# inflammation & IBS



## Talissa (Apr 10, 2004)

Because the information on the ongoing, low-grade inflammation of post-infectious IBS, which may also be present in standard "IBS", isn't getting out there, just wanted to share this~~*World Journal of Gastroenterology, Jan 06**Changing face of irritable bowel syndrome*"...It may come as a real surprise to many to hear that infection and inflammation are now seen as potential factors in the etiology of IBS. With regard to infection, we are now beginning to see the real data to directly support the concept of post-infective or post-dysenteric IBS....In the meantime, as illustrated in Figure 1, I would suggest that a model based on a primary role for intestinal inflammation serves to integrate the various strands which contribute to the presentation of IBS."http://www.wjgnet.com/1007-9327/12/1.asp*American Journal of Gastroenterology, Nov 05*"OBJECTIVES: Imbalances in the genetically controlled pro- and anti-inflammatory cytokine production may promote ongoing low-grade inflammation after an acute gastroenteritis, and subsequently, irritable bowel syndrome (IBS) (post-infectious IBS, PI-IBS)...CONCLUSIONS: Our results support the emerging hypothesis that genetically determined immune activity plays a role in the pathophysiology of IBS. Future studies in larger, clinically relevant, IBS subgroups are warranted to establish definite associations with cytokine gene polymorphisms."http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_docsum*Current Opinion in Gastroenterology, Jan 06*"..._RECENT FINDINGS: Recent studies have overthrown the dogma that irritable bowel syndrome is characterized by no abnormality of structure by demonstrating low-grade lymphocytic infiltration in the gut mucosa, increased permeability and increases in other inflammatory components _ including enterochromaffin and mast cells. Furthermore, increased inflammatory cytokines in both mucosa and blood have been demonstrated in irritable bowel syndrome. While steroid treatment has proved ineffective, preliminary studies with probiotics exerting an anti-inflammatory effect have shown benefit. *SUMMARY: The study of post-infectious irritable bowel syndrome has revealed the importance of low-grade inflammation in causing irritable bowel syndrome symptoms.*"http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_docsum


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## Talissa (Apr 10, 2004)

Here's a pretty good explanation of the low-grade inflammation of IBS~"Humans have evolved a close association with certain disease producing organisms (pathogens), such as bacteria or viruses, leading to immune "tolerance" where there is low grade inflammation in the gut. Inflammation is a normal immune response by the body in reaction to tissue damage such as caused by injury or infection. Some bacteria can be associated with anti-inflammatory production that decrease inflammation by activating anti-inflammatory substances within immune cells (cytokines), while other bacteria can be associated with more inflammatory cytokine production. *However, if this system gets out of balance, there may be increased or destructive immune responses. For example, with IBS with diarrhea a low grade inflammatory response can contribute to the disorder.* With post-infectious IBS, in particular, there is loss of the "good" bacteria (commensals) with increased mucosal inflammation, activation of anti-inflammatory substances, and increased small bowel permeability to bacteria. Probiotics may have a role in improving these symptoms by reversing the inflammatory immune state, by introducing the "good" bacteria."http://www.iffgd.org/symposium2005report.html


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## eric (Jul 8, 1999)

Have you seen this, very up to date IBS infohttp://www.ja-online.com/dukeibs/#


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## Talissa (Apr 10, 2004)

Eric,My pc can't read that format after some virus took over last year. I got rid of the virus, but for ctn pics and text like w/ your link, all I get is a blank box with a tiny red "x" in the corner.







Can you tell me what the previously unknown & "latest" is from your article? If it's too long & time-consuming, I understand.(and if anyone knows how to fix my pc problem, I'd be VERY grateful!!







)Thanks!Tal


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## eric (Jul 8, 1999)

Talissa, it is in flash and you might need to re download a flash player.http://www.macromedia.com/shockwave/downlo...anguage=EnglishHowever its an excellent presentation and very up to date on IBS.There is a new serotonin study that has not been released yet and info on inflammation and the types of inflammation and a whole lot more information on the big picture of IBS.


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## Talissa (Apr 10, 2004)

Thanks Eric.







I tried the download & guess what? The gold bar they said to click on to start the download was a blank box...w/ a little red X in the corner. Grrr!Ah well.


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## 14416 (Jun 21, 2005)

I had visible "chronic inflammation" on my colonoscopy.Here, I'll go get my chart real quick and post what was written:1. "Nonspecific chronic colitis"--based on biopsy.2. "The lamnia propria shows increased number of plasma cells"--biopsy.Clinical notesre operative Diagnosis-DiarrheaPost-op diagnosis-Erythema of sigmoid.Diagnosis:1- Colon, random biopsies: Nonspecific chronic colitis.2- Colon, sigmoid, area of erythema, biopsy: a. Vascular congestion and recent hemorrage into lamnia propria. b. Chronic inflammation.Erythema visible in the sigmoid colon.


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## Talissa (Apr 10, 2004)

Hi Grant,Thanks for the info. Sounds like the inflammation was seen thru biopsy rather than colonoscopy?If inflammation is visual with a naked eye(like in colonoscopy) rather than with the help of a microscope, I thought it was considered IBD?


