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    Study Supports Gluten-free Diet for 'Potential' Celiac Disease Patients


    Jefferson Adams
    Image Caption: New study indicates more people should be gluten-free.

    Celiac.com 12/26/2010 - Should everyone with symptoms of celiac disease go on a gluten-free diet? Current practice allows many patients with symptoms of celiac disease, but no gut damage, and thus no official diagnosis, to forgo a gluten-free diet.


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    In a new study, researchers found that people with celiac disease symptoms have the same distinctive metabolic fingerprint as patients with full-blown disease, and who must follow a gluten-free diet to avoid permanent damage to the gut.

    The new study, by Ivano Bertini and colleagues, is stirring up the discussion about just which patients with symptoms of celiac disease should follow a gluten-free diet.

    Their research shows that people currently diagnosed as "potential" celiac disease patients and not advised to follow a gluten-free diet may not be "potential" patients at all.

    Celiac disease is widely regarded as undiagnosed or misdiagnosed. For their study, the researchers used magnetic resonance metabolic profiling to analyze the biochemical markers in the blood and urine of 61 patients with celiac disease, 29 with potential celiac disease, and 51 healthy people.

    The researchers found that people with unproven celiac disease largely shared the same profile as those with confirmed celiac disease and that the biochemical markers in both groups differed sharply from those of healthy individuals.

    The researchers conclude that their findings "demonstrate that metabolic alterations may precede the development of small intestinal villous atrophy and provide a further rationale for early institution of gluten-free diet in patients with potential celiac disease, as recently suggested by prospective clinical studies."

    The authors do note receiving funding from Boehringer Ingelheim Italy.

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    I would like to know if the patients had any celiac blood panels done, and whether those with the similar metabolic panels as celiacs already had developed antibodies, and whether they were followed up with biopsy... and what they showed. It is not cost effective to test everyone with any one of a dozen or more symptoms... so what will become the best screening tool?

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    Guest Will Smith

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    I do not have celiac disease-wrong genes, no villi damage However, I am highly gluten intolerant. I have lost half of my kidney function from IgA Nephropathy caused by gluten reactions. Mayo Clinic routinely checks people with this condition for celiac disease, but there is no check for gluten intolerance. Have your doctor monitor your kidney function if you are gluten intolerant and continue to eat it anyway.

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  • Related Articles

    Scott Adams
    The following Medline abstract describes a unique study that was done on the quality of life of two groups of people with celiac disease: One that was diagnosed as the result of having symptoms, and the other which had little or no symptoms and whose diagnosis was reached via screen-detection. Both groups were treated for one year with a gluten-free diet, and were then studied to determine their overall response, including their psychological response. Here is the abstract:
    Eff Clin Pract 2002 May-Jun;5(3):105-13
    Mustalahti K, Lohiniemi S, Collin P, Vuolteenaho N, Laippala P, Maki M.
    Department of Pediatrics, Tampere University Hospital, Finland.
    CONTEXT: Since the advent of serologic testing for celiac disease, most persons who receive a diagnosis of celiac disease have few or no symptoms. Although pathologic changes of celiac disease resolve on a gluten-free diet, how a gluten-free diet affects the quality of life for patients with screen-detected celiac disease is unclear.
    OBJECTIVE: To evaluate the effect of a gluten-free diet on the quality of life of patients with screen-detected celiac disease.
    DESIGN: Prospective study of patients before and 1 year after initiating a gluten-free diet.
    PARTICIPANTS: 19 patients with screen-detected celiac disease (found by serologically testing first-degree relatives of celiac patients) and 21 consecutive patients with symptom-detected disease. In all cases, celiac diagnosis was confirmed by finding villous atrophy and crypt hyperplasia on small-bowel biopsy.
    INTERVENTION: Gluten-free diet (explained during a single physician visit). MAIN OUTCOME
    MEASURES: Gastrointestinal Symptoms Rating Scale (GSRS), in which scores range from 0 to 6 (higher scores represent worse symptoms); and quality of life measured with the Psychological General Well-Being Questionnaire (PGWB). Scores range from 22 to 132 (higher scores mean greater well-being).
    RESULTS: At baseline, patients with symptom-detected celiac disease had poorer quality of life and more gastrointestinal symptoms than those with screen-detected celiac disease. Reported compliance with the gluten-free diet was good. All mucosal lesions of the small bowel had resolved at the follow-up biopsy. After 1 year of following the diet, quality of life for patients with screen-detected disease significantly improved (mean PGWB score increased from 108 to 114; P
    CONCLUSIONS: Gluten-free diet was associated with improved quality of life for patients with symptom-detected celiac disease and patients with screen-detected celiac disease. Concerns about the burden of a gluten-free diet, at least over the short term, may be unfounded.
    PMID: 12088289


