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    Latest Data from Multiple Studies Supports Development of Celiac Vaccine


    Jefferson Adams


    • Can increased cytokine levels after gluten ingestion help doctors spot celiac disease?


    Image Caption: Photo: CC--NAIAD

    Celiac.com 10/02/2017 - For anyone following the efforts by ImmusanT to develop a vaccine for celiac disease, the company's recent presentations at the 2017 International Celiac Disease Symposium (ICDS) in New Delhi, India, were welcome news.


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    Nexvax2® is a therapeutic vaccine intended to protect against the effects of gluten exposure while maintaining a gluten-free diet in HLA-DQ2.5+ patients with celiac disease.

    The company announced at ICDS 2017 that it has presented data showing the immunologic basis for the early clinical effects of gluten in celiac disease.

    Presented in two poster presentations and an oral presentation, the company says its data show that "early cytokine changes in blood following gluten ingestion could provide the basis for a new diagnostic for celiac disease in patients on a gluten free diet with an uncertain diagnosis," said Robert Anderson, MBChB, Ph.D., Chief Scientific Officer of ImmusanT.

    The company says its results are "significant" because celiac disease sufferers often adopt a gluten-free diet prior to being diagnosed by a doctor. This can cause problems and lead to unreliable or misleading results with current diagnostic tests.

    ImmusanT says that their data demonstrate that early changes in circulating cytokines after a single gluten exposure may offer a clinical way to assess celiac disease activity.

    The company says that the data, along with the potential to differentiate between celiac disease and non-celiac gluten sensitivity (NCGS) by assessing IL-2 levels, support the science behind targeted immunotherapies such as Nexvax2®.

    Read more at BusinessWire.com

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  • Related Articles

    Jefferson Adams
    Celiac.com 07/19/2016 - The world's first vaccine aimed at curing celiac disease is slated to begin full trials later this year, and residents of the Australian state of Victoria will be among the first humans to give it a try against celiac disease.
    The vaccine, called Nexvax2, was developed by Australian scientist Dr Bob Anderson, and is aimed at giving celiac patients a chance to overcome their immune reaction to the gluten found in products containing wheat, rye and barley. Nexvax2 aims to de-sensitise patients to three peptides contained in gluten that trigger a damaging reaction in their immune system.
    Previous trials on 150 patients from Melbourne, Perth, Adelaide, Brisbane and Auckland were aimed at finding a safe dosage rather than assessing its ability to beat celiac disease. Results from those favorable earlier trials were released in May, and Dr Anderson says that the larger phase II study, also being undertaken in the US and Europe, will assess how well the vaccine works against celiac disease.
    Dr Anderson first identified the peptides triggering coeliac disease and began developing the vaccine while working at Melbourne's Walter and Eliza Hall Institute, before travelling to Boston for six weeks as part of a sister city arrangement through the City of Melbourne, where he made contact with ImmusanT to further the discovery.
    This is certainly exciting news for people with celiac disease, many of whom may benefit from such treatment.
    Stay tuned for news on the progress of these trials.
    Source:
    dailysecrets.press