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## Talissa (Apr 10, 2004)

More on this line of research~"...IBS therefore may begin as an inciting event injuring the bowel followed by an inability to down-regulate the subsequent inflammation. The reason for this ongoing inflammation is not clear, but interestingly, patients with IBS are less likely to have high-producer IL-10 gene alleles (40), similar to patients with inflammatory bowel disease. IL-10 plays a significant anti-inflammatory role; if IL-10 were produced in low levels, mild inflammation could persist.Other potential causes of continued low-level inflammation in the GI tract include food allergies and changes in bacterial microflora. Allergic reactions can evoke inflammatory cell infiltration in the GI tract (41), but the prevalence of food allergies in IBS is unclear (42). Gut microflora may be altered in patients with IBS (43); some findings suggest that IBS patients may have intestinal bacterial overgrowth (44) and increased colonic fermentation (45). Further information is needed to elucidate the role of these environmental factors in promoting and perpetuating the putative low-grade inflammatory process.Much remains unknown about the potential causes of IBS. There may not be a unifying hypothesis to link all the aspects of this diverse syndrome. Nevertheless, markers of low-grade inflammation, which were initially found in diarrhea-predominant and postinfectious cases of IBS, are increasingly being found in constipation-predominant patients as well. Thus, inflammation may figure as an underlying factor in visceral hypersensitivity in more cases of IBS than previously was suspected. These intriguing inroads may be the key to our understanding of the basis for the IBS and may yield exciting therapeutic possibilities."http://www.pulsus.com/Gastro/18_10/andr_ed.htm


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## overitnow (Nov 25, 2001)

From:http://www.drmirkin.com/heart/1812.htmlâ€œA study in The New England Journal of Medicine showed that women with high levels of a blood test called C reactive protein (CRP) which measures inflammation are twice as likely as those with high cholesterol to die from heart attacks and strokes (1). The lowest risk for a heart attack was in women whose CRP was below one-half milligram per liter of blood. Those who had both high cholesterol and high CRP were at very high risk for heart attacksâ€¦â€Since I get my IBS relief from a supplement designed to lower the threat of cholesterol blockages, strengthen the vascular system, and increase circulation, which includes anti-inflammatory agents, I think a good case can be made for IBS being an indicator for subsequent cardio problems. This also may present a further reason, other than binding bicarbonates why aspirin is helpful for Kevin, given it's use in cadiovascular therapy.Mark


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## 14416 (Jun 21, 2005)

Well, that's what was biopsied, the "chronic inflammation".The "erythema" in the sigmoid was where he took the biopsies.He could visibly see inflammation. He told my mom I was really inflammed, but didn't see any visible ulcerations or anything like that.


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## Talissa (Apr 10, 2004)

Grant, sounds like you've got yourself a good doc! At least diagnostically. Thx for the info, that's very interesting.Mark, can't believe you're putting Provex in the same category as aspirin for IBS relief~~"The small intestine is a more common site for nonsteroidal antiinflammatory drug (NSAID) toxicity than the well-recognized effects on the stomach and duodenum. Although NSAID strictures and perforation are rare, two thirds of regular NSAID users may be prone to small bowel enteropathy."http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_DocSum"Long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) is the second most common cause of ulcers and the rate of NSAID-caused ulcers in increasing. About 20 million people take prescription NSAIDs regularly, and over 25 billion tablets of over-the-counter brands are sold each year in America. The most common NSAIDs are aspirin, ibuprofen (Advil), and naproxen (Aleve, Naprosyn), although many others are available."http://www.mercydesmoines.org/ADAM/WellCon...cles/000019.asp


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## eric (Jul 8, 1999)

FYIAliment Pharmacol Ther. 2006 Apr 15;23(8):1067-76. Related Articles, Links Review article: intestinal serotonin signalling in irritable bowel syndrome.Mawe GM, Coates MD, Moses PL.Department of Anatomy and Neurobiology, University of Vermont College of Medicine, Burlington, VT, USA.Summary Alterations in motility, secretion and visceral sensation are hallmarks of irritable bowel syndrome. As all of these aspects of gastrointestinal function involve serotonin signalling between enterochromaffin cells and sensory nerve fibres in the mucosal layer of the gut, potential alterations in mucosal serotonin signalling have been explored as a possible mechanism of altered function and sensation in irritable bowel syndrome. Literature related to intestinal serotonin signalling in normal and pathophysiological conditions has been searched and summarized. Elements of serotonin signalling that are altered in irritable bowel syndrome include: enterochromaffin cell numbers, serotonin content, tryptophan hydroxylase message levels, 5-hydroxyindoleacedic acid levels, serum serotonin levels and expression of the serotonin-selective reuptake transporter. Both genetic and epigenetic factors could contribute to decreased serotonin-selective reuptake transporter in irritable bowel syndrome. A serotonin-selective reuptake transporter gene promoter polymorphism may cause a genetic predisposition, and inflammatory mediators can induce serotonin-selective reuptake transporter downregulation. While a psychiatric co-morbidity exists with IBS, changes in mucosal serotonin handling support the concept that there is a gastrointestinal component to the aetiology of irritable bowel syndrome. Additional studies will be required to gain a more complete understanding of changes in serotonin signalling that are occurring, their cause and effect relationship, and which of these changes have pathophysiological consequences.PMID: 16611266


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## 15677 (Apr 8, 2006)

It sounds as if Inflammation could now part of IBS where it previously was not thought to be part of IBS but only IBD. So if leukocytes (white blood cells) are elevated in the stool (which indicate inflammation)but no other IBD symptoms are present, it may not be IBD but could be IBS which would be a big relief for many.


