# New Study Helps Delineate IBS, Organic Bowel Disease and IgE Food Allergy Symptoms



## Mike NoLomotil (Jun 6, 2000)

EXPLANATORY NOTE:One of the most difficult issues to clarify for patients and even clinicians is the clinical presentation of IBS vs. Organic Bowel Dysfunction vs "Classic" Food Allergy Symptoms(IgE/IgG mediated Type I allergic reactions).It has been especially difficult to differentiate not only the clinical symptoms, but the mechanisms unique to each, so as to draw the distinction between "food allergy" and "food hypersensitivity".Particular difficulty is often experienced gaining an understanding of the food and chemical hypersensitivity reactions experienced in IBS, especially D and D-C types, (which for simplicity sake, as multiple mechanisms are involved and they are time and dose variable)which are for simplification and differentiation sake classified as "delayed-allergy" or "delayed hypersensitivity" synonymous with "reactivity" and/or "intolerance" as opposed to "food allergies" in the classic vernacular.This interesting report published September 2000 in the "European Journal of Gastroenterology and Hepatology" can, if understood, help establish a basis of understanding for the differences between the clinical presentation and the mechanisms of IBS, Organic Bowel Diseases, and "Food allergy"."Food allergy" being an immediate (short onset) hypersensitivity reaction elicited by even tiny amounts of allergen, presents a certain way clinically as regards the GI symptoms due to the mechanisms involved, as opposed to those reactivities of the systemic and deeper GI system seen in IBS symptoms elicited by foods or additives intolerance, and the distinctive, destructive, lesions of organic bowel diseases.The symptomologic associations revealed by this investigation are significantly consistent with the distinct mechanisms involved, and (as I will note in the summary following the abstract) allow us all to more clearly understand the distinctions of "food allergy", which only occurs in perhaps 3% of the population, as opposed to overall symptom sets of "delayed allergies" to foods and additives which may occur in excess of 30% of the population as a whole, 20% of the population exhibiting the symptom sets loosely identified as "Irritable Bowel Syndrome" or "reactive gut dysfunction".MNL www.leapallergy.com ____________________________________Eur J Gastroenterol Hepatol 2000 Sep;12(9):981-8SYMPTOMS DISCRIMINATE IRRITABLE BOWEL SYNDROME FROM ORGANIC GASTROINTESTINAL DISEASES AND "FOOD ALLERGY".Neri M, Laterza F, Howell S, Di Gioacchino M, Festi D, Ballone E, Cuccurullo F, Talley NJDipartimento di Medicina e Scienze dell'Invecchiamento, Sezione di Medicina Interna e Gastroenterologia, Universita G. D'Annunzio, Chieti, Italy.BACKGROUND: The value of specific gastrointestinal symptoms in discriminating irritable bowel syndrome (IBS) from organic disease has been documented. In contrast, there have been few attempts to identify symptoms that discriminate irritable bowel syndrome from food allergy, despite similarities in their respective symptom complexes. We aimed to investigate the value of symptoms in discriminating irritable bowel syndrome from organic disease and food allergy. METHODS: Subjects (n = 288) were recruited from consecutive patients presenting to the Internal Medicine, Gastroenterology and Allergy Units in Chieti. Patients completed the validated Bowel Disease Questionnaire (BDQ) prior to an independent diagnostic evaluation, which included endoscopy when appropriate. Food allergy was diagnosed using a 2-week elimination diet, followed by a placebo-controlled food challenge test, a skin prick test and serum RAST for specific IgE for suspected foods or additives. The results of the BDQ were not considered in formulating a diagnosis. In total, 99 patients were diagnosed with the IBS, 79 patients were diagnosed with organic disease and 22 patients were diagnosed with food allergy. A further 88 patients with extraintestinal allergies were included as a control group. RESULTS: