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Our poor confuse Tal, who is clearly not up to date on IBS research.This is from 97, since then they have found it is not a biological marker IN ALL IBSErs.although when this was posted, it was thought it maybe one.Now they know somewhere between 80 to 90 percent have rectal hypersensitvity.They also thought the brain activation was also, but the jury is still out on that.Breakthroughs in IBS research."By using sophisticated imaging techniques that allow us to visualize the activity of the living human brain (see �Looking Into the Living Human Brain�), researchers at the UCLA Neuroenteric Disease Section have recently identified for the first time the regions within the brain that are involved in the perception and modulation of visceral sensations, including visceral pain. In addition, by comparing brain responses to an acute intestinal stimulus between healthy control subjects, patients suffering from IBS, and patients with ulcerative colitis, they were able to identify specific alterations in how the brains of IBS patients process and respond to acute colonic pain. These research results have recently been published in Gastroenterology. This is the first study which has been able to identify an objective biological marker that is only seen in IBS patients and that is located within brain regions, which are likely to be involved in the alterations in perception and autonomic responses that underlie the most common IBS symptoms. These findings are the first step in a better understanding of how these symptoms develop and how we can treat them by identifying specific targets for pharmacological therapy. The most prominent brain region found to be activated in response to intestinal stimulation in healthy subjects was a specific area within the anterior cingulate cortex which forms part of the limbic system. The limbic system, which has also been referred to as the �visceral cortex� plays a prominent role in a wide range of functions�from maintaining homeostasis, to autonomic control of the digestive system, to pain perception to the generation of feelings and emotions, and to memory of past emotional states. The specific area within the anterior cingulate cortex identified in the brain imaging studies plays a prominent role in several aspects relevant to IBS symptoms: 1. It is the �executive area� in the regulation of colonic motility and water absorption which in turn determines the frequency and consistency of bowel movements. 2. It is part of the medial pain system which determines the affective component (i.e. the degree of suffering or unpleasantness) associated with pain perception. Specific regions with the medial pain system play an important role in suppressing the perception of pain by releasing endorphin molecules (the body�s own painkillers), while other regions participate in the memory formation of past painful experiences. 3. The brain region identified by the UCLA researchers plays a prominent role in the regulation of maternal behaviors and is crucial for mediating communication between newborns and their mother. The results of this study have wide ranging implications for all patients suffering from IBS. The findings for the first time have established IBS as a biological disorder, which can no longer be labeled psychological or �not real� by the healthcare system. The current results are the basis for future research efforts delineating the networks and receptors within the brain that are responsible for such IBS symptoms as abdominal pain and discomfort, sleep disturbance, and altered bowel habits. A range of brain imaging studies are currently underway at UCLA which aim at unraveling these mechanisms. Brain regions and receptor systems identified by functional brain imaging studies are likely to become targets for new drug developments in the near future. " http://www.cns.med.ucla.edu/Articles/Patie...eakthroughs.htm although when this was posted, it was thought it maybe one.Now they know somewhere between 80 to 90 percent have rectal hypersensitvity.To date no biological marker has been found in all IBSers.Nor is rectal hypersensitvity even cosistent with Dysbiosis.Nor is incomplete evacuation.and just fyi, they use HT to study this.Gut. 2002 Nov;51(5):701-4. Related Articles, Links Visceral sensation and emotion: a study using hypnosis.Houghton LA, Calvert EL, Jackson NA, Cooper P, Whorwell PJ.Department of Medicine, University Hospital of South Manchester, Manchester M20 2LR, UK. lahoughton###man.ac.ukBACKGROUND AND OBJECTIVES: We have previously shown that hypnosis can be used to study the effect of different emotions on the motility of the gastrointestinal tract. These studies demonstrated that both anger and excitement increased colonic motility while happiness led to a reduction. The purpose of this study was to investigate the effect of hypnotically induced emotion on the visceral sensitivity of the gut. METHODS: Sensory responses to balloon distension of the rectum and compliance were assessed in 20 patients with irritable bowel syndrome (IBS) (aged 17-64 years; 17 female) diagnosed by the Rome I criteria. Patients were studied on four separate occasions in random order either awake (control) or in hypnosis, during which anger, happiness, or relaxation (neutral emotion) were induced. RESULTS: Hypnotic relaxation increased the distension volume required to induce discomfort (p=0.05) while anger reduced this threshold compared with relaxation (p0.05), happiness (p0.01), and awake conditions (p0.001). Happiness did not further alter sensitivity from that observed during relaxation. There were no associated changes in rectal compliance or wall tension. CONCLUSIONS: Further to our previous observations on motility, this study shows that emotion can also affect an IBS patient's perception of rectal distension and demonstrates the critical role of the mind in modulating gastrointestinal physiology. These results emphasise how awareness of the emotional state of the patient is important when either measuring visceral sensitivity or treating IBS.Publication Types: Clinical Trial Randomized Controlled Trial PMID: 12377810FACT!!!!!!!!!!!!!!!!!!!!!!!!!!!! To date no biological marker has been found in all IBSers. You need to do more studing, you have no idea what your talking about, that twice today, you have been very wrong.
 

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I'm glad you agree that outdated info is useless, when new info is coming out virtually every month.But I would like to know what you think abt what Hunter and Spiller said from my previous post...But while biological markers are imp to you and your experts, here's something you should know~Gastroenterology. 2002 Jun"Visceral hypersensitivity was detected in patients with functional gastrointestinal disorders and has been proposed as a biological marker of irritable bowel syndrome (IBS). " http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12055583 So apparently, there being no bio markers in IBS is not set in stone and absolute as you suggest.
 

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I'm glad you agree that outdated info is useless, when new info is coming out virtually every month.But I would like to know what you think abt what Hunter and Spiller said from my previous post...But while biological markers are imp to you and your experts, here's something you should know~Gastroenterology. 2002 Jun"Visceral hypersensitivity was detected in patients with functional gastrointestinal disorders and has been proposed as a biological marker of irritable bowel syndrome (IBS). " http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12055583 So apparently, there being no bio markers in IBS is not set in stone and absolute as you suggest.
 

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FYIImmunol Lett. 2004"Commensal bacteria (normal microflora), mucosal immunity and chronic inflammatory and autoimmune diseases." "...Involvement of commensal microflora and its components with strong immunoactivating properties (e.g. LPS, peptidoglycans, superantigens, bacterial DNA, Hsp) in etiopathogenetic mechanism of various complex, multifactorial and multigenic diseases, including inflammatory bowel diseases, periodontal disease, rheumatoid arthritis, atherosclerosis, allergy, multiorgan failure, colon cancer has been recently suggested. Animal models of human diseases reared in defined gnotobiotic conditions are helping to elucidate the aetiology of these frequent disorders. An improved understanding of commensal bacteria-host interactions employing germ-free animal models with selective colonisation strategies combined with modern molecular techniques could bring new insights into the mechanisms of mucosal immunity and also into pathogenetic mechanisms of several infectious, inflammatory, autoimmune and neoplastic diseases. Regulation of microflora composition (e.g. by probiotics and prebiotics) offers the possibility to influence the development of mucosal and systemic immunity but it can play a role also in prevention and treatment of some diseases." http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15158604
 

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FYIImmunol Lett. 2004"Commensal bacteria (normal microflora), mucosal immunity and chronic inflammatory and autoimmune diseases." "...Involvement of commensal microflora and its components with strong immunoactivating properties (e.g. LPS, peptidoglycans, superantigens, bacterial DNA, Hsp) in etiopathogenetic mechanism of various complex, multifactorial and multigenic diseases, including inflammatory bowel diseases, periodontal disease, rheumatoid arthritis, atherosclerosis, allergy, multiorgan failure, colon cancer has been recently suggested. Animal models of human diseases reared in defined gnotobiotic conditions are helping to elucidate the aetiology of these frequent disorders. An improved understanding of commensal bacteria-host interactions employing germ-free animal models with selective colonisation strategies combined with modern molecular techniques could bring new insights into the mechanisms of mucosal immunity and also into pathogenetic mechanisms of several infectious, inflammatory, autoimmune and neoplastic diseases. Regulation of microflora composition (e.g. by probiotics and prebiotics) offers the possibility to influence the development of mucosal and systemic immunity but it can play a role also in prevention and treatment of some diseases." http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15158604
 

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From July~~Cell. 2004 Jul"Recognition of commensal microflora by toll-like receptors is required for intestinal homeostasis.""...It is thought that an inflammatory response to commensal bacteria is avoided due to sequestration of microflora by surface epithelia. Here, we show that commensal bacteria are recognized by TLRs under normal steady-state conditions, and this interaction plays a crucial role in the maintenance of intestinal epithelial homeostasis. Furthermore, we find that activation of TLRs by commensal microflora is critical for the protection against gut injury and associated mortality. These findings reveal a novel function of TLRs-control of intestinal epithelial homeostasis and protection from injury-and provide a new perspective on the evolution of host-microbial interactions." http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15260992
 

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From July~~Cell. 2004 Jul"Recognition of commensal microflora by toll-like receptors is required for intestinal homeostasis.""...It is thought that an inflammatory response to commensal bacteria is avoided due to sequestration of microflora by surface epithelia. Here, we show that commensal bacteria are recognized by TLRs under normal steady-state conditions, and this interaction plays a crucial role in the maintenance of intestinal epithelial homeostasis. Furthermore, we find that activation of TLRs by commensal microflora is critical for the protection against gut injury and associated mortality. These findings reveal a novel function of TLRs-control of intestinal epithelial homeostasis and protection from injury-and provide a new perspective on the evolution of host-microbial interactions." http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15260992
 

