Article Text

Effects of prednisolone tapering on effectiveness of infliximab in patients with ulcerative colitis: data from a retrospective cohort
  1. Pernille Dige Ovesen1,
  2. Mohamed Attauabi1,
  3. Johan F K F Ilvemark1,
  4. Mads Damsgaard Wewer2,
  5. David J Warren3,
  6. Johan Burisch2,
  7. Rolf A Klaasen3,
  8. Nils Bolstad3,
  9. Casper Steenholdt1,
  10. Jakob Benedict Seidelin1,4
  1. 1Department of Gastroenterology and Hepatology, Copenhagen University Hospital—Herlev and Gentofte, Herlev Hospital, Copenhagen, Denmark
  2. 2Gastrounit, Hvidovre Hospital Gastro Unit, Hvidovre, Denmark
  3. 3Department of Medical Biochemistry, Oslo University Hospital, Oslo, Norway
  4. 4Department of Clinical Medicine, University of Copenhagen, Kobenhavn, Denmark
  1. Correspondence to Dr Jakob Benedict Seidelin; Jakob.Benedict.Seidelin{at}


Background and objective The influence of concomitant prednisolone on clinical outcomes and safety in infliximab-treated ulcerative colitis (UC) patients is unknown.

Design, setting, participants and outcome measures A retrospective cohort study was performed, including 147 UC patients treated with infliximab at a tertiary inflammatory bowel disease (IBD) centre. Primary outcome was corticosteroid-free clinical remission (CFCR) at week 14 and week 52. Patients were grouped according to prednisolone tapering regimens: standard (≤5 mg/week), fast (>5 mg/week), direct discontinuation or no prednisolone. Patients intolerant to corticosteroids and patients stopping corticosteroids in preparation for surgery including colectomy during their initial admission were excluded.

Results There was no overall association between prednisolone exposure or no exposure and CFCR at weeks 14 or 52 of infliximab. The proportion of patients with C reactive protein ≤5 mg/L was higher in the standard tapering at week 14 as compared with faster regimens or no prednisolone. In subgroup analyses, the standard tapering was associated with a higher rate of CFCR at week 14 compared with the fast-tapering regimen in patients receiving ≥40 mg prednisolone at initiation of infliximab (64.3% vs 26.3%, p=0.04) and among patients admitted with acute severe UC (66.6% vs 23.5%, p<0.05). Similar data were seen at week 52. Prednisolone did not affect infliximab trough levels but increased infection rates (10/77 vs 2/70, p=0.03), in particular C. difficile infection.

Conclusion In UC patients with limited disease burden, prednisolone did not affect effectiveness of infliximab. However, patients with increased disease burden seem to benefit from corticosteroid combination therapy.


Data availability statement

Data are available upon reasonable request. The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See:

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  • Corticosteroids are used to induce remission when patients with ulcerative colitis (UC) experience a moderate to severe flare, but the role of concomitant corticosteroid and tapering regimens in patients initiating infliximab remain unknown.


  • This study is the first to investigate the influence of concomitant prednisolone and tapering regimens on the effectiveness of infliximab in patients with UC, and the results indicate that patients with severe disease burden benefit from longer corticosteroid exposure, whereas the effect of concomitant corticosteroid in patients with lower disease burden does not seem to add efficacy.


  • Concomitant corticosteroid may improve efficacy of infliximab, especially in those UC patients with high disease burden.


Ulcerative colitis (UC) is a chronic, relapsing-remitting immune-mediated disorder affecting the large intestine and caused by a dysregulated immune response to the microbiome in environmentally and genetically susceptible subjects.1 Although colectomy in principle removes the diseased organ, medical treatment remains the cornerstone of treatment. Corticosteroids, due to their immunosuppressive and anti-inflammatory effects,2 are effective in inducing remission and constitute a first line of therapy at moderate to severe flares.3 4 Biologics such as the tumour necrosis factor (TNF)-inhibitor infliximab are commonly used in steroid-refractory patients or in those with repeated frequent flares. More than 50% of patients with UC receive corticosteroids in the first 5 years after their diagnosis and more than 10% receive biologic agents in the same period.5 Furthermore, patients with steroid-refractory acute severe UC (ASUC) are treated with infliximab or cyclosporine.6 Thus, steroids are often used concomitantly when infliximab therapy is initiated and then tapered. However, the role of concomitant steroids, and influence of different tapering regimens, during initiation of infliximab remains unknown, leaving the question whether a longer exposure to corticosteroids will provide an additive effect on infliximab’s immunosuppressive effectiveness or even improve its pharmacokinetics as is the case with conventional immunosuppressives.7–9