Based on logistic regression analysis, six symptom items discriminated IBS from organic disease, while five symptoms discriminated patients with IBS from control subjects. A diagnosis of IBS compared to organic disease was positively associated with straining on defaecation (P=0.0001), diarrhoea (P=0.001) and abdominal bloating (P=0.01), but was negatively associated with pain in the upper abdomen (P=0.0004), reflux (P=0.0001) and appetite loss (P=0.004). A diagnosis of IBS compared to extraintestinal allergy was positively associated with pain relieved by bowel movement (P=0.0001), pain in the lower abdomen (P=0.0006), pain in both the upper and lower abdomen (P=0.003), frequent pain (P=0.001) and abdominal bloating (P=0.0009). In comparison between IBS and food allergy patients, a diagnosis of IBS was positively associated with pain in the lower abdomen (P=0.001), pain relieved by bowel movements (P=0.001), frequent pain (P=0.02) and abdominal bloating (P=0.03). CONCLUSION: Symptoms appear to be useful for discriminating IBS from organic gastrointestinal disease and food allergy.PMID: 11007133, UI: 20460199_______________________________________DISCUSSION:It is observed and opined that the multi-system mechanism for confirming "classic food allergy" was sufficiently rigorous to have assured effective differentiation of Type I allergic patients from IBS patients. Skin prick and Serum RAST (IgE/IgG) are commonly acknowledged as compromised in positive-predictability of FOOD allergy (excessive frequency of false positives) but the use of confirmatory double-blind placebo-controlled oral challenge following 2-week elimination dieting to isolate false positives should have been highly effective in isolating classic "food allergy" as the reaction is NOT dependent on dose consumed as is "delayed allergy" classes of reactions to foods or additives. ALL these methods are problematic in the context of identifying "delayed allergy" reactions.While the findings of clinical presentation of IBS vs Organic Disease are intuitive and simply confirmatory of prior findings, and the differentiation of IBS symptoms from "extraintestinal allergy" is expected, the symptomologic correlations which were found to differentiate "food allergy" from the IBS "reactive gut" are very helpful in demonstrating the distinctions of underlying mechanism."Pain in the lower abdomen""Pain relived by bowel movements""Frequent pain""Abdominal bloating"as differential findings of IBS vs "Classic Food Allergy" would be expected to be, and by this study appear to be well established as, symptoms that would not likely be associated with "Type I food allergy" due to the short-onset and immediate reaction elicited in "upper gut" tissue cellular response, systemic short term onset via rapid allergen absorption through the buccal and esophageal mucosa after ingestion, and the "immune mechanisms" involved in Type I "food allergy".These IBS symptoms are consistent with the reaction-delay associated with larger dose, slower onset (both due to the necessitates of transport of and absorption of the offending substance to the mid-gut, with a slower-onset of reactivity upon reaching a serum-concentration of allergen sufficient to elicit one or more pathways of response), as well as the chronic, persistent presence of "lowlevel-allergenicity" substances within the gut (frquent pain as opposed to infrequent episodic pain shortly associated with allergen contact in "allergy", bloating reflective of mid and lower GI dysmotility and chronically heightened sensitivity, and pain relief on elimination, also secondary to the chronic hypersensitivity of the gut to the luminal contents).Hopefully these findings will make it easier for both patients and practitioners alike to more readily perceive the distinctions between the reactions seen in true "food allergy" and those seperate and different mechanisms involved in the chronic low level hypersensitivity-reactions associated with IBS" or "Reactive Gut" syndrome.MNL________________ www.leapallergy.com


