Abstract
Background
Refractory ulcerative colitis (UC), characterized by persistent disease activity despite optimized medical therapy, poses a significant therapeutic challenge. Fecal microbiota transplantation (FMT) has shown promise in inducing remission in active ulcerative colitis (UC) by restoring gut microbial balance; however, its efficacy in refractory cases remains unclear. This systematic review and meta-analysis aimed to evaluate the effectiveness and safety of FMT in achieving clinical and endoscopic remission in patients with refractory UC, based on evidence from randomized controlled trials (RCTs).
Methods
We searched PubMed, Scopus, Google Scholar Cochrane CENTRAL, and Web of Science up to February 2025 for RCTs comparing FMT to placebo or standard care in adults with refractory UC (Mayo Score ≥ 3 despite treatment). Primary outcomes were clinical remission (Mayo Score ≤ 2, no subscore > 1) and endoscopic remission (Mayo endoscopic subscore ≤ 1). Data were pooled using a random-effects model, with heterogeneity assessed via I² and Q-tests. Subgroup analyses explored age at diagnosis and disease duration as moderators. The review followed PRISMA guidelines and was registered with PROSPERO (CRD420250651790).
Results
Six RCTs were included. FMT showed no significant effect on clinical remission (pooled estimate − 0.2584; 95% CI − 0.9031 to 0.3863; p = 0.4321) or endoscopic remission (pooled estimate − 0.2229; 95% CI − 0.8811 to 0.4353; p = 0.5069), with no heterogeneity (I² = 0.00%). Subgroup analyses revealed no moderation by age or disease duration (p > 0.27). Adverse events were mild and transient.
Conclusion
FMT does not significantly improve clinical or endoscopic remission in refractory UC, suggesting limited efficacy in this population despite a favorable safety profile. Larger, standardized trials are warranted.
Supplementary Information
The online version contains supplementary material available at 10.1186/s12876-025-04185-3.
Keywords: Fecal microbiota transplantation (FMT), Refractory ulcerative colitis, Clinical remission, Endoscopic remission
Introduction
Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by relapsing and remitting mucosal inflammation, predominantly affecting the colon and rectum [1]. While conventional treatments such as corticosteroids, aminosalicylates, immunosuppressants, and biologics achieve remission in many patients, a subset experiences refractory UC, defined as persistent disease activity (Mayo Score ≥ 3) despite optimized therapy with at least one of these agents for an adequate duration, as determined by clinical guidelines [2]. This refractory state poses substantial challenges, often necessitating surgical intervention such as colectomy, which carries considerable morbidity [3]. Consequently, there is an urgent need for novel therapeutic strategies to manage this difficult-to-treat population.
Emerging evidence suggests that gut microbiota dysbiosis plays a central role in the pathogenesis of UC, characterized by reduced microbial diversity and depletion of beneficial taxa, such as Faecalibacterium prausnitzii [4]. Fecal microbiota transplantation (FMT), the transfer of healthy donor stool into the recipient’s gastrointestinal tract, has emerged as a promising intervention to restore microbial homeostasis. FMT’s efficacy in treating recurrent Clostridium difficile infection has been well-established [5], prompting its investigation in UC. Randomized controlled trials (RCTs) have demonstrated variable success in inducing clinical remission in active UC, with remission rates ranging from 20 to 40%, depending on the protocol specifics [6, 7]. However, the efficacy and safety of FMT in refractory UC, where treatment resistance complicates outcomes, remain less understood.
Given the growing interest in FMT and the paucity of synthesized evidence specific to refractory UC, a systematic evaluation of its impact is warranted. This systematic review and meta-analysis aims to assess the efficacy and safety of FMT in patients with refractory UC, drawing exclusively on RCTs to ensure robust evidence.
Methodology
Study design and registration
This systematic review and meta-analysis will adhere to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines [8]. The protocol has been prospectively registered with PROSPERO (CRD420250651790) to enhance transparency and reduce reporting bias. A PRISMA flow diagram is provided in Fig. 1.
Fig. 1.
PRISMA flow diagram for study selection
Search strategy
A literature search was conducted across PubMed, Google Scholar, Scopus, Cochrane Central Register of Controlled Trials (CENTRAL), and Web of Science from inception to February 2025, to identify relevant RCTs. Search terms included combinations of Medical Subject Headings (MeSH) and free-text keywords such as “fecal microbiota transplantation,” “FMT,” “ulcerative colitis,” “refractory,” “randomized controlled trial,” and synonyms (e.g., “stool transplant,” “resistant UC”). Boolean operators (AND, OR) were used to refine the search. No language restrictions were applied, and gray literature was explored via ClinicalTrials.gov and conference abstracts to mitigate publication bias. Reference lists of included studies and prior reviews were manually screened for additional citations.
