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Alterations in mucosal neuropeptides in patients with irritable bowel syndrome and ulcerative colitis in remission: A role in pain symptom generation?
Author(s) -
Keszthelyi D.,
Troost F.J.,
Jonkers D.M.,
Helyes Z.,
Hamer H.M.,
Ludidi S.,
Vanhoutvin S.,
Venema K.,
Dekker J.,
Szolcsányi J.,
Masclee A.A.
Publication year - 2013
Publication title -
european journal of pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.305
H-Index - 109
eISSN - 1532-2149
pISSN - 1090-3801
DOI - 10.1002/j.1532-2149.2013.00309.x
Subject(s) - irritable bowel syndrome , trpv1 , neuropeptide , somatostatin , substance p , abdominal pain , medicine , gastroenterology , nociception , somatization , ulcerative colitis , endocrinology , transient receptor potential channel , disease , receptor , psychiatry , anxiety
Background Irritable bowel syndrome ( IBS ) is a functional gastrointestinal disorder characterized by chronic abdominal pain. The transient receptor potential vanilloid 1 ( TRPV 1) channel, which is involved in visceral pain signalling, has been shown to be up‐regulated in IBS . Activation of TRPV 1 leads to the release of neuropeptides, such as somatostatin and substance P ( SP ). We hypothesized that increased pain perception in IBS could be explained by increased transcription in TRPV 1 and/or altered levels of neuropeptides. We therefore assessed the transcription of TRPV 1 and the mucosal concentration of somatostatin and SP in IBS in comparison to healthy volunteers and patients with ulcerative colitis ( UC ) in remission as disease controls, and to ascertain their relationship to pain symptoms. Method Sigmoid colonic mucosal samples were collected from 12 patients with IBS , 34 patients with UC in remission and 9 healthy volunteers, in which groups TRPV 1 mRNA levels were determined using quantitative polymerase chain reaction and neuropeptide concentrations by radioimmunoassay. Pain symptom intensity was determined by questionnaires. Results Transcription of TRPV 1 as well as the concentration of neuropeptides were significantly higher in IBS , but only the former correlated with pain symptom severity. Conclusion Increased transcription of TRPV 1 may provide a possible explanation for pain generation in IBS . While the neuropeptides SP and somatostatin were both found to be increased in IBS , these changes are not sufficient to explain pain generation. Pain generation in IBS is probably explained by a complex redundancy in the regulation of local nociceptive mechanisms, which remains a subject of intensive investigation.