    Jefferson Adams
    Celiac.com 05/29/2017 - Currently, a gluten-free diet is the only way to manage celiac disease. Can a celiac vaccine change that? One company thinks so. ImmusanT corporation has developed a therapeutic vaccine, Nexvax2, that is specifically designed to treat celiac disease. The vaccine is an adjuvant-free mix of three peptides that include immunodominant epitopes for gluten-specific CD4-positive T cells. The vaccine is designed to neutralize gluten-specific CD4-positive T cells to further antigenic stimulation.
    As part of their efforts to evaluate the vaccine, a team of researchers recently set out to investigate the efficacy of epitope-specific immunotherapy targeting CD4-positive T cells in celiac disease. Specifically, they assessed the safety and pharmacodynamics of the Nexvax2 vaccine in patients with celiac disease on a gluten-free diet.
    An article detailing the findings of their most recent effort, titled Epitope-specific immunotherapy targeting CD4-positive T cells in celiac disease: two randomized, double-blind, placebo-controlled phase 1 studies, appeared in the Lancet.
    The research team included Gautam Goel, PhD, Tim King, MBBChir, A James Daveson, MBBS, Jane M Andrews, MBBS, Janakan Krishnarajah, MBBS, Richard Krause, MD, Gregor J E Brown, MBBS, Ronald Fogel, MDCM, Charles F Barish, MD, Roger Epstein, MD, Timothy P Kinney, MD, Philip B Miner Jr, MD, Jason A Tye-Din, MBBS, Adam Girardin, BS, Juha Taavela, MD, Alina Popp, MD, John Sidney, BS, Prof Markku Mäki, MD, Kaela E Goldstein, BS, Patrick H Griffin, MD, Suyue Wang, PhD, John L Dzuris, PhD, Leslie J Williams, MBA, Prof Alessandro Sette, DrBiolSc, Prof Ramnik J Xavier, MD, Prof Ludvig M Sollid, MD, Prof Bana Jabri, MD, and Dr Robert P Anderson, MBChB.
    To assess the safety and pharmacodynamics of the vaccine in patients with celiac disease on a gluten-free diet, ImmusanT recently conducted two randomized, double-blind, placebo-controlled, phase 1 studies at 12 community sites in Australia, New Zealand, and the USA, in HLA-DQ2·5-positive patients aged 18–70 years who had celiac disease and were following a gluten-free diet.
    The goal of the study was to document the number and percentage of adverse events in the treatment period in an intention-to-treat analysis.
    The study enrolled a total of 108 participants from Nov 28, 2012, to Aug 14, 2014, in the three-dose study, and from Aug 3, 2012, to Sept 10, 2013, in the 16-dose study.
    Overall, 62 (57%) of 108 participants were randomly assigned after oral gluten challenge and 20 (71%) of 28 participants were randomly assigned after endoscopy.
    None of the study participants, investigators, or staff knew which patients received a given treatment; these details were known only by the study’s lead pharmacist.
    In the three-dose study, participants received either Nexvax2 60 μg, 90 μg, or 150 μg weekly, or placebo over 15 days; in a fourth biopsy cohort, patients received either Nexvax2 at the maximum tolerated dose (MTD) or a placebo.
    In the 16-dose study, participants received Nexvax2 150 μg or 300 μg or placebo twice weekly over 53 days; in a third biopsy cohort, patients also received either Nexvax2 at the MTD or a placebo. In both studies, about 5% of the participants reported were vomiting, nausea, and headache.
    Among participants given the MTD, four of eight subjects in the third cohort experienced adverse gastrointestinal treatment-emergent events; zero of three participants had adverse events in the biopsy cohort in the three-dose study, while five events occurred in five (63%) of eight participants in the first cohort, and three events in two (29%) of seven participants in the biopsy cohort of the 16-dose study.
    Those who received the vaccine at the MTD on either schedule showed no significant difference between average villous height to crypt depth ratio in distal duodenal biopsies, as compared with those who received placebo.
    In the 4-week post-treatment period, ascending dose cohorts underwent a further double-blind crossover, placebo-controlled oral gluten challenge, which had a fixed sequence. Meanwhile, biopsy cohorts received a gastroscopy with duodenal biopsies and quantitative histology within 2 weeks without oral gluten challenge. Of the participants who completed the post-treatment oral gluten challenge per protocol, interferon γ release assay to Nexvax2 peptides was negative in two (22%) of nine placebo-treated participants in the three-dose study.
    Compared with two (33%) of six who received Nexvax2 60 μg, five (63%) of eight who received Nexvax2 90 μg, and six (100%) of six who received Nexvax2 150 μg (p=0·007); in the 16-dose study, none (0%) of five placebo-treated participants had a negative assay versus six (75%) of eight who received Nexvax2 150 μg (p=0·021).
    The MTD of Nexvax2 was 150 μg for twice weekly intradermal administration over 8 weeks, which modified immune responsiveness to Nexvax2 peptides with no adverse impact on duodenal histology.
    Patients who received the intradermal administration of the vaccine reported gastrointestinal symptoms were not subtantially different to those seen with oral gluten challenge.
    While the commercial release of a viable vaccine is likely still some time away, early-phase trials have shown promise. Based on these results, ImmusanT will continue clinical development of this potentially therapeutic vaccine for celiac disease.
    Both trials were completed and closed before data analysis. Trials were registered with the Australian New Zealand Clinical Trials Registry, numbers ACTRN12612000355875 and ACTRN12613001331729.
    Source:
    The Lancet Affiliations:
    The researchers are variously affiliated with the Division of Gastroenterology and Center for Computational and Integrative Biology, Massachusetts General Hospital, Boston, MA, USA, the Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA, USA; the Department of Gastroenterology, Auckland City Hospital, Auckland, New Zealand; the School of Medicine, University of Queensland, Brisbane, QLD, Australia; the Department of Gastroenterology & Hepatology, Royal Adelaide Hospital, Adelaide, SA, Australia; the Linear Clinical Research, Nedlands, WA, Australia; the Department of Gastroenterology, Alfred Hospital, Prahran, VIC, Australia; the Clinical Research Institute of Michigan, Chesterfield, MI, USA; the University of North Carolina School of Medicine, Chapel Hill, NC, USA; Wake Gastroenterology and Wake Research Associates, Raleigh, NC, USA; Atlantic Digestive Specialists, Portsmouth, NH, USA; Ridgeview Medical Center, Waconia, MN, USA; Oklahoma Foundation for Digestive Research, Oklahoma City, OK, USA; ClinSearch, Chattanooga, TN, USA; the Immunology Division, Walter and Eliza Hall Institute of Medical Research, Department of Medical Biology, University of Melbourne, Parkville, VIC, Australia; the Murdoch Children's Research Institute and Department of Gastroenterology, Royal Melbourne Hospital, Parkville, VIC, Australia; the Immunology Division, Walter and Eliza Hall Institute of Medical Research, Department of Medical Biology, University of Melbourne, Parkville, VIC, Australia; the Tampere Center for Child Health Research and Department of Pediatrics, University of Tampere Faculty of Medicine and Life Sciences and Tampere University Hospital, Tampere, Finland; the Tampere Center for Child Health Research and Department of Pediatrics, University of Tampere Faculty of Medicine and Life Sciences and Tampere University Hospital, Tampere, Finland; the Alfred Rusescu Institute for Mother and Child Care and Carol Davila University of Medicine and Pharmacy, Bucharest, Romania; Division of Vaccine Discovery, La Jolla Institute for Allergy and Immunology, La Jolla, CA, USA; the Tampere Center for Child Health Research and Department of Pediatrics, University of Tampere Faculty of Medicine and Life Sciences and Tampere University Hospital, Tampere, Finland; the Centre for Immune Regulation, KG Jebsen celiac Disease Research Centre, and Department of Immunology, University of Oslo, Oslo, Norway; the Oslo University Hospital-Rikshospitalet, Oslo, Norway; Department of Pediatrics, Department of Medicine, University of Chicago, Chicago, IL, USA; and ImmusanT in Cambridge, MA, USA.

