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Found 13 results

  1. Ansti

    Sandy poo

    Hi, I was Googling sandy, tarry stool and Celiac threads dominated the search results! I was wondering if I could ask the other parents here a question. In essence, it's 'Do any of your children have seasonal stool symptoms?' I'll explain... My son has had a cluster of symptoms - chronic fatigue, emotional/behavioural problems, black sandy stool, foul smelling breath, joint aches, constipation etc - but it's very markedly worse between February and June. This has happened every year since he turned 2 (although the sandy stool only became obvious last year, so 2 years in a row now), so this is the fourth year that the pattern of ill health is repeating. I'd discounted Celiac as a possibility because of this seasonal pattern. Am I right?
  2. Hello! Hoping some of the more well versed Celiacs here may have a bit of input on my recent situation. Additional and relevant details also included. Quick Celiac Backstory: Mother and sister were diagnosed with Celiac circa 2003. I at the time was blood tested (borderline results) and scoped (negative, no noticeable damage to cilia / villi). I've went through life on a non-gluten free diet as any guy that was told they don't have Celiac would do, am now just shy of turning 30, and decided to get another blood test (this time a newer antibody one). The results were a very strong positive for Celiac, which isn't surprising given my family history. I haven't gotten scoped as I see little actual point in it; I don't doubt I have Celiac. This was about May 1st. I've eaten Gluten Free since then. Relevant Background Information: Main reason how I've went undiagnosed for so long is I've been by and large asymptomatic. My mom and sister were super sick and a wreck GI wise, that's what led to their diagnosis. I probably poop a little more than the average person, but of a normal Type 4/5 Bristol scale (important for later!). My bowel movements don't typically disrupt my life. I didn't feel foggy, nauseous, swollen, or the typical other symptoms. I do have acne flare ups and a hand rash on a few fingers, but not sure they're Celiac related (not sure they aren't, also.) In April I decided I was a bit overweight. I was 5'9", 185 lbs. I started counting calories and eating mostly healthy food. Lot of rice, chicken, and vegetables. I have comfortably lost 10 pounds in 2.5 months, a very safe rate to lose weight. In mid-May I started also cutting added sugars and simple carbs, like white bread, etc. I wouldn't say I was eating Gluten-Free at that point, but definitely a lot less than I ever had before. Around this time of cutting out sugars, my stool started getting a bit softer, and while not diarrhea, definitely a 5-6 on the Bristol scale. I had considered it could be some sort of Candida / yeast / gut flora rebalancing. The soft stool also contains some solids in it, which I later determined to be what I believe is rice husks. I also eat granola with gluten-free oats daily for breakfast with yogurt. After cutting out all gluten, it's looking even a little less solid. I think that today I saw some oat-y looking things in there. While not yellow, it's definitely more yellow-brown than it used to be. My question is this. Does it make sense for my stool to get softer and exhibit the characteristics above while switching to a gluten free diet, or has anyone perhaps experienced this and know what might be up? The only reason I started cutting added sugars and simple carbs in the first place was in attempts to get healthier. I have been eating rice regularly and also greek yogurt and granola for literally years almost day. (Though it wasn't gluten-free granola before.) So it's not a change in the types of fiber going through me. My plan is to cut out oats for a bit as I hear that's a good suggestion for people starting gluten-free diets. I still don't feel ill, nauseous, or really any different than before I went gluten free. Around the time I cut sugars, my stomach was considerably more bubbly and gassy, which I attributed to a change in diet. Unless something stands out to someone as telltale signs of something else, I think it's completely reasonable to carry on with everything else that I've been doing for a month or two and monitor the progress. Thanks for the long read and thanks for any input or advice!
  3. A week ago Johnny Rockets mistakenly served us regular gluten buns, not thinking of the miscoloring, I ate it. I had EXTREME gas pain, bowel movements and blood the night after and have been suffering through tons of blood when having a bowel movement ever since. Tonight though.. I had the weirdest looking poop like seperated in weird ways and I don’t know if it should be a concern? I’m sorry for any graphic images but I need to know asap!