However, improvement in inflammatory markers has been reported in patients with only a partial clinical response to systemic glucocorticoids.10 Combined glucocorticoid and anti-TNF-α could thus be superior to anti-TNF-α alone in the setting where corticosteroids were initially considered necessary. On the other hand, double immunosuppression is prone to increase risk of infections and other serious adverse events,11 which favours a rapid tapering regimen.

A recent systematic review and meta-analysis found no significant difference in the rate of clinical remission between anti-TNF-α monotherapy and anti-TNF-α plus concomitant steroids in patients with Crohn’s disease (CD).12 However, it should be noticed that all patients in the mentioned study were corticosteroid refractory prior to receiving biologics. The way corticosteroids affect outcomes of infliximab treatment in UC remains unreported in clinical trials making a similar study design impossible in UC.

In designing this study, we took advantage of our department having two different approaches to the management of prednisolone use among our consultant gastroenterologists in the light of absence of evidence in the field: one regarding infliximab initiation as an add-on treatment where previous prednisolone is continued without modification to provide maximal anti-inflammatory effect on the intestine (four consultants) and one regarding the need of infliximab as a step-up due to treatment failure prednisolone, thus aiming to quickly terminating corticosteroids to avoid possible side effects of prednisolone itself and possible risk of infectious complications by double immune suppression (two consultants).


The aim of this study was, thus, to determine the influence of concomitant corticosteroid exposure on week 14 and week 52 outcomes in UC patients starting infliximab. Corticosteroid treatment might be stopped due to intolerance or in preparation for imminent colectomy. Therefore, to avoid confounding by indication inherent to corticosteroid therapy, only outpatients and inpatients who completed full induction of infliximab treatment (week 0, 2, and 6) were included and patients who stopped prednisolone due to intolerance were excluded.


Study design, setting, eligibility criteria and bias

All patients with UC receiving infliximab between 2009 and 2019 have routinely been enrolled in our biobank and were included in this retrospective single tertiary centre cohort study. Patients not completing induction with infliximab (week 0, 2 and 6), and patients where corticosteroids were stopped for other reasons (corticosteroid intolerance or preparation for surgery including colectomy) were excluded to avoid confounding by indication. This implies that hospitalised patients with severe colitis colectomized during the admission were not included, as this would automatically bias data towards lesser effect of short-term tapering of corticosteroids, since corticosteroids are typically tapered quickly when the decision is made to operate to minimise corticosteroid exposure during surgery. Also, inclusion of these patients would not answer the question of what the effect is of corticosteroids on infliximab effectiveness after induction and maintenance treatment.

Outcomes and definitions

The primary endpoints were the proportion of patients achieving clinical and biochemical corticosteroid-free clinical remission at week 14 and clinical remission at week 52. Patients were divided into four groups: (1) standard (≤5 mg/week) prednisolone tapering; (2) fast (>5 mg/week) prednisolone tapering; (3) direct discontinuation of prednisolone at start of infliximab in patients receiving an initial course of less than 1 week and (4) infliximab monotherapy. The prednisolone dose registered was at the date of initiation of infliximab. In addition to analysis of the whole cohort, two subgroup analyses were performed: one containing a more homogenous subgroup of patients treated with at least 40 mg of prednisolone at initiation of infliximab. The other containing patients with ASUC and treated with at least 40 mg of prednisolone at initiation of infliximab (online supplemental figure 1).