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Why is there not a higher prevalance of IBS in third world countries and dysbisosis, where there are more enteric infections and again why more women, healcare seeking may be part but not all of the picture?or "It would be counter productive for an animal with a chronic parasite infestation to experince constant viceral pain, and it wouldn't have any advantage for people living in third world countries with frequent enteric infections to suffer from chronic abdominal pain."When I had ameobic dysentarty the start of my IBS, I did not have chronic abdominal pain even though the condition almost killed me, actually I don't remeber any pain from it. And my gut was inflammed for sure and I had severe D and severe projectile nausea.Nor the fact the recent John's hopkins article you cherry picked for intestinal permeability, said IBS is probably a neurologic bowel disorder. regarless IBS is now regonized as brain gut axis disorder anyway you look at it and what ever causes it. Your just not up to date on it yet.Both the brain and gut can cause symptoms.again this is not a competition. That is a fact, both the brain and gut can cause symptoms. You are looking at it withDualism: a theory that proposes a separation between the mind and the body.That it is a only a problem of the gut.as opposed to Holism: a theory built upon the foundation that the mind and body are integrated and utterly inseparable. "IMPLICATIONS FOR FUNCTIONAL GIDISORDERSBased on the concept of dualism, disease was understood in terms of structural abnormalities. Therefore, the validity of a disease rested with the observation of morphological abnormalities. Medical conditions occurring in the absence of such morphological abnormalities and symptoms were not considered legitimate, and were often viewed as psychiatric, consistent with the concept of dualism. The concept of dualism had other effects with regard to treatment. For example, this would include all the functional GI disorders and other somatic syndromes, such as fibromyalgia. Until the latter part of the 20th century, a medical illness was considered amenable to scientific inquiry and treatment. However, patients with psychiatric disorders were interred in insane asylums and considered to no longer be treatable by medical physicians. Unfortunately this concept leads to a clinical dilemma. Specific diseases explain only about 10% of medical illnesses seen by physicians. Furthermore, people with structural (i.e. organic) diagnosis such as inflammatory bowel disease or cancer show considerable variation in their symptom presentation and clinical behavior. Gastroenterologists (as well as other health care practitioners) are all too familiar with the poor correlation between structural findings on endoscopy and their patient's symptoms. "www.med.unc.edu/medicine/fgidc/historyfunctionaldisorders.pdf "Possible causes IBS has no identifiable cause, and endoscopic, radiologic, and laboratory testing is unrevealing. The syndrome has recently been attributed to neurologic or muscular hypersensitivity of the colon. IBS is part of a broader clinical complex known as functional bowel syndrome, which includes nonulcer dyspepsia, an entity with a constellation of upper gastrointestinal tract symptoms such as upper abdominal pain, nausea, and postprandial bloating. People in whom IBS is diagnosed often have symptoms related to nonulcer dyspepsia at various times in their life, and the reverse is true of those in whom nonulcer dyspepsia is diagnosed. This observation suggests that subtypes of functional bowel syndrome--specifically, IBS and nonulcer dyspepsia--do not involve a particular gastrointestinal organ. Thus, IBS is not a disease reflecting intrinsic colonic dysfunction. Instead, the disorder appears to be caused by a central neurologic mechanism that manifests itself as symptoms originating in different organs at various times. "Nor do you understand diagnoses at all in IBS."Diagnostic criteria To characterize IBS and establish criteria for diagnosis, Manning has suggested a constellation of symptoms that differentiate IBS from organic disease (1). These symptoms include lower abdominal pain and irregular bowel evacuation (eg, diarrhea, constipation, straining with bowel movements). Patients often have predominant manifestations of either constipation or diarrhea. Other criteria identified by Manning that are common to IBS include a perception of abdominal distention, the passage of mucus with bowel movements, and a sensation of incomplete evacuation (table 1). Patients often note loose or frequent bowel movements at the onset of abdominal pain, with relief of pain after defecation. Since these complaints also occur with organic disease, each symptom is neither a sensitive nor a specific indicator of IBS. However, with clustering of several symptoms, the likelihood of IBS increases. " "Response to warning indicators Talley and associates (2) also found that people with IBS often have symptoms considered to be warning signs of organic disease. Weight loss, rectal bleeding, recent changes in bowel pattern, and pain or bowel movements that wake a patient are usually attributed to organic disease, especially in older people. Such symptoms always warrant further investigation and are often explainable after evaluation for IBS. In patients with IBS, weight loss may be due to depression, and rectal bleeding is commonly attributed to hemorrhoids or anal fissure caused by straining with a hard bowel movement. However, a thorough evaluation to exclude organic disease is imperative before such symptoms are attributed to IBS. Thus, IBS must be considered a diagnosis of exclusion when these symptoms or other atypical features are present. " http://www.postgradmed.com/issues/2000/03_00/licht.htm This was when they use the manning criteria, they have since use rome l and Rome ll. It is no longer a diagnoses of exclusion either. When the enteric nervous system encounters a pathogen it runs a progam that give a person d and sometimes nausea to dispel the pathogen as quickly as possible. That is not consistent with alternating subtypes in IBS or as mentioned above the cluster of symptoms to diagnose IBS taken together, which using rome ll is a STABLE diagnoses."Irritable Bowel Syndrome: How far do you go in the Workup?Douglas A. Drossman, M.D.Professor of Medicine and PsychiatryCo-Director, UNC Center for Functional GI and Motility DisordersDivision of Digestive DiseasesUniversity of North Carolina at Chapel HillAddress correspondence to: Douglas A. Drossman, M.D.Division of Digestive Diseases726 Burnett-Womack Bldg. CB #7080University of North CarolinaChapel Hill, N.C. 27599-7080 The diagnostic evaluation of patients with irritable bowel syndrome (IBS) can be challenging for several reasons. First, there is no biological marker for the disorder. The diagnosis is based primarily on the presence of a clustered set of symptoms relating to abdominal pain or discomfort and altered bowel habit. Second, it follows that a diagnosis based solely on symptoms can be unsettling; clinicians will struggle with the possibility of missing another diagnosis. This level of uncertainty may increase the risk of overdoing diagnostic studies, though many clinicians believe an extensive diagnostic effort justified: it seeks to satisfy the patient's request for a specific diagnosis, as well as the physician's personal interest to "leave no stone unturned". Unfortunately, this approach contributes to the disproportionately high health care costs for IBS relative to other GI disorders as reported in one Health Maintenance Organization study (1). Finally, developing a diagnostic algorithm for IBS can be challenging given the effect of psychosocial co-factors including psychiatric diagnosis, daily and life stress and other psychosocial domains on IBS (2). Currently, the diagnostic evaluation of patients presenting with IBS symptoms has no simple standard; it is based on the art and science of medicine. Several factors can influence the decision making: a) symptom pattern and severity will influence, for example whether mucosal biopsies are taken for diarrhea-predominant symptoms, or ultrasound or CT are done for pain and weight loss(3),
demographic features such as older age on initial presentation or a family history of IBD or colon cancer may lead to a more extensive (e.g., colonoscopic) evaluation, c) a patient's pain communication style or illness-related behaviors must be appraised in the light of objective screening data; this, for example will reduce the tendency merely to order tests based on urgent requests to "do something" ("furor medicus") (4), and finally d), the clinical setting will influence the prior probability of other medical disorders; so primary care physicians more than gastroenterologists will minimize diagnostic studies, treat the symptoms of IBS, and follow the patient expectantly (5), simply because the likelihood of another serious medical disease in a primary care setting is far less than in a referral practice. Efforts to consolidate these many influences on diagnostic decision making have occurred by creating specific published guidelines obtained by consensus (3;6) (7). Most all authors agree that an initial diagnosis of IBS should be fulfilled by: a) meeting symptom-based diagnostic criteria, such as Rome II (6;8), Rome I (9) (10), or occasionally, Manning (11) criteria, obtaining a negative physical examination, and performing a cost-effective, conservative set of screening studies. These usually include a sigmoidoscopy (or colonoscopy for patients older than 50 years), a few laboratory tests (e.g., CBC, stool for occult blood or ova and parasites) and additional studies if certain "alarm" features are found: fever, an abnormal physical examination, blood in the stool, an abnormal CBC or elevated sedimentation rate, significant weight loss, nocturnal symptoms that awaken the patient, or a family history of cancer or inflammatory bowel disease (12;13). Several prospective studies now offer evidence that the proper application of such recommendations rarely leads to a revision in diagnosis, even for patients followed over many years (14;15) (6). In one study, the positive predictive value for the diagnosis of IBS using Rome I criteria and excluding "red flags" over 1-year follow-up was 98% (12). Of course, the gastroenterologist in referral practice may not be content to accept these probabilities without first excluding those rare conditions overlooked by routine evaluations. So how far should the gastroenterologist go in the workup of patients referred to them who typically present with IBS, and have negative screening studies? One gastroenterologist, recently commented to me: "I order breath hydrogen studies and sprue serologies on all my patients referred with IBS". No doubt this comment reflects the concern that as referral gastroenterologists we have an obligation to contribute additional expertise to the diagnostic effort. Recently, the breath H2 test is being requested more actively by physicians and the public alike possibly because of media attention to a study claiming a 73% rate of bacterial overgrowth in patients with IBS referred for breath H2 testing, and a 50% improvement with antibiotic treatment (16). However, the design limitations of this study, including a high ascertainment bias, use of an uncontrolled and unblinded treatment protocol, and only a 30% follow up rate evaluated over a relatively short period of time, makes it unlikely that clinicians in practice will also obtain such dramatic results. So while this study increases awareness of bacterial overgrowth as an entity that can mimic or exacerbate IBS, clinical experience suggests that the diagnostic yield in general GI practice is probably much lower than reported, perhaps 10% or less. What about celiac disease? This disorder should always be considered in evaluating IBS, because the diarrhea and abdominal discomfort due to proximal small intestinal villous atrophy and inflammation will specifically respond to a gluten-free diet. Therefore, making a diagnosis early may be cost-effective. The prevalence of celiac disease in the US is reported to range from 1:250 to 1:1500 (17). However, this is influenced by the method of assessment as well as the prior probability of the disorder being present in the population under study. With regard to the method of assessment, in a study set in Olmstead County (18), the reported prevalence was 1:4,600, and the cases were identified by clinical and pathological criteria. In contrast, when serological methods are used, the prevalence is at 1:250 or even higher (19), and in one recent study the prevalence for women was 1:125 compared to males at 1:250 (20). So, when clinically suspected, primary care physicians and specialists may now obtain anti-gliadin and anti-endomysial IgA antibody serologies. These are reasonably effective screening tests, given that the sensitivities and positive predictive values range from 90% - 100% (17). However, in populations where the prevalence of this disorder is low, many positive serological tests will be false positives. Therefore, because the gold standard of diagnosis requires upper endoscopy with duodenal biopsy, endoscopy is almost always needed for confirmation of the diagnosis. But can we be satisfied that these studies are enough to exclude celiac disease? In this issue of Gastroenterology, Wahnschaffe et al.(21) raise concerns about the possibility of missing a diagnosis of latent or potential celiac disease among persons thought to have IBS. Patients with latent or potential celiac disease have a genetic susceptibility for the disease, but do not have the histopathological findings (i.e., no villous atrophy or notable mucosal inflammation) when exposed to a gluten diet, so a small bowel biopsy will not make this diagnosis. In contrast to potential celiac disease, latent disease is characterized by mucosal changes that occurred at some point in time and recovered on a gluten-free diet. The authors propose that both these groups may still respond clinically to a gluten free diet. This creative study attempted to identify patients with latent or potential celiac disease (i.e., who presumably had negative serological screens for celiac disease) in a sample of 102 IBS patients. They evaluated a variety of serological, intestinal and genetic markers, and compared the findings to control groups with treated and untreated celiac disease, latent celiac disease and normal controls. They found two surrogate markers: a) the expression of HLA-DQ2 alleles DQA1*050/DQB1*0201, a genetic marker for celiac disease, and
an increased intestinal IgA titer against tissue-transglutaminase and/or gliadin were elevated in the small sample of patients with latent celiac disease. Notably, the assessment of intestinal (rather than serological) antibodies is a unique aspect of this study; it is a diagnostic method for celiac sprue that is not commonly done. Then, when evaluating the IBS patients, they found that 35% had expression of the HLA-DQ2 genotype, and this subgroup of IBS patients had significantly increased IgA antibodies against the celiac disease-associated antigens gliadin and/or tissue-transglutaminase in the duodenal aspirate, as well as increased intra-epithielial lymphocytes (also characteristic of celiac disease) when compared to IBS patients without expression of the HLA-DQ2 genotype. Furthermore, 26 IBS patients were put on a gluten-free diet for 6 months. The 13 patients who were positive for the HLA-DQ2 alleles and for the intestinal celiac disease-associated antibodies had a significant reduction in stool frequency and intestinal IgA antibody titers for the celiac disease-associated antigens. This improvement did not occur in the remaining IBS patients on gluten free diet who were negative for HLA-DQ2 gene expression. They conclude that the presence of these two markers in patients with IBS may identify a subgroup with latent or potential celiac disease that may respond to dietary restriction. These findings must be put into a clinical perspective. First, the authors identified the IBS patients as those who had a "�variable combination of abnormal bowel habits in the absence of endoscopic, histopathological, laboratory and microbiological abnormalities." However, these criteria are not sufficient for diagnosing IBS. We do not know how many of these patients actually had abdominal pain, the key symptom criterion for a diagnosis of IBS. Clinically, patients with diarrhea and no pain are considered separate from IBS ("functional diarrhea"), and they define a group where celiac disease is more likely than patients with typical IBS having abdominal pain. In fact, if many of these patients did not have pain, and therefore did not fulfill criteria for IBS, then the findings of the study and its implications for IBS may be quite different. Second, the sample sizes for some of the cells were small. Only 5 patients had latent celiac disease, and the improvement in response to gluten restriction occurred in a sample of 13 patients with IBS who were HLA-DQ2 positive. It will also be valuable to conduct this study in a controlled fashion using a large group of patients with IBS not having celiac disease markers in order to determine the placebo response rate to a gluten free diet. Even the reduction in serologies with a gluten free diet may not provide complete evidence for a clinical response, since dietary restriction of gluten might reduce the antigenic challenge to the immune system, leading to a serological response that is unrelated to the changes in stool frequency. Despite these limitations, this study has raised some important concerns regarding our sense of "security" in accepting normal histopathology to exclude celiac disease in patients having symptoms of IBS, and has opened the door to pursuing these issues in larger clinical trials. Is it possible that some simple and inexpensive tests will emerge to accurately diagnose IBS? I do not think that IBS can by diagnosed by ordering tests, either to make a unitary diagnosis, or by default by excluding other disorders. There is evidence that IBS is a heterogeneous disorder where different physiological subgroups contribute to the clinical expression of the syndrome. For example, there is a subgroup of patients, called "post-infectious IBS" who appear to respond to an enteric infection such as campylobactor jejuni with an increased inflammatory cell response (22). This is associated with activating enterochromaffin cells to produce 5HT, and CD3 cells to produce cytokines, which in turn leads to enhanced motility and lowered visceral sensation thresholds (22;23). But microscopic inflammation cannot be a diagnostic marker for IBS because it does not typically produce pain in those who have it. All patients with active celiac disease have microscopic inflammation, but a large proportion do not have abdominal pain, and patients with ulcerative colitis who also have microscopic inflammation when compared to patients with IBS appear to have higher pain thresholds (24). In individuals with these disorders, there may be central nervous system counter-regulatory measures responding to the peripheral pain/inflammatory processes that increase pain thresholds. With regard to IBS, the gut-related effects of microscopic inflammation may be only one component of a dysfunctional brain-gut system. In addition, and often in response to stress, there may be a failure to activate descending pain inhibitory systems that enable the clinical experience of pain and other symptoms that typify this disorder (25). In one prospective study of post-infectious IBS, it was found that those who retained their symptoms 3-months after an enteric infection had not only increased mucosal cellularity, but also had increased psychosocial distress at the time of the infection. Furthermore, lowered visceral sensation thresholds and increased motility were present after the infection regardless of whether or not the patients retained their symptoms (26). Therefore, the microscopic inflammation and its physiological effects on motility and sensation contribute to, but are not always sufficient for the clinical expression of IBS pain. At least for post-infectious IBS this provides some evidence that psychological distress alters brain pain regulatory pathways to amplify incoming visceral signals leading to the full clinical expression of this syndrome (27;28). Recent studies using brain imaging (29;30)may help us to understand the physiological mechanisms that modulate these CNS responses to pain, and in the process, identify the subgroup with IBS that are more amenable to psychological and psychopharmacological