  4. A couple months ago, I started having yellow stool and it has not stopped since. I’m 14 and I got my period when I was 12 and have never skipped a period. However, my body frame is quite small and I look like a 11 year old. I have always been at the lower end of the growth percentiles but I’ve never lost a drastic weight but I’ve grown slowly always maintaining my curve. Has anyone with celiac have yellow stool for several months? I’ve always had low appetite and I’ve gained weight slowly. My breasts aren’t quite as developed as they should but I eat plenty to calories. My period wasn’t delayed so I’m not sure if I have celiac but I was wondering if my symptoms point to anything. Am I just slow to mature? Is stool change a first sign that something is not absorbing the way it should or does this mean my intestines are highly damaged? The stool color has me worried. I have no pain just some bloating.
  5. Hi All, For the past two months, I am passing large volume of stool occassionally. For example, I may have one bowl movement today but tomorrow i might have 4 bowl movements. I have done stool test and Upper Abdomen USG and they are showing everything normal. I was feeling gassy but the problem has subsided a lot of late. But the main problem is that when I had 4 BMs, the amount of stool is very large as if I am pooping more than what I am eating. I have seen two gastroentrocologists and they are saying it is because of stress. I am feeling no pain but I have lost 10KG weight in the past two months. Is this normal? thanks a lot for your support.
  6. Hey all, I am noticing much more stringy / mucus with my poop now that I have gone gluten free (about four days now). I know it can take a while to reverse the effects of gluten, so is this normal? To have more of that mucus than before?
  7. Ildiko

    Blood in stool?

    Hi - my 9 year old daughter was diagnosed in February. She had a seemingly routine winter cold and developed stomach pain, diarrhea, and blood in her stool. Blood work and biopsy tested positive for Celiac. We put her on a gluten-free diet right away and she improved significantly and quickly. The blood stopped almost immediately. She still gets almost daily mild stomach pain/gas pain. It lasts only a minute or two. A few days ago her class used flour in science to make play dough (I was not aware). She got diarrhea a day later and a few days later she had some blood again in her stool. Has anyone else had experience with: (1) blood in the stool and (2) ongoing daily mild tummy aches even after gluten-free? I am so worried about her. Thank you!!!
  8. I know this is sort of a gross topic but I would really really appreciated any help. How yellow exactly did your stools look? I keep thinking my stools are yellow (this might be bc im really paranoid and think that my stools gonna be yellow) but my mom thinks that they are just borderline yellow but leaning on brown. It was like a very dark turmeric color. If you mixed turmeric and brown together.She also thinks that it's because of the foods I've been eating which are mainly yellow curries and rice. I'm still on a gluten diet since the doctor said to wait for biopsy results. I'm really really scared. Please help. The poop didn't float but also there was a lot of it so it couldn't really float. I started taking Citrucel on the recommendation of my GI which is why my stool is so large. I don't really have much abdominal pain. Just slight bloating when I wake up.
  9. Two years ago I suffered from a bout of diarrhea and abdominal pain for 7 days. During this time period I ate HEAVY amounts of gluten. Sometimes two sandwiches w/ wheat bread 2 times a day, pasta for dinner, and honey wheat smacks at night. I went to doctor and eventually GI. The tests they ran came in as follows: Total IGA - Normal EMA IGA - Negative tTG IGA - Negative Gliadin DP IgA - Negative Gliadin DP IgG - POSITIVE; Score of 43 U/mL Gene Test: LOW RISK DQ2.2 Heterozygous By the time I saw the GI my symptoms had subsided. He told me not to worry and that Celiac is highly unlikely. Said biopsy wasn't necessary given my genetic markers and lack of symptoms. I wasn't convinced so I monitored my body closely. As 2015 went on symptoms would reoccur but were mild. I'd have abdominal pain and lose stools for one day. Eventually these attacks disappeared even though I continued eating gluten. In 2016 I had my next physical. No flags and no signs of malabsorbtion. Numbers were literally perfect. If I have Celiac, symptoms are EXTREMELY MILD. At least two times a month I get a minor headache. I had a few canker sores last summer. Sometimes I have minor bloating. Had a loose stool last month. But overall, I am very healthy. I run 2-3 miles a day, have a very physically intensive job, and feel great. So obviously I'm getting some mixed signals here. These symptoms appear in healthy people as well! Also there is no consistency in symptoms! I can still eat a big mac and feel fine! I am in the process of getting 2nd opinion. On one hand I fear that I'm in the early stages of Celiac. But at the same time I don't want to follow a highly restrictive diet unless its necessary. On the other hand, I've read studies how high gluten intake can lead to something called leaky gut (even in healthy people). So it is possible I inflamed my gut temporarily and then healed after a few months. Either way I need an answer. Even though I feel good now I don't want to wake up with cancer in ten years! What is your assessment of my situation? Also, do some of you also have VERY MILD symptoms? What did your labs look like and did you have any signs of malabsorbtion? Finally, do any of you have this low risk 2.2 Heterozygous gene? Like I said I'm getting another opinion shortly. But I'd like some peace of mind either way.