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## Talissa (Apr 10, 2004)

Hey rjc,I'm not sure if the inflammation of IBS is to the extent where there'd be a leukocyte response or not. That'd be interesting to find out. Esp since this is an indication of invasive pathogens... ( http://www.medscape.com/viewarticle/407978 )Here's an interesting commentary from last month's issue of Neurogastroenterology & Motility. It discusses the role of enteric microflora & intestinal inflammation~"Advancing knowledge regarding the cellular mechanisms of intestinal inflammation has led to a better understanding of the disease pathology in patients with chronic disorders of the gut including inflammatory bowel disease, coeliac disease, lymphocytic colitis and irritable bowel syndrome. An emerging new paradigm suggests that changes in the homeostasis of bacteria- and host-derived signal transduction at the epithelial cell level may lead to functional and immune disturbances of the intestinal epithelium. *It has become clear from numerous studies that enteric bacteria are a critical component in the development and prevention/treatment of chronic intestinal inflammation.* Signal-specific activation of mitogen-activated protein kinases (MAPK), interferon-regulated factors (IRF) and the transcription factor NF-kappaB through pattern recognition receptor signalling effectively induce inflammatory defence mechanisms. *Unbalanced activation of these innate signalling pathways because of host genetic predispositions and/or the lack of adequate anti-inflammatory feedback mechanisms may turn a physiological response into a pathological situation including failure of bacterial clearance and development of chronic inflammation.* Host-derived regulators from the immune and enteric nerve system crosstalk to the innate signalling network of the intestinal epithelium in order to shape the extent and duration of inflammatory processes."http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_docsum


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## 15677 (Apr 8, 2006)

Talissa:Thanks for the info.I was not able to open the first link re: the leukocyte's, as it requires membership, can you give me the Reader's Digest version? Just because fecal leukocytes are elevated is it a conclusive indication of IBD vs IBS, as there may be other causes of the inflammation/elevated leukocytes, perhaps the body is trying to fight off the bad types of microflora or maybe bleeding hemorrhoids along with IBS are causing enough inflammtion to cause an elevated fecal white blood count ? I don't know if you have access to more info but I would love to know the latest theories pertaining to inflammation/elevated luekocytes and IBS. I also believe the # of leukocytes present is an important factor to consider but still may not be 100% conclusive. I have a feeling IBD is just a greater degree of IBS and are all related...


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## 13540 (Aug 18, 2005)

i had mild inflamtion on my colonscopy not to the naked eye but by biopys and endoscopy came out fine my gi doc said it was from the prep for the colonoscopy caused my mild inflamation


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## Talissa (Apr 10, 2004)

> quote:Just because fecal leukocytes are elevated is it a conclusive indication of IBD vs IBS,


This isn't a test for IBS AT ALL at this point, if it ever will be. The medscape article just backed my saying the leukocytes are elevated with invasive pathogens. It talks about how in IBD, with fecal leukocytes, antibiotics should be considered treatment.(like that's going to help long term)...Fecal calprotectin, on the other hand, is a good test for intestinal inflammation. It's level can indicate the diff btn IBS & IBD. I had this test in 2004. I was pretty close to IBD, but just skirted under the line...


> quote:I have a feeling IBD is just a greater degree of IBS and are all related...


So do I."...There is clinical overlap between IBS and inflammatory bowel disease (IBD), with IBS-like symptoms frequently reported in patients before the diagnosis of IBD, and a higher than expected percentage reports of IBS symptoms in patients in remission from established IBD. Thus,these conditions may coexist with a higher than expected frequency, or may exist on a continuum, with IBS and IBD at different ends of the same spectrum. This article examines these relation-ships using immune activation and inflammation as a common pathogenic process to IBD and a subset of IBS patients."http://www.ncbi.nlm.nih.gov/entrez/query.f...2&dopt=Citation


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## 15677 (Apr 8, 2006)

It's amazing if the MD does not test you when your symptoms are at their worst the results may not be conclusive at all.It sounds like we may share the same level of IBS. The second GI I was seeing was ready to treat me for CD prior to any conclusive data and my original GI who did my colonoscopy, albeit without performing any biopsies for microscopic inflammation, gets very upset when I mention the possibility I have IBD even though I had "many leukocytes" during a stool test and "a few" during another (but of course at that time the symptoms were better) performed by GI# 2 (GI #2 only wanted to do one fecal test and it was I that had to suggest he perform at least three over different times to get a better perspective!)GI#1 still insists I have IBS as my colonoscopy was normal and my bleeding was from internal H's. GI # 2 thought I may have CD in my terminal illeum even though the flouroscopic spot image test that he ordered showed a normal terminal illeum! GI#2 made me try a capsule endoscopy which never made it all the way through before running out of battery, he then tells me if I do it again there's a med to help make sure it passes all the way through! I was amazed he did not suggest this the first time! I was about to take the capsule endoscopy again when GI#2 started writting me an RX for Entocort (a somewhat strong albeit 90% localized steroid), I asked him why are you giving me a steroid, he replied "to help you get some relief", but I said we haven't got any conclusive tests to indicate CD/IBD at all; that's when I told him thanks, but no thanks and went back to GI #1. Sorry for the rambling but I wanted to give you the full perspective


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## Talissa (Apr 10, 2004)

Hey rjc,Wow, that's some story! Doesn't say much for GIs, or I should say for the current knowledge about our complex, perplexing GI problems...I'm so glad you didn't take the steroids. I sometimes check out the colitisfoundation.com site & the people that do best there are the ones treating IBD naturally--w/ probiotics, fiber, diet changes, exercise, and sometimes natural antiinflammatories/antibacterials. The exact same things that help out IBSrs...