    Roy Jamron
    Celiac.com 07/31/2006 - A two-year study in the July 2006 Endoscopy showed older celiac patients on a gluten-free diet have an incomplete histological recovery even after two years. Only the younger patients (5 - 30 years) showed significant improvement of histology within 12 months (P < 0.034); older patients (>30 years) showed histological improvement but this was not statistically significant, even after 24 months on a gluten-free diet. This study was also previously discussed in an article by Dr. Antonio Tursi in the Spring 2006 Celiac.com Scott-Free Newsletter. This also means increased intestinal permeability and associated problems such as liver damage may continue to be a lasting problem in older patients beyond two years on a gluten-free diet. Below is the abstract:
     

    Endoscopy 2006 July; 38(7): 702-707
    Endoscopic and histological findings in the duodenum of adults with celiac disease before and after changing to a gluten-free diet: a 2-year prospective study
    Tursi, A.; Brandimarte, G.; Giorgetti, G. M.; Elisei, W.; Inchingolo, C. D.; Monardo, E.; Aiello, F.
     


    Background and study aims: Published follow-up data on small-intestinal recovery in patients with celiac disease are scarce and contradictory. This is especially the case for adult patients, who often show incomplete histological recovery after starting a gluten-free diet (GFD). We conducted a 2-year prospective study to evaluate the effectiveness of a GFD in improving the endoscopic and histological duodenal findings in adults with celiac disease.
    Patients and methods: We studied 42 consecutive adults with newly diagnosed celiac disease (13 men, 29 women; mean age 32.7 years, range 15 - 72 years). All the patients underwent esophagogastroduodenoscopy and small bowel biopsy. We devised our own grading system for the endoscopic appearance of the duodenum, which ranged from "normal" appearance to "mild", "moderate", or "severe" alterations. Small bowel biopsies were obtained from the second part of the duodenum (and from the duodenal bulb when it had a micronodular appearance). The histopathological appearances were described according to modified Marsh criteria.
    Results: A normal endoscopic appearance in the duodenum was found in 5/42 patients (11.9 %) at entry and in 32/42 patients (76.2 %) after 2 years on a GFD. Subdividing the patients according to age, patients aged from 15 years to 60 years showed significant improvement within 12 months (P < 0.0001 for patients aged from 15 years to 45 years; P < 0.003 for patients in the 46 years to 60 years group), whereas the improvement in endoscopic findings in patients older than 60 years was not statistically significant, even 24 months after starting the GFD. "Normal" histology was reported in none of the patients at entry, but in 25 patients (59.5 %) after 24 months on a GFD, but this parameter did not show a significant improvement until the patients had been on the GFD for 12 months (P < 0.0001). Only the younger patients (5 - 30 years) showed significant improvement of histology within 12 months (P < 0.034); older patients (>30 years) showed histological improvement but this was not statistically significant, even after 24 months on a GFD.
    Conclusions: This study shows for the first time that endoscopic recovery is faster than histological recovery in adults with celiac disease who go on a GFD. Moreover, older patients showed incomplete endoscopic and histological recovery even 24 months after starting a GFD. We therefore advise, as a minimum recommendation, that follow-up biopsies should be taken 1 - 2 years after starting a GFD in adults with celiac disease.

    Jefferson Adams
    Celiac.com 05/02/2012 - Doctors and researchers are still debating the usefulness of active blood screening for spotting celiac disease in older populations. Studies do suggest that many cases of celiac disease go undetected, especially in the older population. One unanswered question is whether screening does any good for older people who have been eating gluten many decades.
    A team of researchers recently studied the clinical benefit of a gluten-free diet in screen-detected older celiac disease patients. The research team included Anitta Vilppula, Katri Kaukinen, Liisa Luostarinen, Ilkka Krekelä, Heikki Patrikainen, Raisa Valve, Markku Luostarinen, Kaija Laurila, Markku Mäki, and Pekka Collin.
    They are affiliated with the Department of Neurology, the Department of Internal Medicine and the Department of Surgery at Päijät-Häme Central Hospital, and the University of Helsinki's Department of Education and Development in Lahti, Finland, the Department of Gastroenterology and Alimentary Tract Surgery the School of Medicine, and the Paediatric Research Centre at the University of Tampere and Tampere University Hospital, Tampere, Finland.
    For their study, the researchers evaluated the benefit of active detection and implementation of a gluten-free diet in elder populations with for celiac disease.
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    Using surveys, the team established gastrointestinal symptom ratings and quality of life by psychological general well-being. The used this information to rate symptoms.
    They found patient dietary compliance to be good overall.  Initial tests on the patients showed reduced serum ferritin levels, pointing to subclinical iron deficiency. This trend reversed after patients followed a gluten-free diet.
    Initially low vitamin B12, vitamin D and erythrocyte folic acid levels increased significantly on a gluten-free diet.
    Patient histories showed that those with celiac disease had sustained more low-energy fractures, and sustained such fractures more frequently than the general population. A gluten-free diet brings with it a beneficial increase in bone mineral density.
    The team also noticed that many gastrointestinal symptoms disappeared, even though though many patients reported only subtle symptoms upon diagnosis.
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    Results showed that patients who had celiac disease detected by mass blood screen did, in fact, benefit from a gluten-free diet. For doctors evaluating older patients, the team advocates a high index of suspicion and active case-finding in celiac disease as an alternative to mass screening.
    Source:
    BMC Gastroenterology 2011, 11:136. doi:10.1186/1471-230X-11-136

