# Post infectious colitis--result IBS



## cfro (Dec 28, 2006)

I am a 65 year old female with no problems before October of 2006 when I went to Africa and got a bacterial infection--was cleared up with Livaquin and everything was find until I got home. The D started with nausea and not wanting to eat. Went for a colonoscopy and the doctor (awful doctor) said I had ulcerated colitis and possibly Chrons and prescribed Asacol. I kept getting sicker and sicker--broke out in a rash and asked if I could be put on Flagyl (sp?) as I think I was alergic to the medicine. He took me off the Asacol and I went on Flagly for 15 days. Was finally feeling better and than he puts me on Colozal same ASA, but different delievery system. Anyway I finally went to a new GI and he said the colonoscopy was inconcusive for UC and ordered a blood test that determined that I did not have either.(75per cent accuracy). He gave the diagnosis as post infectious colitis and also gave my Xyflaxin. For the most part everything is fine as I have been taking the calcium pills which seem to help. I still get D and then cramping out of the blue after feeling fine for 2 weeks or more. Cannot figure what causes the flare. It also takes me days if not weeks to get back to a decent feeling again. Sorry this is so long, but I am wondering if this is going to continue and was it the infection that caused the IBS or was it the wrong medication for 5 weeks that caused the IBS. Will this go away since I am much older in getting this ailment? One more question--does anyone get a funny sensation in the inside of their mouth (cheeks)? Crazy I know!!! Thanks for any help. I was originally on the IBD board until I found I have the IBS D.


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## eric (Jul 8, 1999)

I am not sure about the funny sensation in the ceheeks, you have to ask your doctor about that one, although some meds can have effects.There is something called post infectious IBS.You might want to read this thread and the links. http://www.ibsgroup.org/forums/index.php?showtopic=89591Hope that helps and you recover.


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## cfro (Dec 28, 2006)

Thank you for your response and the link information. I was just wondering it anyone who has gotten IBS after infectious colitis has ever gone back to normal. Since this has happened so much later in life than most people that get this syndrome, if it could get better on it's own. Thank you--this is such a helpful forum.


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## newgirl60 (Jun 30, 2007)

Hi cfro,I also developed ibs d after acute gastritis following a trip to Mexico. Was on 2 antibiotics ( cipro and flagyl) that may have started problem by wiping out the good bacteria in my gut. I am 60 yrs old and was completely healthy before this. Physicians keep wanting more tests, etc for celiac disease and other problems but I am skeptical after over 2 years of this. Read online about post infectious ibs and am sure that is how this all started. No constipation only d and only at certain times. Can't figure food or emotional triggers so have been living on imodium, probiotics, and trying calcium. Calcium is helping but I still get flareups. Seeing a new gastroenterologist next month and taking tons of info with me from this and other sites. Since most patients start ibs at a young age there must be some link to having the severe gastriitis then starting symptoms. Hang in there and keep reading, these forums are very helpful


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## cfro (Dec 28, 2006)

Keep me posted on your progress with the new GI doc. I have thought several times I had my licked only to have it come back with a vengence. The calcium does help alot and I do the Activa and also have been taking some probotics. Cannot seem to figure out when I have a flare as for as foods go. However, it does take me quite awhile to get over a flare up. I can get the "D" under control, but the cramping stays for a while and the upset tummy. Still able to go on, but never feeling 100 per cent. I can not help but to think that if I had the right doc to start with that I could have gotten it under control alot faster. As you I was in perfect helath before I got the bacterial infection in Africa.Thanks for your reply.


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## MexicoWasn'tWorthIt (Jul 11, 2007)

Hi Newgirl60,You can find my posts but my issues started after a bug from Mexico and then same antibiotics--flagyl and cipro. I saw a gastro. I've seen in the past and am on Prevacid/Align (probiotic). I go in for an endoscopy next week. He thinks I have post infectious gastritis/IBS. The Prevacid should calm things down since I do have some heartburn w/ this and the Align should give me some good bacteria. I'll keep updating but so far all I feel is bloated and a bit constipated from the Align.Fun fun : (--Mexico--


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## eric (Jul 8, 1999)