Clinical remission was defined as a partial Mayo (pMayo) score ≤1 or a Simple Clinical Colitis Activity Index (SCCAI) score ≤3. A partial response was defined as a reduction in a clinical pMayo score from baseline ≥30% and ≥3 points or a decrease in total SCCAI to ≤4 points or a 50% drop from baseline value. No decrease in pMayo or SCCAI at week 14 was defined as primary non-response.

Patients with no pMayo or SCCAI were given a Global Physician Evaluation (GPE), based on serological measures, Mayo Endoscopic Subscore, prior and later pMayo or SCCAI scores and the attending physician’s assessment of disease severity.

ASUC was defined as patients with a disease activity of such severity that they were admitted to hospital ward and treated with ≥40 mg intravenous corticosteroids. Biochemical remission was defined as having C reactive protein (CRP) less than 5 mg/L. Loss of response (LOR) during induction or maintenance therapy was reported as either colectomy, dose escalation or discontinuation of infliximab due to inadequate response need of new course of systemic corticosteroids or swich in biologic due to flare.

Data sources

A retrospective chart review was performed using the joined EPIC patient file system (Epic Systems Corporation, Verona, Wisconsin), which covers 47.4% of the Danish population and contains data from 2005 and onwards. The following data were collected at initiation of infliximab and during induction therapy: gender, age, weight, height, smoking status, disease duration and previously worst extent according to Montreal classification, admission to hospital ward, pMayo and SCCAI score, haemoglobin, albumin, CRP, faecal calprotectin, concomitant medication, dose and tapering of corticosteroids and concomitant infections.

Measurements of serum infliximab concentrations

Circulating serum infliximab and anti-drug antibodies (ADA) were measured in biobanked trough samples. Infliximab was measured using a fully validated three-step time resolved fluorometric assay automated on the AutoDELFIA (PerkinElmer, Waltham, Massachusetts) immunoassay platform. The assay, performed in streptavidin-coated 96-well microplates, uses biotinylated recombinant TNF-α as solid-phase reagent and europium-labelled protein-A as tracer. At infliximab concentrations of 2.5 and 13 mg/L, the method has an intra-assay coefficient of variation (CV) of 2.7% at both levels and inter-assay CV% of 3.4 and 3.0%, respectively. Samples with infliximab ≤5 mg/L were assessed for ADA using an automated inhibition assay on the AutoDELFIA platform.13 All analyses were done simultaneously and under blinded conditions (Dept. Medical Biochemistry, Oslo University Hospital, Oslo, NO).

Quantitative variables and statistical methods

Data were reported by descriptive statistics. Categorical data were presented as proportions and compared using Fisher’s exact test, while continous data were presented as medians with IQRs and compared through the Student’s t test or the Mann-Whitney U-test if the variables were non-normally distributed. The different tapering regimens were all compared with the standard tapering regimen.

Missing data were excluded. Cox regression analysis investigating time to LOR to infliximab was performed. A priori selected variables such as gender, smoking, disease duration and severity, concomitant medication and tapering regimens were included, and the outcomes were reported as HR with 95%CIs. Differences in outcome with p<0.05 were considered significant.

Multiple propensity scores followed by matching were carried out to reduce bias by indication. This resulted in subcohort in which patients were matched according to use of steroids yes/no and subcohort where patients were matched according to tapering regimen. The matching was performed using the R packages ‘MatchIt’ using the method ‘optimal’ with a ratio 1:1. Patients were matched as closely as possible for age, gender and severity scores (eg, pMayo, SCAAI or GPE) while exact matching was used for Montreal classification.


Study population and baseline characteristics

In all, 147 patients with UC were included, of which 77 (52%) received prednisolone at time of initiation of infliximab. Of these, 43 (55.8%) patients underwent standard tapering, 25 (32.5%) fast tapering and 9 (11.7%) direct tapering. Seventy patients (48%) started infliximab as monotherapy. All patients initiated infliximab due to refractory active disease despite prior treatment with conventional therapy (mesalazine, corticosteroids, thiopurines or methotrexate).

