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Discussion Starter · #1 ·
"IS IRRITABLE BOWEL SYNDROME A MILD FORM OF IRRITABLE BOWEL DISEASE?The authors believe that IBD and at least a subset of IBS patients exist at two ends of the same spectrum of pathophysiology, which involves immune activation and inflammation. This is prompted by the observation that IBS symptoms may precede IBD, which reflects gut dysfunction generated by subclinical inflammation. It also has been observed that IBS occurs in patients in remission from IBD. This concept is underpinned by results of basic scientific studies in animal models showing that immune activation and inflammation restricted to the mucosal compartment result in profound changes in neuromuscular function that may persist after recovery of the mucosa. Emerging evidence shows similarities in genotype between IBD and a subset of IBS patients; polymorphisms of genes that encode cytokine secretion may result in an imbalance of pro- and counter-inflammatory signals. This in turn would lead to inefficient down-regulation of inflammatory responses and promote low-grade inflammation. It is a matter of the severity of inflammation that separates IBD and this IBS subset, and this may reflect additional genetic abnormalities or greater exposure to environmental factors in the case of IBD. This prompts the question as to whether IBD is more common in patients with IBS, and there is some evidence to support this [65]. Clearly in IBD the brunt of immune-mediated injury is borne by the mucosal compartment, whereas in IBS, the mucosal compartment may play a role in initiating events, but the brunt of injury is taken by the deeper neuromuscular tissues. Further work is required to elucidate differences in the regulation of immune activity between these compartments to better understand the relationship of IBD and IBS."Abstract of the above article below : http://www.ncbi.nlm.nih.gov/entrez/query.f...2932&query_hl=1
 

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I respect DR Collins. However" But microscopic inflammation cannot be a diagnostic marker for IBS because it does not typically produce pain in those who have it. All patients with active celiac disease have microscopic inflammation, but a large proportion do not have abdominal pain, and patients with ulcerative colitis who also have microscopic inflammation when compared to patients with IBS appear to have higher pain thresholds (24). In individuals with these disorders, there may be central nervous system counter-regulatory measures responding to the peripheral pain/inflammatory processes that increase pain thresholds. With regard to IBS, the gut-related effects of microscopic inflammation may be only one component of a dysfunctional brain-gut system. In addition, and often in response to stress, there may be a failure to activate descending pain inhibitory systems that enable the clinical experience of pain and other symptoms that typify this disorder (25). ""Visceral Sensations and Brain-Gut MechanismsBy: Emeran A. Mayer, M.D., Professor of Medicine, Physiology and Psychiatry; Director, Center for Neurovisceral Sciences & Women's Health, David Geffen School of Medicine at UCLA"http://www.aboutibs.org/Publications/VisceralSensations.html
 

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Discussion Starter · #3 ·
First of all no one is saying that microscopic inflammation is a diagnostic marker for IBS. The authors are saying it is a continuum with mild IBS on one end and IBD on the other.Note that an intact epithelium in the absence of mucosal inflammation does not mean that inflammation is not present in deeper layers of the gut. This can lead to altered gut function see this studyhttp://www.ncbi.nlm.nih.gov/entrez/query.f...4854&query_hl=7As for visceral hypersensitivity it s true that the studies are controversial but visceral hypersensitivity correlated with the number of mast cells located in close proximity to the enteric nerves in this very recent study http://www.ncbi.nlm.nih.gov/entrez/query.f...8823&query_hl=5The presence of visceral hypersensitivity in IBD depends on whether the disease is acute or chronic and on the region involved. "Intuitively, different immune or inflammatory cell infiltrates will impose different effects on sensory nerve functionâ€"a concept supported by recent preliminary reports in animals " the quote is from the article in the first post.
 

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quote:The presence of visceral hypersensitivity in IBD depends on whether the disease is acute or chronic and on the region involved.
Who said there is hypersensitivity in IBD?
 

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Discussion Starter · #6 ·
eric Re: stress downregulating pain inhibition, psychosocial factors play a big role in IBS and IBD. Just type in Depression AND IBD in Pubmed and you will come across many articles. In fact depression is associated with relapses of colitis or other disease activity in IBD. Activation of the immune system may be the common pathway mediating behavioral-induced changes in these conditions.
 

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Why not?I can be worst that an IBD sufferer in term of symptoms.
 

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quote:"Although UC activity index scores negatively correlated with perceptual thresholds for discomfort (r=-0.76, p=0.016), "
Exactly. UC patients are hyposensitive.
 

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Discussion Starter · #9 ·
I assume if activity index increases the disease is more active? And doesn't negative correlation mean when one increases the other decreases? So when the disease became more active the pain threshold decreased. I.e when disease became more active they became more hypersensitive.
 

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quote:I.e when disease became more active they became more hypersensitive.
Oh yeah, it does. Anyway, it's irrelevant because the UCers are so hyposensitive to begin with. I guess you can say UC could be used to treat IBS.
 
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