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## eric (Jul 8, 1999)

RJCwere you able to view thishttp://www.ja-online.com/dukeibs/#and this is also new, but in medscape"Review Article: Intestinal Serotonin Signalling in Irritable Bowel SyndromePosted 04/13/2006G. M. Mawe; M. D. Coates; P. L. Moses Summary and IntroductionSummaryAlterations in motility, secretion and visceral sensation are hallmarks of irritable bowel syndrome. As all of these aspects of gastrointestinal function involve serotonin signalling between enterochromaffin cells and sensory nerve fibres in the mucosal layer of the gut, potential alterations in mucosal serotonin signalling have been explored as a possible mechanism of altered function and sensation in irritable bowel syndrome. Literature related to intestinal serotonin signalling in normal and pathophysiological conditions has been searched and summarized.Elements of serotonin signalling that are altered in irritable bowel syndrome include: enterochromaffin cell numbers, serotonin content, tryptophan hydroxylase message levels, 5-hydroxyindoleacedic acid levels, serum serotonin levels and expression of the serotonin-selective reuptake transporter. Both genetic and epigenetic factors could contribute to decreased serotonin-selective reuptake transporter in irritable bowel syndrome. A serotonin-selective reuptake transporter gene promoter polymorphism may cause a genetic predisposition, and inflammatory mediators can induce serotonin-selective reuptake transporter downregulation.While a psychiatric co-morbidity exists with IBS, changes in mucosal serotonin handling support the concept that there is a gastrointestinal component to the aetiology of irritable bowel syndrome. Additional studies will be required to gain a more complete understanding of changes in serotonin signalling that are occurring, their cause and effect relationship, and which of these changes have pathophysiological consequences."http://www.medscape.com/viewarticle/528890?src=mp


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## 15677 (Apr 8, 2006)

> quote:Originally posted by Talissa:Hey rjc,Wow, that's some story! Doesn't say much for GIs, or I should say for the current knowledge about our complex, perplexing GI problems...I'm so glad you didn't take the steroids. I sometimes check out the colitisfoundation.com site & the people that do best there are the ones treating IBD naturally--w/ probiotics, fiber, diet changes, exercise, and sometimes natural antiinflammatories/antibacterials. The exact same things that help out IBSrs...


Thanks Talissa. What are some natural anti inflammatories?


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## 15677 (Apr 8, 2006)

> quote:Originally posted by Talissa:
> 
> 
> > quote:Just because fecal leukocytes are elevated is it a conclusive indication of IBD vs IBS,
> ...


GI#2 never mentioned calprotien levels, just his concern about the "many" leukocytes! It appears GI#1 is leading me toward the correct dx.Thanks


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## 15677 (Apr 8, 2006)

> quote:Originally posted by eric:RJCwere you able to view thishttp://www.ja-online.com/dukeibs/#and this is also new, but in medscape"Review Article: Intestinal Serotonin Signalling in Irritable Bowel SyndromePosted 04/13/2006G. M. Mawe; M. D. Coates; P. L. Moses Summary and IntroductionSummaryAlterations in motility, secretion and visceral sensation are hallmarks of irritable bowel syndrome. As all of these aspects of gastrointestinal function involve serotonin signalling between enterochromaffin cells and sensory nerve fibres in the mucosal layer of the gut, potential alterations in mucosal serotonin signalling have been explored as a possible mechanism of altered function and sensation in irritable bowel syndrome. Literature related to intestinal serotonin signalling in normal and pathophysiological conditions has been searched and summarized.Elements of serotonin signalling that are altered in irritable bowel syndrome include: enterochromaffin cell numbers, serotonin content, tryptophan hydroxylase message levels, 5-hydroxyindoleacedic acid levels, serum serotonin levels and expression of the serotonin-selective reuptake transporter. Both genetic and epigenetic factors could contribute to decreased serotonin-selective reuptake transporter in irritable bowel syndrome. A serotonin-selective reuptake transporter gene promoter polymorphism may cause a genetic predisposition, and inflammatory mediators can induce serotonin-selective reuptake transporter downregulation.While a psychiatric co-morbidity exists with IBS, changes in mucosal serotonin handling support the concept that there is a gastrointestinal component to the aetiology of irritable bowel syndrome. Additional studies will be required to gain a more complete understanding of changes in serotonin signalling that are occurring, their cause and effect relationship, and which of these changes have pathophysiological consequences."http://www.medscape.com/viewarticle/528890?src=mp


Thanks Eric, great presentation.


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## 15677 (Apr 8, 2006)

Has anyone had an rx for Levsen?Since serotonin appears to influence IBS could a serotonin supplement be helpful or even harmful?