  10. maddierozell

    Suspected Celiac In Toddler

    I have a 19 month old son that I am suspecting may have Celiac. He is very small. He is 19lbs and only 27" tall. He has been sick since the day he was born. He is constantly constipated and vomits almost daily. He also has chronic respiratory infections. As of about 4 months ago, I started seeing these small liquid filled sacs in his stools. They are comparatively about the size of a grain of rice. The will pop if you squeeze them and a clearish yellow liquid will come out. I have had him tested for parasites and it came back negative. My son has always had issues with constipation and gas. His stomach stays big and swollen. We have an appointment at Texas Children's with a GI next month, I am just trying to narrow down things I can bring up to the doctor. When looking at the symptoms of Celiac's everything seemed to click. Right down to his asthma and size issues. When I asked his pediatrician about the sacs in his stool he was at a loss and could not even begin to make a guess. I myself also have had a diagnosis of IBS with bad episodes of constipation and diarrhea. Celiac is the first thing in my mind and I am kind of just wondering if these things sound like this may be the answer to our problems? Any help would be extremely helpful and appreciated.
  11. Celiac.com 02/02/2013 - The possible link between the makeup of gut bacteria and celiac has been a subject of past discussion in "More Evidence Links Gut Bacteria to Celiac Disease"[1] and other articles. Certain gut bacteria appear to enhance the immune response to gluten which may contribute to the onset of celiac disease. Vitamin D may reduce or eliminate this enhanced gluten response, and, therefore, vitamin D deficiency may be a significant factor contributing to the onset and development of celiac disease.[2] "Fecal transplantation", probiotics, and vitamin D have been advocated as possible therapy, treatment, and/or preventative measures against celiac disease. While vitamin D and probiotics may have potential as preventative measures against the onset of celiac disease early in life, the option of a fecal transplant provides the actual possibility of restoring tolerance to gluten or curing celiac disease later in life following long-term intestinal mucosal recovery on a gluten-free diet. In particular, fecal transplantation might make it possible to treat refractory celiac disease which does not respond to a gluten-free diet. Fecal transplant therapy for gastrointestinal disorders was pioneered by the world reknown Australian gastroenterologist, Prof. Thomas J. Borody, M.D., and is now used most successfully for treatment of persistant C. difficile infections of the gastrointestinal tract. Fecal transplantation involves the actual transfer of screened and filtered fecal material from a healthy donor into the gut of a patient, previously treated with antibiotics to clear gut bacteria, replacing the patient's own gut bacteria with a healthy mix of donor gut bacteria. The fecal material may be administered either orally or anally, via tubes. Selecting and screening a healthy donor, usually a spouse or close relative, as well as the "disgust" factor have limited use of this therapy in past years, but its high anecdotal success rate for treating stubborn C. difficile cases is finally bringing fecal transplantation into the mainsteam of routine gastrointestinal practice. The first clinical trial of fecal transplant therapy involving 43 C. difficile patients compared to conventional vancomycin antibiotic therapy has just been published finding fecal transplantation 3 times more effective than vancomycin in resolving C. difficile infections.[3,4] To date, there does not appear any record of an attempt or clinical trial to treat celiac disease via fecal transplant therapy. A big problem preventing any significant clinical trial of fecal transplantation for celiac disease is there is no way to "standardize" the healthy donor fecal material. The mix of bacteria from every donor is unique. Each donor must also undergo careful screening for harmful fecal pathogens. But, now, recent developments may make such a clinical trial feasible. A synthetic stool substitute was successfully used to clear C. difficile infections in 2 patients as part of a "proof-of-principle" study which may lead the way to eliminate the need for individual healthy feces donors and the need for screening tests. The synthetic stool consisted of a mix of 33 bacteria species isolated from the stool of one healthy donor and cultured under simulated intestinal conditions.