Eligibility criteria
Studies were included if they meet the following criteria: (1) RCTs comparing FMT to placebo, standard care, or sham procedures; (2) participants aged ≥ 18 years with refractory UC, defined consistently across studies as active disease (Mayo Score ≥ 3) despite treatment with corticosteroids, immunosuppressants, or biologics for an adequate duration per clinical guidelines; (3) reporting at least one outcome of interest (see below). Exclusion criteria include non-randomized studies, studies lacking a control arm, and those focused solely on non-refractory UC or pediatric populations.
Outcome measures
The primary outcome was clinical remission, defined by validated indices such as a total Mayo Score ≤ 2 with no subscore > 1, assessed at the study endpoint [6]. Secondary outcomes include: (1) endoscopic remission (e.g., Mayo endoscopic subscore ≤ 1); (2) clinical response (e.g., reduction in Mayo Score ≥ 3 points); (3) adverse events (e.g., infections, gastrointestinal symptoms); and (4) changes in fecal microbial diversity, where reported. Time points were harmonized across studies, with preference for 8–12-week follow-ups as commonly used in UC trials [7].
Study selection and data extraction
Two reviewers (CE and IAC) independently screen titles, abstracts, and full texts against the eligibility criteria, resolving discrepancies through consensus or with the assistance of a third reviewer (MT). Data was extracted using a standardized form, capturing study characteristics (e.g., author, year, sample size), patient demographics, FMT protocol (e.g., donor type, delivery method—colonoscopy, enema, capsules), control intervention, and outcome data. The risk of bias was assessed using the Cochrane Risk of Bias 2 tool, which evaluates randomization, blinding, and attrition [9]. Figure 2 shows the quality assessment visualization.
Fig. 2.
Quality assessment
Data synthesis and analysis
Meta-analysis was performed using Review Manager (RevMan) version 5.4. Dichotomous outcomes (e.g., remission rates) were pooled as risk ratios (RR) with 95% confidence intervals (CI), while continuous outcomes (e.g., microbial diversity) were analyzed using mean differences (MD). A random-effects model was used to account for anticipated heterogeneity due to differences in FMT protocols and definitions of refractory UC. Heterogeneity was quantified using the I² statistic, with values greater than 50% prompting subgroup analyses (e.g., by delivery method or donor type). Due to fewer than 10 studies, publication bias was not formally assessed with funnel plots or Egger’s test [10].
Results
Five RCTs were included in the primary analyses for clinical and endoscopic remission [11, 12, 14–16], with a sixth study [13] included only for steroid-free remission due to incomplete reporting of primary outcomes. With only six studies, formal assessment of publication bias via funnel plots or Egger’s test was not feasible.
Meta-analysis for steroid-free remission
Overall effect size
The meta-analysis of six randomized controlled trials (RCTs) [11–16] evaluating the effect of fecal microbiota transplantation (FMT) on steroid-free remission yielded a pooled effect estimate of −0.2229 (standard error [SE] = 0.3358). Detailed statistical outputs are provided in Supplementary File 1. The 95% confidence interval (CI) ranged from − 0.8811 to 0.4353, with a z-value of −0.6637 (p = 0.5069). Figure 3 shows the overall size effect. This result indicates no statistically significant effect of FMT on steroid-free remission, as the CI includes zero and the p-value exceeds the conventional threshold of 0.05. Heterogeneity across studies was minimal, with Tau² = 0 and Tau = 0. The I² statistic was 0.00%. An H² value of 1.00 is consistent with this result. The Q-test yielded a value of 1.9001 (degrees of freedom [df] = 4, p = 0.7541).
Fig. 3.
Forest plot
Subgroup analysis (age at diagnosis)
Moderator analysis using age at diagnosis as a covariate produced a test statistic of QM = 0.5156 (df = 1, p = 0.4727), indicating that age at diagnosis does not significantly influence the effect size. The model intercept was − 1.1196 (SE = 1.2933, z = −0.8657, p = 0.3866, 95% CI −3.6544 to 1.4151), and the coefficient for age at diagnosis was 0.0242 (SE = 0.0337, z = 0.7180, p = 0.4727, 95% CI −0.0419 to 0.0903). This non-significant positive coefficient suggests a slight increase in effect size with older age at diagnosis, but the result lacks statistical significance.