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## Kathleen M. (Nov 16, 1999)

I've used Levsin, it works pretty well for me, but it can make my mouth dry.It isn't just serotonin levels in the whole body that is the issue, it is where/when released by nerve cells.I don't know that the precursors sold OTC help much, but they may not hurt, but I would avoid them if you take any medication that alters serotonin as you can get too much in the wrong place and get symptoms from that (serotonin syndrome).K.


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## 15677 (Apr 8, 2006)

> quote:Originally posted by Kathleen M.:I've used Levsin, it works pretty well for me, but it can make my mouth dry.It isn't just serotonin levels in the whole body that is the issue, it is where/when released by nerve cells.I don't know that the precursors sold OTC help much, but they may not hurt, but I would avoid them if you take any medication that alters serotonin as you can get too much in the wrong place and get symptoms from that (serotonin syndrome).K.


Did you use the Levsin as needed or 3x's per day everyday until the flare ups ended?It apppears from what I just viewed, the experts don't know if there is too much serotonin being released or not enough with degradation also being a possible factor...


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## Talissa (Apr 10, 2004)

rjc, I'm assuming you have diarrhea? Acc to this drug info, you shouldn't take levsin if you've got diarrhea(neither should peeps w/ UC)~http://www.healthsquare.com/newrx/lev1223.htmAlso, from Eric's post above, it says, "changes in mucosal serotonin handling support the concept that there is a gastrointestinal component to the aetiology of irritable bowel syndrome." This in my mind is another consequence of the submucosal inflammation of IBS. It's the handling of serotonin gone bad, due to the inflammation.


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## 15677 (Apr 8, 2006)

> quote:Originally posted by Talissa:rjc, I'm assuming you have diarrhea? Acc to this drug info, you shouldn't take levsin if you've got diarrhea(neither should peeps w/ UC)~http://www.healthsquare.com/newrx/lev1223.htm


I do have mild to moderate D sometimes only during flare up's, mostly just extra mucus production with gas and the GI MD knows this. Now after reading the warnings you've posted I'm wondering why he prescribed Levsin knowing I get mild D???


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## Talissa (Apr 10, 2004)

rjc, Maybe because its not chronic diarrhea. I'm sure he wouldn't Rx it if he thought it'd be dangerous.Re: what "they" know about serotonin~"...If these findings are indeed correct, they represent a landmark observation. The findings suggest that patients with constipation and IBS may have a reduced capacity to reuptake serotonin, leading to excess free serotonin and then desensitization of these receptors, thus reducing motor function. In contrast, in the setting of diarrhea, serotonin uptake was normal. If the underlying abnormality in serotonin transporter function alternated, then this would in turn explain alternating constipation and diarrhea. These data strongly suggest that IBS is a "real" gut disease and a potential diagnostic disease marker."http://www.medscape.com/viewarticle/444514ps, from the same article, re: IBS vs IBD~" IBD and IBS: Common Link?...Therefore, it may be difficult to distinguish these diseases unless colonoscopy and biopsy are performed. ...Therefore, it appears that the pain experience is similar in IBS and Crohn's disease and that using pain descriptors to differentiate IBS from IBD is unlikely to be effective. ...*In patients with IBS compared with active IBD, the symptoms were remarkably similar, suggesting that it can be difficult to differentiate IBD based on gastrointestinal symptoms alone."*


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## 15677 (Apr 8, 2006)

> quote:Originally posted by Talissa:rjc, Maybe because its not chronic diarrhea. I'm sure he wouldn't Rx it if he thought it'd be dangerous.________________________________________________True as it appears Levsin is being used my many with IBS D________________________________________________Re: what "they" know about serotonin~"...If these findings are indeed correct, they represent a landmark observation. The findings suggest that patients with constipation and IBS may have a reduced capacity to reuptake serotonin, leading to excess free serotonin and then desensitization of these receptors, thus reducing motor function. In contrast, in the setting of diarrhea, serotonin uptake was normal. If the underlying abnormality in serotonin transporter function alternated, then this would in turn explain alternating constipation and diarrhea. These data strongly suggest that IBS is a "real" gut disease and a potential diagnostic disease marker."http://www.medscape.com/viewarticle/444514ps, from the same article, re: IBS vs IBD~" IBD and IBS: Common Link?...Therefore, it may be difficult to distinguish these diseases unless colonoscopy and biopsy are performed. ________________________________________________Is a biopsy helpful in determing UC and CD or just UC?_________________________________________________...Therefore, it appears that the pain experience is similar in IBS and Crohn's disease and that using pain descriptors to differentiate IBS from IBD is unlikely to be effective. ...*In patients with IBS compared with active IBD, the symptoms were remarkably similar, suggesting that it can be difficult to differentiate IBD based on gastrointestinal symptoms alone."*


 ______________________Isn't life fun...______________________


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## eric (Jul 8, 1999)