I developed IBS from Post infectious IBS when I was ten and am now 46. Probably from e-coli, but they called it dysentary.I am posting this because I highly believe after tons reading IBS research, this information might help you both. Its also taking me a little bit of time to put it all together for you both.It is very complex however. "6th International Symposium on Functional Gastrointestinal Disorders""Demonstration of PI IBS as a brain gut axis disorder"http://www.iffgd.org/store/viewproduct/199It can be very important in the begining stages of PI IBS to do stress reduction and to calm the brain gut axis. You might have a better chance of recovery. IT is one of the things that can be part of developing PI IBS in the first place. Chronic stress, which is a threat to the organism either real or perceived, can cause permeability, but more importantly reactive inflammation. Stress and Diseasehttp://www.medicinenet.com/script/main/art...rticlekey=60918Stress, Health and Diseasehttp://www.cellscience.com/reviews6/Stress...th_Disease.htmlThis is called Psychoneuroimmunology.The stress system helps fight infections as well as well as its role in stress itself.In PI IBS they have found an increase of certain important cells. This is complicated and you might want to bring it to the doctor with you perhaps. One of those cells is called an enterochromaffin (EC) cells. The other is called a mastt cell.Distinctive Features of Postinfective Irritable Bowel Syndrome "Using conventional criteria, biopsy results for all patients were normal, but there were increased EC cells in the PI-IBS group compared with the non-PI-IBS group (P = .017) and with controls (P = .02). Lamina propria T lymphocytes were increased in PI-IBS (P = .026) and in non-PI-IBS (P = .011) patients compared with control patients, and mast cells were increased in non-PI-IBS patients (P = .054) compared with control patients."http://www.medscape.com/viewarticle/459230Relative importance of enterochromaffin cell hyperplasia, anxiety, and depression in postinfectious IBS.http://www.medscape.com/medline/abstract/14724817The enterochromaffin cells store the majority of serotonin in the gut. "Serotonin is directly involved in initiating the ENS-mediated peristaltic reflex"There is strong evidence that serotonin regulation from ec cells is a major part of d/c and d/c as well as its role in signaling pain to the brain.altered serotonin signaling and ibs compilationhttp://www.ibsgroup.org/forums/index.php?showtopic=80198Next is the mast cell. The bodies stress system is the HPA axis or Hypothalamic-pituitary-adrenal axis. That can activate mast cells in the gut. Part of that importantly is the fight or flight responce."FYI"You have two brains: one in your head and another in your gut. Dr. Jackie D. Wood is a renowned physiologist at The Ohio State University. He calls the second brain, "the-little-brain-in-the-gut." This enteric nervous system is part of the autonomic nervous system and contains over one hundred million neurons, which is as many as are in the spinal cord. This complex network of nerves lines the walls of the digestive tract form the esophagus all the way down to the colon. This little brain in the gut is connected to the big brain by the vagus nerves, bundles of nerve fibers running from the GI tract to the head. All neurotransmitters, such as serotonin that are found in the brain are also present in the gut.Dr Wood has discovered that this little-brain-in-the-gut has programs that are designed for our protection and which are very much like computer programs. They respond to perceived threats in the same way that the limbic system or the emotional brain does. So the threat of a gastrointestinal infection can activate the program that increases gut contractions in order to get rid of the infection. The symptoms are abdominal cramping and diarrhea. Dr. Wood has determined that a type of cell found in the body and the gut, *called the mast cell, is a key to understanding the connection of the big brain in the head with the little-brain-in-the-gut. Mast cells are involved in defense of the body. In response to certain threats or triggers, such as pollen or infection, mast cells release chemicals, such as histamine, that help to fight off the invader. Histamine is one of the chemicals that causes the symptoms of an allergy or a cold. When an infection of the gut occurs, such as food poisoning or gastroenteritis, the mast cells of the gut release histamine. The little-brain-in-the-gut interprets the mast cell signal of histamine release as a threat and calls up a protective program designed to remove the threat â€" at the expense of symptoms: abdominal pain and diarrhea. **The brain to mast cell connection has a direct clinical relevance for irritable bowel syndrome and other functional gastrointestinal syndromes. It implies a mechanism for linking allostasis and the good stress response to irritable states (e.g., abdominal pain and diarrhea) of the gut. Mast cells can be activated to release histamine in response to perceived psychological stress, whether the stressor or trigger is consciously perceived or not. So the end result is the same as if an infection activated the program in the-little-brain-in-the-gut: abdominal pain and diarrhea."*http://www.parkviewpub.com/nuggets/n5.html It is also worth reading my story. Gut directed HT has helped me tremendously and may help PI IBS at the begining stages. Although not a ton of research has been done on this yet with PI IBS a lot has been done on IBS itself, I know in the future it will take place.Part of this is breaking the vicious IBS cycle before it gets a chance to become embedded in the person. This will also boost your immune system, and reduce pain and attacks.Ponderings of an IBSerhttp://www.ibsgroup.org/forums/index.php?showtopic=35700I personally wish I would have known this a lot sooner in my life.


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## cfro (Dec 28, 2006)

Is the audio 100 that is mentioned in the link, the way to hypnosis or do you have to go to someone? I am a bit confused. I read all the links and since i am retired, I don't feel like I am in any stress condition, but than when I think about this condition, it does make me a bit anxious for sure. If this tape has worked for you, I would certainly like to give it a try.