Baseline characteristics are shown in table 1. The median age was between 26 and 38 years, with the direct discontinuation regimen as the youngest (IQR: 26–40 years) and the group with infliximab monotherapy as the oldest (IQR: 30–45 years) although the differences were not statistically significant. Patients treated with infliximab monotherapy were less likely to be treated as inpatients (8.6%, p=0.004) as compared with those being treated with prednisolones standard regimen (30.2%), fast regimen (72%, p=0.001) and directly tapering (88.8%, p=0.002).

Table 1

Patient baseline demographics and disease characteristics

The cumulated dose of prednisolone in relation to infliximab initiation showed heterogeneity among the tapering regimens. The standard tapering had median prednisolone dose of 1680 mg, IQR 1015–2135 mg; the fast regimen had a median dose of 700 mg, IQR of 595–805 mg (p<0.00001 compared with standard); the direct discontinuation had a median at 320 mg and an IQR from 240 mg to 420 mg (p<0.00001 compared with standard).

Clinical outcomes

Full cohort

The influence of prednisolone exposure on infliximab’s effectiveness is summarised in table 2.

Table 2

Clinical outcomes at week 14 and week 52

Although there was a numerical higher proportion of patients achieving corticosteroid-free clinical remission at week 14 in the group with standard tapering (55.8%), neither of the different tapering regimens differed significantly in terms of corticosteroid-free clinical remission with the fast tapering being 36% (p=0.1), direct discontinuation regimen 44.4% (p=0.7) and infliximab monotherapy 40.0% (p=0.1; figure 1A,B).

Figure 1

Clinical outcomes in full cohort at (A) week 14 and (B) week 52, in subgroup analysis stratified for ≥40 mg prednisolone at infliximab initiation at (C) week 14 and (D) week 52 and in subgroup analysis stratified for ≥40 mg prednisolone at infliximab initiation and ASUC at (E) week 14 and (F) week 52. † Pooled data include fast tapering and directly discontinuation.*Significant with p<0.05. **Significant with p<0.01. ‡Compared with remission in group with standard tapering. §Compared with no response in group with standard tapering. ASUC, acute severe ulcerative colitis.

However, a higher proportion of patients in the standard tapering group achieved a CRP level less than 5 mg/L at week 14 (23/23, 100%) as compared with the fast-tapering regimen (14/18 (77.8 %), p=0.03) and the directly tapering (3/5 (60%), p=0.03). Furthermore, four patients (21.1 %) in the fast-tapering regimen had severe disease activity at week 14, while no patients in the standard (0%, p=0.03) and the direct discontinuation regimen had severe disease activity.

Eleven patients stopped infliximab before week 14 but were still in clinical remission at week 14. Six stopped due to remission and one due to pregnancy. One had elevated ALAT, two stopped due to serious infections (Clostridiodes difficile (C. difficile) and severe ethmoiditis) and one due to an anaphylactic reaction towards infliximab. All patients completed the three-dose induction.

After completion of maintenance therapy for 52 weeks, 23 (53.5%) patients in the standard tapering regimen had a sustained steroid-free response or remission on infliximab treatment. Neither the fast-tapering, the directly tapering nor the patients with no prednisolone at initiation of infliximab differed significantly from the standard tapering group (44%, 66.6%, 42.8%, respectively; p>0.05). The cumulated treatment failure rates in the first 52 weeks are shown in online supplemental figure 2. No predictors of LOR to infliximab were found using Cox regression (online supplemental table 1).

In the subcohort of propensity score-matched patients controlling for disease severity, the use of corticosteroids showed no significant deference in clinical remission on either week 14 or 52 when compared with infliximab monotherapy, equally to what was observed in the full cohort (table 3, online supplemental figure 3, n=134). Furthermore, a similar propensity score-matched analysis on standard tapering versus fast regimens (fast and direct tapering combined) revealed no differences in clinical remission rates at week 14 within standard tapering (18/32 (56.2%) vs 13/32 (41.9%), p=0.32; table 3, online supplemental figure 4, n=64). However, a significant difference in patients with the standard tapering regimen being in biochemical remission with CRP levels <5 mg/L was observed in the propensity score-matched analysis.

