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Found 6 results

  1. Celiac.com 09/12/2017 - Are we at the beginning of the end for celiac disease? The last few years have seen numerous advances in celiac diagnosis and treatment. People diagnosed recently and in the future face a very different world than that faced by celiacs just five or ten years ago. In the old days, the process of properly diagnosing involved blood tests, endoscopies, and biopsies. In the near future, a simple blood test may do the trick. In the old days, the only treatment was a life-long gluten-free diet. That is still true, but the writing of change is on the wall. Here are five advances that will change the way celiac disease is diagnosed and treated in the future. These advances may well signal the beginning of the end of celiac disease as we know it. Blood Test Diagnosis (Without Biopsy) Researchers are getting better at identifying likely celiac cases using blood tests alone, without biopsy. As these techniques are refined and integrated into medicine, chances are pretty good that in the near future, large numbers of people will be diagnosed for celiac disease without the need for biopsy confirmation. Can Antibodies Spot Celiac Disease in Kids Without a Biopsy? Kids Can Get Accurate Celiac Diagnosis Without Biopsy Celiac Diagnosis Without Biopsy Can Be Useful in Some Cases Portable Gluten Detectors Imagine a future where you can take a bit of food you're not sure about, and pop it in a portable tester that will tell you if the food is gluten-free. A few years ago, that might have been the future of science fiction. With several companies looking to introduce just such kits, that future looks a lot more certain. Innovative Device Eliminates Gluten-Free Guesswork This Device Can Help Tell You If Your Food Is Actually Gluten-Free nimasensor.com Enzymes Enzymes that break down gluten might help people with celiac disease to enjoy a more normal life by protecting them from minor gluten contamination, and allowing them a bit more confidence when eating away from home. A number of manufacturers are currently working on enzyme treatments that are specifically designed to break down gluten for people with celiac disease. AN-PEP Shows Promise in Breaking Down Gluten in Stomach Enzyme Shows Promise In Dissolving Gliadin Peptides in Celiac Patients Could Carnivorous Plant Enzymes Act Like Beano for Gluten? Could Enzymes from Oral Bacteria Treat Celiac Disease Bio-Therapeutics—Hookworms They sound gross. The thought of having their guts infected with a parasitic worm makes people's skin crawl. However, researchers have documented the gut healing abilities of parasites like hookworm. When hookworms are introduced into the gut of people with celiac disease in the right amount, and kept at therapeutic levels, patients see their celiac symptoms disappear and their guts return to a healthy, normal condition. While still very much in the experimental phase, researchers are keen to investigate various strains and to determine the best therapeutic levels for these treatments. If all goes well, treatments based on parasitic worms will likely become more viable and more common in the future. Celiac Patients Tolerate Wheat Spaghetti After Hookworm Treatment Have Celiac Disease? Try a Little Hookworm with that Pasta! Can Bloodsucking Parasites Help Treat Asthma and Celiac Disease? Controversial Pig Parasite May Soon Be Sold In Germany To Treat Disease Bio-Therapeutics—Fecal Transplant Could fecal transplants be used to cure or to treat celiac disease? Much like hookworms, once you get past the 'yuck' factor, fecal transplants are proving to be cheap, easy, reliable way to treat gut conditions like C-Diff and, possibly celiac disease. The idea is to get some healthy poop in your gut to inoculate it with beneficial microbes. The effects are nothing short of astonishing. As they are studied, developed and refined, look for bio-therapeutic approaches like fecal transplant to play a role in treating gut contains like celiac disease. A Case of Refractory Celiac Disease Cured By Fecal Microbiota Transfer Vaccine A vaccine against celiac disease would be a holy grail of sorts. Receive a dose, or maybe multiple doses over time and become immune to the adverse effects of gluten. Several companies are working on a vaccine that would basically eliminate celiac disease. Many of these have moved through the early trial phases and several have shown enough promise to move to trials in humans. This is a very exciting area of research that may pay huge dividends in the near future. Celiac Disease Vaccine Set to Begin Full Human Trials Would You Try a Vaccine for Celiac Disease? Celiac Vaccine Clears First Big Clinical Trial This Vaccine Could Be a Game-Changer for People with Celiac Disease The main takeaway from these developments is that we are now living in an age where the diagnosis and treatment of celiac disease is the focus of tremendous research and development on numerous fronts. Many of these will likely result in products, tests, or treatments for celiac disease that were unimaginable just 5 or 10 years ago.
