更新于：2024-11-01

Colitis, Collagenous

胶原性结肠炎

更新于：2024-11-01

基本信息

别名

CC - Collagenous colitis、COLLAGENOUS COLITIS、Colitis collagenous

+ [15]

简介

A subtype of MICROSCOPIC COLITIS, characterized by chronic watery DIARRHEA of unknown origin, a normal COLONOSCOPY but abnormal histopathology on BIOPSY. Microscopic examination of biopsy samples taken from the COLON show larger-than-normal band of subepithelial COLLAGEN.

关联

项与胶原性结肠炎相关的药物

Budesonide

布地奈德

靶点

作用机制

GR激动剂

在研机构

Calliditas Therapeutics AB [+28]

原研机构

阿斯利康制药有限公司

在研适应症

免疫球蛋白a肾病 [+9]

非在研适应症

急性移植物抗宿主病 [+19]

最高研发阶段批准上市

首次获批国家/地区

美国

首次获批日期1994-02-14

项与胶原性结肠炎相关的临床试验

NCT03658993 / Unknown status临床3期IIT

Rifaximin-treatment of Collagenous Colitis:

The hypothesis of this study is that an altered gut microbiota is a contributory factor in initiating an inflammatory process in the colonic mucosa leading to collagenous colitis. The investigators suggest that treatment with budesonide reduces the inflammation without treating the underlying cause. In this trial the investigators will try to modullate gut microbiota by adding rifaximin. The aim of this study is to assess if 4 weeks treatment with rifaximin as a supplement to a standard course of budesonide against active CC can reduce the risk of relapse after treatment cessation.

开始日期2018-11-01

申办/合作机构-

EUCTR2018-001891-39-DK / Not yet recruiting临床2期IIT

Rifaximin-treatment of Collagenous colitis: A prospective, double-blind, placebo-controlled study

开始日期2018-09-14

申办/合作机构-

NL-OMON45110 / CompletedN/AIIT

Risk Factors for Microscopic Colitis. A Dutch Case-Control Study - Risk factors for MC

开始日期2014-07-03

申办/合作机构-

100 项与胶原性结肠炎相关的临床结果

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100 项与胶原性结肠炎相关的转化医学

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0 项与胶原性结肠炎相关的专利（医药）

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1,170

项与胶原性结肠炎相关的文献（医药）

2024-12-31·Annals of Medicine

Factors associated with long-term clinical outcome in microscopic colitis

Article

作者: Sakuraba, Atsushi ; Micic, Dejan ; Komaki, Yuga ; Keyashian, Kian ; Miyatani, Yusuke ; Komaki, Fukiko

BACKGROUND AND AIMSMicroscopic colitis has been increasingly recognized as a cause of chronic diarrhoea. We aimed to characterize the role of disease-related factors and treatments on the clinical outcomes of microscopic colitis.METHODSWe retrospectively reviewed the medical records of patients with microscopic colitis who were treated at the University of Chicago and Oregon Health & Science University between August 2010 and May 2016. Patient characteristics and treatments were evaluated as predictors of clinical outcomes using univariate and multivariate analyses. Clinical remission was defined as no symptoms associated with microscopic colitis based on physician assessment and histologic remission was defined as no evidence of histological inflammation of microscopic colitis.RESULTSSeventy-two patients with microscopic colitis were included in the study (28 with lymphocytic colitis and 44 with collagenous colitis). Non-steroidal anti-inflammatory drugs, proton pump inhibitors and selective serotonin reuptake inhibitors were used in 23 (31.9%), 14 (19.4%) and 15 (20.8%), respectively, at the time of diagnosis. Among 46 patients with adequate follow-up data, 25 (54.3%) patients achieved clinical remission. Response to budesonide (p = .0002) and achieving histologic remission (p = .0008) were associated with clinical remission on univariate analysis. On multivariate analysis, budesonide response (p = .0052) was associated with clinical remission (odds ratio 25.00, 95% confidence interval 2.63-238.10). Among 22 patients who underwent a follow-up colonoscopy, five patients (22.7%) achieved histologic remission. All patients with histologic remission maintained clinical remission without medication, whereas only two patients (11.8%) were able to discontinue medical therapy when histologic inflammation was present (p = .0002).CONCLUSIONSIn the present cohort of patients with microscopic colitis, a favourable response to budesonide was significantly associated with long-term clinical remission, and all patients achieving histological remission were able to maintain clinical remission without further medical therapy. Larger studies are required to confirm these findings.

2024-08-01·JPGN Reports

Co‐occurrence of collagenous gastrointestinal disease in siblings in early childhood: New insight into a rare condition

Article

作者: Luitingh, Taryn L. ; Ng, Jessica ; McGrath, Kathleen H.

AbstractCollagenous gastrointestinal (GI) disease is a rare inflammatory condition characterized by subepithelial collagen deposition and inflammatory cell infiltrates of the GI mucosa, which typically occurs in the stomach in children. There are few published reports of more extensive involvement in children, and descriptions of familial involvement are rare, with no previous reported cases of affected siblings in early childhood. We describe two siblings with contrasting medical backgrounds, who were simultaneously diagnosed with collagenous GI disease in early childhood. Both children demonstrated gastric and colonic involvement on serial endoscopies, however, had distinct patterns of clinical presentation, disease course, and histological progression, providing new insights into the pediatric phenotype of collagenous GI disease and further, its relationship to microscopic colitis. Although rare, this condition should be considered as a differential in children presenting with severe or refractory iron deficiency anemia, chronic non‐bloody watery diarrhea, or unexplained nonspecific chronic abdominal pain.

2024-07-01·United European Gastroenterology Journal

Lymphocytic colitis can be transcriptionally divided into channelopathic and inflammatory lymphocytic colitis

Article

作者: Koch, Stefan ; Bhardwaj, Archana ; Münch, Andreas ; Rosenstiel, Philip ; Escudero‐Hernández, Celia ; Montague, Julia

AbstractBackgroundThe pathobiology of the non‐destructive inflammatory bowel disease (IBD) lymphocytic colitis (LC) is poorly understood. We aimed to define an LC‐specific mucosal transcriptome to gain insight into LC pathology, identify unique genomic signatures, and uncover potentially druggable disease pathways.MethodsWe performed bulk RNA‐sequencing of LC and collagenous colitis (CC) colonic mucosa from patients with active disease, and healthy controls (n = 4–10 per cohort). Differential gene expression was analyzed by gene‐set enrichment and deconvolution analyses to identify pathologically relevant pathways and cells, respectively, altered in LC. Key findings were validated using reverse transcription quantitative PCR and/or immunohistochemistry. Finally, we compared our data with a previous cohort of ulcerative colitis and Crohn's disease patients (n = 4 per group) to distinguish non‐destructive from classic IBD.ResultsLC can be subdivided into channelopathic LC, which is governed by organic acid and ion transport dysregulation, and inflammatory LC, which is driven by microbial immune responses. Inflammatory LC displays an innate and adaptive immunity that is limited compared to CC and classic IBD. Conversely, we noted a distinct induction of regulatory non‐coding RNA species in inflammatory LC samples. Moreover, compared with CC, water channel and cell adhesion molecule gene expression decreased in channelopathic LC, whereas it was accentuated in inflammatory LC and associated with reduced intestinal epithelial cell proliferation.ConclusionsWe conclude that LC can be subdivided into channelopathic LC and inflammatory LC that could be pathomechanistically distinct subtypes despite their shared clinical presentation. Inflammatory LC exhibits a dampened immune response compared to CC and classic IBDs. Our results point to regulatory micro‐RNAs as a potential disease‐specific feature that may be amenable to therapeutic intervention.