This" This in my mind is another consequence of the submucosal inflammation of IBS. It's the handling of serotonin gone bad, due to the inflammation."Isn't correct however.Because these cells which are called ec or enterochromaffin cells are not inflammed, two different problems. The mast cells which can be macroscopically inflammed and release certain toxins onto the smooth muscle which can contribute to pain and can be triggered by chronic stress without a pathogen. The mast cells can also be triggered by foods, stress, heat, cold, and certain medications. They are also connected to irritable bladder.IN IBD conditions also you can get red flag symptoms, weight loss and malabsorbtion and others. The Rome Criteria has a high positive predictive value of 98% and a probablity of 100% as you saw RJC in the presenation.The calprotectin testing looks like its going to be very useful.and Clin Lab. 2005;51(3-4):117-26. Related Articles, Links Fecal leukocyte proteins in inflammatory bowel disease and irritable bowel syndrome.Silberer H, Kuppers B, Mickisch O, Baniewicz W, Drescher M, Traber L, Kempf A, Schmidt-Gayk H.University of Heidelberg, Germany.The aim of this prospective study was to compare five different leukocyte proteins in feces of patients with chronic inflammatory bowel disease (IBD), irritable bowel syndrome (IBS) and healthy persons who underwent prophylactic colonoscopy. METHODS: The leukocyte proteins calprotectin, lactoferrin, lysozyme, myeloperoxidase, and PMN-elastase were determined with immunoassays in fecal samples of three consecutive feces (e.g. three days) in 40 healthy persons, 39 patients with chronic IBD (of these 21 with Crohn's disease and 18 with ulcerative colitis), and 40 patients with IBS. RESULTS: ROC curves calculated for healthy persons and patients with IBD yielded the following areas under the curves (AUCs): PMN-elastase 0.916, calprotectin 0.872, myeloperoxidase 0.750, lysozyme 0.726, and lactoferrin 0.693. The AUCs of PMN-elastase and calprotectin were not significantly different (p = 0.327), whereas PMN-elastase or calprotectin vs. the other proteins were significantly different (p < 0.001). PMN-elastase and calprotectin correlated with the endoscopically classified severity of inflammation. All fecal leukocyte markers in IBS were found in the range of the healthy persons. Data on storage stability of leukocyte proteins in fecal supernatants are given. *CONCLUSION: Fecal PMN-elastase and calprotectin support the differentiation of chronic IBD from IBS and correlate with the severity of inflammation.*PMID: 15819166


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## eric (Jul 8, 1999)

FYI Nat Clin Pract Gastroenterol Hepatol. 2005 Feb;2(2):96-102. Related Articles, Links Technology insight: calprotectin, lactoferrin and nitric oxide as novel markers of inflammatory bowel disease.Lundberg JO, Hellstrom PM, Fagerhol MK, Weitzberg E, Roseth AG.Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden. jon.lundberg###fyfa.ki.seDistinguishing patients with inflammatory bowel disease from those with irritable bowel syndrome can be difficult. A simple and reliable test that detects intestinal inflammation would therefore be very useful in the clinic. If such a test parameter correlated with the intensity of the inflammatory reaction it could also be used to monitor disease activity. Calprotectin, lactoferrin and nitric oxide are produced and released locally in much greater quantities in the inflamed gut than in the noninflamed gut. These compounds can be readily measured in fecal samples (calprotectin and lactoferrin) or directly in the intestinal lumen (nitric oxide gas). Here, we discuss what is known about these markers, how they could be used in clinical practice and how they can complement existing techniques used for the diagnosis and monitoring of inflammatory bowel disease.Publication Types: ReviewPMID: 16265127


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## eric (Jul 8, 1999)

RJC here is another one for you.Report from the 6th International Symposium on Functional Gastrointestinal Disordershttp://www.iffgd.org/symposium2005report.html


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## 15677 (Apr 8, 2006)

> quote:Originally posted by eric:This" This in my mind is another consequence of the submucosal inflammation of IBS. It's the handling of serotonin gone bad, due to the inflammation."Isn't correct however.Because these cells which are called ec or enterochromaffin cells are not inflammed, two different problems. The mast cells which can be macroscopically inflammed and release certain toxins onto the smooth muscle which can contribute to pain and can be triggered by chronic stress without a pathogen. The mast cells can also be triggered by foods, stress, heat, cold, and certain medications. They are also connected to irritable bladder.IN IBD conditions also you can get red flag symptoms, weight loss and malabsorbtion and others. The Rome Criteria has a high positive predictive value of 98% and a probablity of 100% as you saw RJC in the presenation.The calprotectin testing looks like its going to be very useful.and Clin Lab. 2005;51(3-4):117-26. Related Articles, Links Fecal leukocyte proteins in inflammatory bowel disease and irritable bowel syndrome.Silberer H, Kuppers B, Mickisch O, Baniewicz W, Drescher M, Traber L, Kempf A, Schmidt-Gayk H.University of Heidelberg, Germany.The aim of this prospective study was to compare five different leukocyte proteins in feces of patients with chronic inflammatory bowel disease (IBD), irritable bowel syndrome (IBS) and healthy persons who underwent prophylactic colonoscopy. METHODS: The leukocyte proteins calprotectin, lactoferrin, lysozyme, myeloperoxidase, and PMN-elastase were determined with immunoassays in fecal samples of three consecutive feces (e.g. three days) in 40 healthy persons, 39 patients with chronic IBD (of these 21 with Crohn's disease and 18 with ulcerative colitis), and 40 patients with IBS. RESULTS: ROC curves calculated for healthy persons and patients with IBD yielded the following areas under the curves (AUCs): PMN-elastase 0.916, calprotectin 0.872, myeloperoxidase 0.750, lysozyme 0.726, and lactoferrin 0.693. The AUCs of PMN-elastase and calprotectin were not significantly different (p = 0.327), whereas PMN-elastase or calprotectin vs. the other proteins were significantly different (p < 0.001). PMN-elastase and calprotectin correlated with the endoscopically classified severity of inflammation. All fecal leukocyte markers in IBS were found in the range of the healthy persons. Data on storage stability of leukocyte proteins in fecal supernatants are given. *CONCLUSION: Fecal PMN-elastase and calprotectin support the differentiation of chronic IBD from IBS and correlate with the severity of inflammation.*PMID: 15819166


