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Letter
Thiopurine monotherapy has a limited place in treatment of patients with mild-to-moderate Crohn’s disease
  1. Bram Verstockt1,2,
  2. Liesbeth Boets1,
  3. João Sabino1,2,
  4. Séverine Vermeire1,2,
  5. Marc Ferrante1,2
  1. 1 Dpt Gastroenterology and Hepatology, University Hospitals Leuven, KU Leuven, Leuven, Belgium
  2. 2 Dpt Chronic Diseases, Metabolism and Ageing, Translational Research in Gastrointestinal Disorders (TARGID), IBD, KU Leuven, Leuven, Belgium
  1. Correspondence to Dr Marc Ferrante, KU Leuven University Hospitals Leuven, Leuven B3000, Belgium; marc.ferrante{at}uzleuven.be

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We read with interest the multicentre UK study by Stournaras et al on the long-term effectiveness of thiopurine monotherapy for the treatment of patients with IBD.1 Through a similar retrospective, single-centre design at the tertiary IBD referral centre of the University Hospitals Leuven (Leuven, Belgium), we evaluated the outcome of patients with active Crohn’s disease (CD) who initiated thiopurine monotherapy between 1988 and 2016. Response was defined as continuation of thiopurine monotherapy for at least 1 year,2 with minimal corticosteroids use (<2 corticosteroids courses/year) and without additional treatment (surgery, biological agents). Patients had to be exposed to thiopurines for at least 4 months before response could be evaluated, as thiopurines are not recommended for induction of response.3 In total, 823 CD patients (99.9% azathioprine) with a median follow-up of 13.0 (IQR 7.7–18.0) years were screened (figure 1).

Figure 1

Flowchart summarising the main findings of the current observational study on thiopurine monotherapy in Crohn’s disease.

Similar to the discontinuation rates linked to intolerance reported in the UK study,1 229 patients (29.4%) discontinued thiopurine therapy after a median of 31.0 (IQR 13.0–74.7) days, mainly because of leucopenia (n=13), liver function abnormalities (n=26), pancreatitis (n=62) or GI intolerance (n=59). On the long term, three patients were diagnosed …

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Footnotes

  • Twitter @bverstockt, ibdleuven, @JoaoPGSabino

  • Presented at These data have been presented as an oral presentation at the 13th European Crohn’s and Colitis Organization congress 2018 (Vienna, Austria) and the 30th Belgian Week of Gastroenterology (Antwerp, Belgium).

  • Contributors BV contributed to study design, data acquisition and interpretation, statistical analysis and drafting of the manuscript. LB contributed to data acquisition. JS contributed to critical revision of the manuscript. SV and MF contributed to study design, data interpretation, supervision and critical revision of the manuscript. All authors agreed with the final version of the manuscript prior to submission.

  • Funding SV and MF are senior clinical investigators of the research foundation Flanders (FWO), Belgium.

  • Competing interests BV reports financial support for research from Pfizer; lecture fees from Abbvie, Ferring, Takeda Pharmaceuticals, Janssen and R Biopharm; consultancy fees from Janssen and Sandoz. JS reports lecture fees from Abbvie, Takeda, Janssen and Nestle Health Sciences. SV reports financial support for research: MSD, AbbVie, Takeda, Pfizer, J&J; Lecture fee(s): MSD, AbbVie, Takeda, Ferring, Centocor, Hospira, Pfizer, J&J, Genentech/Roche; Consultancy: MSD, AbbVie, Takeda, Ferring, Centocor, Hospira, Pfizer, J&J, Genentech/Roche, Celgene, Mundipharma, Celltrion, SecondGenome, Prometheus, Shire, Prodigest, Gilead, Galapagos. MF reports financial support for research: Amgen, Biogen, Janssen, Pfizer, Takeda, Consultancy: Abbvie, Boehringer-Ingelheim, MSD, Pfizer, Sandoz, Takeda and Thermo Fisher; Speakers fee: Abbvie, Amgen, Biogen, Boehringer-Ingelheim, Falk, Ferring, Janssen, Lamepro, MSD, Mylan, Pfizer, Sandoz, and Takeda.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

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