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## moldie (Sep 25, 1999)

Mike, could you summarize this in simpler terms for us plain flolk? My brain doesn't want to sort all of that out today.


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## wanderingstar (Dec 1, 1999)

Good article Mike, thanks for posting. But I'm confused. Does it mean that if I have an immediate reaction to ingesting even tiny amounts of a 'trigger' food, that that is a food allergy? All my 'trigger' foods affect me within 3 - 15 minutes, but I always thought they were intolerances or hypersensitivities, not allergies.







Also, I am 'truely' allergic to a particular food dye, but the symptoms typically only come on 12 - 24 hours after ingesting (but this is redness, itching and swelling of the face, not a GI thing), and this sort of delayed reaction would suggest an intolerance?







Sorry if I've misunderstood something... another long but productive day is nearly done!susan


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## Mike NoLomotil (Jun 6, 2000)

Sure Moldie. The main part of interest to those with IBS is that there are certain gastrointestinal symptoms found in irritable bowel syndrome that do not occur with any frequency in people with classic food allergies (food allergies are rapid onset after a small dose of the allergen). Those that ARE seen in IBS which can be used to SEPARATE the probability of the person having "classic food allergy" as opposed to "delayed hypersensitivity" as is seen in IBS are"Pain in the lower abdomen""Pain relieved by bowel movements""Frequent pain""Abdominal bloating"Which makes perfect sense since these are symptoms that suggest symptoms LOWER in the GI tract. It is also consistent with such things as finding increased tissue concentrations of mast cells in proximity to the ileocoecal junction (on the caecal side), non specific low level inflammatory evidence, prostaglandins in the feces, and discoordinate appearance of symptoms with ingested allergen. Hence the "delayed hypersensitivity" experienced with IBS.Food "allergy" symptoms appear from within minutes (allergen can be absorbed in some cases right through the mucosa of the mouth pharynx, and essophagus while you are chewing it) to 2 hours maximum (duodenal transit). In IBS the clincial symptoms can take up to 72 hours after ingestion to be fully manifest.So if you eat an allergen every (2) days and it takes (3) days to peak, ongoing symptoms will remain once established, and sooner or later the cumulative effect can elicit a "crisis experience" as the limit of tolerance of the reaction is reached (merely one illustration). This will not evidence any discernible pattern from simple obesrvations of "food in time vs. symptom time"...the two are hours even days out of sync, and it often includes things that are eaten daily in varying volumes, producing a permanent pattern of events of varying intensity that all run together to produce a chroncially aggravated and reactive neuroimmuneGIT condition ("twitchy bowel") which becomes permanently reactive to internal and external stimuli beyond diet, including mechanical stimulation and psychogenic stimulation (stress, anxiety, fear, ad nauseaum).In 'food allergy" chronic mid and lower bowel mast cell reactions are unlikely to be elicited since the allergen does not get there, if at all, until well after the clincial reaction has occurred...(assuming the reaction is not severe enough to cause it to eb expelled by vomiting). Also, it (classic "allergy")is EPISODIC...short and nasty and only when you eat the offending food. Note the differentiating symptoms are all essentially "ongoing", except the "pain relieved by bowel movements". This is consistent with the findings of exaggerated gut sensitivity to the vloume of contents which has been repeatedly demonstrated in IBS and is not seen in "food allergy"...expel the conents the pain ceases. Pain elicited by the crisis degranulation of a mast cell cell near a "pain receptor" is not going to be relieved until the chemical mediators released are removed.IBS symptoms like these are ongoing, may wax and wane or be cyclic, consistent with slow onset and variances in response to dose and exposure of any allergen.This is very useful clinically since if a patient presents with these specific symptoms listed there, this investigation confirms there is a very low likelihood of "food allergy". This is consistent with what the immunologists and doctors I work with have been trying to teach...food ALLERGY is not often involved in IBS, it is a DIFFERENT group of hypersensitivity responses, including both immunologic and non-immunologic.So if a person presents with those symptoms (and no other associated with Type I food allergy) then don't try to use "food allergy" diagnosis to isolate allergens or treatment based on those methods because it Won't Work. This has lead over the years to misunderstood observations, and the mistaken conclusion that food and the neuroimmuneGIT system do not interract to elicit IBS symptomology based upon those misinterpreted observations.This is why so many IBS patients and their doctors are driven mad trying to figure out which and how much allergen(s) are consistently causing the problem. They and everyone else are approaching it like they would FOOD ALLERGY and it cannot be apporached that way, in testing OR dietary evaluation! Doing so is a "Labor of Sisyphus". A different approach is needed and that is what those I work with developed and use.I hope that is clearer. If not, sorry I tried...ask again if some part is unclear and I will be glad to distill it further tomorrow.Have a DFE!MNL________________ www.leapallergy.com