Table 3

Clinical outcomes at week 14 and week 52 in matched cohorts

Subgroup analysis of patients receiving standard dose of corticosteroid at infliximab initiation

A subgroup analysis containing patients treated with ≥40 mg of prednisolone at baseline (n=42 of 77, 54.5%) was performed in order to harmonise the exposure time and cumulated dose of prednisolone prior to infliximab initiation (online supplemental table 2). In this subgroup, the direct discontinuation regimen had a shorter duration of prednisolone treatment prior to infliximab with a median of 4 days (IQR: 4–6 days, p=0.009) compared with the standard tapering regimen with 12 days (IQR: 7–16 days) of treatment. The standard and the fast-tapering regimen did not differ in terms of duration (p=0.40).

At week 14, in patients receiving ≥40 mg prednisolone, the standard tapering regimen was associated with a higher rate of corticosteroid-free clinical remission as compared with the fast-tapering regimen (9/14 (64.3%) vs 5/19 (26.3%), p=0.04). This difference remained significant through maintenance therapy and at week 52, the standard tapering regimen had 12/14 (85.7%) in clinical remission or response, as compared with the fast tapering with 7/19 (36.8%, p=0.01) and the group treated with no prednisolone with 30/70 (42.8%, p=0.007). The difference was maintained in a sensitivity analysis of week 52 corticosteroid-free remission where fast-tapering and direct-tapering were pooled and compared with standard tapering (12/28 (42.9%, p=0.01); figure 1C,D).

Subgroup analysis of ASUC patients

Additional subgroup analyses including patients treated with at least 40 mg of prednisolone and ASUC (baseline characteristics presented in online supplemental table 3) were in line with the above findings and with significantly higher corticosteroid-free clinical remission at week 14 among standard tapering (6/9, 66.7%) than fast tapering (4/17, 23.5%, p<0.05) (table 4). Finally, close to 90% of the patients in the standard tapering were in clinical remission or response at week 52, compared with 35.3% (p=0.02) in the fast-tapering regimen (figure 1E,F).

Table 4

Clinical outcomes at week 14 and week 52, prednisolone≥40 mg and ASUC

The week 52 superiority of standard tapering remained after pooling the data from the fast-tapering and direct-tapering regimens (66.7% vs 41.7%, p=0.02).

Taken together, these subgroup analyses indicate that longer exposure to corticosteroid may have a beneficial effect on infliximab’s effectiveness in patients with high disease burden.

Infliximab trough levels and corticosteroids

Exploring any interaction of prednisolone tapering regimens on infliximab trough levels showed no association with infliximab concentrations in patients with the standard tapering regimen as compared with the other regimens or none-exposure to corticosteroid at week 14 (table 2 and online supplemental table 4). It is notable, however, that the group not treated with prednisolone had a numerical, but not statistically significant, higher median of trough level as compared with the other groups treated with prednisolone, regardless of tapering, through the first 14 weeks.

Subgrouping the patients according to prednisolone dosage at baseline (>40 mg at infliximab initiation) showed some differences between the standard tapering and infliximab monotherapy at week 2 (median (IQR): 17.7 mg/L (14.7–21.3) vs 29.0 mg/L (20.5–33.1), p=0.006). However, concomitant use of thiopurines at baseline likely explains this difference, as dividing the subgroup according to thiopurine use showed a significant difference in trough levels favouring thiopurine use. At week 2, patients on infliximab monotherapy had higher trough levels in the sensitivity analysis only including patients on standard infliximab dosing, whereas no differences in trough levels were found at later time points (online supplemental table 4). This difference might be explained by intestinal loss and inflammatory burden in corticosteroid exposed patients, both known to decrease T½ of infliximab, as corticosteroid exposed patients had a higher disease burden than the patients on infliximab monotherapy (table 1). Similar findings were observed in the full cohort including high-dose infliximab (10 mg/kg) and accelerated regimens (data not shown).