Thank you Eric. So just because a fecal test may show many leukocytes does that indicate any specific conclusion without a measure of calprotectin and pmn elastase and or perhaps lactoferrin? BTW my colonoscopy showed no visual inflammation; I was somewhat concerned the MD did not take a biopsy during the colonoscopy and did not go far enough to check the terminal ileum but he told me that my colon looked very healthy right after the procedure. What are your thoughts. Thanks


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## Talissa (Apr 10, 2004)

I was glad to take the calprotectin stool test in 2004. It was just good to know.Re:


> quote: This in my mind is another consequence of the submucosal inflammation of IBS. It's the handling of serotonin gone bad, due to the inflammation."Isn't correct however.


Actually, it's my opinion on a matter that acc to your original article, says the cause & effect hasn't been established yet~"We have searched and summarized relevant literature related to 5-HT signalling in the mucosa of the intestines under normal conditions and *changes in key elements of 5-HT signalling that have been reported in IBS and in response to inflammation.*...*The studies summarized here provide compelling evidence for a role for altered mucosal 5-HT signalling in IBS, as well as in IBD * and other GI disorders. While the data reported in these studies represent snapshots of 5-HT signalling in what are generally chronic conditions, it is clear that the sequence of events responsible for 5-HT signalling can be remodelled in response to various physiological and pathophysiological conditions. *Although the cause and effect relationship of these changes has not been established*..."http://www.medscape.com/viewarticle/528890_1Btw, they go on to say "One part of the picture that is missing is the status of 5-HT receptors in IBS, and also in IBD. *Similar to SERT, 5-HT receptor expression is dynamic and could be affected by the amount of 5-HT that is available and by other factors such as inflammatory mediators*..."***Also important to note is this research on previous research was *funded in LARGE part by Novartis Pharmaceuticals, the makers of Zelnorm, who are very interested in serotonin signaling(what zelnorm messes with)*. If they slant the article to the signaling problem rather than the inflammation causing the signaling problem, that -may- be why.Let the research continue...all answers aren't in yet, that's for sure!


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## 15677 (Apr 8, 2006)

> quote:So just because a fecal test may show many leukocytes does that indicate any specific conclusion without a measure of calprotectin and pmn elastase and or perhaps lactoferrin? BTW my colonoscopy showed no visual inflammation; I was somewhat concerned the MD did not take a biopsy during the colonoscopy and did not go far enough to check the terminal ileum but he told me that my colon looked very healthy right after the procedure.


Talissa I'd appreciate your opinion on this too. Thanks


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## eric (Jul 8, 1999)

RJC, there can be transient inflammation in everyday living or from meds or drinking or many reason.You should ask your doc the above question just to see what they say.Sounds like you had a normal colonoscopy though.RJC, did you know about Post Infectious IBS? Was that how you developed it?http://www.medscape.com/viewarticle/518355_print


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## Talissa (Apr 10, 2004)

rjc,I also had a clear colonoscopy and from a standard lab, a clear stool test for pathogens following antibiotic treatment for Giardia infection.However, the calprotectin test I took a few years later showed high inflammation. If I'd originally been biopsied along diff sections of the colon, this may have been established earlier.I've never been tested for fecal leukocytes. I imagine mine are high as well. I say this because I have bacterial imbalance, which was established when I took a more specialized type of stool test(which incl'd the calprotectin test).From what I've read about fecal leukocytes, they are more elevated in IBD than in IBS. They are present in elevated #s with enteric pathogens(mine are klebsiella & citrobactor), and also in "idiopathic" IBD. Idiopathic is defined as a medical adjective that indicates that a recognized cause has not yet been established.So, like you said earlier, I think you & I have simlar cases. High inflammation, dysbiosis, but not enough to cause IBD that shows up with a colonoscopy.Regardless of what it is though or what its called, you can treat it naturally with success. It just takes more personal effort to try the different dietary changes & supplements to find what works for you, more effort than taking an Rx.


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## 15677 (Apr 8, 2006)

> quote:Originally posted by eric:RJC, there can be transient inflammation in everyday living or from meds or drinking or many reason.You should ask your doc the above question just to see what they say.Sounds like you had a normal colonoscopy though.RJC, did you know about Post Infectious IBS? Was that how you developed it?http://www.medscape.com/viewarticle/518355_print


Thanks Eric. I'm not sure how I got this wonderful disorder it reared it's ugly head about 3 years ago, I am now in my mid forties. The first GI (he's the one that performed my colonoscopy) is adamant that I have IBS and feel's GI #2 is an alarmist as all the tests GI #2 administered have not come up with any concrete findings illustrating IBD vs IBS; except for elevated Leukocytes, which only occurs during flares. Everytime I mention the leukocytes to GI#1 he dismisses it indicating many things can cause them to elevate; he also says 2 of the fecal tests (I did 3) show "few"; vs. another showing "many". I have expalined to him that during a very bad flare is when "many" were shown. The calprotectins were never mentioned by either GI and I'd imagine they were part of the fecal tests but I'n not sure. I wish a biopsy was done during my colonoscopy to check for microscopic inflammation but since my colon looked so healthy GI#1 did not feel it was indicated. Couple of questions: Would a biopsy during the colonoscopy pick up CD or just UC or both?