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## betterthroughscience (Jan 13, 2006)

Dear cfro,Many people who have had symptoms like yours after an infection are able to re-establish the healthy balance of their intestinal tract and alleviate their symptoms. You are going to get all sorts of interesting advice. My best advice to you is to find a doctor who has a substantial track record of helping people to overcome their IBS and work with that doctor. Doctors don't like to admit that they don't know and there are huge numbers that keep focusing on the symptoms and the proximal issues, rather than looking at the whole system and how to return it to proper function.You will be told that IBS is just a stress problem and that the only thing to do is reduce stress. I do not advocate this point of view. There is usually a biochemical reason why your body is producing the symptoms. Often it can be uncovered with simple (but for some reason very rare) stool testing to determine what the ecosystem is like in your gut. Sometimes there is a parasite that is simply overlooked through lack of good testing. And your funny sensation in the cheeks could be a significant sign (to the right doctor).Best of luck.


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## eric (Jul 8, 1999)

Nobody what so ever should tell you IBS is caused by stress!Betterthroughscience however doesn't understand or care about the stress to mast cell conection, which can generate more macroscopic inflammation of mast cells which then release histimine unto the smooth muscle of the colon and inflammes the tissue there locally, which can contribute to pain and the continual bidirectional communication between the gut and the brain that keeps you safe. The tissue is irritated and the brain see's it as a threat and continues to downregulate via in part the immune system to go after it. That is part of the bodies stress systems function in all people.So betterthrough science, stress does not cause biochemical reactions?Physician's Weekly Article - Irritable Bowel Syndrome "IBS was once considered a catch-all diagnosis in situations where physicians were unable to make a complete and accurate diagnosis," says Dr. Drossman.""Three physiological mechanisms may potentially be involved in the development of IBS symptoms: impaired motility throughout the gastrointestinal tract, increased visceral sensitivity, and impaired intestinal secretion. These abnormalities in the gut may be related to breakdown in communication along the brain-gut axis and to alterations in the levels or function of serotonin-5-hydroxy-tryptamine (5-HT)-a naturally occurring signaling molecule. * "We're moving away from just treating the symptoms of IBS and we're now focusing on attacking the mechanism of action," *says Dr. Drossman. "While anti-diarrhea medication and fiber can still help treat symptoms, the newer agents on the market are engineered to act at receptors of the gut in order to modify functioning of the mucosal bowel. We now have 5-HT3 antagonists that reduce the amount of serotonin activity, slow diarrhea, and reduce pain. 5-HT4 receptor agonists are also available and increase the activity in the bowel to treat constipation. Psychological interventions and antidepressants are also playing a critical role in treatment of IBS because they work at the central perceptual level to reduce disease symptoms." Other agents to treat IBS are also under investigation, adds Dr. Drossman. "A class of potential visceral analgesics called the tachykinin receptor antagonists are being evaluated in the treatment of IBS. *Corticotropin releasing hormone (CRH) helps mediate stress responses in the brain-gut axis and there is evidence that suggests this hormone can improve gastrointestinal motility, visceral perception, and negative moods."* Dr. Drossman says there is greater interest in looking at centrally active agents for the treatment of IBS in the future. "We need to further evaluate CRH antagonists and the newer antidepressants in order to see if these agents can be added to the treatment armamentarium. While there will never be one universal drug that effectively treats IBS, the hope is that we'll be able to control as many of the mechanisms as possible in order to effectively manage the disease and improve our patients' quality of life."http://www.physiciansweekly.com/article.as...;articleid=1703


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## eric (Jul 8, 1999)