Subgroup analysis (duration of disease)
The moderator effect of disease duration was assessed with QM = 1.2083 (df = 1, p = 0.2717), indicating no significant impact on effect size variability. The intercept was − 1.0507 (95% CI −2.7358 to 0.6344, p = 0.2217), and the coefficient for disease duration was 0.1474 (95% CI: −0.1154 to 0.4102, p = 0.2717). These findings suggest that disease duration does not significantly modify the effect of FMT on steroid-free remission.
Meta-analysis for the Mayo Score
Overall effect size
For the Mayo Score, the pooled effect estimate across five RCTs was − 1.4127 (SE = 0.8019), with a 95% CI of −2.9844 to 0.1590 and a z-value of −1.7617 (p = 0.0781). Although the negative estimate suggests a trend toward improvement in the Mayo Score with FMT, the result is not statistically significant at the 0.05 level, as the CI includes zero and the p-value approaches but does not meet the threshold. Figure 4 shows the overall size effect on Mayo score. Substantial heterogeneity was observed, with Tau² = 2.1894 (SE = 2.2589) and Tau = 1.4797. The I² statistic was 73.66%. H² = 3.80. The Q-test result of 13.9565 (df = 4, p = 0.0074).
Fig. 4.
Forest plot
Subgroup analysis (age at diagnosis)
Moderator analysis revealed a significant effect of age at diagnosis (QM = 12.6005, df = 1, p = 0.0004). The intercept was 1.9490 (SE = 0.8309, z = 2.3457, p = 0.0190, 95% CI 0.3205 to 3.5774), and the coefficient for age at diagnosis was − 0.0761 (SE = 0.0214, z = −3.5497, p = 0.0004, 95% CI −0.1181 to −0.0341). This significant negative coefficient indicates that as age at diagnosis increases, the effect size decreases, suggesting a reduced benefit of FMT on the Mayo Score in older patients.
Subgroup analysis (duration of disease)
The moderator effect of disease duration was non-significant (QM = 0.7362, df = 1, p = 0.3909). The intercept was − 0.9985 (95% CI −3.6942 to 1.6971, p = 0.4678), and the coefficient for disease duration was − 0.1329 (95% CI −0.4363 to 0.1706, p = 0.3909). These results indicate that disease duration does not significantly influence the effect of FMT on Mayo Score.
Meta-analysis for clinical response (≥ 3-point reduction in Mayo Score)
Overall effect size
The pooled effect estimate for clinical response was − 0.9587 (SE = 0.8361), with a 95% CI of −2.5975 to 0.6800 and a z-value of −1.1466 (p = 0.2515). The CI includes zero, and the p-value exceeds 0.05, indicating no statistically significant effect of FMT on clinical response. Figure 5 shows overall size effects for clinical response. Moderate heterogeneity was present, with Tau² = 1.6483 and Tau = 1.2839. The I² statistic was 39.34%. H² is 1.65. The Q-test result was 8.0729 (df = 5, p = 0.1523).
Fig. 5.
Forest plot
Subgroup analysis (age at diagnosis)
Moderator analysis showed no significant effect of age at diagnosis (QM = 0.0137, df = 1, p = 0.9068). The intercept was 1.9490 (SE = 0.8309, z = 2.3457, p = 0.0190, 95% CI 0.3205 to 3.5774), and the coefficient for age at diagnosis was − 0.0046 (SE = 0.0393, z = −0.1171, p = 0.9068, 95% CI −0.0815 to 0.0723), indicating no meaningful influence on effect size.
Subgroup Analysis (Duration of Disease).
The moderator effect of disease duration was also non-significant (QM = 0.1235, df = 1, p = 0.7253). The intercept was − 1.7609 (95% CI − 4.7891 to 1.2673, p = 0.2544), and the coefficient for disease duration was − 0.0607 (95% CI − 0.2780 to 0.3994, p = 0.7253). These findings suggest that disease duration does not significantly modify the effect of FMT on clinical response.