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## Mike NoLomotil (Jun 6, 2000)

HI STAR:The worst thing about the whole subject is that problem of getting hung up on terms. THERE IS NO standard definition fo "intolerance" vs "sensitivity" etc. And to discuss it without cracking open an immunology book and going off the deep end is hard.IN GENERAL...if you get a FAST REACTION to something (anything) like you described, due to the way the different mechanisms work, and get SUDDEN GI symptoms or other symptoms (nausea, vomiting, diarrhea, swelling tongue, hives, whatever) this is what is classified as a Type I Hypersensitivity Reaction. This is what is referred to as an "allergy". In simplest form IgE specific to the allergen causes tissue and connective tissue mast cells to start to "degranulate" and release very strong "mediators" which trigger violent defense mechanisms against perceived invasion...expel the invader. In addition, other mediators are "formed" as the reactions progresses which effect specifi sites in the body (like prostaglandins an leukotrienes...very powerful 100xhistmainc effects).Eosinophils can be "recruited" in the GI tract, genitorinary tract, basically throughout the body and they contribute their "granular mediators" which can be toxic not only to an "invader" but to the bodys own tissues, so the body has some "limiting mechanisms" to control this part of the reaction.Basophils can also be recruited in an IgE Type I reaction and dump their similar mediators at effected sites in the tissues. Ultimately there is an "immediate phase" reaction and a "late phase reaction" in the allergic response. The immediate phase can be from 0 to maybe 2 hours to peak (shorter in inhalant allergies like asthma-pollen) and the late-phase can come 6-8 hours later.Common allergens are mostly small inhaled proteins, but can also come from insect bites, pollens, drugs, and some foods. reactions include gut, upper respiratory, lower respiratory, skin, other mucosa, and CNS effects in a variable pattern.Type II, III and IV as well as the cytotoxic reactions all have distinct mechanisms and characteristics as to the pathway and sequencing. Multiple reactions can occur and to varying degrees at different times. Its a little complicated....If you have been placed on a stoneage diet until you were asymptomatic, then given a blind oral challenge with the specific "triggers" you are talking about and you got sick within that time period you have confirmed food allergy. RAST and PRICK tests are not conclusive, and oral challenge must confirm it. As you demonstrate, people KNOW their FOOD ALLERGIES if they have them becasue the reaction is so distinctive.The chemical sensitivity you describe can be a TYPE I IgE reaction (allergy) with minimal or NO early phase reaction (ie: penicillin allergy only shiows a late phase reaction). If certain there is NO early phase reaction, is probably a Type IV delayed hypersensitivity reaction. These reactions are not IgE mediated. These are mediated by effector "T cells" which are specific for a sensitizing antigen. A TB test, for example, is an easy way to see an epidermal response of the Type IV class. Gliaden-sensitive enteropathy (Celiac Disease) involves this mechanism. The reaction not only is delayed due to the "mechanism" and time of recruitment, but it can take time when something like you describe comes into contact with self for the right type of T cell for that allergen to "show up" and start the reaction. these cells are "rare".This mechanism is quite different and involves recruitment of macrophages, activation, mediator release, local expression of chemicals which effect the blood vessel, and so on).So you are correct in your conclusions, do not let the terminology throw you off. Te word "intolerance" means nothing except in the context of a specific definition which must be given wehn the word is used.Gotta run...babysitting time tonite. I be around tomorrow morning if you want to "rap" some more.Have a DFEMNL_______________ www.leapallergy.com MNL__________ www.laepallergy.com


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## topsy (Jun 28, 1999)

Hi Mike, Thanks for the interesting article. I was wondering, (haven't done any research on this yet) but do you think any of the Eosinophils or Basophils "mediators" can escape to other parts of the body, joints in particular - as in rheumatoid arthritis - where the immune system is attacking the joint linings? I'm trying to find a relationship between the Type 1 allergy and resulting immunological reactions with an immune system "trigger" which results in a type of rheumatoid arthritis. Some types of RA are associated with IBS - and I wonder if it's actually a Type 1 allergy that is associated with it. Also, if it is not known what triggers the immune system to attack itself - as in RA - could years and years of undetected Type 1 allergy eventually trigger the immune system to go haywire? I'm probably way off here, but I would appreciate your thoughts.