treatments. As we continue to develop the means to assess the pathophysiological determinants of IBS symptoms, we will continue to identify subgroups that will change our diagnostic assessment, and may even redefine what we mean by IBS. Post-infectious IBS, and patients having concurrent psychosocial disturbances (among others to be determined) characterize subgroups that will be more responsive to more specific treatments. For the present, we must still make a diagnosis of IBS based on established guidelines including symptom-based (e.g., Rome) criteria. We must also remain vigilant to identifying other relevant disorders like celiac disease that may mimic or exacerbate IBS, and will use clinical judgment (e.g., ordering anti-endomysial antibodies for patients with predominant diarrhea), rather than routinely ordering tests in all IBS patients just to exclude other disease. With careful appraisal of the historical and laboratory data and good clinical judgment, a positive diagnosis of IBS can be made in a cost-effective manner and with confidence. " http://www.romecriteria.org/reading1.html The above is less then three years old."Gastroenterology Expert ColumnDiagnosing Irritable Bowel Syndrome: What's Too Much, What's Enough?Posted 03/12/2004 Susan Lucak, MD IntroductionIrritable bowel syndrome (IBS) is the most common gastrointestinal disorder diagnosed in clinical practice in the United States. Because there is no biological marker to confirm the diagnosis of IBS, it is a diagnosis that has challenged clinicians for decades. In the past, IBS was a "waste-basket" diagnosis given to patients with unexplained gastrointestinal symptoms. It was considered to be "the diagnosis of exclusion" when extensive work-up for organic disease yielded no diagnosis.In recent decades, it was recognized that patients with IBS experienced a constellation of specific gastrointestinal symptoms. Manning criteria were described in 1978,1 followed by Rome I in 19892 and Rome II criteria in 1999.3 Rome I and Rome II criteria were initially developed by multinational working groups to provide a framework for the selection of patients in diagnostic and therapeutic trials. These criteria are being continuously modified as we gain new knowledge about functional bowel disorders.Recently published diagnostic guidelines4,5 recommend using symptom-based criteria in making the diagnosis of IBS in clinical practice. Using these criteria in conjunction with "alarm features" allows a physician to minimize the extent of diagnostic testing needed to make the diagnosis of IBS. Furthermore, recent systematic review of the literature indicates that performing a number of diagnostic tests did not result in a significant increase in the diagnosis of organic gastrointestinal disease.6EpidemiologyWhen making the diagnosis of IBS, it is helpful to consider it in the context of its epidemiology. IBS is a very common gastrointestinal disorder in the United States, affecting 10% to 20% of the population.7 Female patients outnumber male patients by 1.5-3.0:1.0 in most epidemiologic studies.8 Although it is not well understood why more women present with IBS, differences in healthcare-seeking behavior may partly account for this predominance.Smith and colleagues9 found that psychosocial factors were determinants of healthcare seeking for patients with both organic gastrointestinal disorders and functional gastrointestinal disorders. History of abuse is another important determinant in healthcare seeking.10Symptom-based CriteriaIn a given patient, the diagnosis of IBS is suggested by identification of specific symptoms. The Rome II criteria for diagnosis of IBS include presence of abdominal pain or discomfort for 12 weeks (need not be consecutive) in the preceding 12 months, and at least 2 of the following 3 features regarding symptoms: (1) relieved with defecation, (2) associated with change in frequency of defecation, and /or (3) associated with a change in form or appearance of stool. Patients with IBS may have additional symptoms, including passage of mucus and bloating or abdominal distension (Table 1).3 Although refinement and validation of these criteria are necessary, Rome II criteria are widely accepted as a diagnostic instrument in IBS."Alarm Features"An important aspect of making the diagnosis of IBS is the absence of "red flag" or "alarm features" (Table 2).4,11,12 Unexplained weight loss may reflect disorders such as malignancy, inflammatory bowel disease (IBD), or celiac disease. Persistent diarrhea or severe constipation may be associated with an organic disease.IBS is generally an intermittent and recurrent disorder. Symptoms of IBS tend to disappear at night when the patient is asleep. Thus, nocturnal gastrointestinal symptoms warrant search for a diagnosis other than IBS. The onset of new gastrointestinal symptoms after the age of 50 should prompt the physician to look for organic disease, particularly colorectal cancer. Blood in stool may reflect IBD or an infectious process or colon cancer. Family history of IBD, celiac disease, or gastrointestinal malignancy requires evaluation for these diseases. Fever suggests the possibility of an infectious or inflammatory disorder. Anemia should alert the physician to look for IBD or colorectal cancer. Signs of bowel obstruction, malabsorption, extraintestinal signs of IBD, or thyroid dysfunction should all prompt organic disease work-up. Any laboratory test abnormalities should be pursued appropriately. Absence of these "alarm features" serves to support, not establish, the diagnosis of IBS.Physical ExaminationThe American Gastroenterological Association (AGA) Technical Review on IBS recommends that a physical examination be performed, primarily to rule out organic disease.4 For instance, the presence of abdominal mass, signs of obstruction, or enlarged liver should trigger further investigation. A rectal examination identifying lax sphincter may confirm complaints of fecal incontinence, whereas paradoxical pelvic floor muscle contraction may suggest pelvic floor dyssynergia. In the latter case, anorectal motility study may be appropriate. Digital rectal examination is of further value in the assessment for fecal occult blood. A pelvic examination (performed by a gastroenterologist or a gynecologist) should be performed if symptoms point to the pelvic/lower abdominal area and are associated with menses.Diagnostic TestingReview of the current literature does not support performance of extensive testing in patients who meet symptom-based criteria for IBS and who lack "alarm features."6,13 Cash and colleagues[6] performed a systematic literature review of frequently ordered diagnostic tests as part of IBS work-up (Table 3). After careful assessment of the quality and validity of the selected studies, it was concluded that the pretest probability of organic disorders (such as IBD, colon cancer, thyroid disease, and lactose malabsorption) was not significantly increased in patients suspected of having IBS when compared with the general population. In other words, when patients fulfilled symptom-based criteria for the diagnosis of IBS, performing tests such as flexible sigmoidoscopy, barium enema, colonoscopy, rectal biopsy, complete blood count (CBC), serum chemistries, fecal occult blood test (FOBT), TSH, stool ova and parasites (O&P), hydrogen breath test for lactose malabsorption, or abdominal ultrasound did not result in a significant increase in the diagnosis of organic gastrointestinal disease. Specifically, performing a colonoscopy did not result in identifying gastrointestinal organic disease in more than 1% to 2% of cases.Widespread testing for celiac disease in patients who fulfill symptom-based criteria for IBS is not recommended.4,5 A matched case-control study in the United Kingdom showed 66 of 300 IBS patients had positive celiac disease auto-antibodies and 14 had biopsy-proven celiac disease compared with 2 out of 300 control subjects.14 This demonstrates a 7-fold increase in occurrence of celiac disease in patients suspected of having IBS. This study was, however, conducted in a secondary care setting. Given availability of effective therapy for celiac disease and prevention of long-term morbidity, testing for celiac disease with celiac disease auto-antibodies may not be unreasonable.The most recent AGA Technical Review on IBS4 recommends the performance of screening and other diagnostic tests as listed in Table 4. Colonic visualization with colonoscopy or flexible sigmoidoscopy/barium enema should be performed according to colorectal cancer screening guidelines. A colonoscopy is recommended for patients over the age of 50 years, but in younger patients, performing flexible sigmoidoscopy or colonoscopy needs to be determined by clinical presentation and sound clinical judgment.4,5 In many cases, therapy can be instituted before diagnostic studies are done or completed.The American College of Gastroenterology (ACG) Task Force comments on the value of "reassurance" derived from negative evaluation for organic disease.5 It is pointed out that the value of this "reassurance" is unclear and should be assessed in future clinical trials.The extent to which a diagnostic work-up is performed also depends on the severity of symptoms and where a patient with IBS presents.Primary Care SettingMost patients with IBS (about 70%) present to primary care physicians.4 Patients with IBS in this group have symptoms that tend to be mild in severity. A recently published evidence-based review by the ACG IBS Task Force concluded that routine testing among patients with symptoms "fitting" the Rome II criteria and no "alarm features" is not necessary in the primary care setting.5Secondary Care SettingMore difficult or more severe cases of IBS are generally seen by gastroenterologists referred from primary care physicians. The estimated prevalence of this subgroup is about 25% of all patients with IBS.If screening and other diagnostic tests were done by the primary care physician, they do not need to be repeated. The need for colonic visualization should be determined according to guidelines outlined above. Further evaluation may be warranted if a patient presents with any of the following features: (1) short duration of symptoms or worsening severity of symptoms, (2) onset of symptoms at an older age ( 50 years), (3) family history of colon cancer or IBD, or (4) absence of psychosocial features or absence of healthcare seeking.4During the first visit, it is important to explore with the patient possible contributing factors such as psychosocial issues (stress, anxiety, depression) and history of abuse. Up to 40% of patients may have a history of sexual, physical, or mental abuse.10Clearly, the right balance needs to be struck between making an accurate diagnosis of IBS and, at the same time, not missing other diagnoses that may mimic IBS. It is important to recognize, however, that if a patient diagnosed with IBS does not respond to a therapy, the diagnosis may be reassessed in 3 to 6 weeks and additional evaluation can be performed (see Table 5).4Tertiary Care SettingThe most severe cases of IBS and those most difficult to treat are seen in referral centers. The latter group comprises approximately 5% of all IBS cases. The clinical symptoms for this patient group do not tend to correlate with gut physiology. Rather, these patients tend to have constant symptoms, more psychosocial difficulties, greater healthcare-seeking behavior, more illness behavior (illness behavior is a way in which an individual perceives, interprets, and reacts to physical sensations that can be interpreted as symptoms of disease), and more psychiatric diagnoses.4Generally, most diagnostic studies have been performed by the time a patient with IBS presents to a referral center. Specialized studies such as defecating proctography, rectoanal angle measurement, anorectal motility and balloon expulsion, and investigational testing may be performed depending on clinical presentation and lack of response to previous treatments (see Table 5).4Differential Diagnosis and Durability of DiagnosisDifferential DiagnosisSymptoms of IBS are nonspecific and may mimic a number of disease entities (Table 6).15 It is important to recognize that in a given patient with IBS, these diagnoses need not be "excluded" before a diagnosis of IBS can be established.Durability of DiagnosisA number of studies conducted in community-based and specialty-based clinics over the past 3 decades have demonstrated that once the diagnosis of IBS is made, only a small percentage (0.7% to 6.5%) of patients subsequently receive a diagnosis of organic disease.16-20 These studies provide evidence that once the diagnosis of IBS is established, additional studies are not necessary unless the clinical symptoms change.Legal Risks in Diagnosing IBSSome physicians who see patients with IBS are concerned about the risk of malpractice. Feld21 recently described sources of risk under which physicians may be sued, including negligence, duty to provide care to a patient, and medical practice below standard of care, among others. But the idea that more testing is better in IBS may not always be the case. For example, colonoscopy leads to a change in diagnosis about 1% to 2% of the time and may represent performance of substandard care based on testing guidelines for IBS diagnosis recommended by gastroenterological associations in the United States. Therefore, any complication resulting from "unnecessary" testing may expose a physician to a malpractice suit. Alternatively, if a physician explains to a patient why only limited testing is necessary, this allows a patient to participate in the process and understand inherent uncertainties and thus share in the responsibility when a reasonable decision results in an adverse outcome.21 Feld's risk management recommendations are outlined in Table 7.Summary and ConclusionsWhat's too much when we think about diagnosing IBS is to do exhaustive and duplicate testing. In a retrospective, community-based study in Olmsted County, Minnesota, two thirds of patients who consulted for gastrointestinal symptoms had to wait at least 2 years to have their IBS diagnosed, despite averaging nearly 5 healthcare visits per year.20 Such an approach is not only costly and inefficient, but it delays treatment and fosters frustration on the part of the patient and the physician.What's enough is to use symptom-based criteria, "alarm features," and guidelines proposed by the ACG IBS Task Force and the AGA Technical Review on IBS in making a more timely diagnosis of IBS. Although additional studies are necessary to validate Rome II criteria and to assess diagnostic testing in prospective studies, the expert guidelines allow the diagnosis of IBS to be made with greater efficiency, certainty, and confidence. Furthermore, once a diagnosis of IBS is made, it is retained in more than 93% of cases with a long-term follow-up. Considering legal aspects of IBS diagnosis, symptom-based criteria and guidelines set forth by the ACG and AGA are becoming key elements in establishing standard of care. It has become clear that the diagnosis of IBS can and should be made quickly so that treatment can be initiated as soon as possible. This promotes greater patient confidence in the physician. http://www.medscape.com/viewarticle/465760_9 "In the new IFFGD Digestive Health Matters.Visceral Sensations and Brain-Gut Mechanisms By: Emeran A. Mayer, M.D., Professor of Medicine, Physiology and Psychiatry; Director, Center for Neurovisceral Sciences & Women's Health, David Geffen School of Medicine at UCLA IntroductionOver the past several years, different mechanisms located within the gut, or gut wall have been implicated in as possible pathoophysiologic mechanisms underlying the charecteristic IBS symptoms of abdominal pain and discomfort. The list ranges from altered transit of intestinal gas, alterations in colonic flora, immune cell activation in the gut mucosa, and alterations in serotonin containing enterochromaffin cells lining the gut. For those investigators with a good memory, these novel mechanisms can be added to an older list of proposed pathomechanisms, including altered gut motility('Sapstic Colitus') and alterations in mucus secretion. While the jury is still out, one unique aspect about the gut and its connection to the brain are often forgotten: Our brain gut axis is not designed to generate concious perceptions of every alteration in gut homeostasis and internal enviroment, in particlur when these changes are chronic, and when there is no adaptive behavioral response an affected organism could generate.Evolution has not designed our brain gut axis to experience abdominal pain every time the number of mast cells in our ileum goes up, or the number of our serotonin containing cells goes down. It would be counter productive for an animal with a chronic parasite infestation to experince constant viceral pain, and it wouldn't have any advantage for people living in third world countries with frequent enteric infections to suffer from chronic abdominal pain. It has been suggested that viceral pain maybe a secondary phenomenon of an elaborate system of signaling non painful signals to the brain: hunger and fullness (satiety), well being after a meal, urge to evacuate, ect. At the same time, powerful mechanisms have evolved that keep many other aversive signals out of concious perception: contractions, luminal distension, gas volume, low grade inflammation, ect..The most common symptoms of IBS patients are related to altered perception of sensations, arising from the GI tract, and frequently from sites outside the GI tract, such as the genitourinary system or the musculskeletal system. Sensations of bloating, fullness, gas, incomplete rectal evacuation, and crampy abdominal pain are the most common symptoms patients experience. Numerous reports have demonstarted that a significant percentage of functional bowel disorders (FBD) patients about (60) percent rate experimental distensions of the colon as uncomfortable at lower distension volumes or pressure when compared to healthy control subjects. This finding of an increased perception of viceral signals ("viceral hypersensitvity") has been demonstrated during baloon distension tests of the respective part of the GI tract regarless of where the primary symptoms are- the esophagus, the stomach, or the lower abdomen.In contrast to the current emphasis on mechanisms that may result in sensitization of viceral Afferent pathways in the gut, it may well be that alterations in the way the nervous system normally suppresses the perception of the great majority of sensory activity arising from our viscera are essential for the typical symptom constellation of IBS and other functional disorders to develop."It goes into a lot more detail and I highly recommend people get a copy and read the whole article."SummaryIn summary, it is clear that we still have a long way to go to understand the intricate connections between our digestive system and the brain, and how alterations in this two way communication result in functional bowel disorders symptoms. While more alterations in peripheral mechanisms involved in gut function are being reported, rapid progress has occured in our uunderstanding of the multiple mechanisms by which the brain can increase the concious perception of viceral stimuli, which is normally rarely perceieved." http://www.aboutibs.org/Publications/currentParticipate.html On the inflammation you still don't get it Tal and nor are they my researchers on IBS they are everyones and one of if not the top center in the US.I have told you this before, you have not put enough time in to be careful of how to interpret a lot of studies you post. You also suffer from extreme tunnel vision that IBS is only dysbiosis and bacteria.Even the people studying it think its a small part of the puzzle"Marshall is the lead author of a new study that may help explain how those symptoms start.The study involved 132 Walkerton residents with IBS and 86 residents without the condition. Average age was 46 years and about 60 per cent were female.Nearly 36 per cent of IBS cases had abnormal intestinal permeability, or "leaky gut syndrome," a condition in which the lining of the intestines allows more bacteria, toxins and food to leak in and potentially irritate the deeper tissue layers. In comparison, less than 19 per cent of non-IBS participants had a leaky gut.Marshall says his findings represent only a small piece of the entire IBS puzzle, but he hopes they will provide the basis for future research in the Walkerton population. "Why did NON IBS patients have "leaky gut"?This was also a virus outbreak.This also does not go into PI IBS infromation.
 