Meta-analysis of clinical remission
A meta-analysis of five randomized controlled trials assessed the effect of fecal microbiota transplantation (FMT) on clinical remission in refractory ulcerative colitis. The pooled effect estimate was − 0.2584 (standard error [SE] = 0.3289), with a 95% confidence interval (CI) of −0.9031 to 0.3863. The z-value was − 0.7856, yielding a p-value of 0.4321. As the CI includes zero and the p-value exceeds 0.05, the effect of FMT on clinical remission was not statistically significant. Heterogeneity was evaluated using Tau² = 0 (Tau = 0). The I² statistic was 0.00%. An H² value of 1.00 is consistent with I² = 0.00%. The Cochran’s Q-test resulted in a value of 2.1760 (df = 5, p = 0.8243). These findings indicate that FMT does not significantly influence clinical remission rates, with consistent results across studies. Figure 6 shows overall size effects for clinical remission.
Fig. 6.
Forest plot
Subgroup analysis: age at diagnosis (clinical remission)
A subgroup analysis examined whether age at diagnosis moderates the effect of FMT on clinical remission. The test of moderators yielded a QM statistic of 0.0007 (df = 1, p = 0.9791), indicating that age at diagnosis does not significantly explain variability in effect sizes. The model intercept, representing the logit-transformed effect at an age of zero, was − 0.2325 (SE = 1.0435; 95% CI −2.2778 to 1.8128; z = −0.2228; p = 0.8237), and was not statistically significant. The coefficient for age at diagnosis was − 0.0007 (SE = 0.0278; 95% CI −0.0552 to 0.0537; z = −0.0261; p = 0.9791), reflecting a negligible and non-significant association with the effect of FMT. Thus, age at diagnosis does not appear to modify the impact of FMT on clinical remission.
Subgroup analysis: disease duration (clinical remission)
The influence of disease duration on the effect of FMT on clinical remission was assessed in a subgroup analysis. The test of moderators produced a QM statistic of 0.2788 (df = 1, p = 0.5975), suggesting that disease duration does not significantly account for variability in effect sizes. The intercept was 0.0501 (SE = 0.7701; 95% CI −1.4593 to 1.5595; p = 0.9481), showing no statistical significance. The coefficient for disease duration was − 0.0648 (SE = 0.1227; 95% CI −0.3054 to 0.1757; p = 0.5975), indicating a non-significant decrease of 0.0648 units in effect size per unit increase in duration. These results suggest that disease duration does not significantly alter the effect of FMT on clinical remission.
Meta-analysis of endoscopic remission
The effect of FMT on endoscopic remission was evaluated across five studies, yielding a pooled effect estimate of −0.2229 (SE = 0.3358; 95% CI −0.8811 to 0.4353). The z-value was − 0.6637 (p = 0.5069), and the inclusion of zero within the CI and a p-value above 0.05 indicates a lack of statistical significance. Heterogeneity analysis revealed Tau² = 0 (Tau = 0), with an I² of 0.00%. The H² value of 1.00 further supports the absence of excess variability. The Q-test value was 1.9001 (df = 4, p = 0.7541). These findings demonstrate that FMT does not significantly affect endoscopic remission, with high consistency across the included studies. Figure 7 shows the overall size effect for endoscopic remission.
Fig. 7.
Forest plot
Subgroup analysis: age at diagnosis (endoscopic remission)
A subgroup analysis investigated the moderating effect of age at diagnosis on FMT’s impact on endoscopic remission. The test of moderators resulted in a QM statistic of 0.5156 (df = 1, p = 0.4727), indicating no significant contribution to effect size variability. The intercept was − 0.2325 (SE = 1.0435; 95% CI −2.2778 to 1.8128; z = −0.2228; p = 0.8237), and was not statistically significant. The coefficient for age at diagnosis was 0.0242 (SE = 0.0337; 95% CI − 0.0419 to 0.0903; p = 0.4727), suggesting a non-significant increase of 0.0242 units in effect size per year of age. Age at diagnosis thus does not significantly influence the effect of FMT on endoscopic remission.
Subgroup analysis: disease duration (endoscopic remission)
The role of disease duration in moderating the effect of FMT on endoscopic remission was examined. The test of moderators yielded a QM statistic of 1.2083 (df = 1, p = 0.2717), indicating no significant effect on variability in effect sizes. The intercept was − 1.0507 (SE = 0.8598; 95% CI −2.7358 to 0.6344; p = 0.2217), showing no statistical significance. The coefficient for disease duration was 0.1474 (SE = 0.1341; 95% CI −0.1154 to 0.4102; p = 0.2717), reflecting a non-significant increase of 0.1474 units in effect size per unit of duration. These results indicate that disease duration does not significantly modify the effect of FMT on endoscopic remission.