CfroI personally used the tapes and lot of others have used them on this forum. You can also ask questions there as well and get any help you need both on seeing one in person or using the home program. These are gut specific though for IBS and have other benefits as well to them.http://www.ibsgroup.org/forums/index.php?showforum=9I reread what you orginally posted again and its just hard for anyone to answer some of those questions, sometimes you have to wait and see what happens and do your best to get yourself well.Taking probiotics would be a good thing especially ones with a certain strain I will look it up for you.It was probably the intial infection that started the IBS.The condition itself puts a person into threat mode, will I have d or pain or be consitpated along with worry antisipatory anxiety, anxiety and negative reaction to the symptoms themselves all qualify as stressors. There can also be physical stressors such as hot and cold, humidity and other outside sources. There is also good stress excitement even. Not all stress is bad though.This is some more info. Once again I know this is all complex, but you can also just bring it to the doctor with you perhaps. These are top PI IBS Research experts. This is a little dated and more has been learned since this was written.With Permission from the The UNC Center for Functional GI & Motility DisordersPOST INFECTIOUS IRRITABLE BOWEL SYNDROMERobin C. Spiller, MD Reader in Gastroenterology at the University Hospital, Nottingham, UK An important subgroup of patients with Irritable Bowel Syndrome describe a previously entirely normal bowel habit with all their symptoms developing immediately after an acute bout of diarrhea and vomiting. This phenomenon has been recognized by clinicians for many years and was well described by Truelove and Chaudary who studied 130 patients with Irritable Bowel Syndrome, 34 of whom were described as having post-infective IBS. Most of the infections were bacillary dysentery but some were amoebic. Interestingly, they found there was an important interaction between psychological problems and infection. They found that a post-infectious origin and absence of anxiety, depression or neurotic features both predicted a good outcome. The commonest causes of gastroenteritis are viral, followed by Campylobacter, Salmonella and Shigella. Viral gastroenteritis typically heals rapidly with little residual injury, while the bacterial infections often produce ulceration and bleeding. They are generally associated with more prolonged illness and it is these infections which have been associated with post-infective Irritable Bowel Syndrome. The first prospective study was reported by McKendrick(1)who studied 38 individuals following a salmonella outbreak. He found that 11 out of the 38 met the Rome I criteria for IBS 6 months after the initial illness. Two further prospective studies of hospitalized patients from an infectious disease unit in Sheffield also confirmed this high incidence of post-infective IBS(2,3). Our own study of 386 cases of bacterial gastroenteritis obtained from a community survey showed a lower incidence of post infective IBS (7%) possibly reflecting a less severe illness, since only 1 in 10 of these patients were hospitalized However these were not trivial illnesses since the average duration of illness was 7 days with a third reporting bloody diarrhea and a median weight loss of 6kg. Interpreting this data requires knowledge of the normal incidence of new IBS, as was obtained in a large survey based on the British general practice database. This study of 584,308 patients found the incidence of new IBS per annum in non-infected patients to be 0.35%. However, in 300 patients who had a culture positive infectious gastroenteritis, the annual incidence was 4% giving a relative risk of 11.9% 95% CI (6.9-21)(4). Traveler's diarrhea is of course extremely common in Canadian citizens traveling to Mexico and Ilnyckyj prospectively surveyed this group. Nearly 50% developed travelers diarrhea and in this group the incidence of new IBS three months later was 17.5% compared with just 2.7% for those who did not get travelers diarrhea, a relative risk of 6.6(0.8-53)(5). RISK FACTORSMost patients with bacterial gastroenteritis recover fully and only a small minority develop post-infective Irritable Bowel Syndrome. Female sex, hypochondriasis and adverse life events in the previous year all give an increased risk(6,7)with a relative risk of 3.4, 2.0 and 2.0 respectively. A much stronger risk factor is the duration of the initial illness, with a steadily increasing relative risk for each week of illness, reaching 11.4 for those with diarrhe a lasting more than 21 days. Bacterial factors are likely to be important http://www.med.unc.edu/ibsThe UNC Center for Functional GI& Motility Disorderssince we found around 1 in 10 of Campylobacter infected individuals developed post-infective IBS compared with just 1 out of 100 with Salmonella. It is likely therefore that the severity of tissue damage and ulceration is a major predictor. PATHOPHYSIOLOGYDiarrheal illnesses are characterized by accelerated GI transit and increased gut sensitivity. This gradually returns to normal but at a variable rate. By three months most of those who are going to recover will have done so and thereafter the rate of recovery is much slower. As Gwee found colonic transit is accelerated in all infected individuals at 3 months, but those who meet the Rome I criteria for IBS have a faster transit than those who do not. Similarly rectal sensitivity is increased in those meeting Rome criteria, though again all those infected show a similar trend. Although conventional histological examination of mucosal biopsies in IBS shows no abnormality, when detailed quantification is undertaken changes are noted. We performed serial rectal biopsies in individuals recovering from Campylobacter gastroenteritis at 2, 6, 12 and 52 weeks. We note initial increases in both inflammatory cells and enteroendocrine cells, which mostly returned towards normal, but remained abnormal in a few markedly symptomatic individuals(8). Similar abnormalities were noted in patients attending the outpatients with a history of post-infectious Irritable Bowel Syndrome. There is a good correlation between the inflammatory cells and the enteroendocrine cells suggesting that cytokines might drive the enteroendocrine cell hyperplasia. The main content of the enteroendocrine cells is 5HT, an agent that stimulates peristalsis and intestinal secretion causing diarrhea in normal subjects. Drugs, which inhibit the action of 5HT such as Alosetron, are likely to show benefit in this group thought they have