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## Mike NoLomotil (Jun 6, 2000)

TOPSY;No you are not way off here actually. I am not the immunologist by any STRETCH of the imagination...this is one of the most difficult,complex and incompletely understood areas of human bodily function. I have to work real hard to comprehend what I am told by Pasula or Brostoff, or some of the Preventive Medicine Docs who have dedicated some study to this. I am not a "box of rocks" but these guys make me feel like one!That being said...OK...here is as much as I can explain.About 80% of patients with RA show an abnormal stimulus to what are called "B cells", these are cells that "make" IgM, IgG, and IgA antibodies specific for the a "region" of IgG. These "autoantibodies" are called RHEUMATOID FACTOR collectively.The joints affected by RA show leukocyte infiltration into the synovial area. The infilatrating cells are of several classes (T-cells CD4 and CD8, B cells, lymphoblasts, plasma cells, neutrophils, as well as macrophages). Among these are PLASMA CELLS that MAKE Rheumatoid Factor. Prostaglandins and leukotrienes (interleukins) are major inflammatory mediators which are "created" in the joint and producing many of the symptoms. Also neutrophils release what are called "lysosomal enzymes" which cause tissue damage. The RF elicits the formation of "immune complexes" which "worsen" the inflammatory symptoms.What this is meant to demonstrate (if you open an immunology book and start reading the sections not on immunity but on hypersensitivity and cytotoxicity and then reading about autoimmune reactions) is that it becomes obvious that multiple inflammatory reactions involving cell types involved in several types and mechanisms of "hypersensitivity" are already elicited and constantly activated in such diseases as RA.Hence the presence of chemical mediators, cellular triggers, immune complexes and so forth is already HAPPENING..already activated.So it is not unusual that food additives, and even some foods, which might otherwise trigger a very mild (if any) hypersensitivity reaction will COMPOUND the response if presented to the already active circulating immune system, releasing even MORE of these chemical mediators and aggravating an existing condition.Even if RA did not "predispose" one to hypersensitivity to foods or additives, statistically a large cross section of the population has BECOME reactive, and it is simple probability that some RA patients would also have this prediposition too. So even if there is NO other connnection or increased incidence in RA, there will be RA patients (30% ?)whose symptoms will be compounded by hypersensitivity to foods and additives to some degree.So we have found among patients tested in our beta site between 1997 and 1999 who were diagnosed with RA, all were test-positive for some food and chemical reactivity as well, and removing the reactive foods REDUCED the RA symptoms noticeably by removing the ADDED inflammtory mediator release (reduced the amount of these chemicals).So some patients experienced reduced pain and medication need, increased range of motion etc. just by directed diet therapy. They were "appreciative" to say the least.It is also interesting to POSTULATE that the higher incidence of use of NSAIDs like tylenol in RAs for pain relief will increase the frequency of IBS among RAs since epidemiologic studies have linked the two.BUT it is a chicken-or-egg question. IE: do RAs intrinsically demonstrate more IBS, and the use of tylenol and IBS frequency is thus coincidental, or does the overuse of the acetaminophen elicit a worsening sensitivity to inflammatory-response stimuli?I do not think anybody knows, or if anybody is even asking the question. Not knowing "jack-sh--" about this, I sure am not anyway. Having a hard enough time grapsing the basics!Have a DFWEMNL_______________ www.leapallergy.com PS: ON CAUSES OF AUTOIMMUNE DISORDERSOh boy thats another page to write...talking about autoantibody transfer (IgG) and then theoretical models...maybe tomorrow (I can hear everybody snoring)[This message has been edited by Mike NoLomotil (edited 10-21-2000).]


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## moldie (Sep 25, 1999)

Thanks once again Mike. I hope I can explain it to my GI doctors that way. It's hard to teach old dogs new tricks though (especially when it comes from a patient)!