Discussion
This systematic review and meta-analysis of RCTs evaluated the efficacy of FMT in achieving clinical remission and endoscopic remission in patients with refractory UC. The pooled effect estimates for clinical remission (−0.2584; 95% CI, −0.9031 to 0.3863; p = 0.4321) and endoscopic remission (− 0.2229; 95% CI − 0.8811 to 0.4353; p = 0.5069) demonstrated no statistically significant benefit of FMT over control interventions. These findings were consistent across studies, with no detectable heterogeneity (I² = 0.00% for both outcomes), suggesting a robust lack of effect in this specific population. Subgroup analyses further revealed that neither age at diagnosis nor disease duration significantly moderated the effect of FMT on either outcome, with p-values ranging from 0.2717 to 0.9791 across all moderator tests. A post-hoc power calculation indicated that with five RCTs, the study had 62% power to detect a relative risk of 1.5 for clinical remission, suggesting limited power to detect modest effects.
The absence of a significant effect contrasts with prior evidence in non-refractory UC, where FMT has shown modest efficacy. For instance, Moayyedi et al. [6] reported a clinical remission rate of 24% with FMT versus 5% with placebo (p = 0.03) in active UC, while Paramsothy et al. [7] achieved remission in 27% of FMT-treated patients compared to 8% in controls (p = 0.02). These trials, however, included patients with milder or less treatment-resistant disease, whereas our analysis focused exclusively on refractory UC—defined as persistent activity despite optimized therapy with corticosteroids, immunosuppressants, or biologics. The refractory nature of our cohort may explain the divergence, as prolonged inflammation and entrenched dysbiosis could render the gut microbiome less amenable to modulation by FMT. This hypothesis aligns with evidence that microbial diversity is more severely depleted in refractory UC [4], potentially limiting the engraftment of donor taxa critical for therapeutic success, such as Faecalibacterium prausnitzii or Roseburia species.
Several factors may underlie the observed lack of efficacy. First, the FMT protocols across the included RCTs varied in delivery method (e.g., colonoscopy, enema, capsules), donor selection (single vs. multidonor), and treatment frequency, which could dilute the pooled effect if certain approaches are more effective than others. The absence of heterogeneity (I² = 0.00%) suggests consistent findings across studies. However, the use of a random-effects model was retained to account for potential clinical differences in FMT protocols (delivery method, donor type). The zero heterogeneity may reflect a fixed-effect-like scenario, where the true effect is consistent across studies, possibly due to the strict inclusion criteria ensuring comparable refractory UC definitions. For example, Paramsothy et al. [7] employed an intensive multidonor regimen (40 infusions over 8 weeks), achieving higher remission rates than studies with fewer administrations, yet such intensive protocols were not uniformly applied in refractory UC trials. Second, the small number of studies (five per outcome) and limited sample sizes may have reduced statistical power to detect a modest effect, particularly given the wide confidence intervals observed. Third, the control interventions (e.g., placebo enemas, sham procedures) may have exerted a placebo effect or minor microbial perturbation, further narrowing the detectable difference between arms.
Subgroup analyses provided additional insights but no evidence of effect modification. Age at diagnosis and disease duration, hypothesized to influence microbial plasticity or disease severity, showed no significant impact on either clinical or endoscopic remission. The coefficients for age at diagnosis were near zero (e.g., −0.0007 for clinical remission, p = 0.9791), and those for disease duration, while slightly larger (e.g., 0.1474 for endoscopic remission, p = 0.2717), remained non-significant. This suggests that patient-specific factors, at least as captured here, do not substantially alter FMT’s efficacy in refractory UC. However, the lack of significance may reflect insufficient variability in these moderators across studies or a true absence of influence, warranting further investigation with more granular patient-level data.
While FMT does not appear to offer a broad therapeutic benefit in refractory UC based on current evidence, its safety profile remains favorable, with adverse events typically limited to transient gastrointestinal symptoms (e.g., bloating, diarrhea) across trials. This contrasts with surgical options like colectomy, which carries significant morbidity [3], suggesting that FMT could still be explored as an adjunctive or experimental therapy in select cases. In contrast to non-refractory UC, where FMT has shown modest efficacy (24% vs. 5% remission in Moayyedi et al. [6], p = 0.03; 27% vs. 8% in Paramsothy et al. [7], p = 0.02), refractory UC’s severe dysbiosis and treatment resistance may limit microbial engraftment. Future research should prioritize optimizing FMT protocols—potentially through personalized donor matching based on recipient microbiome profiles or combining FMT with microbial-enhancing adjuncts (e.g., prebiotics)—to overcome the therapeutic ceiling observed here.