    Jefferson Adams
    Celiac.com 10/15/2014 - A team of researchers recently set out to assess the benefits of a gluten-free diet for people whose blood screens show markers for celiac disease, but who show no physical symptoms. Specifically, they investigated whether screen-detected and apparently asymptomatic adults with endomysial antibodies (EmA) benefit from a gluten-free diet.
    The research team included K. Kurppa, A. Paavola, P. Collin, H. Sievänen, K. Laurila, H. Huhtala, P. Saavalainen, M. Mäki, and K. Kaukinen. They are variously associated with the Tampere Center for Child Health Research, the Tampere School of Health Sciences of the University of Tampere and Tampere University Hospital, the Department of Gastroenterology and Alimentary Tract Surgery at Tampere University Hospital and School of Medicine, University of Tampere, the UKK Institute in Tampere, Finland, the Research Program Unit of the Immunobiology and Haartman Institute at the Department of Medical Genetics of the University of Helsinki in Helsinki, Finland, and the Department of Gastroenterology and Alimentary Tract Surgery, Tampere University Hospital and School of Medicine, University of Tampere, Tampere, Finland and Seinäjoki Central Hospital, Seinäjoki, Finland.
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    After 1 year on the gluten-free diet, the mean mucosal villous height:crypt depth values increased (P < .001), levels of celiac-associated antibodies decreased (P < .003), and gastrointestinal symptoms improved compared to patients on gluten-containing diets (P = .003).
    The gluten-free diet group showed less indigestion (P = .006), reflux (P = .05), and anxiety (P = .025), and better overall health, based on the visual analog scale (P = .017), compared gluten-containing diet group.
    Only social function scores improved more in the gluten-containing diet group than in the gluten-free diet group (P = .031). There were no differences between groups in terms of lab test results, bone mineral density, or body composition.
    Most measured parameters improved when patients in the gluten-containing diet group were placed on gluten-free diets.
    No subjects considered their experience to be negative and most expected to continue eating gluten-free.
    The results show that a gluten-free diet benefits asymptomatic EmA-positive patients, and show the benefits of actively screening patients at risk for celiac disease.
    Source:
    Gastroenterology. 2014 Sep;147(3):610-617.e1. doi: 10.1053/j.gastro.2014.05.003. 

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/19/2018 - Could baking soda help reduce the inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease? Scientists at the Medical College of Georgia at Augusta University say that a daily dose of baking soda may in fact help reduce inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease.
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    Read more at: Sciencedaily.com

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    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. 
    The research team included P Singh, A Arora, TA Strand, DA Leffler, C Catassi, PH Green, CP Kelly, V Ahuja, and GK Makharia. They are variously affiliated with the Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Lady Hardinge Medical College, New Delhi, India; Innlandet Hospital Trust, Lillehammer, Norway; Centre for International Health, University of Bergen, Bergen, Norway; Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Gastroenterology Research and Development, Takeda Pharmaceuticals Inc, Cambridge, MA; Department of Pediatrics, Università Politecnica delle Marche, Ancona, Italy; Department of Medicine, Columbia University Medical Center, New York, New York; USA Celiac Disease Center, Columbia University Medical Center, New York, New York; and the Department of Gastroenterology and Human Nutrition, All India Institute of Medical Sciences, New Delhi, India.
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    This systematic review and meta-analysis showed celiac disease to be reported worldwide. Blood test data shows celiac disease rate of 1.4%, while biopsy data shows 0.7%. The prevalence of celiac disease varies with sex, age, and location. 
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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
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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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    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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    To that end, a research team recently set out to try to get some information about the frequency and importance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. The research team included Shafinaz Hussein, Tatyana Gindin, Stephen M Lagana, Carolina Arguelles-Grande, Suneeta Krishnareddy, Bachir Alobeid, Suzanne K Lewis, Mahesh M Mansukhani, Peter H R Green, and Govind Bhagat.
    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. 
    Clonal TCR-GRs are not infrequent in cases lacking features of RCDII, while PCPs are frequent in all disease phases. TCR-GR results should be assessed in conjunction with immunophenotypic, histological and clinical findings for appropriate diagnosis and classification of RCD.
    The team divided the TCR-GR patterns into clonal, polyclonal and prominent clonal peaks (PCPs), and correlated these patterns with clinical and pathological features. In all, they detected clonal TCR-GR products in biopsies from 67% of patients with RCDII, 17% of patients with RCDI and 6% of patients with gluten-free diet. They found PCPs in all disease phases, but saw no significant difference in the TCR-GR patterns between the non-RCDII disease categories (p=0.39). 
    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