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Why is there not a higher prevalance of IBS in third world countries and dysbisosis, where there are more enteric infections and again why more women, healcare seeking may be part but not all of the picture?or "It would be counter productive for an animal with a chronic parasite infestation to experince constant viceral pain, and it wouldn't have any advantage for people living in third world countries with frequent enteric infections to suffer from chronic abdominal pain."When I had ameobic dysentarty the start of my IBS, I did not have chronic abdominal pain even though the condition almost killed me, actually I don't remeber any pain from it. And my gut was inflammed for sure and I had severe D and severe projectile nausea.Nor the fact the recent John's hopkins article you cherry picked for intestinal permeability, said IBS is probably a neurologic bowel disorder. regarless IBS is now regonized as brain gut axis disorder anyway you look at it and what ever causes it. Your just not up to date on it yet.Both the brain and gut can cause symptoms.again this is not a competition. That is a fact, both the brain and gut can cause symptoms. You are looking at it withDualism: a theory that proposes a separation between the mind and the body.That it is a only a problem of the gut.as opposed to Holism: a theory built upon the foundation that the mind and body are integrated and utterly inseparable. "IMPLICATIONS FOR FUNCTIONAL GIDISORDERSBased on the concept of dualism, disease was understood in terms of structural abnormalities. Therefore, the validity of a disease rested with the observation of morphological abnormalities. Medical conditions occurring in the absence of such morphological abnormalities and symptoms were not considered legitimate, and were often viewed as psychiatric, consistent with the concept of dualism. The concept of dualism had other effects with regard to treatment. For example, this would include all the functional GI disorders and other somatic syndromes, such as fibromyalgia. Until the latter part of the 20th century, a medical illness was considered amenable to scientific inquiry and treatment. However, patients with psychiatric disorders were interred in insane asylums and considered to no longer be treatable by medical physicians. Unfortunately this concept leads to a clinical dilemma. Specific diseases explain only about 10% of medical illnesses seen by physicians. Furthermore, people with structural (i.e. organic) diagnosis such as inflammatory bowel disease or cancer show considerable variation in their symptom presentation and clinical behavior. Gastroenterologists (as well as other health care practitioners) are all too familiar with the poor correlation between structural findings on endoscopy and their patient's symptoms. "www.med.unc.edu/medicine/fgidc/historyfunctionaldisorders.pdf "Possible causes IBS has no identifiable cause, and endoscopic, radiologic, and laboratory testing is unrevealing. The syndrome has recently been attributed to neurologic or muscular hypersensitivity of the colon. IBS is part of a broader clinical complex known as functional bowel syndrome, which includes nonulcer dyspepsia, an entity with a constellation of upper gastrointestinal tract symptoms such as upper abdominal pain, nausea, and postprandial bloating. People in whom IBS is diagnosed often have symptoms related to nonulcer dyspepsia at various times in their life, and the reverse is true of those in whom nonulcer dyspepsia is diagnosed. This observation suggests that subtypes of functional bowel syndrome--specifically, IBS and nonulcer dyspepsia--do not involve a particular gastrointestinal organ. Thus, IBS is not a disease reflecting intrinsic colonic dysfunction. Instead, the disorder appears to be caused by a central neurologic mechanism that manifests itself as symptoms originating in different organs at various times. "Nor do you understand diagnoses at all in IBS."Diagnostic criteria To characterize IBS and establish criteria for diagnosis, Manning has suggested a constellation of symptoms that differentiate IBS from organic disease (1). These symptoms include lower abdominal pain and irregular bowel evacuation (eg, diarrhea, constipation, straining with bowel movements). Patients often have predominant manifestations of either constipation or diarrhea. Other criteria identified by Manning that are common to IBS include a perception of abdominal distention, the passage of mucus with bowel movements, and a sensation of incomplete evacuation (table 1). Patients often note loose or frequent bowel movements at the onset of abdominal pain, with relief of pain after defecation. Since these complaints also occur with organic disease, each symptom is neither a sensitive nor a specific indicator of IBS. However, with clustering of several symptoms, the likelihood of IBS increases. " "Response to warning indicators Talley and associates (2) also found that people with IBS often have symptoms considered to be warning signs of organic disease. Weight loss, rectal bleeding, recent changes in bowel pattern, and pain or bowel movements that wake a patient are usually attributed to organic disease, especially in older people. Such symptoms always warrant further investigation and are often explainable after evaluation for IBS. In patients with IBS, weight loss may be due to depression, and rectal bleeding is commonly attributed to hemorrhoids or anal fissure caused by straining with a hard bowel movement. However, a thorough evaluation to exclude organic disease is imperative before such symptoms are attributed to IBS. Thus, IBS must be considered a diagnosis of exclusion when these symptoms or other atypical features are present. " http://www.postgradmed.com/issues/2000/03_00/licht.htm This was when they use the manning criteria, they have since use rome l and Rome ll. It is no longer a diagnoses of exclusion either. When the enteric nervous system encounters a pathogen it runs a progam that give a person d and sometimes nausea to dispel the pathogen as quickly as possible. That is not consistent with alternating subtypes in IBS or as mentioned above the cluster of symptoms to diagnose IBS taken together, which using rome ll is a STABLE diagnoses."Irritable Bowel Syndrome: How far do you go in the Workup?Douglas A. Drossman, M.D.Professor of Medicine and PsychiatryCo-Director, UNC Center for Functional GI and Motility DisordersDivision of Digestive DiseasesUniversity of North Carolina at Chapel HillAddress correspondence to: Douglas A. Drossman, M.D.Division of Digestive Diseases726 Burnett-Womack Bldg. CB #7080University of North CarolinaChapel Hill, N.C. 27599-7080 The diagnostic evaluation of patients with irritable bowel syndrome (IBS) can be challenging for several reasons. First, there is no biological marker for the disorder. The diagnosis is based primarily on the presence of a clustered set of symptoms relating to abdominal pain or discomfort and altered bowel habit. Second, it follows that a diagnosis based solely on symptoms can be unsettling; clinicians will struggle with the possibility of missing another diagnosis. This level of uncertainty may increase the risk of overdoing diagnostic studies, though many clinicians believe an extensive diagnostic effort justified: it seeks to satisfy the patient's request for a specific diagnosis, as well as the physician's personal interest to "leave no stone unturned". Unfortunately, this approach contributes to the disproportionately high health care costs for IBS relative to other GI disorders as reported in one Health Maintenance Organization study (1). Finally, developing a diagnostic algorithm for IBS can be challenging given the effect of psychosocial co-factors including psychiatric diagnosis, daily and life stress and other psychosocial domains on IBS (2). Currently, the diagnostic evaluation of patients presenting with IBS symptoms has no simple standard; it is based on the art and science of medicine. Several factors can influence the decision making: a) symptom pattern and severity will influence, for example whether mucosal biopsies are taken for diarrhea-predominant symptoms, or ultrasound or CT are done for pain and weight loss(3),
demographic features such as older age on initial presentation or a family history of IBD or colon cancer may lead to a more extensive (e.g., colonoscopic) evaluation, c) a patient's pain communication style or illness-related behaviors must be appraised in the light of objective screening data; this, for example will reduce the tendency merely to order tests based on urgent requests to "do something" ("furor medicus") (4), and finally d), the clinical setting will influence the prior probability of other medical disorders; so primary care physicians more than gastroenterologists will minimize diagnostic studies, treat the symptoms of IBS, and follow the patient expectantly (5), simply because the likelihood of another serious medical disease in a primary care setting is far less than in a referral practice. Efforts to consolidate these many influences on diagnostic decision making have occurred by creating specific published guidelines obtained by consensus (3;6) (7). Most all authors agree that an initial diagnosis of IBS should be fulfilled by: a) meeting symptom-based diagnostic criteria, such as Rome II (6;8), Rome I (9) (10), or occasionally, Manning (11) criteria, obtaining a negative physical examination, and performing a cost-effective, conservative set of screening studies. These usually include a sigmoidoscopy (or colonoscopy for patients older than 50 years), a few laboratory tests (e.g., CBC, stool for occult blood or ova and parasites) and additional studies if certain "alarm" features are found: fever, an abnormal physical examination, blood in the stool, an abnormal CBC or elevated sedimentation rate, significant weight loss, nocturnal symptoms that awaken the patient, or a family history of cancer or inflammatory bowel disease (12;13). Several prospective studies now offer evidence that the proper application of such recommendations rarely leads to a revision in diagnosis, even for patients followed over many years (14;15) (6). In one study, the positive predictive value for the diagnosis of IBS using Rome I criteria and excluding "red flags" over 1-year follow-up was 98% (12). Of course, the gastroenterologist in referral practice may not be content to accept these probabilities without first excluding those rare conditions overlooked by routine evaluations. So how far should the gastroenterologist go in the workup of patients referred to them who typically present with IBS, and have negative screening studies? One gastroenterologist, recently commented to me: "I order breath hydrogen studies and sprue serologies on all my patients referred with IBS". No doubt this comment reflects the concern that as referral gastroenterologists we have an obligation to contribute additional expertise to the diagnostic effort. Recently, the breath H2 test is being requested more actively by physicians and the public alike possibly because of media attention to a study claiming a 73% rate of bacterial overgrowth in patients with IBS referred for breath H2 testing, and a 50% improvement with antibiotic treatment (16). However, the design limitations of this study, including a high ascertainment bias, use of an uncontrolled and unblinded treatment protocol, and only a 30% follow up rate evaluated over a relatively short period of time, makes it unlikely that clinicians in practice will also obtain such dramatic results. So while this study increases awareness of bacterial overgrowth as an entity that can mimic or exacerbate IBS, clinical experience suggests that the diagnostic yield in general GI practice is probably much lower than reported, perhaps 10% or less. What about celiac disease? This disorder should always be considered in evaluating IBS, because the diarrhea and abdominal discomfort due to proximal small intestinal villous atrophy and inflammation will specifically respond to a gluten-free diet. Therefore, making a diagnosis early may be cost-effective. The prevalence of celiac disease in the US is reported to range from 1:250 to 1:1500 (17). However, this is influenced by the method of assessment as well as the prior probability of the disorder being present in the population under study. With regard to the method of assessment, in a study set in Olmstead County (18), the reported prevalence was 1:4,600, and the cases were identified by clinical and pathological criteria. In contrast, when serological methods are used, the prevalence is at 1:250 or even higher (19), and in one recent study the prevalence for women was 1:125 compared to males at 1:250 (20). So, when clinically suspected, primary care physicians and specialists may now obtain anti-gliadin and anti-endomysial IgA antibody serologies. These are reasonably effective screening tests, given that the sensitivities and positive predictive values range from 90% - 100% (17). However, in populations where the prevalence of this disorder is low, many positive serological tests will be false positives. Therefore, because the gold standard of diagnosis requires upper endoscopy with duodenal biopsy, endoscopy is almost always needed for confirmation of the diagnosis. But can we be satisfied that these studies are enough to exclude celiac disease? In this issue of Gastroenterology, Wahnschaffe et al.(21) raise concerns about the possibility of missing a diagnosis of latent or potential celiac disease among persons thought to have IBS. Patients with latent or potential celiac disease have a genetic susceptibility for the disease, but do not have the histopathological findings (i.e., no villous atrophy or notable mucosal inflammation) when exposed to a gluten diet, so a small bowel biopsy will not make this diagnosis. In contrast to potential celiac disease, latent disease is characterized by mucosal changes that occurred at some point in time and recovered on a gluten-free diet. The authors propose that both these groups may still respond clinically to a gluten free diet. This creative study attempted to identify patients with latent or potential celiac disease (i.e., who presumably had negative serological screens for celiac disease) in a sample of 102 IBS patients. They evaluated a variety of serological, intestinal and genetic markers, and compared the findings to control groups with treated and untreated celiac disease, latent celiac disease and normal controls. They found two surrogate markers: a) the expression of HLA-DQ2 alleles DQA1*050/DQB1*0201, a genetic marker for celiac disease, and