Fourteen patients were found positive for ADA during the first 14 weeks, 5 (10.6%) patients treated with no prednisolone had detectable ADA, while 9 (17.0%, p=0.4) patients in the prednisolone-treated group were found ADA-positive.

Safety of infliximab in combination with corticosteroids

In total, 22 adverse events were reported during the first 52 weeks of maintenance therapy (online supplemental table 5). Six patients (7.8%) treated with prednisolone and three (4.3%) with no prednisolone experienced an acute severe anaphylactoid reaction. One patient treated with prednisolone had non-inflammatory bowel disease (IBD)-related cancer.

Ten patients treated with prednisolone experienced severe infections. Seven had C. difficile, one had a severe ethmoiditis, one had herpes zoster reactivation and one had an intercurrent non-C. difficile gastrointestinal infection. In comparison, the no-prednisolone group had only one patient with C. difficile and one with a staphylococcus infection of the skin (infection rate: 10/77 (13.0%) vs 2/70 (2.9%), p=0.03).


We conducted a retrospective cohort study exploring the influence of prednisolone tapering on the effectiveness and safety of infliximab. No overall association between standard tapering, fast-tapering or no prednisolone, and clinical response or remission was found throughout the first year of therapy. Matching for disease severity by propensity score within the whole cohort did not change these findings. However, subgroup analyses showed that patients receiving high dose of corticosteroids at baseline and patients admitted with ASUC might have a beneficial effect of longer corticosteroid exposure after infliximab initiation.

Our findings in the general UC population are in line with a recent meta-analysis, indicating no synergetic effect between infliximab and concomitant steroids in patients with CD.12 In the meta-analysis, only 32.0% of the pooled patients with CD were in clinical remission after completion of induction therapy despite still being on corticosteroids, as compared with the 35.5% in infliximab-monotherapy.

Infliximab and corticosteroids in combination are associated with a 64% higher risk of serious infections, and our data support this finding revealing a significant difference in infection rate between prednisolone and no prednisolone (p=0.03).11 14 The main infection was C. difficile being accountable for 70% of the infections in the prednisolone-treated group. Even though the evidence is contradictory, large cohorts and guidelines suggest that the use of corticosteroids results in an increased risk of infection with C. difficile in patients with IBD.15

Our data show that the use of corticosteroids, despite being immunosuppressant, does not seem to significantly influence infliximab trough levels during the induction phase. However, the infliximab-treated control group that did not receive concomitant prednisolone tended to have higher infliximab levels, but this difference did not reach statistical significance. In the subgroup analyses, the significantly higher infliximab trough level at week 2 in patients without prednisolone versus prednisolone exposed is likely explained by the heterogenous use of thiopurines in the groups and increased inflammatory burden in corticosteroid-exposed patients.7–9 16 Infliximab clearance might in addition be higher in the corticosteroid-treated group as they were more often admitted to the hospital and had a lower level of albumin (p=0.001). The formation of ADA was equal between patients treated with and without prednisolone. Farrell et al17 found intravenous hydrocortisone to reduce the concentration of ADA, but with only a numerical difference in the formation of ADA across patients pre-treated with hydrocortisone prior to infliximab as compared with infliximab without prednisolone and are thus in line with our findings. Taken together, our data indicate that the possible positive effect on infliximab effectiveness within the subgroup analyses is likely to be explained by an additive immunosuppressant effect targeting multiple pathways rather than influencing the pharmacokinetics of infliximab.

