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IBS-like Symptoms in Patients with Ulcerative Colitis in Deep Remission Are Associated with Increased Levels of Serum Cytokines and Poor Psychological Well-being

Jonefjäll, Börje MD; Öhman, Lena PhD; Simrén, Magnus MD, PhD; Strid, Hans MD, PhD

doi: 10.1097/MIB.0000000000000921
Original Clinical Articles

Background: Gastrointestinal symptoms (GI) compatible with irritable bowel syndrome (IBS) are common in patients with ulcerative colitis (UC) in remission. The causes of these symptoms remain to be clarified. Our aim was to investigate prevalence and factors associated with IBS-like symptoms in patients with UC in deep remission.

Methods: We included 298 patients with UC and used Mayo score, sigmoidoscopy, and fecal calprotectin to define deep remission versus active disease. Presence of IBS-like symptoms according to the Rome III criteria, severity of GI, extraintestinal and psychological symptoms, stress levels, and quality of life were measured with validated questionnaires. Serum cytokines and high-sensitive C-reactive peptide were determined.

Results: The criteria for deep remission was fulfilled by 132 patients (44%) and 24 of these fulfilled the Rome III criteria for IBS (18%). Patients with UC in deep remission with IBS-like symptoms had comparable levels of GI symptoms, non-GI somatic symptoms, and quality of life as patients with active UC. The patients with UC in deep remission with IBS-like symptoms had similar levels of fecal calprotectin as patients in deep remission without IBS-like symptoms (18 versus 31 μg/g, P = 0.11), but higher levels of serum cytokines (interleukin [IL]-1β, IL-6, IL-13, IL-10 and IL-8, P < 0.05) and higher levels of anxiety (P < 0.001), depression (P = 0.02) and perceived stress (P = 0.03).

Conclusions: IBS-like symptoms in patients with UC in deep remission are common, but not as prevalent as previously reported. Poor psychological well-being and increased serum cytokine levels, but not colonic low-grade inflammation, were associated with IBS-like symptoms.

Article first published online 15 September 2016.

*Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden;

Department of Internal Medicine, Kungälv Hospital, Kungälv, Sweden;

Department of Microbiology and Immunology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden;

§School of Health and Education, University of Skövde, Skövde, Sweden;

Center for Functional GI and Motility Disorders, University of North Carolina, Chapel Hill, North Carolina; and

Department of Internal Medicine, Södra Älvsborg Hospital, Borås, Sweden.

Address correspondence to: Börje Jonefjäll, MD, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, 413 45 Gothenburg, Sweden (e-mail: borje.jonejall@vgregion.se).

Supported by the Swedish Medical Research Council (Grants 13409, 21691 and 21692), the Health & Medical Care Committee of the Regional Executive Board Region in Västra Götaland (119011), the Göteborg Medical Society and foundation of Elin and Carl Linder (GLS-406621), the Swedish Society of Medicine (SLS-329111), and by the Faculty of Medicine, University of Gothenburg.

Author disclosures are available in the Acknowledgments.

Received April 07, 2016

Accepted July 21, 2016

© Crohn's & Colitis Foundation of America, Inc.
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