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    What are the Best Predictors of Persistent Villous Atrophy in Celiac Disease?


    Jefferson Adams

    Celiac.com 05/26/2014 - Villous atrophy with intraepithelial lymphocytosis is the classic confirmation of of celiac disease. However, data show varying rates of mucosal recovery among individuals.


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    A research team recently sought gauge the impact of age and other demographic variables on the likelihood of persistent villous atrophy in celiac disease with follow-up biopsy.

    Photo: Wikimedia CommonsThe research team included B. Lebwohl, J. A. Murray, A. Rubio-Tapia, P. H. R. Green, and J. F. Ludvigsson. They are variously affiliated with the Celiac Disease Center of the Department of Medicine at Columbia University College of Physicians and Surgeons in New York, NY., the Clinical Epidemiology Unit of the Department of Medicine at Karolinska University Hospital and Karolinska Institutet in Stockholm, Sweden, the Division of Gastroenterology and Hepatology of the Department of Medicine at the Mayo Clinic College of Medicine in Rochester, Minnesota, and the Department of Pediatrics of Örebro University Hospital in Örebro, Sweden.

    For their study, the team reviewed data on patients with villous atrophy on duodenal histology from all 28 Swedish pathology departments from 1969–2008. They looked at age, gender, calendar period, duration of disease and educational attainment to determine predictors of persistent villous atrophy.

    They found that, of 7,648 celiac disease patients who received follow-up biopsy, 3,317 patients showed clear persistent villous atrophy (43%; 95% CI 42–44%).

    Persistent villous atrophy rise with patient age, with 56% of those 70 years of age or older, compared to 17% among those younger than 2 years.

    In contrast, persistent villous atrophy did not vary widely by age in earlier years. Multivariate analysis showed that, 2–5 years after celiac disease diagnosis, persistent villous atrophy was more common among males (OR 1.43; 95% CI 1.07–1.90), and less common in more highly educated patients (OR for college degree vs.

    Overall, rates of persistent villous atrophy have changed over time, with greater rates of healing in recent years.

    Social differences in persistent villous atrophy suggest that levels of education regarding the importance of a gluten-free diet can influence mucosal healing.

    Source:

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  • Related Articles

    Jefferson Adams
    Celiac.com 01/14/2011 - Researchers recently presented information at the American College of Gastroenterology that indicates that more people with celiac disease might stop responding to gluten-free diets. Their new study, in the form of a retrospective chart review, turned up 17 cases of refractory celiac disease, each of which was eventually treated successfully with thiopurines.
    Researchers Christopher Hammerle, MD, and Sheila Crowe, MD, of the University of Virginia in Charlottesville, reported the results at a meeting at the American College of Gastroenterology. Hammerle called thiopurines her "treatment-of-choice for refractory celiac disease to avoid long-term steroids." The researchers stated that refractory disease appear to be on the rise. Patients with refractory celiac disease have recurrent symptoms such as abdominal pain, severe malabsorption, and intestinal damage.
    While some people note that refractory sprue might be caused by non-compliance to the gluten-free diet, current guidelines for treating refractory sprue call for doctors to review the dietary compliance of their patients, and to press for stricter adherence, and to search for other triggers of non-responsiveness only once dietary adherence issues are ruled out. In order to best understand the natural history of the celiac disease and to establish best practices for treatment, the researchers examined non-responsive celiac patients who had been seen at the University of Virginia Medical Center over the previous 10-year period.
    They found 17 such patients; 16 of whom had intraepithelial lymphocytes, four with the polyclonal phenotype and 12 with the monoclonal phenotype. One patient was untyped, while five patients also suffered autoimmune disease. The average age for diagnosis of a polyclonal phenotype was 45 years, and for the monoclonal phenotype mean age at diagnosis was 59. Overall, patients received a diagnosis of refractive disease an average of 4.7 years after receiving their diagnosis of celiac disease.
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    Source:

    American College of Gastroenterology. Hammerle C, Crowe S "Natural history and treatment of refractory celiac disease: Experience with 17 patients at a single center" ACG 2010; Abstract 235.