not been specifically studied. Other authors have noted increased enteroendocrine cells in unselected irritable bowel patients(9)but this needs confirmation. *More important than increase in numbers may be the increase in release of 5HT. Several pilot studies(10)including some reported at DDW this year suggested that there was an exaggerated release of 5HT following a meal particularly in those who got meal related symptoms(11). *MANAGEMENT*It is important that patients should understand the important roles of anxiety, stress, and diet and persisting low-grade inflammation in this condition*. Providing the Rome criteria are met and general physical examination is normal then the probability of another diagnosis is low. However, infections can unmask other disease particularly coeliac disease, inflammatory bowel disease such as Crohn's and tropical sprue together with hypolactasia. Such patients should therefore undergo a minimum set of screening tests including endomysial antibodies, hemoglobin, CRP, ESR, albumin and stool culture. In the absence of alarm features such as weight loss, fever, rectal bleeding and nocturnal diarrhea, only 5% of all these tests will be abnormal. Since microscopic colitis has also been reported to develop acutely after an infectious illness it is important to do a colonic biopsy and, if suspicions are high, also a duodenal biopsy to exclude coeliac disease. Lactose intolerance developing after a viral gastroenteritis is well recognized by pediatricians. This occurs because lactase, the enzyme responsible for digesting lactose, is expressed fully only in the mature enterocyte at the tip of the villus. Since viral gastroenteritis generally specifically damages the villi, lactose levels remain low for some months. *A low lactose diet is therefore worth trying, particularly in those racial groups with an a priori greater risk of lactose intolerance such as Asians, Africans and Chinese. A low lactose diet is only relevant if the subjects take more than 240mls of milk. Even those with documented lactose intolerance can tolerate amounts smaller than this when spread throughout the day. **Since psychological factors are so important, it is necessary to make some formal assessment of this.* Where anxiety and depression levels are high they should be treated on their own merits since it is unlikely the patient will recover without addressing these issues. *There are no specific diets recommended for post infective IBS but reduction of poorly absorbed carbohydrates, particularly wheat, potatoes together with other items such as citrus fruits have been reported to be beneficial in patients with diarrhoea-predominant IBS and should be tried*(12). Loperamide and codeine are well tried treatments for diarrhea predominant IBS regardless of origin and are likely to be effective though at the risk of some side-effects, including sedation and nausea in the case of codeine and abdominal pain in the case of Loperamide. Alosetron has also been reported to be effective in diarrhea predominate IBS but again has not been specially tried in post infective patients. *PROGNOSISWhatever treatments are offered, the clinician can afford to be reassuring since the prognosis is relatively good. Chaudary's original study found 77% had recovered within 2 years(13)while Harvey also found 82% of those with acute illness at onset had recovered by 5 years(14). In our own follow-up 5 to 6 years following the initial survey we found that 11 out of 17 post infective Irritable Bowel Syndrome patients had actually recovered though we also noted that a past history of psychiatric disorder predicted a poor outcome. *KEY POINTS•Post infective Irritable Bowel Syndrome accounts for around 1 in 10 of all cases of IBS. •Females with prolonged illnesses and previous adverse life events are more likely to develop post-infective IBS. •Low-grade inflammatory changes may persist in some of these patients. •Overall prognosis is good with 2 out of 3 recovering over a period of 3-5 years. Reference List 1.McKendrick MW,.Read NW. Irritable bowel syndrome - Post salmonella infection. Journal of Infection 1994;29:1-3. 2.Yeoh KG, Kang JY, Tay HH, Gwee KA, Tan CC, Wee A et al. Effect of Cisapride on functional dyspepsia in patients with and without histological gastritis: a double-blind placebo-controlled trial. J. Gastroenterol. Hepatol. 1997;12:13-8. http://www.med.unc.edu/ibsThe UNC Center for Functional GI& Motility Disorders3.Gwee KA, Leong YL, Graham C, McKendrick MW, Collins SM, Walters SJ et al. The role of psychological and biological factors in postinfective gut dysfunction. Gut 1999;44:400-6. 4.Rodriguez LA,.Ruigomez A. Increased risk of irritable bowel syndrome after bacterial gastroenteritis: cohort study. BMJ. 1999;318:565-6. 5.Ilnyckyj A, Choudri SH, Duerksen D. Association of travel related diarrhea(TD) with irritable bowel syndrome (IBS): Is post-infectious IBS a true entity? Gastroenterology 1999; 116:A1011-A1011. 6.Neal KR, Hebden J, Spiller R. Prevalence of gastrointestinal symptoms six months after bacterial gastroenteritis and risk factors for development of the irritable bowel syndrome: postal survey of patients [see comments]. BMJ. 1997;314:779-82. 7.Gwee KA, Graham JC, McKendrick MW, Collins SM, Marshall JS, Walters SJ et al. Psychometric scores and persistence of irritable bowel after infectious diarrhea Lancet 1996;347:150-3. 8.Spiller RC, Jenkins D, Thornley JP, Hebden JM, Wright T, Skinner M et al. Increased rectal mucosal enteroendocrine cells, T lymphocytes and increased gut permeability following acute Campylobacter enteritis and in post-dysenteric irritable bowel syndrome. Gut 2000;47:804-11. 9.Bose M, Nickols C, Feakins R, Farthing MJG. 5-hydroxytryptamine and enterochromaffin cells in the irritable bowel syndrome. Gastroenterology 2000;118:A563. 10.Bearcroft CP, Perrett D, Farthing MJ. Postprandial plasma 5-hydroxytryptamine in diarrhea predominant irritable bowel syndrome: a pilot study. Gut 1998;42:42-6. 11.Houghton LA, Atkinson W, Whitaker P, Whorwell PJ, Rimmer M, Fricker J et al. A role for 5-hydroxytryptamine (5-HT) in the postprandial exacerbation of symptoms in femal patients with diarrhea predominant irritable bowel syndrome. Gastroenterology 2003;120:A-67. 12.Parker TJ, Naylor SJ, Riordan AM, Hunter JO. Management of patients with food intolerance in irritable bowel syndrome: The development and use of an exclusion diet. Journal of Human Nutrition & Dietetics 1995;8:159-66. 13.Chaudary NA,.Truelove SC. The irritable colon syndrome. Quart.J.Med. 1962;123:307-22. 14.Harvey RF, Maudad EC, Brown AM. Prognosis in the irritable bowel syndrome: a 5 year prospective study. Lancet. 1987;1:963-5.