an increased intestinal IgA titer against tissue-transglutaminase and/or gliadin were elevated in the small sample of patients with latent celiac disease. Notably, the assessment of intestinal (rather than serological) antibodies is a unique aspect of this study; it is a diagnostic method for celiac sprue that is not commonly done. Then, when evaluating the IBS patients, they found that 35% had expression of the HLA-DQ2 genotype, and this subgroup of IBS patients had significantly increased IgA antibodies against the celiac disease-associated antigens gliadin and/or tissue-transglutaminase in the duodenal aspirate, as well as increased intra-epithielial lymphocytes (also characteristic of celiac disease) when compared to IBS patients without expression of the HLA-DQ2 genotype. Furthermore, 26 IBS patients were put on a gluten-free diet for 6 months. The 13 patients who were positive for the HLA-DQ2 alleles and for the intestinal celiac disease-associated antibodies had a significant reduction in stool frequency and intestinal IgA antibody titers for the celiac disease-associated antigens. This improvement did not occur in the remaining IBS patients on gluten free diet who were negative for HLA-DQ2 gene expression. They conclude that the presence of these two markers in patients with IBS may identify a subgroup with latent or potential celiac disease that may respond to dietary restriction. These findings must be put into a clinical perspective. First, the authors identified the IBS patients as those who had a "�variable combination of abnormal bowel habits in the absence of endoscopic, histopathological, laboratory and microbiological abnormalities." However, these criteria are not sufficient for diagnosing IBS. We do not know how many of these patients actually had abdominal pain, the key symptom criterion for a diagnosis of IBS. Clinically, patients with diarrhea and no pain are considered separate from IBS ("functional diarrhea"), and they define a group where celiac disease is more likely than patients with typical IBS having abdominal pain. In fact, if many of these patients did not have pain, and therefore did not fulfill criteria for IBS, then the findings of the study and its implications for IBS may be quite different. Second, the sample sizes for some of the cells were small. Only 5 patients had latent celiac disease, and the improvement in response to gluten restriction occurred in a sample of 13 patients with IBS who were HLA-DQ2 positive. It will also be valuable to conduct this study in a controlled fashion using a large group of patients with IBS not having celiac disease markers in order to determine the placebo response rate to a gluten free diet. Even the reduction in serologies with a gluten free diet may not provide complete evidence for a clinical response, since dietary restriction of gluten might reduce the antigenic challenge to the immune system, leading to a serological response that is unrelated to the changes in stool frequency. Despite these limitations, this study has raised some important concerns regarding our sense of "security" in accepting normal histopathology to exclude celiac disease in patients having symptoms of IBS, and has opened the door to pursuing these issues in larger clinical trials. Is it possible that some simple and inexpensive tests will emerge to accurately diagnose IBS? I do not think that IBS can by diagnosed by ordering tests, either to make a unitary diagnosis, or by default by excluding other disorders. There is evidence that IBS is a heterogeneous disorder where different physiological subgroups contribute to the clinical expression of the syndrome. For example, there is a subgroup of patients, called "post-infectious IBS" who appear to respond to an enteric infection such as campylobactor jejuni with an increased inflammatory cell response (22). This is associated with activating enterochromaffin cells to produce 5HT, and CD3 cells to produce cytokines, which in turn leads to enhanced motility and lowered visceral sensation thresholds (22;23). But microscopic inflammation cannot be a diagnostic marker for IBS because it does not typically produce pain in those who have it. All patients with active celiac disease have microscopic inflammation, but a large proportion do not have abdominal pain, and patients with ulcerative colitis who also have microscopic inflammation when compared to patients with IBS appear to have higher pain thresholds (24). In individuals with these disorders, there may be central nervous system counter-regulatory measures responding to the peripheral pain/inflammatory processes that increase pain thresholds. With regard to IBS, the gut-related effects of microscopic inflammation may be only one component of a dysfunctional brain-gut system. In addition, and often in response to stress, there may be a failure to activate descending pain inhibitory systems that enable the clinical experience of pain and other symptoms that typify this disorder (25). In one prospective study of post-infectious IBS, it was found that those who retained their symptoms 3-months after an enteric infection had not only increased mucosal cellularity, but also had increased psychosocial distress at the time of the infection. Furthermore, lowered visceral sensation thresholds and increased motility were present after the infection regardless of whether or not the patients retained their symptoms (26). Therefore, the microscopic inflammation and its physiological effects on motility and sensation contribute to, but are not always sufficient for the clinical expression of IBS pain. At least for post-infectious IBS this provides some evidence that psychological distress alters brain pain regulatory pathways to amplify incoming visceral signals leading to the full clinical expression of this syndrome (27;28). Recent studies using brain imaging (29;30)may help us to understand the physiological mechanisms that modulate these CNS responses to pain, and in the process, identify the subgroup with IBS that are more amenable to psychological and psychopharmacological treatments. As we continue to develop the means to assess the pathophysiological determinants of IBS symptoms, we will continue to identify subgroups that will change our diagnostic assessment, and may even redefine what we mean by IBS. Post-infectious IBS, and patients having concurrent psychosocial disturbances (among others to be determined) characterize subgroups that will be more responsive to more specific treatments. For the present, we must still make a diagnosis of IBS based on established guidelines including symptom-based (e.g., Rome) criteria. We must also remain vigilant to identifying other relevant disorders like celiac disease that may mimic or exacerbate IBS, and will use clinical judgment (e.g., ordering anti-endomysial antibodies for patients with predominant diarrhea), rather than routinely ordering tests in all IBS patients just to exclude other disease. With careful appraisal of the historical and laboratory data and good clinical judgment, a positive diagnosis of IBS can be made in a cost-effective manner and with confidence. " http://www.romecriteria.org/reading1.html The above is less then three years old."Gastroenterology Expert ColumnDiagnosing Irritable Bowel Syndrome: What's Too Much, What's Enough?Posted 03/12/2004 Susan Lucak, MD IntroductionIrritable bowel syndrome (IBS) is the most common gastrointestinal disorder diagnosed in clinical practice in the United States. Because there is no biological marker to confirm the diagnosis of IBS, it is a diagnosis that has challenged clinicians for decades. In the past, IBS was a "waste-basket" diagnosis given to patients with unexplained gastrointestinal symptoms. It was considered to be "the diagnosis of exclusion" when extensive work-up for organic disease yielded no diagnosis.In recent decades, it was recognized that patients with IBS experienced a constellation of specific gastrointestinal symptoms. Manning criteria were described in 1978,1 followed by Rome I in 19892 and Rome II criteria in 1999.3 Rome I and Rome II criteria were initially developed by multinational working groups to provide a framework for the selection of patients in diagnostic and therapeutic trials. These criteria are being continuously modified as we gain new knowledge about functional bowel disorders.Recently published diagnostic guidelines4,5 recommend using symptom-based criteria in making the diagnosis of IBS in clinical practice. Using these criteria in conjunction with "alarm features" allows a physician to minimize the extent of diagnostic testing needed to make the diagnosis of IBS. Furthermore, recent systematic review of the literature indicates that performing a number of diagnostic tests did not result in a significant increase in the diagnosis of organic gastrointestinal disease.6EpidemiologyWhen making the diagnosis of IBS, it is helpful to consider it in the context of its epidemiology. IBS is a very common gastrointestinal disorder in the United States, affecting 10% to 20% of the population.7 Female patients outnumber male patients by 1.5-3.0:1.0 in most epidemiologic studies.8 Although it is not well understood why more women present with IBS, differences in healthcare-seeking behavior may partly account for this predominance.Smith and colleagues9 found that psychosocial factors were determinants of healthcare seeking for patients with both organic gastrointestinal disorders and functional gastrointestinal disorders. History of abuse is another important determinant in healthcare seeking.10Symptom-based CriteriaIn a given patient, the diagnosis of IBS is suggested by identification of specific symptoms. The Rome II criteria for diagnosis of IBS include presence of abdominal pain or discomfort for 12 weeks (need not be consecutive) in the preceding 12 months, and at least 2 of the following 3 features regarding symptoms: (1) relieved with defecation, (2) associated with change in frequency of defecation, and /or (3) associated with a change in form or appearance of stool. Patients with IBS may have additional symptoms, including passage of mucus and bloating or abdominal distension (Table 1).3 Although refinement and validation of these criteria are necessary, Rome II criteria are widely accepted as a diagnostic instrument in IBS."Alarm Features"An important aspect of making the diagnosis of IBS is the absence of "red flag" or "alarm features" (Table 2).4,11,12 Unexplained weight loss may reflect disorders such as malignancy, inflammatory bowel disease (IBD), or celiac disease. Persistent diarrhea or severe constipation may be associated with an organic disease.IBS is generally an intermittent and recurrent disorder. Symptoms of IBS tend to disappear at night when the patient is asleep. Thus, nocturnal gastrointestinal symptoms warrant search for a diagnosis other than IBS. The onset of new gastrointestinal symptoms after the age of 50 should prompt the physician to look for organic disease, particularly colorectal cancer. Blood in stool may reflect IBD or an infectious process or colon cancer. Family history of IBD, celiac disease, or gastrointestinal malignancy requires evaluation for these diseases. Fever suggests the possibility of an infectious or inflammatory disorder. Anemia should alert the physician to look for IBD or colorectal cancer. Signs of bowel obstruction, malabsorption, extraintestinal signs of IBD, or thyroid dysfunction should all prompt organic disease work-up. Any laboratory test abnormalities should be pursued appropriately. Absence of these "alarm features" serves to support, not establish, the diagnosis of IBS.Physical ExaminationThe American Gastroenterological Association (AGA) Technical Review on IBS recommends that a physical examination be performed, primarily to rule out organic disease.4 For instance, the presence of abdominal mass, signs of obstruction, or enlarged liver should trigger further investigation. A rectal examination identifying lax sphincter may confirm complaints of fecal incontinence, whereas paradoxical pelvic floor muscle contraction may suggest pelvic floor dyssynergia. In the latter case, anorectal motility study may be appropriate. Digital rectal examination is of further value in the assessment for fecal occult blood. A pelvic examination (performed by a gastroenterologist or a gynecologist) should be performed if symptoms point to the pelvic/lower abdominal area and are associated with menses.Diagnostic TestingReview of the current literature does not support performance of extensive testing in patients who meet symptom-based criteria for IBS and who lack "alarm features."6,13 Cash and colleagues[6] performed a systematic literature review of frequently ordered diagnostic tests as part of IBS work-up (Table 3). After careful assessment of the quality and validity of the selected studies, it was concluded that the pretest probability of organic disorders (such as IBD, colon cancer, thyroid disease, and lactose