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/16/2018 - Summer is the time for chips and salsa. This fresh salsa recipe relies on cabbage, yes, cabbage, as a secret ingredient. The cabbage brings a delicious flavor and helps the salsa hold together nicely for scooping with your favorite chips. The result is a fresh, tasty salsa that goes great with guacamole.
    Ingredients:
    3 cups ripe fresh tomatoes, diced 1 cup shredded green cabbage ½ cup diced yellow onion ¼ cup chopped fresh cilantro 1 jalapeno, seeded 1 Serrano pepper, seeded 2 tablespoons lemon juice 2 tablespoons red wine vinegar 2 garlic cloves, minced salt to taste black pepper, to taste Directions:
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    Cover and refrigerate for at least 1 hour. 
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    Dr. Ron Hoggan, Ed.D.
    Celiac.com 06/15/2018 - There seems to be widespread agreement in the published medical research reports that stuttering is driven by abnormalities in the brain. Sometimes these are the result of brain injuries resulting from a stroke. Other types of brain injuries can also result in stuttering. Patients with Parkinson’s disease who were treated with stimulation of the subthalamic nucleus, an area of the brain that regulates some motor functions, experienced a return or worsening of stuttering that improved when the stimulation was turned off (1). Similarly, stroke has also been reported in association with acquired stuttering (2). While there are some reports of psychological mechanisms underlying stuttering, a majority of reports seem to favor altered brain morphology and/or function as the root of stuttering (3). Reports of structural differences between the brain hemispheres that are absent in those who do not stutter are also common (4). About 5% of children stutter, beginning sometime around age 3, during the phase of speech acquisition. However, about 75% of these cases resolve without intervention, before reaching their teens (5). Some cases of aphasia, a loss of speech production or understanding, have been reported in association with damage or changes to one or more of the language centers of the brain (6). Stuttering may sometimes arise from changes or damage to these same language centers (7). Thus, many stutterers have abnormalities in the same regions of the brain similar to those seen in aphasia.
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    With the advent of the Internet a whole new field of anecdotal information was emerging, connecting a variety of neurological symptoms to celiac disease. While many medical practitioners and researchers were casting aspersions on these assertions, a select few chose to explore such claims using scientific research designs and methods. While connections between stuttering and gluten consumption seem to have been overlooked by the medical research community, there is a rich literature on the Internet that cries out for more structured investigation of this connection. Conversely, perhaps a publication bias of the peer review process excludes work that explores this connection.
    Whatever the reason that stuttering has not been reported in the medical literature in association with gluten ingestion, a number of personal disclosures and comments suggesting a connection between gluten and stuttering can be found on the Internet. Abid Hussain, in an article about food allergy and stuttering said: “The most common food allergy prevalent in stutterers is that of gluten which has been found to aggravate the stutter” (10). Similarly, Craig Forsythe posted an article that includes five cases of self-reporting individuals who believe that their stuttering is or was connected to gluten, one of whom also experiences stuttering from foods containing yeast (11). The same site contains one report of a stutterer who has had no relief despite following a gluten free diet for 20 years (11). Another stutterer, Jay88, reports the complete disappearance of her/his stammer on a gluten free diet (12). Doubtless there are many more such anecdotes to be found on the Internet* but we have to question them, exercising more skepticism than we might when reading similar claims in a peer reviewed scientific or medical journal.
    There are many reports in such journals connecting brain and neurological ailments with gluten, so it is not much of a stretch, on that basis alone, to suspect that stuttering may be a symptom of the gluten syndrome. Rodney Ford has even characterized celiac disease as an ailment that may begin through gluten-induced neurological damage (13) and Marios Hadjivassiliou and his group of neurologists and neurological investigators have devoted considerable time and effort to research that reveals gluten as an important factor in a majority of neurological diseases of unknown origin (14) which, as I have pointed out previously, includes most neurological ailments.
    My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question.
    Sources:
    1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44.
    2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15.
    3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23.
    5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26.
    6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11.
    7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48
    9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4.
    10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
    13. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
    14. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.