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## cfro (Dec 28, 2006)

Thank you so very much for posting the information. I am going to order the Audio as I cannot help but think it could only help. Also, I was encouraged that PI IBS was found in the one study to improve over time or was that wishful thinking))As I mentioned in a previous post, it is not bad "D", but it does take it out of me as it does seem to upset my entire system. The cramping I get comes after the "D" not before and that too is not severe. This forum is just so helpful.


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## cfro (Dec 28, 2006)

Thank you for your reply. I have had alot of stool testing done as the original thought was that it was a parasite of some sort esp. since I had been to Africa. I have been to several doctors and this last GI seems to be fairly good, but I don't think really has any more answers than what has been on this BB. There just doesn't seem to be any reason when I do get a flare up which drives me crazy as I have been very careful of what I eat.


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## eric (Jul 8, 1999)

Cfro, I type out a post and lost it.So this is the shorten version. I really believe that the tapes will help you and hopefully help you fully recover. They help work on brain gut communications and a side effect is anxiety at a deep level. They are also safe with basically no side effects. It is very much worth a shot at it with this approach. Any relaxation techniques, but Gut directed HT is a deeper approach to this.I would also take probiotics with these strains. Lactobillus salivaris and Bifidobacterium infantis"Anti-inflammatory Effect of ProbioticsNumerous studies have shown an anti-inflammatory effect but the study by McCarthy et al.[30] is of particular interest since it showed a benefit in the interleukin-10-knockout mouse model of colitis using two probiotic bacteria, Lactobillus salivaris and Bifidobacterium infantis, which have since been used in IBS patients (see below). The same group also demonstrated that bacteria did not need to be living to be effective. Nor did they need to be administered orally but could be effective when given subcutaneously,[31] showing that the anti-inflammatory effect is systemic with a generalized decrease in proinflammatory cytokines."http://www.medscape.com/viewarticle/518355_printThe above link is newer PI IBS information then my last post. Its updated.I would also be careful of taking any otc nasids or any med or OTC that can cause irritation. You might talk to your doctor about this if you are on anything or taking any otc's.Anything that is irritating.


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## cfro (Dec 28, 2006)

Again, thank you for the information. I was wondering if you had tried the 5-hydroxy-trytamine that one of the links mention to increase the seratonin? What do you mean by the nasids? Right now I am taking just the calcium. Looking forward to trying these tapes.


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## eric (Jul 8, 1999)

Actually the problem is the release of serotonin from specific cells in the gut, that signal via serotonin to the brain and back as well as intiate gut contractions.So its not an amount problem, but regulation problem.Taking 5ht can increase or drcrease anxiety but cause more bowel problems.Nasids are like aleve or nanoproxen. Taking calcium shouldn't be a problem, calcium can also help nerve signaling.Hope that helps


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## MexicoWasn'tWorthIt (Jul 11, 2007)

I need to go back and read through what Eric posted on the PI IBS (thank you!). But I wanted to quickly update. I've been on Prevacid for a little over a mth and the Align (probiotic from the gastro.) for a little over a week. The first days on Align made things worse--much more bloating/gas/a bit of constipation.However, I've noticed significant improvement the past couple of days. The only thing that has changed is a little more time on Prevacid and starting the Align. I have an endoscope scheduled for Wednesday and will update after this. I am starting to feel more optimistic though and ordered three months worth of the probiotic!







-Mexico-


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## cfro (Dec 28, 2006)

I have one more question (at least for now)--what brand name carries the bacteria strains that you mention.? I had a flare yesterday, but I seem to be better today, so the flares seen to be getting shorter. I am in hopes that the hp will help and this will all go away in time or at least get to the point where I am dealing with it better. Thanks again!!!!


