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my little penguin

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Abstract and Introduction
Abstract

Objectives: Symptoms compatible with irritable bowel syndrome (IBS) may co-exist in patients with inflammatory bowel disease (IBD), presenting a clinical dilemma for physicians. We conducted a systematic review and meta-analysis to examine this issue.

Methods: MEDLINE, EMBASE, and EMBASE Classic were searched (through February 2012) to identify cross-sectional surveys or case-control studies reporting the prevalence of symptoms meeting diagnostic criteria for IBS in ≥50 unselected adult IBD patients. The number of individuals with symptoms meeting criteria for IBS was extracted for each study, and pooled prevalence and odds ratios (ORs), with 95% confidence intervals (CIs), were calculated.

Results: The search identified 3,045 articles. Thirteen studies, containing 1,703 patients, were eligible. The pooled prevalence for IBS in all IBD patients was 39% (95% CI 30–48%), with an OR compared with controls of 4.89 (95% CI 3.43–6.98). In IBD patients in remission, the OR was 4.39 (95% CI 2.24–8.61). For IBD patients with active disease, the pooled prevalence of IBS was 44%, compared with 35% in those felt to be in remission (OR 3.89; 95% CI 2.71–5.59). The prevalence in patients with Crohn's disease (CD) was higher than in those with ulcerative colitis (UC; 46 vs. 36%, OR 1.62; 95% CI 1.21–2.18).

Conclusions: Symptoms compatible with IBS were significantly higher in patients with IBD compared with non-IBD controls, even among those felt to be in remission. IBS-type symptoms were also significantly more common in CD than in UC patients, and in those with active disease. Management strategies for IBD patients with symptoms suggestive of IBS are required.

From:
http://www.medscape.com/viewarticle/777071?src=nl_topic
 
Data from randomized controlled trials demonstrate that such patients tend to respond poorly to therapy,[20,21] and evidence for other therapies that appear to be of benefit in IBS remains lacking in IBD patients

From link above
 
Another possibility is that existing diagnostic criteria for IBS perform poorly in distinguishing between occult disease activity in IBD and true IBS. In other words, it may be that these criteria are fulfilled purely owing to symptoms that are causally related to active IBD. If this were the case, undetected low-level inflammation in those patients judged by investigators in these studies to be in remission could be the cause of an excess of symptoms in this group. The findings in one of the studies identified in this meta-analysis support this,[23] with significantly higher levels of fecal calprotectin observed among IBD patients in remission with symptoms of IBS, compared with those without. However, in the only other study to examine this issue, levels were no different between these two groups.[42] This is an area for future research, but our finding that prevalence of IBS symptoms in patients with active IBD were almost fourfold than those of patients in remission adds weight to this potential explanation, although the prevalence among IBD patients felt to be in remission was still significantly higher than in non-IBD controls. Alternatively, patients with IBD who report these symptoms may have co-existent conditions, such as celiac disease, small intestinal bacterial overgrowth, or bile acid malabsorption. Meta-analyses suggest that all of these can produce symptoms that may be confused with IBS.[49–51] This could partly explain the reason for the higher prevalence of IBS-type symptoms in patients with CD, compared with UC, as patients with small bowel CD may be at risk of small intestinal bacterial overgrowth, and those undergoing terminal ileal surgery are likely to develop bile acid malabsorption as a result. However, as the studies did not report prevalence of IBS in CD patients according to disease distribution or history of previous terminal ileal resection this is speculative, and more research exploring possible explanations for this observation is required.

From link above :)
 
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.
 

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