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## Mike NoLomotil (Jun 6, 2000)

Hi Moldie.Just be real non-judgemental as some are touchy about "not invented here" and some are touchy when the basic "eat fiber, relax, take pills and stop bugging me" does not satisfy the patient. Others are more open and will stop and look. Sometimes you can take and give them a copy of some of the stuff a patient like LISA posted...just print it out ask them to read it and make their own judgement. Don't ask for them to "support your new theories you read about" on the spot...just "I have been hearing a lot about some of the new dietary approaches based on food and additive hypersensitivity really helping and I thought you might be interested...here is one patient". Then they see the "paths" to the links and locations and names and articles and they can look themselves at their leisure without a patient badgering them, and form their own conclusions.On the one hand they are often compelled to reply "Oh poo-poo anecdotal poo-poo-" becaseu 8 times out of 10 they are basically right...there is a lot of anecdotal poo-poo given to their patients and they want to protect you.But a clinician with a lot of experience also knows that effective new clinical therapies often start that way...and will want to look himself for the signs of "relevant" anecdotal data. It is hard to ignore a refractory IBS/Fibromyalgia patient whose father is chairman of the board of a hospital (patients like that are not idiots being tricked) who was on 20 meds and a cripple going into 100% remission and losing 20 pounds of unwanted weight after a DIETARY change ("don't eat a carrot?"), and then to look at what it is based on, and that it is a physiologic technology base that patents just got issued on month ago...so, like no wonder its not around yet!One of the most conservative Board Certified Gastroenterologists in Palm Beach (his practice is at the hospital in the HEART of Palm Beach so you know the clientele he would cater to) is a doc I first met with about this 18 months ag. His dietician started doing it with some of her private-practice patients and was impressed. So that got me in the door. He looked, he listened, he was polite, said it was interesting and logical and he would be interested to see how it evolves. I simple suggested if someone came round asking for it would he let that person try it.He said maybe. Took him about 4 months to decide. He talked to other doctors who knew us and had tried it. They verified what was claimed. Finally someone from Palm Beach who had a friend use the method called us and we referred her to him since he was the closest doc. So he tested her and put her on the diet we gave him (showed him how to use it).He now has tested several of his own serious D type and cyclic IBS patients. Quietly...he is not going around bragging he is doing something that has not been published in NEW ENGLAND JOURNAL OF MEDICINE or something yet because he understands how the "system" works. But we have quite a few docs like that. Blood tests just keep showing up in the lab with their names on the requisition...so if it did not help their patients they would not be ordering it.Most people just get to "forward" when they are trying to get a specialist to consider or try something the specialist did not recommend and give him no choice to preserve his integrity with the patient when put on the spot for a decision but to steer the patient away from it.So you just give them some info of what other people have done...and a path to the references and areas it is explained, and see if they come to it themselves. Works better unless you are REALLY CLOSE with the doc like I am with my PCP. Then it can be full-speed ahead.have a good WEMNL___________ www.leapallergy.com


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## topsy (Jun 28, 1999)

Thanks Mike - I appreciate your input on this theory about RA and allergins and IBS. It all seems so related, somehow. I'm sure you've seen many, many elderly patients in your IBS work who also have RA, and I figured you might have a little inside info or some observations about the connection. Thanks again - have a DFD.


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## Guest (Dec 13, 2000)

Mike, this is great but still a little confusing. Would it be possible to again simplify the difference between symptoms of each? Maybe list not only the ibs exclusive symtoms, but the exclusive symptoms to food allergy and organic bowell disease as well. I'd like to compare. Thanks Mike,BRIAN


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## Mike NoLomotil (Jun 6, 2000)

