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    DQ8 Causes More Than Just Celiac Disease


    Hallie Davis

    Celiac.com 08/18/2009 - Many of you know that DQ8 is one of the two major genes which may lead to celiac disease. You may also know that celiac disease is often associated with various other autoimmune diseases. What you may not know is that DQ8 may be the direct cause of these other autoimmune diseases, for these autoimmune diseases are found in increased incidence not just in celiac disease, but also with DQ8 itself.


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    What follows is a list I have compiled showing the various diseases that are found in increased frequency among people who have the DQ8 gene (DQB1*0302). I will show the reference number next to each, and the corresponding references will appear below:

    • Celiac disease (1)
    • Scleroderma (2)
    • Rheumatoid arthritis (1)
    • Autoimmune thyroiditis (3)
    • Pemphigus (4)
    • Lupus (6)
    • Pemphigoid (5)
    • Focal myositis (7)
    • Multiple sclerosis (8)
    • Myasthenia gravis (1)
    • Insulin dependant latent autoimmune diabetes of adults and adult Type 1 diabetes (9)
    • Type 1 juvenile diabetes (1)
    • Sjogren’s syndrome (10)
    • Addisons’s disease (11)
    • Complex regional pain syndrome with dystonia (12)
    • Latex allergy (13)
    This list is not intended to be exhaustive. It is a starter list. Hopefully more research will be done on these, including carefully controlled research as to whether gluten plays any role in triggering these other autoimmune diseases even in the absence of gluten blood antibodies or positive duodenal biopsies. I, for one have DQ8 and numerous of these autoimmune diseases, even though my gluten blood antibodies and duodenal biopsies are negative. We who have this gene need to know for certain #1 whether a gluten free diet will help prevent the triggering of these other various autoimmune diseases, and #2 whether a gluten-free diet will help mitigate autoimmune symptoms that have already developed. I feel no better on the gluten-free diet than before I started it a year and a half ago. However, if I had not been on the diet, perhaps I would be feeling even worse now. Only controlled research will give us the answer.

    References:

    1. http://en.wikipedia.org/wiki/HLA-DQ8
    2. Autoantibodies to fibrillarin in systemic sclerosis (scleroderma). An immunogenetic, serologic, and clinical analysis. Frank C. Arnett, MD, John D. Reveille, MDet al. See abstract at http://www3.interscience.wiley.com/journal/112212324/abstract.
    3. A strong association between thyrotropin receptor-blocking antibody- positive atrophic autoimmune thyroiditis and HLA-DR8 and HLA-DQB1*0302 in Koreans. Cho, JH Chung, YK Shong, YB Chang, H Han, JB Lee, HK Lee and CS Koh. See abstract at http://jcem.endojournals.org/cgi/content/abstract/77/3/611.
    4. Association between HLA-DRB1, DQB1 genes and pemphigus vulgaris in Chinese HansBy Zhou SH, Lin L, Jin PY, Ye SZ. See abstract at: http://www.ncbi.nlm.nih.gov/pubmed/12579512.
    5. Polymorphisms of HLA-DR and -DQ Genes in Japanese Patients with Bullous Pemphigoid. By Okazaki A, Miyagawa S, et al. See abstract at: http://sciencelinks.jp/j-east/article/200017/000020001700A0339663.php.
    6. HLA-DRB1*03 and DQB1*0302 associations in a subset of patients severely affected with systemic lupus erythematosus from western India. By U Shankarkumar, K Ghosh, S S Badakere, D Mohanty. See abstract at: http://ard.bmj.com/cgi/content/extract/62/1/92.
    7. HLA typing in focal myositis. By Kenji Sekiguchi, Fumio Kanda, Kenichi Oishi, Hirotoshi Hamaguchi, Kenichiro Nakazawa, Nobuya Maeda, Hiroyuki Ishihara and Kazuo Chihara. See abstract at: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T06-4DB5B4F-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=975695599&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=36883393fca9b990607eeb0d38116c5a.
    8. HLA-DRB1*1501, -DQB1*0301, -DQB1*0302, -DQB1*0602, and -DQB1*0603 alleles are associated with more severe disease outcome on MRI in patients with multiple sclerosis. By Zivadinov Robert; Uxa Laura et al. See abstract at: http://www.biomedexperts.com/Abstract.bme/17531857/HLA-DRB1_1501_-DQB1_0301_-DQB1_0302_-DQB1_0602_and_-DQB1_0603_alleles_are_associated_with_more_severe_disease_outcome.
    9. Similar Genetic Features and Different Islet Cell Autoantibody Pattern of Latent Autoimmune Diabetes in Adults (LADA) Compared With Adult-Onset Type 1 Diabetes With Rapid ProgressionBy Nóra Hosszúfalusi, MD, PHD, Ágnes Vatay, MD1, et al. See abstract at http://care.diabetesjournals.org/content/26/2/452.full.
    10. Specific amino acid residues in the second hypervariable region of HLA- DQA1 and DQB1 chain genes promote the Ro (SS-A)/La (SS-B) autoantibody responses. ByJD Reveille, MJ Macleod, K Whittington and FC Arnett. See abstract at http://www.jimmunol.org/cgi/content/abstract/146/11/3871.
    11. Analysis of extended human leukocyte antigen haplotype association with Addison’s disease in three populations. ByGombos, Hermann, et al. See study at: http://www.eje-online.org/cgi/reprint/157/6/757.pdf.
    12. HLA-B62 and HLA-DQ8 are associated with Complex Regional Pain Syndrome with fixed dystonia. By Rooij, Gosso, et al. See study at: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T0K-4WH0JWP-2&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=c869b6d3a38081820fad17c162b510ba.
    13. HLA-DQ8 and the HLA-DQ8-DR4 haplotype are positively associated with the hevein-specific IgE immune response in health care workers with latex allergy. By  Rihs Hans-Peter; Chen Zhiping; Ruëff Franziska; et al. See abstract at: http://www.biomedexperts.com/Abstract.bme/12209103/HLA-DQ8_and_the_HLA-DQ8-DR4_haplotype_are_positively_associated_with_the_hevein-specific_IgE_immune_response_in_health_c