[5,6] Such a standardized synthetic stool potentially administered orally in capsule form could make large scale fecal transplantation clinical trials possible. An "off-the-shelf" bacteria mixture specifically developed for the treatment of celiac disease might become a reality. In the case of refractory celiac disease, a gluten-free diet does not stop the continued destruction of the intestinal mucosa. Research has not yet found the reason for refractory celiac disease, but "molecular mimicry" may be one possible cause. Celiac disease is an immune response to particular sequences of amino acids in gluten peptides called epitopes. In the absence of gluten, if there exist peptides from other sources with amino acid sequences matching or "mimicking" these gluten epitopes, the destructive immune response may continue to damage the mucosa. This is molecular mimicry in action. It is possible that some gut bacteria may express some of these epitopes on their surface, or, more likely, secrete peptides that contain these epitopes. These bacterial secretions might then coat the lining of the intestine sustaining the immune response. Secreted epitopes are the more likely cause of refractory celiac disease than bacteria surface epitopes because the immune system would eventually destroy the bacteria if bacteria surface epitopes were involved. But if the cause were the bacterial secretion epitopes, the bacteria itself would not be attacked and would continue to produce the secretions indefinitely perpetuating the mucosal damage. Fecal transplant therapy might cure refractory celiac disease by eliminating the gut bacteria producing the epitope mimicking secretions. How likely are such gut bacteria molecular mimics to exist? One study has investigated this for the case of multiple sclerosis and concluded there is a strong likelihood that "normally occurring gut bacterium" could produce epitopes that might cause MS through molecular mimicry.[7] One case of molcular mimicry between human peptides and wheat peptides has been found.[8] In the case of normal celiac disease (non-refractory celiac disease) treatable by a gluten-free diet, after some length of time on a gluten-free diet when the antibodies to gluten epitopes have cleared and when the intestinal mucosa has sufficiently healed, it may be possible to reprogram the immune system to tolerate gluten through fecal transplantation, along with vitamin D supplementation, providing a new healthy gut bacteria mix. One problem, however, is that in many cases the damage to the intestinal mucosa from celiac disease does not entirely heal.[9,10] This means that a long-term or permanent state of increased intestinal permeablity or "leaky gut" exists after beginning a gluten-free diet. "Leaky-gut" is by no means a benign condition. It puts a strain on the liver's detoxification abilities having to continually deal with toxins readily passing through the "leaky" intestinal mucosa. The toxins come from gut bacteria as well as from drugs and environmental chemicals including household products and cosmetics. Inhaled environmental toxins can be ingested when mucus expelled from the lungs is swallowed. The overload on the liver and its inability to keep up with detoxification can lead to long-term debilitating medical conditions such as wide-spread chronic pain, muscle pain and weakness, neuropathies, fatigue, dry mouth, frequent urination, swelling, allergies, and even to other autoimmune disorders[11] due to fat soluble toxins accumulating in adipose tissue where they remain causing inflammation and raising havoc indefinitely. The result is an unfavorable pro-inflammatory immune system environment which could impede any chance of restoring gluten tolerance. A promising treatment that could entirely heal the intestinal mucosa and "leaky gut" is a treatment based on a novel protein called R-spondin1. Prior to January 2009 a small San Francisco pharmaceutical company, Nuvelo, was developing an R-spondin1 therapy drug with the designation, NU206. NU206 had shown some great promise and success in lab studies. Dramatic mucosal healing was demonstrated in an experimental colitis model with mice.[12] Nuvelo's first targets were to use NU206 to heal and reduce intestinal mucosal damage from cancer chemotherapy and radiation therapy and to treat short-bowel syndrome. In December 2008 Nuvelo had actually announced results from Phase 1 clinical safety trials on 32 healthy male volunteers demonstrating administration of NU206 caused no adverse effects.[13] Unfortunately, Nuvelo, which also has other drugs in development, ran short of funding and, in January 2009, merged with a Colorado company, ARCA biopharma.