Interventions for treating lymphocytic colitis

Abstract

Background Lymphocytic colitis is a cause of chronic diarrhea. It is a subtype of microscopic colitis characterized by chronic, watery, non-bloody diarrhea and normal endoscopic and radiologic findings. The etiology of this disorder is unknown.Therapy is based mainly on case series and uncontrolled trials, or by extrapolation of data for treating collagenous colitis, a related disorder. This review is an update of a previously published Cochrane review. Objectives To evaluate the efficacy and safety of treatments for clinically active lymphocytic colitis. Search methods The MEDLINE, PUBMED and EMBASE databases were searched from inception to 11 August 2016 to identify relevant papers. Manual searches from the references of included studies and relevant review articles were performed. Abstracts from major gastroenterological meetings were also searched to identify research submitted in abstract form only. The trial registry web site www.ClinicalTrials.gov was searched to identify registered but unpublished trials. Finally, the Cochrane Central Register of Controlled Trials and the Cochrane Inflammatory Bowel Disease and Functional Bowel Disorders Group Specialized Trials Register were searched for other studies. Selection criteria Randomized controlled trials assessing medical therapy for patients with biopsy-proven lymphocytic colitis were considered for inclusion Data collection and analysis Data was independently extracted by at least two authors. Any disagreements were resolved by consensus. Data were analyzed on an intention-to-treat (ITT) basis. The primary outcome was clinical response as defined by the included studies. Secondary outcome measures included histological response as defined by the included studies, quality of life as measured by a validated instrument and the occurrence of adverse events. Risk ratios (RR) and 95% confidence intervals (CI) were calculated for dichotomous outcomes. The methodological quality of included studies was evaluated using the Cochrane risk of bias tool. The overall quality of the evidence supporting the primary outcome and selected secondary outcomes was assessed using the GRADE criteria. Data were combined for analysis if they assessed the same treatments. Dichotomous data were combined using a pooled RR along with corresponding 95% CI. A fixed-effect model was used for the pooled analysis.

<p>Management of microscopic colitis: challenges and solutions</p>

“…A recent 2017 Cochrane review echoed these sentiments and demonstrated that budesonide 9 mg/day for 6–8 weeks was effective in inducing both clinical and histologic remission. In two examined studies with a total of 57 patients, 88% showed clinical response to budesonide as opposed to 38% to placebo and 78% showed histologic response compared with 33% with placebo 50. The “number needed to treat” was two for CC and three for LC.…”

“…At week 8, 70% of patients were in remission 55. While beclomethasone does appear to induce remission, a 2010 trial demonstrated that only 26% of patients (from the 84% with initial response) maintained clinical remission at 1 year, bringing its longevity into question 50. While beclomethasone dipropionate is promising, it is not available in the USA and to date is only in use in Europe.…”

Editorial: The Dark Side of Microscopic Colitis

“…Treatment is guided by response to symptoms, with budesonide identified as the most effective drug to control MC (19)(20)(21). Unfortunately, as reported by Mihaly et al not enough data have been received from extensive trials on alternative drugs including immunomodulators, aminosalicylates, and biological treatment such as TNF-alpha antagonists and integrin inhibitors.…”

Long‐term oral budesonide treatment and risk of osteoporotic fractures in patients with microscopic colitis

“…The controlled-release formulations of oral budesonide are proven both effective and well tolerated in patients with ileoceacal Crohn´s disease 1,2 and have been a breakthrough in the treatment of microscopic colitis (MC). 3,4 Unlike most other oral corticosteroids, budesonide has a substantial first-pass metabolism. Thereby, it exerts an immunosuppressant effect in the gut wall and is subsequently metabolised in the liver, thus resulting in quite a low systemic bioavailability, about 10% 1 compared to more than 80% for prednisolone.…”

“…5 This ingenious leveraging of first-pass metabolism has enabled us to use budesonide for maintenance treatment of MC without undue toxicity. 3,4 However, adverse effects related to long-term use of corticosteroids are of concern. Oral corticosteroids in general are known to increase the risk of osteoporotic fractures through a reduction in bone formations and osteocyte apoptosis.…”