malabsorption) was not significantly increased in patients suspected of having IBS when compared with the general population. In other words, when patients fulfilled symptom-based criteria for the diagnosis of IBS, performing tests such as flexible sigmoidoscopy, barium enema, colonoscopy, rectal biopsy, complete blood count (CBC), serum chemistries, fecal occult blood test (FOBT), TSH, stool ova and parasites (O&P), hydrogen breath test for lactose malabsorption, or abdominal ultrasound did not result in a significant increase in the diagnosis of organic gastrointestinal disease. Specifically, performing a colonoscopy did not result in identifying gastrointestinal organic disease in more than 1% to 2% of cases.Widespread testing for celiac disease in patients who fulfill symptom-based criteria for IBS is not recommended.4,5 A matched case-control study in the United Kingdom showed 66 of 300 IBS patients had positive celiac disease auto-antibodies and 14 had biopsy-proven celiac disease compared with 2 out of 300 control subjects.14 This demonstrates a 7-fold increase in occurrence of celiac disease in patients suspected of having IBS. This study was, however, conducted in a secondary care setting. Given availability of effective therapy for celiac disease and prevention of long-term morbidity, testing for celiac disease with celiac disease auto-antibodies may not be unreasonable.The most recent AGA Technical Review on IBS4 recommends the performance of screening and other diagnostic tests as listed in Table 4. Colonic visualization with colonoscopy or flexible sigmoidoscopy/barium enema should be performed according to colorectal cancer screening guidelines. A colonoscopy is recommended for patients over the age of 50 years, but in younger patients, performing flexible sigmoidoscopy or colonoscopy needs to be determined by clinical presentation and sound clinical judgment.4,5 In many cases, therapy can be instituted before diagnostic studies are done or completed.The American College of Gastroenterology (ACG) Task Force comments on the value of "reassurance" derived from negative evaluation for organic disease.5 It is pointed out that the value of this "reassurance" is unclear and should be assessed in future clinical trials.The extent to which a diagnostic work-up is performed also depends on the severity of symptoms and where a patient with IBS presents.Primary Care SettingMost patients with IBS (about 70%) present to primary care physicians.4 Patients with IBS in this group have symptoms that tend to be mild in severity. A recently published evidence-based review by the ACG IBS Task Force concluded that routine testing among patients with symptoms "fitting" the Rome II criteria and no "alarm features" is not necessary in the primary care setting.5Secondary Care SettingMore difficult or more severe cases of IBS are generally seen by gastroenterologists referred from primary care physicians. The estimated prevalence of this subgroup is about 25% of all patients with IBS.If screening and other diagnostic tests were done by the primary care physician, they do not need to be repeated. The need for colonic visualization should be determined according to guidelines outlined above. Further evaluation may be warranted if a patient presents with any of the following features: (1) short duration of symptoms or worsening severity of symptoms, (2) onset of symptoms at an older age ( 50 years), (3) family history of colon cancer or IBD, or (4) absence of psychosocial features or absence of healthcare seeking.4During the first visit, it is important to explore with the patient possible contributing factors such as psychosocial issues (stress, anxiety, depression) and history of abuse. Up to 40% of patients may have a history of sexual, physical, or mental abuse.10Clearly, the right balance needs to be struck between making an accurate diagnosis of IBS and, at the same time, not missing other diagnoses that may mimic IBS. It is important to recognize, however, that if a patient diagnosed with IBS does not respond to a therapy, the diagnosis may be reassessed in 3 to 6 weeks and additional evaluation can be performed (see Table 5).4Tertiary Care SettingThe most severe cases of IBS and those most difficult to treat are seen in referral centers. The latter group comprises approximately 5% of all IBS cases. The clinical symptoms for this patient group do not tend to correlate with gut physiology. Rather, these patients tend to have constant symptoms, more psychosocial difficulties, greater healthcare-seeking behavior, more illness behavior (illness behavior is a way in which an individual perceives, interprets, and reacts to physical sensations that can be interpreted as symptoms of disease), and more psychiatric diagnoses.4Generally, most diagnostic studies have been performed by the time a patient with IBS presents to a referral center. Specialized studies such as defecating proctography, rectoanal angle measurement, anorectal motility and balloon expulsion, and investigational testing may be performed depending on clinical presentation and lack of response to previous treatments (see Table 5).4Differential Diagnosis and Durability of DiagnosisDifferential DiagnosisSymptoms of IBS are nonspecific and may mimic a number of disease entities (Table 6).15 It is important to recognize that in a given patient with IBS, these diagnoses need not be "excluded" before a diagnosis of IBS can be established.Durability of DiagnosisA number of studies conducted in community-based and specialty-based clinics over the past 3 decades have demonstrated that once the diagnosis of IBS is made, only a small percentage (0.7% to 6.5%) of patients subsequently receive a diagnosis of organic disease.16-20 These studies provide evidence that once the diagnosis of IBS is established, additional studies are not necessary unless the clinical symptoms change.Legal Risks in Diagnosing IBSSome physicians who see patients with IBS are concerned about the risk of malpractice. Feld21 recently described sources of risk under which physicians may be sued, including negligence, duty to provide care to a patient, and medical practice below standard of care, among others. But the idea that more testing is better in IBS may not always be the case. For example, colonoscopy leads to a change in diagnosis about 1% to 2% of the time and may represent performance of substandard care based on testing guidelines for IBS diagnosis recommended by gastroenterological associations in the United States. Therefore, any complication resulting from "unnecessary" testing may expose a physician to a malpractice suit. Alternatively, if a physician explains to a patient why only limited testing is necessary, this allows a patient to participate in the process and understand inherent uncertainties and thus share in the responsibility when a reasonable decision results in an adverse outcome.21 Feld's risk management recommendations are outlined in Table 7.Summary and ConclusionsWhat's too much when we think about diagnosing IBS is to do exhaustive and duplicate testing. In a retrospective, community-based study in Olmsted County, Minnesota, two thirds of patients who consulted for gastrointestinal symptoms had to wait at least 2 years to have their IBS diagnosed, despite averaging nearly 5 healthcare visits per year.20 Such an approach is not only costly and inefficient, but it delays treatment and fosters frustration on the part of the patient and the physician.What's enough is to use symptom-based criteria, "alarm features," and guidelines proposed by the ACG IBS Task Force and the AGA Technical Review on IBS in making a more timely diagnosis of IBS. Although additional studies are necessary to validate Rome II criteria and to assess diagnostic testing in prospective studies, the expert guidelines allow the diagnosis of IBS to be made with greater efficiency, certainty, and confidence. Furthermore, once a diagnosis of IBS is made, it is retained in more than 93% of cases with a long-term follow-up. Considering legal aspects of IBS diagnosis, symptom-based criteria and guidelines set forth by the ACG and AGA are becoming key elements in establishing standard of care. It has become clear that the diagnosis of IBS can and should be made quickly so that treatment can be initiated as soon as possible. This promotes greater patient confidence in the physician. http://www.medscape.com/viewarticle/465760_9 "In the new IFFGD Digestive Health Matters.Visceral Sensations and Brain-Gut Mechanisms By: Emeran A. Mayer, M.D., Professor of Medicine, Physiology and Psychiatry; Director, Center for Neurovisceral Sciences & Women's Health, David Geffen School of Medicine at UCLA IntroductionOver the past several years, different mechanisms located within the gut, or gut wall have been implicated in as possible pathoophysiologic mechanisms underlying the charecteristic IBS symptoms of abdominal pain and discomfort. The list ranges from altered transit of intestinal gas, alterations in colonic flora, immune cell activation in the gut mucosa, and alterations in serotonin containing enterochromaffin cells lining the gut. For those investigators with a good memory, these novel mechanisms can be added to an older list of proposed pathomechanisms, including altered gut motility('Sapstic Colitus') and alterations in mucus secretion. While the jury is still out, one unique aspect about the gut and its connection to the brain are often forgotten: Our brain gut axis is not designed to generate concious perceptions of every alteration in gut homeostasis and internal enviroment, in particlur when these changes are chronic, and when there is no adaptive behavioral response an affected organism could generate.Evolution has not designed our brain gut axis to experience abdominal pain every time the number of mast cells in our ileum goes up, or the number of our serotonin containing cells goes down. It would be counter productive for an animal with a chronic parasite infestation to experince constant viceral pain, and it wouldn't have any advantage for people living in third world countries with frequent enteric infections to suffer from chronic abdominal pain. It has been suggested that viceral pain maybe a secondary phenomenon of an elaborate system of signaling non painful signals to the brain: hunger and fullness (satiety), well being after a meal, urge to evacuate, ect. At the same time, powerful mechanisms have evolved that keep many other aversive signals out of concious perception: contractions, luminal distension, gas volume, low grade inflammation, ect..The most common symptoms of IBS patients are related to altered perception of sensations, arising from the GI tract, and frequently from sites outside the GI tract, such as the genitourinary system or the musculskeletal system. Sensations of bloating, fullness, gas, incomplete rectal evacuation, and crampy abdominal pain are the most common symptoms patients experience. Numerous reports have demonstarted that a significant percentage of functional bowel disorders (FBD) patients about (60) percent rate experimental distensions of the colon as uncomfortable at lower distension volumes or pressure when compared to healthy control subjects. This finding of an increased perception of viceral signals ("viceral hypersensitvity") has been demonstrated during baloon distension tests of the respective part of the GI tract regarless of where the primary symptoms are- the esophagus, the stomach, or the lower abdomen.In contrast to the current emphasis on mechanisms that may result in sensitization of viceral Afferent pathways in the gut, it may well be that alterations in the way the nervous system normally suppresses the perception of the great majority of sensory activity arising from our viscera are essential for the typical symptom constellation of IBS and other functional disorders to develop."It goes into a lot more detail and I highly recommend people get a copy and read the whole article."SummaryIn summary, it is clear that we still have a long way to go to understand the intricate connections between our digestive system and the brain, and how alterations in this two way communication result in functional bowel disorders symptoms. While more alterations in peripheral mechanisms involved in gut function are being reported, rapid progress has occured in our uunderstanding of the multiple mechanisms by which the brain can increase the concious perception of viceral stimuli, which is normally rarely perceieved." http://www.aboutibs.org/Publications/currentParticipate.html On the inflammation you still don't get it Tal and nor are they my researchers on IBS they are everyones and one of if not the top center in the US.I have told you this before, you have not put enough time in to be careful of how to interpret a lot of studies you post. You also suffer from extreme tunnel vision that IBS is only dysbiosis and bacteria.Even the people studying it think its a small part of the puzzle"Marshall is the lead author of a new study that may help explain how those symptoms start.The study involved 132 Walkerton residents with IBS and 86 residents without the condition. Average age was 46 years and about 60 per cent were female.Nearly 36 per cent of IBS cases had abnormal intestinal permeability, or "leaky gut syndrome," a condition in which the lining of the intestines allows more bacteria, toxins and food to leak in and potentially irritate the deeper tissue layers. In comparison, less than 19 per cent of non-IBS participants had a leaky gut.Marshall says his findings represent only a small piece of the entire IBS puzzle, but he hopes they will provide the basis for future research in the Walkerton population. "Why did NON IBS patients have "leaky gut"?This was also a virus outbreak.This also does not go into PI IBS infromation.
 