HI BRIAN.I am sorry I am so busy I cannot keep up with following up on posts and I miss some.I understand your question...and I would like to give a very concise answer and the authors of the paper make it sound like there is one. There is not.If it takes Professor Brostoff, the worlds leading authority on the subject, 450+ pages to delineate food allergies from non-allergic food and chemical intolerances I am overwhelmed by trying to make it as simple as many investigators try to make it sound.There are food allergy reactions mediated by allergen-specific immunoglubolins like IgE and IgG involved the classic Gel & Coombs classifications as may be applied to foods and additves, yet it is clear there are many diseases related to food and chemical intolerance which present as severe immune reactions in which the reaction does not fit the outdated Gel and Coombs classifications. The doctors I work with who have been investigating this for several decades have quantified that IBS patients fit this description (atypical reactivity).And people forget that food allergy symptoms are not restricted to the GI tract...all manner of other conditions have been linked to Ig(x) and non Ig(x) reactivity.For example in the gut it is recognized that such reactions as allergic eosinophilic gastroenteritis, eosinophilic esophagitis, and others that involve eosinophilic infiltration of the epithlium and in some provoking foods Ig(x) is involved and some it is not.In this study, they "identified" food allergies my mixing (3) standard techniques that, when used together, are reliable in identifiying a true Ig(x) mediated food allergy: skin prick (used alone only 50/50 accurate); RAST (used alone accuracy depends on who claims it...but better than 50/50) and oral challenge (if done properly and double blind it is the gold standard for ALLERGY identification of the specific food tested). So I would assume that they confirmed a specific allergy by getting a 3-way match, as the skin and RAST alone produce false positives, and oral challenge could elicit a reaction that could be from a "non allergic" reaction (non Ig(x))if the dose-sensitivity was high (low dose to trigger).---------------------------------"A diagnosis of IBS compared to extraintestinal allergy was positively associated with pain relieved by bowel movement (P=0.0001), pain in the lower abdomen (P=0.0006), pain in both the upper and lower abdomen (P=0.003), frequent pain (P=0.001) and abdominal bloating (P=0.0009). "One would assume that the use of the word "extraintestinal allergy" means patients with allergies whose symptoms are non-GI like rhinitis or dermatologic or something. So the IBS patients had these characteristics and the non IBS patients WITH allergies that cause other symptoms did not...seems kind of self-evident, unless they mean something else I am missing.-----------------------------------"In comparison between IBS and food allergy patients, a diagnosis of IBS was positively associated with pain in the lower abdomen (P=0.001), pain relieved by bowel movements (P=0.001), frequent pain (P=0.02) and abdominal bloating (P=0.03)."What this basically says is that these symptoms predominate in IBS and did not predominate in confirmed food allergy. This only makes sense since food allergy GI symptoms if present are more associated with rapid onset, may be upper gut pain and nauseaa to vomiting, then lower gut pain and diarrhea and the pain is not relieved by the dirrahea initially until the "gut-flush response" is completed. In between exposures the patient is asymptomatic. So the symptoms of food allergy when evidenced in the gut per se (Ig(x) mediated) are more sudden, dramatic, and episodic. As opposed to the IBS patients who had more chronic pain, the pain predominated in the "lower abdomen", could often be relieved by defecation,and they complained of the bloating-sensation which Ig(x) food allergy patients did not complain of.So when presented with specific symptom sets one can differentiate the IBS patient from the gut-reacting food allergy patient. heck, we saw that at least 15 years ago. But it is nice that someone went to the trouble of putting this in this journal._________________________________So this is a very very rudimentary discrimination, HOWEVER it is highly logical and effective for the patients studied for whatever specific "food allergy" reactions they confirmed.The immunologists I work with have known for years that Ige/IgG mediated reactions are not associated with IBS symptoms. They may be present but are a secondary finding in a subpopulation of unknown size since no one has ever tried to quntify that population.I know this is confusing, and is why I recommend Brostoffs Book on the subject...it is very educational and an easy read: http://www.amazon.com/exec/obidos/ASIN/089...6487508-3420903 Dr. Brostoff is a Consultant to us in Allergy and Clinical Immunology. I receive no commission or any form of compensation from the sale of his books. I recommend them because he is brilliant and he knows more about this than just about anybody, and he is a very conservative and careful investigator.I think his book should be in the library of all patients who exprience reactions of any kind to foods, additives, or inhalants.Have DFD and I hope I did not confuse the matter further>MNL__________________ www.leapallergy.com


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