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## 15677 (Apr 8, 2006)

> quote:Originally posted by Talissa:rjc,I also had a clear colonoscopy and from a standard lab, a clear stool test for pathogens following antibiotic treatment for Giardia infection.However, the calprotectin test I took a few years later showed high inflammation. If I'd originally been biopsied along diff sections of the colon, this may have been established earlier.I've never been tested for fecal leukocytes. I imagine mine are high as well. I say this because I have bacterial imbalance, which was established when I took a more specialized type of stool test(which incl'd the calprotectin test).From what I've read about fecal leukocytes, they are more elevated in IBD than in IBS. They are present in elevated #s with enteric pathogens(mine are klebsiella & citrobactor), and also in "idiopathic" IBD. Idiopathic is defined as a medical adjective that indicates that a recognized cause has not yet been established.So, like you said earlier, I think you & I have simlar cases. High inflammation, dysbiosis, but not enough to cause IBD that shows up with a colonoscopy.Regardless of what it is though or what its called, you can treat it naturally with success. It just takes more personal effort to try the different dietary changes & supplements to find what works for you, more effort than taking an Rx.


Thanks Talissa. I wish we had something else in common rather than this stuff, like we were billionaires and were trying to figure out how to spend our money







.Here's an interesting detail with regard to me. I have been using a topical antibiotic (erythromycin) for very slight adult acne, but I was told to use it everyday twice a day, I've been using it for more than 7 years+!! I just read the insert and found a warning that if one has UC etc not to use the product. Even though I've been taking a probiotic for the last year and a half I was using this stuff everyday! So I would imagine the probiotic was not doing much other than keeping the current bad level of flora as is vs being able to restore the good to appropriate levels! Since a week ago I am off the topical antibiotic and am hoping and praying this was a major factor. Do the probiotics need to be enterically coated to stay in tact in the stomach acids and what have you been using naturally to help you?Thanks


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## Talissa (Apr 10, 2004)

Billions? Sounds like fun!! A yacht? A chalet in Switzerland? A convertible BMW? No, better than all of these--fund all animal shelters so they could be no-kill, with soft clean beds for our furry friends! Oh the possibilities...I think we have something else in common--antibiotics did us in. I took antibiotics(tetracycline) for a year in my teens, & the year leading to IBS, antibiotics 3 separate times.Every type of topical antibiotic for acne has to carry the following warning~~"In view of the potential for diarrhea, bloody diarrhea and pseudomembranous colitis, the physician should consider whether other agents are more appropriate."They have to say that because dysbiosis, or bacterial imbalance, can occur. Low natural probiotic bacteria w/an overgrowth of facultive bacteria. Like what happened to me. Thank goodness you're stopping now. Better late than never. But unfortunately, just stopping the antibiotic probably won't be enough.You really need good probiotics. There are arguments for and ag enteric coating for probiotics, and now it looks like the DNA alone is what's needed so the probiotics don't even have to be alive. They just have to be there to begin with. Many brands aren't truthful w/ their labeling. I use nature's way primadophilus reuteri & florastor atm. Good results. They're also both clinically tested w/ good feedback in diff forums. Others have had good luck with other brands. You need to give them at least a month to work. And I firmly believe in taking more than the bottle says.I don't think I'll ever try SBO's like Primal Defense. Too many dirt variables and not enough clinical data.Fiber helps me greatly. It's more than just a bulking agent. It also helps reduce intestinal inflammation & create SCFA's which create butyrates, which help protect ag colon cancer...I've got great studies on these products if interested.But its just a matter of reading as much as possible, learning, and trying diff things out. No victims allowed, right?!







Talissa


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## 15677 (Apr 8, 2006)

> quote:Billions? Sounds like fun!! A yacht? A chalet in Switzerland? A convertible BMW? No, better than all of these--fund all animal shelters so they could be no-kill, with soft clean beds for our furry friends! Oh the possibilities...


 _______________________________________________________________________________________________________________________St Moritz in Switzerland is one of my favorite places on earth and I've ALWAYS wanted to help animals in a big way...don't get me started on cars, especially German one's which has always been a big weakness for me.GI#1 is big advocate of soluable fiber. I take Benefiber every morning with my low acid OJ, oatmeal, banana and vitamins. I found Citracel has sucralose or some other artificial sweetner in it; I've had to avoid all artificial sweetners and most dairy products since I was about 16; the artificial sweetners just kill me.I hope and pray (I do alot of that for both human's and creatures







)that stopping the topical erythro makes a big difference for me. I am now using Mega Flora brand probiotics which has 14 strains and a 20 billion count but it does not have the special coating. Should I use the Nature's Way primadophilus reuteri & florastor atm too? What about these flavanoids I've been reading about here?Thanks







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## CheckMyMath (Jun 15, 2015)

You all sound like just the folks to help check my math on my first health issue -- in my late 40s. Is this the right place to present a case?


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