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If your going to tell people what IBS is Tal or even suggest it or how people get it, you better learn more about what they know and how they diagnose it, because you have not even grasped that yet, and while your at it study how digestion works in the first place.
 

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If your going to tell people what IBS is Tal or even suggest it or how people get it, you better learn more about what they know and how they diagnose it, because you have not even grasped that yet, and while your at it study how digestion works in the first place.
 

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Ask your experts at UNC or Spiller--both are researching now if inflammation can be the cause IBS symptoms. They must not think it's out of the question if they are studying it.And let's not forget JAMA's publication last month of Lin's work. He is my expert, whose research is funded solely by one family's riches, no Rx companies involved~~AUG 2004"CONCLUSIONS: The gastrointestinal and immune effects of small intestinal bacterial overgrowth provide a possible unifying framework for understanding frequent observations in IBS, including postprandial bloating and distension, altered motility, visceral hypersensitivity, abnormal brain-gut interaction, autonomic dysfunction, and immune activation." http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15316000 He believes dysbiosis of the small intestine can explain it all.(Although I believe the low bifidobacteria of the colon also needs to be addressed. I also believe the solution lie in probiotics, not antibiotics...maybe a combination, followed by a longer term on probiotics to prevent recurrence)
 

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Ask your experts at UNC or Spiller--both are researching now if inflammation can be the cause IBS symptoms. They must not think it's out of the question if they are studying it.And let's not forget JAMA's publication last month of Lin's work. He is my expert, whose research is funded solely by one family's riches, no Rx companies involved~~AUG 2004"CONCLUSIONS: The gastrointestinal and immune effects of small intestinal bacterial overgrowth provide a possible unifying framework for understanding frequent observations in IBS, including postprandial bloating and distension, altered motility, visceral hypersensitivity, abnormal brain-gut interaction, autonomic dysfunction, and immune activation." http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15316000 He believes dysbiosis of the small intestine can explain it all.(Although I believe the low bifidobacteria of the colon also needs to be addressed. I also believe the solution lie in probiotics, not antibiotics...maybe a combination, followed by a longer term on probiotics to prevent recurrence)
 

