A few more articles for your reading pleasure regarding IBD and IBS.
I've been watching the literature on IBS and IBD casually so I am certainly not any expert.
But it would appear to me that the bottom line - at this point in time - is that the top researches in this field think IBS and IBD may exist on a continuum in some people and that IBS may even be a pre-cursor or put you at risk for developing IBD.
It has been suggested that IBS in people with Crohn's could be caused by inflammation that is somehow different than the inflammation associated with active Crohn's. In that case, elevated calprotectin level's don't signify active Crohn's - just IBS.
Other researchers are like - duh, :duh: it's inflammation from the Crohn's dummy.
Right, she says sarcastically.
My practical side says that of course it would make sense that IBS and IBD might be connected somehow at least in some patients. And it can be very helpful to be able to sort out these things without putting people through scopes and MRE, etc.
What I can't figure out is why no one appears to be attempting to coordinate this research with the people trying to create the perfect test to diagnose Crohns (i.e. Prometheus). Maybe they are and I don't know about it. Because the one thing the Prometheus test does seem to do OK on is ruling out IBD. If it says you don't have IBD then there's a good chance that you don't. Not perfect of course but a higher rate of success at that than the other aspects of the test perform.
So why not pair that with these questions about which patients with IBS and inflammation test positive for IBD or not.
My reasoning is probably off somewhere. Perhaps the better minds than mine that populate the forum can make better sense of it all.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3444908/
BMC Gastroenterol. 2012; 12: 55.
Published online 2012 May 28. doi: 10.1186/1471-230X-12-55
PMCID: PMC3444908
Risk of inflammatory bowel disease following a diagnosis of irritable bowel syndrome
Chad K Porter,1 Brooks D Cash,2 Mark Pimentel,3 Akintunde Akinseye,4 and Mark S Riddle1
Conclusions
These data reflect a complex interaction between illness presentation and diagnosis of IBS and IBD and suggest intercurrent IGE may increase IBD risk in IBS patients. Additional studies are needed to determine whether IBS lies on the causal pathway for IBD or whether the two are on a pathophysiological spectrum of the same clinical illness. These data suggest consideration of risk reduction interventions for IGE among IBS patients at high disease risk.
http://www.ncbi.nlm.nih.gov/pubmed/20389294
Am J Gastroenterol. 2010 Aug;105(8):1788, 1789-94; quiz 1795. doi: 10.1038/ajg.2010.156. Epub 2010 Apr 13.
Irritable bowel syndrome-type symptoms in patients with inflammatory bowel disease: a real association or reflection of occult inflammation?
Keohane J, O'Mahony C, O'Mahony L, O'Mahony S, Quigley EM, Shanahan F
Conclusions:
IBS-like symptoms are common in patients with IBD who are thought to be in clinical remission, but abnormal calprotectin levels suggest that the mechanism in most cases is likely to be occult inflammation rather than coexistent IBS.
.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3468846/
World J Gastroenterol. 2012 October 7; 18(37): 5151–5163.
Published online 2012 October 7. doi: 10.3748/wjg.v18.i37.5151
PMCID: PMC3468846
Irritable bowel syndrome: Diagnosis and pathogenesis
Magdy El-Salhy
Abstract
Irritable bowel syndrome (IBS) is a common gastrointestinal (GI) disorder that considerably reduces the quality of life. It further represents an economic burden on society due to the high consumption of healthcare resources and the non-productivity of IBS patients. The diagnosis of IBS is based on symptom assessment and the Rome III criteria. A combination of the Rome III criteria, a physical examination, blood tests, gastroscopy and colonoscopy with biopsies is believed to be necessary for diagnosis. Duodenal chromogranin A cell density is a promising biomarker for the diagnosis of IBS. The pathogenesis of IBS seems to be multifactorial, with the following factors playing a central role in the pathogenesis of IBS: heritability and genetics, dietary/intestinal microbiota, low-grade inflammation, and disturbances in the neuroendocrine system (NES) of the gut. One hypothesis proposes that the cause of IBS is an altered NES, which would cause abnormal GI motility, secretions and sensation. All of these abnormalities are characteristic of IBS. Alterations in the NES could be the result of one or more of the following: genetic factors, dietary intake, intestinal flora, or low-grade inflammation. Post-infectious IBS (PI-IBS) and inflammatory bowel disease-associated IBS (IBD-IBS) represent a considerable subset of IBS cases. Patients with PI- and IBD-IBS exhibit low-grade mucosal inflammation, as well as abnormalities in the NES of the gut.