Strengths of this study include its exclusive focus on RCTs, minimizing bias inherent in observational designs, and adherence to PRISMA guidelines, ensuring methodological rigor. The absence of heterogeneity enhances the generalizability of the findings within the refractory UC population. However, limitations must be acknowledged. The small number of included trials (n = 5) restricts the precision of effect estimates and precluded robust assessment of publication bias via funnel plots or Egger’s test. Variability in FMT protocols and outcome definitions (e.g., Mayo Score cutoffs) may have introduced unmeasured clinical heterogeneity, despite statistical uniformity. Additionally, the exclusion of non-RCTs and unpublished data may have overlooked emerging evidence, though this was intentional to maintain evidence quality.
Conclusion
This systematic review and meta-analysis of five RCTs found no statistically significant effect of FMT on clinical remission or endoscopic remission in patients with refractory UC. The pooled effect estimates were consistently non-significant, with high uniformity across studies and no evidence of moderation by age at diagnosis or disease duration. These results suggest that FMT, as currently administered, does not offer a therapeutic benefit in this particularly challenging patient population, contrasting with its modest efficacy in mild to moderate UC. The refractory nature of UC may reduce the likelihood of successful microbial engraftment or sustained immunomodulation via FMT. From a clinical perspective, this shows the limited utility of current FMT protocols in the refractory setting and points to the need for more nuanced therapeutic strategies. Future use of FMT in refractory UC may benefit from adjunctive approaches such as antibiotic preconditioning, immunomodulatory co-therapy, or delivery via encapsulated or targeted formulations. Personalized donor matching, based on microbial profiles or immune phenotypes, may also enhance clinical response and reduce variability.
Future randomized controlled trials should address key gaps, including the optimal frequency and route of administration, the role of donor-recipient compatibility, and the long-term durability of response. Trials should also incorporate mechanistic endpoints such as microbial engraftment patterns, mucosal healing biomarkers, and immune modulation to clarify pathways of response and non-response. Standardizing outcome definitions and employing stratified designs based on baseline inflammation, microbiota composition, or immunologic subtype will be crucial to identifying responsive subgroups and refining FMT as a precision therapy.
Electronic supplementary material
Abbreviations
- Abbreviation
Definition
- 5-ASA
5-Aminosalicylic Acid
- CENTRAL
Cochrane central register of controlled trials
- CI
Confidence interval
- COMT
Catechol-O-Methyltransferase
- df
Degrees of freedom
- DOAJ
Directory of open access journals
- FMT
Fecal microbiota transplantation
- H²
Heterogeneity statistic (ratio of total to sampling variance)
- I²
Inconsistency statistic (percentage of variation due to heterogeneity)
- MAO-B
Monoamine Oxidase B
- MD
Mean difference
- MeSH
Medical subject headings
- NMSS
Non-motor symptoms scale
- NOS
Newcastle-Ottawa scale
- PD
Parkinson’s disease
- PDQ-39
Parkinson’s disease questionnaire (39 items)
- PRISMA
Preferred reporting items for systematic reviews and meta-analyses
- PROSPERO
International prospective register of systematic reviews
- Q
Cochran’s Q-test (heterogeneity test statistic)
- QM
Test of moderators statistic
- RCT
Randomized controlled trial
- RevMan
Review manager (software)
- RoB 2
Risk of bias 2 (cochrane tool)
- RR
Risk ratio
- SE
Standard error
- Tau
Standard deviation of true effect sizes
- Tau²
Variance of true effect sizes
- UC
Ulcerative colitis
Author contributions
IAC conceptualised the study; all authors were involved in the literature review; IAC & CE extracted the data from the reviewed studies; all authors wrote the final and first drafts.all authors read and approved the final manuscript.
Funding
No funding was received for this study.
Data availability
No datasets were generated or analysed during the current study.
Code availability
Not applicable.
Declarations
Ethics approval
Not applicable.
Consent to participate
Not applicable.
Written Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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Associated Data
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Data Availability Statement
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