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From the the International foundation of functional GI disorders."Characteristicsof IBS How common is IBS?Most people with IBS have mild symptoms. Many people don't recognize IBS symptoms. Yet, IBS is one of the most common disorders seen by physicians. Irritable bowel syndrome is characterized by symptoms of abdominal discomfort or pain, usually in the lower abdomen (although the location and intensity are variable, even at different times within the same person), and altered bowel habit (change in frequency or consistency) -- chronic or recurrent diarrhea, constipation, or both in alternation. Abdominal pain has been reported as primarily crampy or a generalized ache with superimposed periods of abdominal cramps, although sharp, dull, gas-like, or nondescript pains are also common..The abdominal discomfort or pain are usually relieved with a bowel movement. "Irritable Bowel" refers to a disturbance in the regulation of bowel function that results in unusual sensitivity and muscle activity. "Syndrome" refers to a number of symptoms and not one symptom exclusively.Everyone suffers from an occasional bowel disturbance. However, for those with IBS the symptoms are more severe, or occur more often -- either continuously or off and on. IBS affects men and women of all ages. Some or all of IBS symptoms can occur at the same time -- some symptoms may be more pronounced than others. There are no physical findings or diagnostic tests that confirm the diagnosis of IBS. Diagnosis involves identifying certain symptoms consistent with the disorder and excluding other medical conditions that may have a similar clinical presentation. The symptom-based Rome II diagnostic criteria for IBS emphasize a positive diagnosis rather than exhaustive tests to rule out other diseases. These criteria are based on the presentation of a specific set of symptoms. In addition, a detailed history, a physical examination, and limited diagnostic tests help confirm this diagnosis with a high level of confidence. Extensive testing may be reserved for specific situations. The Rome II Diagnostic Criteria (a system for diagnosing functional gastrointestinal disorders based on symptoms) for IBS is as follows:At least 12 weeks or more, which need not be consecutive, in the preceding 12 months of abdominal discomfort or pain that is accompanied by at least two of the following features: 1) It is relieved with defecation, and/or2) Onset is associated with a change in frequency of stool, and/or 3) Onset is associated with a change in form (appearance) of stool. Other symptoms that are not essential but support the diagnosis of IBS: Abnormal stool frequency (greater than 3 bowel movements/day or less than 3 bowel movements/week); Abnormal stool form (lumpy/hard or loose/watery stool); Abnormal stool passage (straining, urgency, or feeling of incomplete evacuation); Passage of mucus; Bloating or feeling of abdominal distension. Upper GI symptoms are commonly reported by IBS patients with 25% to 50% of patients reporting heartburn, early feeling of fullness (satiety), nausea, abdominal fullness, and bloating. Many patients also report intermittent upper abdominal discomfort or pain (dyspepsia). Feelings of urgency, and a feeling of "incomplete" emptying may also be experienced.Many IBS patients also report non-gastrointestinal symptoms such as fatigue, muscle pain, sleep disturbances, and sexual dysfunction. These symptoms may be due to the coexistence or overlap of IBS with another condition such as fibromyalgia, chronic fatigue syndrome, or interstitial cystitis. Symptoms can vary and sometimes seem contradictory, such as alternating diarrhea and constipation. The symptoms of IBS are produced by abnormal functioning of the nerves and muscles of the bowel. In IBS there is no evidence of an organic disease, yet, something -- a "dysregulation" between the brain, the gut, and the central nervous system -- causes the bowel to become "irritated," or overly sensitive to stimuli. Symptoms may occur even in response to normal events. IBS is not caused by stress. It is not a psychological or psychiatric disorder. It is not, "All in the mind." IBS is not caused by stress. It is not a psychological or psychiatric disorder. It is not, "All in the mind." Because of the connection between the brain and the gut, symptoms in some individuals can be exacerbated or triggered by stress. Dietary and hormonal factors can affect symptoms of IBS. IBS is not an indication of another more serious disease, like cancer. Irritable bowel syndrome can, however, seriously compromise a person's quality of life. Chronic and recurrent symptoms can disrupt personal or professional activities, upset emotional well being, and limit individual potential.A significant proportion -- 35% to 40% -- of individuals who report IBS in the community are male. Approximately 60% to 65% of individuals who report IBS in the community are female.IBS is a major women's health issue. Data reveals an increased risk of unnecessary surgery for extra-abdominal and abdominal surgery in IBS patients. For example, hysterectomy or ovarian surgery has been reported in female patients with IBS as high as 47% to 55% and has been performed more often in the IBS patient than in comparison groups.There is a pressing need to support educational programs about IBS to the public and health care providers. Anemia, bleeding, weight loss, or fever are not characteristic of IBS. You should alert your physician immediately if you are experiencing these symptoms. Other factors that may suggest the presence of an organic disease include awakening from sleep at night, family history of colon cancer or inflammatory bowel disease, and onset of symptoms (or change in symptoms) over the age of 50. " http://www.aboutibs.org/characteristics.html
 

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From the the International foundation of functional GI disorders."Characteristicsof IBS How common is IBS?Most people with IBS have mild symptoms. Many people don't recognize IBS symptoms. Yet, IBS is one of the most common disorders seen by physicians. Irritable bowel syndrome is characterized by symptoms of abdominal discomfort or pain, usually in the lower abdomen (although the location and intensity are variable, even at different times within the same person), and altered bowel habit (change in frequency or consistency) -- chronic or recurrent diarrhea, constipation, or both in alternation. Abdominal pain has been reported as primarily crampy or a generalized ache with superimposed periods of abdominal cramps, although sharp, dull, gas-like, or nondescript pains are also common..The abdominal discomfort or pain are usually relieved with a bowel movement. "Irritable Bowel" refers to a disturbance in the regulation of bowel function that results in unusual sensitivity and muscle activity. "Syndrome" refers to a number of symptoms and not one symptom exclusively.Everyone suffers from an occasional bowel disturbance. However, for those with IBS the symptoms are more severe, or occur more often -- either continuously or off and on. IBS affects men and women of all ages. Some or all of IBS symptoms can occur at the same time -- some symptoms may be more pronounced than others. There are no physical findings or diagnostic tests that confirm the diagnosis of IBS. Diagnosis involves identifying certain symptoms consistent with the disorder and excluding other medical conditions that may have a similar clinical presentation. The symptom-based Rome II diagnostic criteria for IBS emphasize a positive diagnosis rather than exhaustive tests to rule out other diseases. These criteria are based on the presentation of a specific set of symptoms. In addition, a detailed history, a physical examination, and limited diagnostic tests help confirm this diagnosis with a high level of confidence. Extensive testing may be reserved for specific situations. The Rome II Diagnostic Criteria (a system for diagnosing functional gastrointestinal disorders based on symptoms) for IBS is as follows:At least 12 weeks or more, which need not be consecutive, in the preceding 12 months of abdominal discomfort or pain that is accompanied by at least two of the following features: 1) It is relieved with defecation, and/or2) Onset is associated with a change in frequency of stool, and/or 3) Onset is associated with a change in form (appearance) of stool. Other symptoms that are not essential but support the diagnosis of IBS: Abnormal stool frequency (greater than 3 bowel movements/day or less than 3 bowel movements/week); Abnormal stool form (lumpy/hard or loose/watery stool); Abnormal stool passage (straining, urgency, or feeling of incomplete evacuation); Passage of mucus; Bloating or feeling of abdominal distension. Upper GI symptoms are commonly reported by IBS patients with 25% to 50% of patients reporting heartburn, early feeling of fullness (satiety), nausea, abdominal fullness, and bloating. Many patients also report intermittent upper abdominal discomfort or pain (dyspepsia). Feelings of urgency, and a feeling of "incomplete" emptying may also be experienced.Many IBS patients also report non-gastrointestinal symptoms such as fatigue, muscle pain, sleep disturbances, and sexual dysfunction. These symptoms may be due to the coexistence or overlap of IBS with another condition such as fibromyalgia, chronic fatigue syndrome, or interstitial cystitis. Symptoms can vary and sometimes seem contradictory, such as alternating diarrhea and constipation. The symptoms of IBS are produced by abnormal functioning of the nerves and muscles of the bowel. In IBS there is no evidence of an organic disease, yet, something -- a "dysregulation" between the brain, the gut, and the central nervous system -- causes the bowel to become "irritated," or overly sensitive to stimuli. Symptoms may occur even in response to normal events. IBS is not caused by stress. It is not a psychological or psychiatric disorder. It is not, "All in the mind." IBS is not caused by stress. It is not a psychological or psychiatric disorder. It is not, "All in the mind." Because of the connection between the brain and the gut, symptoms in some individuals can be exacerbated or triggered by stress. Dietary and hormonal factors can affect symptoms of IBS. IBS is not an indication of another more serious disease, like cancer. Irritable bowel syndrome can, however, seriously compromise a person's quality of life. Chronic and recurrent symptoms can disrupt personal or professional activities, upset emotional well being, and limit individual potential.A significant proportion -- 35% to 40% -- of individuals who report IBS in the community are male. Approximately 60% to 65% of individuals who report IBS in the community are female.IBS is a major women's health issue. Data reveals an increased risk of unnecessary surgery for extra-abdominal and abdominal surgery in IBS patients. For example, hysterectomy or ovarian surgery has been reported in female patients with IBS as high as 47% to 55% and has been performed more often in the IBS patient than in comparison groups.There is a pressing need to support educational programs about IBS to the public and health care providers. Anemia, bleeding, weight loss, or fever are not characteristic of IBS. You should alert your physician immediately if you are experiencing these symptoms. Other factors that may suggest the presence of an organic disease include awakening from sleep at night, family history of colon cancer or inflammatory bowel disease, and onset of symptoms (or change in symptoms) over the age of 50. " http://www.aboutibs.org/characteristics.html
 
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