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## eric (Jul 8, 1999)

Mexicowasn't worth it.Good to hear your feeling a little better. Keep plugging away at it, but like I said its benefical to reduce stressors. They are so deep it can be conciously percevied or even not conciously perceived. Threats to the organism that trigger the fight or flight reponce.Cfro, I honestly am not exactly sure, you might create another post and ask on the main forum here or the probiotics forum.


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## eric (Jul 8, 1999)

This is new on this again from Dr Spiller Curr Treat Options Gastroenterol. 2007 Aug;10(4):312-21. LinksIrritable bowel syndrome: bacteria and inflammation--clinical relevance now.Spiller RC.Robin C. Spiller, MB BChir, MSc, MD Wolfson Digestive Diseases Centre, University Hospital, Nottingham, NG7 2UH, England. [email protected] bowel syndrome (IBS) is a ubiquitous but heterogeneous syndrome characterized by abdominal pain and erratic bowel habits that affects 5% to 10% of the population. Although current definitions specify that there are no structural or biochemical abnormalities to account for the symptoms, there is growing evidence that in at least a subset of IBS patients, there is low-grade inflammation characterized by increased T lymphocytes and mast cells. Whether this is cause or effect is uncertain, as *there is also clear evidence of bidirectional communication between the immune and nervous systems, and at least some of the mucosal changes could be secondary to psychological stress. A small percentage (6%-17%) of patients develop IBS symptoms for the first time after an acute episode of infective gastroenteritis (postinfective IBS), which appears to be directly responsible for low-grade immune activation. However, even in this group, preexisting psychological factors are as important as mucosal ones. Specific anti-inflammatory treatments have not been systematically evaluated, but there is no evidence of benefit currently.*PMID: 17761124


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## eric (Jul 8, 1999)