[14] ARCA biopharma is dedicated to developing genetically-targeted therapies for cardiovascular diseases. [http://www.nuvelo.com/] It appears that all NU206 research and development and clinical trials were suspended with the merger. NU206, an extremely promising drug that might enable full intestinal mucosal healing and recovery in celiac disease now sits idly on a shelf with no indication clinical trials will ever resume. While there has been some very limited research on R-spondin1 in other medical applications by other scientists, there has been no new R-spondin1 research on intestinal healing since the merger. Any celiac disease interest group with access to funding for celiac disease research should consider contacting ARCA biopharma to see what efforts might be implemented to restart this very important R-spondin1 research. Sources: 1. More Evidence Links Gut Bacteria to Celiac Disease Roy S. Jamron Celiac.com 2008 Nov 6. https://www.celiac.com/articles/21685/ 2. Do Vitamin D Deficiency, Gut Bacteria, and Gluten Combine in Infancy to Cause Celiac Disease? Roy S. Jamron Celiac.com 2008 Jun 16. https://www.celiac.com/articles/21605/ 3. Fecal Transfer Proves Potent Clostridium difficile Treatment Jenni Laidman Medscape Medical News 2013 Jan 16. http://www.medscape.com/viewarticle/777772 4. Duodenal Infusion of Donor Feces for Recurrent Clostridium difficile Els van Nood, Anne Vrieze, Max Nieuwdorp, Susana Fuentes, Erwin G. Zoetendal, Willem M. de Vos, Caroline E. Visser, Ed J. Kuijper, Joep F.W.M. Bartelsman, Jan G.P. Tijssen, Peter Speelman, Marcel G.W. Dijkgraaf, Josbert J. Keller NEJM 2013 Jan 16; Published Online http://www.nejm.org/doi/full/10.1056/NEJMoa1205037 5. C difficile: Synthetic Stool Substitute Clears Infection Jenni Laidman Medscape Medical News 2013 Jan 10. http://www.medscape.com/viewarticle/777515 6. Stool substitute transplant therapy for the eradication of Clostridium difficile infection: "RePOOPulating" the gut Elaine O Petrof, Gregory B Gloor, Stephen J Vanner, Scott J Weese, David Carter, Michelle C Daigneault, Eric M Brown, Kathleen Schroeter and Emma Allen-Vercoe Microbiome 2013 Jan 9;1:3. http://www.microbiomejournal.com/content/1/1/3 7. Molecular mimicry revisited: gut bacteria and multiple sclerosis. Westall FC. J Clin Microbiol. 2006 Jun;44(6):2099-104. http://jcm.asm.org/content/44/6/2099.long 8. IgA cross-reactivity between a nuclear autoantigen and wheat proteins suggests molecular mimicry as a possible pathomechanism in celiac disease. Natter S, Granditsch G, Reichel GL, Baghestanian M, Valent P, Elfman L, Gronlund H, Kraft D, Valenta R. Eur J Immunol. 2001 Mar;31(3):918-28. http://www.ncbi.nlm.nih.gov/pubmed/11241297 9. Mucosal healing and mortality in coeliac disease. Lebwohl B, Granath F, Ekbom A, Montgomery SM, Murray JA, Rubio-Tapia A, Green PH, Ludvigsson JF. Aliment Pharmacol Ther. 2013 Feb;37(3):332-9. http://www.ncbi.nlm.nih.gov/pubmed/23190299 10. Complete recovery of intestinal mucosa occurs very rarely in adult coeliac patients despite adherence to gluten-free diet. Lanzini A, Lanzarotto F, Villanacci V, Mora A, Bertolazzi S, Turini D, Carella G, Malagoli A, Ferrante G, Cesana BM, Ricci C. Aliment Pharmacol Ther. 2009 Jun 15;29(12):1299-308. http://www.ncbi.nlm.nih.gov/pubmed/19302264 11. Chemical-induced allergy and autoimmunity Marty Bernardus Franciscus Wulferink [s.l.] : [s.n.], 2001 - Tekst. - Proefschrift Universiteit Utrecht http://igitur-archive.library.uu.nl/dissertations/1975053/inhoud.htm 12. R-spondin1, a novel intestinotrophic mitogen, ameliorates experimental colitis in mice. Zhao J, de Vera J, Narushima S, Beck EX, Palencia S, Shinkawa P, Kim KA, Liu Y, Levy MD, Berg DJ, Abo A, Funk WD. Gastroenterology. 2007 Apr;132(4):1331-43. http://www.ncbi.nlm.nih.gov/pubmed/17408649 13. Nuvelo Announces Positive Results from Phase 1 Clinical Trial of NU206 in Healthy Volunteers 2008 Dec 10. http://www.evaluatepharma.com/Universal/View.aspx?type=Story&id=172716 14. Biotechs Arca, Nuvelo complete reverse merger 2009 Jan 28. http://www.bizjournals.com/sanfrancisco/stories/2009/01/26/daily64.html
  12. American Journal of Clinical Pathology, April 2000 - A New Method of Quantitative Fecal Fat Microscopy and its Correlation with Chemically Measured Fecal Fat Output, by Kenneth Fine, M.D. and Frederick Ogunji Ph.D (Celiac.com 07/09/2000) Patients with gluten sensitivity should be evaluated for nutrient malabsorption because if present, this means there is small intestinal damage and institution of a gluten-free diet is imperative to prevent osteoporosis and other nutrient deficiency syndromes. Furthermore, a test at the time of diagnosis serves as a baseline to be compared to later if needed. For more than 50 years, the primary method used to assess for the presence of small intestinal damage and nutrient malabsorption in patients with celiac disease has been a 72-hour