  2. Celiac.com 08/31/2017 - A possible mechanism behind the cause of refractory celiac disease and why fecal transplantation (fecal microbiota transfer) may provide a cure was presented in "Synthetic Stool May Advance Fecal Transplant Therapy for Celiac Disease" 02/13/2013.[1] In September 2016, the article "Serendipity in Refractory Celiac Disease: Full Recovery of Duodenal Villi and Clinical Symptoms after Fecal Microbiota Transfer" was published in the Journal of Gastrointestinal and Liver Disease[2] describing the first known case of refractory celiac disease cured by a fecal transplant. The patient in that case was being treated for a recurrent Clostridium difficile infection. This very important milestone article somehow missed the light of the news media at that time. The 68-year old woman patient was a 10-year diagnosed victim of refractory celiac disease on a gluten-free diet. On admission for treatment of severe diarrhea, the patient exhibited Marsh IIIA villous atrophy. The patient was already receiving on-going treatment for refractory celiac disease with drugs. Additional drugs and antibiotics were given to treat the diarrhea. Eventually, the patient tested positive for C. difficile. Antibiotics were ineffective to treat the recurrent C. difficile infection. A fecal microbiota transfer was then performed. The C. difficile infection and diarrhea resolved, and, 6 months after the fecal transplant, villous atrophy resolved and went to Marsh 0. All symptoms of refractory celiac disease were eliminated. The patient remains symptom free on a continuing gluten-free diet. The case clearly demonstrates the need to fully investigate the use of fecal microbiota transfers to treat celiac disease. As suggested in my earlier reference[1], a standardized synthetic stool should be developed to enable full scale clinical trials. Also a full scale research effort into completely healing and restoring the intestinal mucosa with the novel protein R-spondin1 needs to be funded and restarted. Sources: 1. Synthetic Stool May Advance Fecal Transplant Therapy for Celiac Disease. Roy S. Jamron. Celiac.com 2013 Feb 13. 2. Serendipity in Refractory Celiac Disease: Full Recovery of Duodenal Villi and Clinical Symptoms after Fecal Microbiota Transfer. van Beurden YH, van Gils T, van Gils NA, Kassam Z, Mulder CJ, Aparicio-Pages N J Gastrointestin Liver Dis. 2016 Sep;25(3):385-8.
  3. Celiac.com 09/16/2016 - Great news about poop transplants: They work! And now doctors kind of understand how and why they work. This is good news about a humor provoking, but very serious matter. Clostridium difficile infection is one of the most common health care-associated infections, and up to 40% of patients suffer from recurrence of disease following standard antibiotic therapy. C. difficile infection has proven to be very difficult to treat. Fecal microbiota transplantation (FMT) has been successfully used to treat recurrent C. difficile infection. Doctors hypothesize that FMT promotes recovery of a microbiota capable of colonization resistance to C. difficile. However, they didn't really understand how it worked. Recently, a research team investigated changes in the fecal microbiota structure following FMT in patients with recurrent C. difficile infection, and imputed a hypothetical functional profile based on the 16S rRNA profile, using a predictive metagenomic tool. After FMT, they also noted increased relative abundance of Bacteroidetes and decreased abundance of Proteobacteria. The research team included Anna M. Seekatz, Johannes Aas, Charles E. Gessert, Timothy A. Rubin, Daniel M. Saman, Johan S. Bakken, and Vincent B. Young. They are variously affiliated with the Department of Internal Medicine, Division of Infectious Diseases, Department of Microbiology and Immunology, University of Michigan, Ann Arbor, Michigan, USA; Essentia Health, Department of Gastroenterology, Duluth, Minnesota, USA; Essentia Institute of Rural Health, Duluth, Minnesota, USA; and St. Luke's Hospital, Section of Infectious Diseases, Duluth, Minnesota, USA. Their results showed that, after transplantation, fecal microbiota