This is also extremely newThis is in medscape and you have to register and suplly a password, but its free, they have an excellent IBS resource center and they don't sapm you when you sign up.Systematic Review and Meta-Analysis: The Incidence and Prognosis of Post-Infectious Irritable Bowel SyndromeSummaryBackground: Individual studies suggest that post-infectious irritable bowel syndrome is common, but symptoms gradually improve.Aim: To review evidence for an association between intestinal infection and development of irritable bowel syndrome, assess the prognosis of post-infectious irritable bowel syndrome and explore factors that increase the risk.Methods: MEDLINE (1966-2007) and EMBASE (1980-2007) databases were searched to identify the studies of post-infectious irritable bowel syndrome epidemiology. Data were extracted by two independent reviewers. Pooled odds ratios (POR) and corresponding 95% CI for incidence of irritable bowel syndrome were estimated among the exposed and unexposed groups.Results: Eighteen of 26 studies identified were eligible for inclusion. Intestinal infection was associated with increased odds of developing irritable bowel syndrome at study end (POR = 5.86; 95% CI: 3.60-9.54). In subgroup analysis, the odds of developing irritable bowel syndrome was increased at 3 months (POR = 7.58; 95% CI: 4.27-13.45), 6 months (POR = 5.18; 95% CI: 3.24-8.26), 12 months (POR = 6.37; 95% CI: 2.63-15.40) and 24-36 months (POR = 3.85; 95% CI: 2.95-5.02). Among all studies (controlled and uncontrolled), the pooled incidence of irritable bowel syndrome at study conclusion was 10% (95% CI: 9.4-85.6). Subjects with post-infectious irritable bowel syndrome were younger and more anxious and depressed than those without post-infectious irritable bowel syndrome.Conclusion: The odds of developing irritable bowel syndrome are increased sixfold after acute gastrointestinal infection. Young age, prolonged fever, anxiety and depression are risk factors for post-infectious irritable bowel syndrome.Summary and IntroductionMaterials and MethodsResultsDiscussionFiguresTablesReferencesRelated Links"DiscussionThe findings of this systematic review are consistent with those of individual published studies of PI-IBS, and also with the systematic review by Halvorson et al.[26]. We have demonstrated a strong association between intestinal infection and development of symptoms consistent with IBS. A pooled estimate from nine published prospective studies suggests that the odds of developing IBS are increased about sixfold after acute gastrointestinal infection and remain significantly increased for up to 3 years. The estimated incidence of IBS after enteric infection is 10% (95% CI: 9.4-85.6).*This review supports the previously observed association between PI-IBS and psychological disturbance. Indeed, a recent landmark study by Spence and Moss-Morris[35] suggests that combinations of psychological profiles such as emotion, cognitive and behavioral profiles are significant risk factors for development of IBS after GE, and support an interactive model of biology and psychology in the onset of IBS. While intestinal infection may trigger the initial symptoms, cognition, behaviour and emotions may help prolong and maintain them over time*.[35]We have confirmed an association between increasing risk of PI-IBS and younger age. Evidence from this review suggests that subjects who develop PI-IBS are younger than those who do not. In part, this difference could be explained by the age gender effect. Many functional disorders including bloating and constipation are more common among females, and could be partially attributed to gender-specific factors such as circulating female sex hormones and changes in rectal sensitivity during menstrual cycles.[36-38] Furthermore, the increased prevalence of psychological distress among young women can also contribute to functional presentations.[35,39-41]The nature of the acute gastrointestinal illness may be an important determinant of PI-IBS risk. We found that prolonged fever during acute gastroenteritis increased the risk of PI-IBS, perhaps as a marker of illness severity. Associations between microbial virulence factors and subsequent development of IBS have been previously described.[16,27] Most recently, Soyturk et al.[42] demonstrated an association between a parasite trichinella infection and development of IBS in humans. However, most such studies have considered differences within species rather than differences among a spectrum of pathogens. Halvorson et al.[26] demonstrated in their meta-analysis that the risk of PI-IBS was increased with bacterial vs. non-bacterial pathogens, and that bacterial dysentery is more likely to be associated with fever, diarrhoea abdominal pain and vomiting.[41] We did not find significant association between increasing risk of PI-IBS and duration of diarrhoeal illness, but we may have been underpowered to detect an effect as not all studies assessed this risk factor. Our pooled estimates were based on univariate analysis reported by individual studies and do not control for potential confounders.When interpreting the results of this review, certain limitations need to be taken into account. Because studies of PI-IBS are initiated after exposure to an enteric pathogen, they rely heavily on participants" recollection of their previous gastrointestinal symptoms and their episode of acute infection. In fact, the time interval from exposure to data collection among these studies ranges from 3 months[13,18,21] to 2 years.[23] Recall bias can misclassify both cases and controls, as people with more severe chronic symptoms are more motivated than controls to recall exposure and may exaggerate its intensity[43] and overestimate risk. We observed no association between recall interval and risk of PI-IBS, but may have been underpowered to detect such an effect. Future studies should strive to initiate data collection immediately after exposure, and to access public health and primary care health records to confirm details of acute and antecedent illness. Prospective designs that enroll cohorts before infection, such as that by Ilnyckyj et al.[18], may circumvent this problem but face other methodological challenges such as high drop rates out and non-response.Some studies included in this review recruited patients with enteric infection from public health or general primary healthcare databases based on positive stool culture. Although this approach is convenient and offers the most reliable approach to confirming exposure to infection, it could suffer from ascertainment biases because of differences in reporting and/or healthcare access. Patients who take time to submit stool cultures or consult a physician for acute infection may not be representative of the broader population who suffer enteric infection. If patients with severe illness are disproportionately likely to seek health care and submit stool samples, the risk of PI-IBS could be inflated. Furthermore, at least one study has suggested that patients with premorbid IBS are more likely to seek health care for acute gastroenteritis.[19] Without careful assessment of premorbid functional symptoms, this phenomenon will also serve to overestimate the risk of PI-IBS.The estimated incidence of IBS can vary substantially depending on the criteria used to define the disorder. For example, Rome II criteria are more restrictive and yield lower estimates of prevalence than Rome I or Manning.[44,45] Rome II criteria require both abdominal pain and changes in bowel habit lasting 12 weeks over 12 months, while Rome I consider abdominal pain and changes in bowel habit independently. Among studies assessed in this review, the incidence of PI-IBS ranged from 3% to 14% among studies that used Rome II criteria, vs. 16% to 32% among those that used Rome I criteria (excluding Ilnyckyj et al., who reported 4%). The recent Rome III criteria may also be less restrictive than Rome II, as they require only 6 months of symptoms (active for at least 3 months).[46] To date, no study of PI-IBS has used Rome III criteria.Eight of the 18 studies included in this review did not assess a control group (see Table 1 ) and hence do not allow estimation of attributable risk. Seven of the 10 controlled studies selected both exposed and unexposed subjects from the same population. This approach has methodological merits because controls are better compared with cases on potential confounding factors and allows exposed cases to be compared with those of their source population, with controls having the same opportunity to develop the disease and are representative of the exposure distribution in that population. Two controlled studies matched controls from a research database. This approach is convenient and inexpensive and reduces observer bias as exposure and outcome data are collected independent of any specific hypothesis. It would be ideal for future studies to use multiple control groups to estimate attributable risk, but this approach is complex, costly and rarely feasible. In summary, this review supports the strong association between acute gastroenteritis and new onset of IBS. However, we also identify strengths and limitations of study design that should provide direction to future research. There remains much to understand about the risk factors and mechanisms that lead to PI-IBS, so that we can better prevent and treat this common phenomenon."http://www.medscape.com/viewarticle/561853_4


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