quantitative stool collection. However, because this method requires that patients accurately collect all the stools they pass for 3 days (missed stools lead to falsely low results), the test is logistically difficult for medical centers unaccustomed to the procedure, and the voluminous specimens usually are abhorred by patients and laboratory technicians. It poses obvious problems for children who cannot or will not collect all their stools, as well as for patients with chronic diarrhea, who may have bowel movement frequencies reaching 15 or more per day and/or fecal volumes as high as 2 or 3 liters per day. For these reasons, physicians evaluating patients with suspected or proven gluten sensitivity often avoid tests for intestinal malabsorption altogether. Recently, researchers at the Intestinal Health Institute in Dallas, Texas have developed a new method for quantitating fecal fat excretion that requires collection of only a single stool specimen. Development of this method was based on the fact that as more fat is malabsorbed, the fat globules in stool become more numerous and larger. In a study published in the April 2000 issue of the American Journal of Clinical Pathology entitled A New Method of Quantitative Fecal Fat Microscopy and its Correlation with Chemically Measured Fecal Fat Output, Kenneth Fine, M.D. and Frederick Ogunji Ph.D. tested 180 patients and found a highly statistically significant linear correlation between quantitative fecal fat microscopy (the new method) and chemically measured fecal fat output (the old method). They also showed that their microscopic analysis of just one stool gives comparable results to analysis of an entire 3-day collection. These researchers have, thus, shown that a dedicated quantitative analysis of one stool under a microscope can detect the rise in fecal fat due to intestinal malabsorption (or pancreatic maldigestion) as accurately as 3-day stool collections, making this latter test a thing of the past for most patients. This new stool test for intestinal malabsorption and other celiac-testing is available for order online from a laboratory set up by Drs. Fine and Ogunji to serve the needs of celiac patients. It is called EnteroLab and can be accessed at http://www.enterolab.com/.
  13. Celiac.com 02/27/2006 - Kappler M, Krauss-Etschmann S, Diehl V, Zeilhofer H, Koletzko S. Detection of secretory IgA antibodies against gliadin and human tissue transglutaminase in stool to screen for celiac disease in children: validation study. BMJ. 2006 January 28; 332(7535): 213-14. Study Abstract: Objective: To evaluate two commercial stool tests for detection of secretory IgA antibodies against gliadin and human tissue transglutaminase for diagnosis of celiac disease in children with symptoms. Setting: Tertiary care childrens hospital. Participants: Coded stool samples from 20 children with newly diagnosed celiac disease and 64 controls. Six children with celiac disease had stool tests every two weeks for three months after starting a gluten-free diet. Main Outcome Measures: Secretory IgA antibodies against gliadin and human tissue transglutaminase in stool samples, determined in duplicate by using recommended cut-off limits. Results: Sensitivity of fecal antibodies against human tissue transglutaminase was 10% (95% confidence interval 1% to 32%), and specificity was 98% (91% to 100%). For antibodies against gliadin, sensitivity was 6% (0% to 29%) and specificity was 97% (89% to 100%). Optimisation of cut-off limits by receiver operating characteristic analysis and use of results of both tests increased sensitivity to 82%, but specificity decreased to 58%. All follow-up stool tests remained negative, except for two positive anti-gliadin results in one patient, six and 10 weeks after the gluten-free diet was started. Conclusions: Neither stool test was suitable for screening for celiac disease in children with symptoms. Dr. Kenneth Fine Comments on this Study: Dont Throw the Baby Out With the Bath Water! Letter to the Editor BMJ Kamran Rostami, M.D., Ph.D. Department of Medicine, Gloucestershire Royal Hospital Gloucester, UK Kenneth Fine, M.D. The Intestinal Health Institute, Dallas, Texas, USA We have read with interest the article by Kappler et al recently published in your journal (1) and feel several issues deserve mention. This article is very timely in light of the growing worldwide awareness of immunologic sensitivity to dietary gluten and celiac disease, as well as appreciation of its high prevalence; these facts are driving the need for more widely available, low cost, non-invasive screening tests. Stool testing for these disorders holds great promise for screening because it does not require any invasion of body