of recipients was more diverse, and more similar to the donor profile, than the microbiota before transplantation. Additionally, they observed differences in the imputed metagenomic profile. In particular, amino acid transport systems were over-represented in samples collected prior to transplantation. These results Indicate that functional changes accompany microbial structural changes following this therapy. Further identification of the specific microbiota, and functions that promote colonization resistance, may help to create better treatment methods for C. difficile infection. Source: mBio. 2014 May-Jun; 5(3): e00893-14. Published online 2014 Jun 17. doi: 10.1128/mBio.00893-14. PMCID: PMC4068257
  4. Hi! WARNING! EXTREMELY HIGH ICK-FACTOR! I'm new to Celiac Disease, and thus this site as well. Though I'm still waiting on blood work to come back, I'm nearly a week into a gluten-free diet and can already tell a major difference. My doctor told me to do some research on a gluten free diet and I must admit that I have been experiencing an amalgamation of excitement for a conclusion to a 15 year search, a fear of the implications of having celiac disease, and an intense dread of having a lifetime of a gluten-free diet. All that said, in researching cure research progress, I came across several inferences and references to a cure. Unfortunately, however, that cure is a fecal transplant from a perfectly healthy donor. Here is a starter link to one article, if anyone is curious: http://www.mayoclinic.org/medical-professionals/clinical-updates/digestive-diseases/quick-inexpensive-90-percent-cure-rate It seems to take a good bit of research to piece together tidbits from here and there to get an idea of where this procedure is headed. There is also a video on YouTube of a woman showing how to do this from home. The only drawback I am aware of, so far and beyond the obvious ICK-factor, is that antibiotics could necessitate another transplant. I am wondering if anyone has any experience or insight into this. If a fecal transplant really can cure celiac disease, what an equally gross and amazing thing! What could this mean for those with celiac, and what can we do to further this along?
  5. 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
  6. Celiac.com 02/09/2005 – The following abstract supports the use of fecal scIgA AGA combined with fecal IgA AGA, IgG AGA and IgM AGA to diagnose celiac disease, as they may be detected there even before they can be in the blood of celiac patients. This research adds support for the use of fecal testing as an early diagnostic tool, and perhaps also supports the work that has been done in this area by doctors like Kenneth Fine. Clin Lab. 2004;50(9-10):551-7. Comparison of different salivary and fecal antibodies for the diagnosis of celiac disease. Halblaub JM, Renno J, Kempf A, Bartel J, Schmidt-Gayk H. Clin Lab. 2004;50(9-10):551-7. ABSTRACT: To investigate the detectability and expressiveness of salivary and fecal anti-gliadin (AGA), anti-endomysium (EMA) and anti-tissue-transglutaminase (ATA) antibodies, 127 salivary and 160 fecal samples of healthy volunteers and salivary and fecal samples of 17 patients with histologically proven and 9 patients with suggested celiac disease were investigated in this study. With all salivary parameters and fecal IgA AGA, IgM AGA, IgA EMA and IgG EMA, healthy volunteers and patients showed partially overlapping results. The most promising results in our study with higher concentrations in patients with celiac disease were obtained by fecal scIgA AGA and a combined determination of fecal IgA AGA, IgG AGA and IgM AGA. Further investigations should be performed with fecal IgA EMA and scIgA ATA based on human recombinant tissue-transglutaminase. One patient with histologically proven celiac disease had normal serological but high fecal scIgA AGA and scIgA ATA values. This patient emphasizes the importance of fecal antibody determination for the diagnosis of celiac disease, at least in patients with suggested celiac disease and negative serum antibodies.
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