    Jefferson Adams
    Celiac.com 06/14/2018 - Refractory celiac disease type II (RCDII) is a rare complication of celiac disease that has high death rates. To diagnose RCDII, doctors identify a clonal population of phenotypically aberrant intraepithelial lymphocytes (IELs). 
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    They are variously affiliated with the Department of Pathology and Cell Biology, and the Department of Medicine at the Celiac Disease Center, New York Presbyterian Hospital/Columbia University Medical Center, New York, USA. Their team analyzed results of TCR-GR analyses performed on SB biopsies at our institution over a 3-year period, which were obtained from eight active celiac disease, 172 celiac disease on gluten-free diet, 33 RCDI, and three RCDII patients and 14 patients without celiac disease. 
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    They also noted a higher frequency of surface CD3(−) IELs in cases with clonal TCR-GR, but the PCP pattern showed no associations with any clinical or pathological feature. 
    Repeat biopsy showed that the clonal or PCP pattern persisted for up to 2 years with no evidence of RCDII. The study indicates that better understanding of clonal T cell receptor gene rearrangements may help researchers improve refractory celiac diagnosis. 
    Source:
    Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023

    Jefferson Adams
    Celiac.com 06/13/2018 - There have been numerous reports that olmesartan, aka Benicar, seems to trigger sprue‐like enteropathy in many patients, but so far, studies have produced mixed results, and there really hasn’t been a rigorous study of the issue. A team of researchers recently set out to assess whether olmesartan is associated with a higher rate of enteropathy compared with other angiotensin II receptor blockers (ARBs).
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    Source:
    Alimentary Pharmacology & Therapeutics

    Jefferson Adams
    Celiac.com 06/12/2018 - A life-long gluten-free diet is the only proven treatment for celiac disease. However, current methods for assessing gluten-free diet compliance are lack the sensitivity to detect occasional dietary transgressions that may cause gut mucosal damage. So, basically, there’s currently no good way to tell if celiac patients are suffering gut damage from low-level gluten contamination.
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    The ability to use GIP in urine to reveal gluten consumption will likely help lead to new and non-invasive methods for monitoring gluten-free diet compliance. The test is sensitive, specific and simple enough for clinical monitoring of celiac patients, as well as for basic and clinical research applications including drug development.
    Source:
    Gut. 2017 Feb;66(2):250-257.  doi: 10.1136/gutjnl-2015-310148.