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      Gastrointestinal hypoalgesia in inflammatory bowel disease

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          Abstract

          Background:

          Pain perception is critical for detection of noxious bodily insults. Gastrointestinal hypoalgesia in inflammatory bowel disease (IBD) is a poorly understood phenomenon previously linked to poor patient outcomes. We aimed to evaluate the risk factors associated with this condition and to discern characteristics that might differentiate these patients from pain-free quiescent counterparts.

          Methods:

          We performed a retrospective analysis using an IBD natural history registry based in a single tertiary care referral center. We compared demographic and clinical features in 3 patient cohorts defined using data from simultaneous pain surveys and ileocolonoscopy: a) active IBD without pain (hypoalgesic IBD); b) active IBD with pain; and c) inactive IBD without pain.

          Results:

          One hundred fifty-three IBD patients had active disease and 43 (28.1%) exhibited hypoalgesia. Hypoalgesic IBD patients were more likely to develop non-perianal fistulae (P=0.03). On logistic regression analysis, hypoalgesic IBD was independently associated with male sex, advancing age and mesalamine use, and inversely associated with anxious/depressed state and opiate use. Hypoalgesic IBD patients were demographically and clinically similar to the pain-free quiescent IBD cohort (n=59). Platelet count and C-reactive protein were more likely to be pathologically elevated in hypoalgesic IBD (P=0.03), though >25% did not exhibit elevated inflammatory markers.

          Conclusions:

          Hypoalgesia is common in IBD, particularly in male and older individuals, and is associated with an increased incidence of fistulae and corticosteroid use. Novel noninvasive diagnostic tools are needed to screen for this population, as inflammatory markers are not always elevated.

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          Most cited references28

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          Clinical disease activity, C-reactive protein normalisation and mucosal healing in Crohn's disease in the SONIC trial.

          The Crohn's Disease Activity Index (CDAI) has been criticised due to heavy weighting on subjective clinical symptoms. C-reactive protein (CRP) and endoscopic lesions are objective measures of inflammation. We investigated the relationships between clinical disease activity, CRP normalisation and mucosal healing in Crohn's disease (CD).
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            Pain and inflammatory bowel disease.

            Abdominal pain is a common symptom of inflammatory bowel disease (IBD: Crohn's disease, ulcerative colitis). Pain may arise from different mechanisms, which can include partial blockage and gut distention as well as severe intestinal inflammation. A majority of patients suffering from acute flares of IBD will experience pain, which will typically improve as disease activity decreases. However, a significant percentage of IBD patients continue experiencing symptoms of pain despite resolving inflammation and achieving what appears to be clinical remission. Current evidence suggests that sensory pathways sensitize during inflammation, leading to persistent changes in afferent neurons and central nervous system pain processing. Such persistent pain is not only a simple result of sensory input. Pain processing and even the activation of sensory pathways is modulated by arousal, emotion, and cognitive factors. Considering the high prevalence of iatrogenic as well as essential neuropsychiatric comorbidities including anxiety and depression in IBD patients, these central modulating factors may significantly contribute to the clinical manifestation of chronic pain. The improved understanding of peripheral and central pain mechanisms is leading to new treatment strategies that view pain as a biopsychosocial problem. Thus, improving the underlying inflammation, decreasing the excitability of sensitized afferent pathways, and altering emotional and/or cognitive functions may be required to more effectively address the difficult and disabling disease manifestations.
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              The narcotic bowel syndrome: clinical features, pathophysiology, and management.

              Narcotic bowel syndrome (NBS) is a subset of opioid bowel dysfunction that is characterized by chronic or frequently recurring abdominal pain that worsens with continued or escalating dosages of narcotics. This syndrome is underrecognized and may be becoming more prevalent. In the United States this may be the result of increases in using narcotics for chronic nonmalignant painful disorders, and the development of maladaptive therapeutic interactions around its use. NBS can occur in patients with no prior gastrointestinal disorder who receive high dosages of narcotics after surgery or acute painful problems, and among patients with functional gastrointestinal disorders or other chronic gastrointestinal diseases who are managed by physicians who are unaware of the hyperalgesic effects of chronic opioids. The evidence for the enhanced pain perception is based on the following: (1) activation of excitatory antianalgesic pathways within a bimodal opioid regulation system, (2) descending facilitation of pain at the rostral ventral medulla and pain facilitation via dynorphin and cholecystokinin activation, and (3) glial cell activation that produces morphine tolerance and enhances opioid-induced pain. Treatment involves early recognition of the syndrome, an effective physician-patient relationship, graded withdrawal of the narcotic according to a specified withdrawal program, and the institution of medications to reduce withdrawal effects.
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                Author and article information

                Journal
                Ann Gastroenterol
                Ann Gastroenterol
                Annals of Gastroenterology
                Hellenic Society of Gastroenterology (Greece )
                1108-7471
                1792-7463
                Jan-Feb 2020
                29 November 2019
                : 33
                : 1
                : 45-52
                Affiliations
                [a ]Department of Medicine, Division of Gastroenterology and Hepatology (Matthew D. Coates, Shannon Dalessio, August Stuart, Nana Bernasko, Andrew Tinsley, Kofi Clarke, Emmanuelle D. Williams)
                [b ]Department of Medicine (Christopher Soriano)
                [c ]Public Health Sciences and Department of Biochemistry (Vonn Walter)
                [d ]Department of Surgery, Division of Colorectal Surgery (Walter Koltun), Pennsylvania State University College of Medicine, Hershey, PA, USA
                Author notes
                Correspondence to: Matthew D. Coates, MD, PhD, Assistant Professor of Medicine, Penn State University Hershey Medical Center, Division of Gastroenterology and Hepatology, 500 University Drive, Hershey, PA 17033, USA, e-mail: mcoates@ 123456pennstatehealth.psu.edu
                Article
                AnnGastroenterol-33-45
                10.20524/aog.2019.0442
                6928483
                31892797
                0fde5ea6-7606-4a96-a42b-45b369549578
                Copyright: © Hellenic Society of Gastroenterology

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 19 August 2019
                : 04 October 2019
                Categories
                Original Article

                abdominal pain,hypoalgesia,hyposensitivity,inflammatory bowel disease,crohn’s disease

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