285e72b0e0/WJGE-12-542-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b06f/7739142/eea1c0bd0d71/WJGE-12-542-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b06f/7739142/171c8f721516/WJGE-12-542-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b06f/7739142/6d7ded765e54/WJGE-12-542-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b06f/7739142/40285e72b0e0/WJGE-12-542-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b06f/7739142/eea1c0bd0d71/WJGE-12-542-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b06f/7739142/171c8f721516/WJGE-12-542-g004.jpg

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