tissues, is of relatively low cost, and could be widely available combining medical care delivery of such tests with home testing. While our first criticism of this study is its small cohort size (20 patients), the results are intriguing, but in our opinion have been misinterpreted by the authors. First, there is a potential methodological flaw in this study whereby a serologic method was apparently transferred intact to analyze stool. The aspects of a serologic ELISA method possibly requiring modification for use in stool include but are not limited to: degree to which the sample is diluted prior to analysis; technique and amount of washing of plates during ELISA analysis (because of greater solid contaminant of fecal fluid vs. serum); mathematical conversion of detected optical density to a Unit; and how that calculated Unit is interpreted relative to a normal vs. abnormal cutoff. Utilizing fecal antigliadin and antitissuetransglutaminase IgA antibody testing in this way were reported to be very insensitive (6-10%) but highly specific (97-98%) for celiac disease. Such results should be interpreted as possibly possessing either a misassigned cutoff value (i.e., one that was too high), or possibly introduction of an artificial element that drove fecal antibody concentrations down (such as over-diluting the stool, improper handling or storage of specimens allowing ex vivo destruction of antibody, or centrifuging the stool at the wrong speed driving antibody into the pellet; the authors mentioned destruction of antibody during transit within the GI tract, but antibody is very stable within the GI tract, and has been detected in stool by many authors). Nevertheless, as performed in this study, such a highly specific stool test for celiac disease could be used as a pre-screening test of sorts, able to specifically and non-invasively detect celiac disease, perhaps with a home collected stool specimen. At the worst, 6-10% of celiac patients could be identified even before presenting to a medical institution. The authors went on to correct a potential cutoff error, using optimization of cut-off limits by receiver operating characteristic analysis, and found that resetting the cut-off value and combining the tests could possess an 82% sensitivity and 58% specificity. Again the authors discounted these findings, in our opinion failing to grasp their importance. Although they did not report the corrected accuracy results of antigliadin test alone, their stool test may have outperformed serum antigliadin antibody, the serologic test in longest use in screening for celiac disease. Many investigators have lost confidence in the presumed lack of specificity of antigliadin antibody alone as a screening test for celiac disease because of the paradigm within which it has been applied, that is, villous atrophic celiac disease. It is also known that its sensitivity is highly dependent on the degree of small intestinal villous atrophy present (2). Most importantly today however, in our opinion, with the wealth of expanding knowledge on the broadening clinical spectrum of gluten-sensitive disorders (3), it should at least have been considered and/or discussed by Kappler et al that in their optimized cut-off analysis, a positive fecal antigliadin antibody may have been a true sign of immunologic sensitivity to gluten either in an evolutionary phase before the onset of villous atrophic celiac disease (4), or in gluten sensitive individuals who may never develop classic celiac disease but who suffer symptoms and associated autoimmune disorders nevertheless. When interpreted in this context, the authors results may have been clinically important. We feel further study of this method with improved attention to methodological issues pertaining to stool, and broader clinical application beyond classic celiac disease is warranted. References: 1. Kappler M, Krauss-Etschmann S, Diehl V, Zeilhofer H, Koletzko S. Detection of secretory IgA antibodies against gliadin and human tissue transglutaminase in stool to screen for celiac disease in children: validation study. BMJ. 2006 January 28; 332(7535): 213-14. 2. Rostami K, Kerckhaert J, Tiemessen R, von Blomberg BM, Meijer JW, Mulder CJ. Sensitivity of antiendomysium and antigliadin antibodies in untreated celiac disease: disappointing in clinical practice. Am J Gastroenterol. 1999 Apr;94(4):888-94. 3. Ferguson A, Arranz E, OMahony S. Clinical and pathological spectrum of celiac disease--active, silent, latent, potential. Gut. 1993 Feb;34(2):150-1. 4. Arranz E, Ferguson A. Jejunal fluid antibodies and mucosal gamma/delta IEL in latent and potential celiac disease. Adv Exp Med Biol. 1995;371B:1345-8.
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