    Jefferson Adams
    Celiac.com 03/25/2011 - A group of researchers recently set out to evaluate cladribine [2-chlorodeoxyadenosine (2-CdA)] therapy in refractory celiac disease (RCD) â…¡.
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    Source:

    World J Gastroenterol. 2011 January 28; 17(4): 506–513. doi: 10.3748/wjg.v17.i4.506.

    Diana Gitig Ph.D.
    Celiac.com 05/27/2011 - Refractory Celiac Disease (RCD) is exactly what it sounds like: persistent malabsorption symptoms and intestinal villous atrophy even after following a gluten free diet. It is divided into two subtypes. RCDI has normal intraepithelial lymphocytes (IELs) while RCDII has abnormal IELs. RCDII is by far the more severe - there is no effective treatment, and it is often fatal within five years. Recent studies in Amsterdam and Paris have reported that RCDII can account for 28-75% of RCD patients. A group of researchers led by Ciaran Kelly at the Celiac Center at Beth Israel Deaconess Medical Center in Boston, the only specialized celiac center in New England, set out to determine if the same was true in the United States. They found a much lower incidence, 17%, of RCD patients with RCDII.
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    Sources:

    Roshan et al. The Incidence and Clinical Spectrum of Refractory Celiac Disease in a North American Referral Center. The American Journal of Gastroenterology 2011; 106: 923-928. Malamut and Cellier. Is Refractory Celiac Disease More Severe in Old Europe? The American Journal of Gastroenterology 2011; 106: 929-932.

    Jefferson Adams
    Celiac.com 04/07/2014 - Histologically non-responsive celiac disease (NRCD) is a potentially serious condition found in celiac disease patients who suffer persistent villous atrophy despite following a gluten-free diet (GFD).
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    Source:
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  • Recent Articles

    Jefferson Adams
    Celiac.com 06/18/2018 - Celiac disease has been mainly associated with Caucasian populations in Northern Europe, and their descendants in other countries, but new scientific evidence is beginning to challenge that view. Still, the exact global prevalence of celiac disease remains unknown.  To get better data on that issue, a team of researchers recently conducted a comprehensive review and meta-analysis to get a reasonably accurate estimate the global prevalence of celiac disease. 
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    Source:
    Clin Gastroenterol Hepatol. 2018 Jun;16(6):823-836.e2. doi: 10.1016/j.cgh.2017.06.037.

    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:
    Purée all ingredients together in a blender.
    Cover and refrigerate for at least 1 hour. 
    Adjust seasoning with salt and pepper, as desired. 
    Serve is a bowl with tortilla chips and guacamole.

    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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    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 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).
    The research team included Y.‐H. Dong; Y. Jin; TN Tsacogianis; M He; PH Hsieh; and JJ Gagne. They are variously affiliated with the Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School in Boston, MA, USA; the Faculty of Pharmacy, School of Pharmaceutical Science at National Yang‐Ming University in Taipei, Taiwan; and the Department of Hepato‐Gastroenterology, Chi Mei Medical Center in Tainan, Taiwan.
    To get solid data on the issue, the team conducted a cohort study among ARB initiators in 5 US claims databases covering numerous health insurers. They used Cox regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for enteropathy‐related outcomes, including celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy. In all, they found nearly two million eligible patients. 
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    After PS matching comparing olmesartan to other ARBs, hazard ratios were 1.21 (95% CI, 1.05‐1.40), 1.00 (95% CI, 0.88‐1.13), 1.22 (95% CI, 1.10‐1.36) and 1.04 (95% CI, 1.01‐1.07) for each outcome. Patients aged 65 years and older showed greater hazard ratios for celiac disease, as did patients receiving treatment for more than 1 year, and patients receiving higher cumulative olmesartan doses.
    This is the first comprehensive multi‐database study to document a higher rate of enteropathy in olmesartan initiators as compared to initiators of other ARBs, though absolute rates were low for both groups.
    Source:
    Alimentary Pharmacology & Therapeutics