Treatment of ASUC requires rapid systemic corticosteroids, and when used in combination with rescue infliximab, our findings suggest that a longer exposure to prednisolone might be beneficial to this subgroup of UC patients. The standard tapering resulted in 66.6% of the patients in corticosteroid-free clinical remission at week 14 with a significant difference from the fast-tapering regimen even though the latter had a less severe disease activity at baseline. Pooling the fast-tapering and direct-tapering maintained the difference. The small population of patients with fast-tapering and direct-tapering constitutes a potential bias with risk of type II error, nonetheless, the results indicate that a rapid tapering of corticosteroids could potentially lower the response rate to infliximab, which merits further exploration. Since ASUC occurs in up to 25% of patients with UC, and the colectomy rate is about 20% and rising to almost 50% with multiple Truelove and Witts’ criteria present, optimising the effectiveness of infliximab is important in the biologic era, whether it is the dosing regimen, the prediction of response by biomarkers or the use of concomitant medication.3 18 19

The rate of colectomies of 10% in our ASUC cohort was lower than reported elsewhere.18 19 This lower rate is well explained by the study design, since only patients treated with rescue infliximab and being discharged receiving full infliximab induction were included. Thus, patients considered too ill to receive rescue infliximab and patients being colectomized during the admission for ASUC despite receiving infliximab were not included in our study. This design was chosen to investigate the influence on corticosteroid tapering on infliximab effectiveness but at the same time minimising the risk of bias by indication, since patients colectomized during admission often will have rapid tapering to avoid high-dose corticosteroids during surgery.

There are several limitations to our study, including those mentioned above, which should be borne in mind when interpreting the results. First, the retrospective design limits the ability to make cause-effect assumptions compared with randomised clinical trials. Second, stratifying patients according to tapering scheme lowered the number of patients in subgroups. Furthermore, the deviation of tapering of prednisolone from the standard regimen might have been influenced by side effects not mentioned in data source files. Most importantly, the retrospective design does imply a risk of bias by indication. We have, however, sought to control for this by the use of propensity score-based analyses limiting effects of differences in disease severity in the different tapering regimens. On the other hand, real-life clinical data might have a better generalisability than data from RCTs.

In conclusion, we observed no association between duration of prednisolone exposure or tapering regimen and corticosteroid-free clinical remission during infliximab induction or maintenance therapy. Patients with increased disease burden not needing imminent colectomy seem, however, to potentially benefit from the longer additional immunosuppressant effect of corticosteroids when tapering with 5 mg/week after infliximab initiation. Prednisolone did not influence the pharmacokinetics of infliximab or the risk of ADA formation.

Data availability statement

Data are available upon reasonable request. The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.

Ethics statements

Patient consent for publication


Lab technicians Fadime Pinar and Mina Hossiniyon are thanked for their assistance in handling biobank samples.


Supplementary materials

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  • Contributors JBS is the guarantor of this article. PDO helped with study concept design, data extraction, analysis and interpretation of data, drafting of the manuscript. MA, MDW and JB helped with study concept design, analysis and interpretation of data. JFKFI and CS helped with study concept design and supervision. DJW, RAK and NB helped with resources and analyses of data. JBS. helped with study concept design, analysis and interpretation of data, supervision. All authors helped with critical revision of the manuscript. All authors have approved the final version of this manuscript, including the authorship list.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests JFKF Ilvemark has received research grants from Takeda, Janssen, Abbvie, ParaTech, the Danish Research Council, and the Capital Region of Denmark. MDW has received grants from Bristol Myers Squibb, Novo Nordisk Foundation, Aage og Johanne Louis-Hansens Fond, Boehringer Ingelheim. JB: reports grants and personal fees from AbbVie, grants and personal fees from Janssen-Cilag, personal fees from Celgene, grants and personal fees from MSD, personal fees from Pfizer, grants and personal fees from Takeda, grants and personal fees from Tillots Pharma, personal fees from Samsung Bioepis, grants, and personal fees from Bristol Myers Squibb, grants from Novo Nordisk, personal fees from Pharmacosmos, personal fees from Ferring, personal fees from Galapagos CS: Speaker and advisory board for MSD and Janssen-Cilag. Jakob Benedict Seidelin: Research grants from Takeda and the Capital Region Denmark, national coordinator of studies from AbbVie, Arena Pharmaceuticals, Ely Lilly, and Boehringer Ingelheim. PDO, MA, DJW, RAK, NB: no disclosures.

  • Provenance and peer review Not commissioned; externally peer-reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.