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    You say that you are feeling no better on a gluten-free diet. Many of us have found that in order to feel well we need to eliminate more than gluten. I discovered I react strongly to yeast. In fact, when I first went gluten-free I though all yeast breads were contaminated with wheat because of the reaction I had. I have also discovered that I feel best when I eat no grains and no dairy. Have you looked into the possibility that you may be reacting to other foods?

     

    Thanks you for this article and references.

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    I too had the negative results on my blood work, but my attacks stopped once I went on the gluten free diet. About a year into the diet I found that I also had issues with Xanthan gum. Now two years in, I have begun to struggle with hypoglycemia attacks and extreme fatigue. I was recently put on a structured diet including protein supplements. The attacks have stopped but the fatigue is becoming worse. I've been to several doctors that all say my lab work checks out, but have no suggestions or answers to why I feel so poorly. So, if the new diet doesn't work they are sending me off for more tests. So, I think that celiac can just be the tip of the iceberg. Any suggestions or insight is welcome.

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    My personal opinion is that if you don't feel any better/get worse/no clinical lab or test results improve on the gluten free diet than gluten is not your problem. I hear of so many "gluten intolerant" people who think they have some form of celiac say "but I didn't start to feel better until I cut out dairy/yeast/fruit, etc. Well, then maybe that was what the problem was...what indicates it would be gluten then? It just doesn't make any sense. Just having the genes for celiac or some symptoms of celiac doesn't mean you have celiac or NCGI. And if you still are getting sick, it's entirely possible that food plays little to no role in your illness to begin with unless allergy or intolerance testing proves otherwise. Do I think that a subset of people with autoimmunity/genes/family history for autoimmunity will improve or be helped by being gluten free? Yes. Definitely. I bet some of those people definitely should most certainly be gluten free. However, I suspect that a lot of people are thinking gluten is the problem when really it's not. I mean, if you don't actually have celiac, and if you don't improve or you continue to be ill, what is the point of being gluten free? Likely there is something else going on that requires testing, not cutting out more foods. Although there are people out there who truly have an immune (IgE, IgA, IgM, etc.) reaction to multiple and many (if not all) foods. But they need to be under the care of a specialist anyway. I know because I am one of those people. I also think people in general eat a lot of junk and processed foods, which have additives that bother some people. It's not necessarily gluten that people are reacting to. I do agree 100% with the author that more research does need to be done.

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    Guest Lisa Cairncross

    Posted

    Having gone undiagnosed or misdiagnosed for 42 years, I'll never know when my Celiac Disease became active. Once dx'd I removed all gluten from my diet and did indeed get worse and was subsequently diagnosed with Fibromyalgia. The endoscopy performed at one year gluten free revealed increased damage/blunting of my villi. I continued to get sicker and sicker until I had maybe an hour of vertical time per day (right when I awoke and there was no food in my body).

     

    I was gluten free two and a half years before I eliminated all possible food intolerances at once to trial them each separately over a six month period. Within three days of eliminating Grains, Nightshades, Legumes, Nuts, Dairy and Citrus I was up out of bed (had been bedridden for over a year) and have continued to slowly improve with the exception of some horrible days during food trial.

     

    I now believe that a lifetime of gluten destroyed my digestive system which led to other food intolerances. Now that I have removed these foods I have new hope that my digestive system will have an opportunity to heal and I will gain some foods back, but never Gluten. If I am incorrect and never get these foods back -- at least I am out of bed, feeling great (most days) and have a life once again.

     

    PS All three of my children and two grandchildren had negative celiac panels, but have all had greatly improved health on a gluten free diet. Two children had to remove a few other foods through elimination...and are also now healthier than ever before. I am certain they were on the same path as me and would have only got sicker as the decades passed.

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    This probably explains why having one autoimmune disease increases your risk for others. They're all closely related (genetic profile wise). I am Pakistani, positive for the HLA-DQ8 gene. Celiac disease is fairly prominent in South Asia too, and I think it's the only gene that is related to Celiac there (HLA-DQ2 is fairly absent).

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    Guest Dee Hayes

    Posted

    Having gone undiagnosed or misdiagnosed for 42 years, I'll never know when my Celiac Disease became active. Once dx'd I removed all gluten from my diet and did indeed get worse and was subsequently diagnosed with Fibromyalgia. The endoscopy performed at one year gluten free revealed increased damage/blunting of my villi. I continued to get sicker and sicker until I had maybe an hour of vertical time per day (right when I awoke and there was no food in my body).

     

    I was gluten free two and a half years before I eliminated all possible food intolerances at once to trial them each separately over a six month period. Within three days of eliminating Grains, Nightshades, Legumes, Nuts, Dairy and Citrus I was up out of bed (had been bedridden for over a year) and have continued to slowly improve with the exception of some horrible days during food trial.

     

    I now believe that a lifetime of gluten destroyed my digestive system which led to other food intolerances. Now that I have removed these foods I have new hope that my digestive system will have an opportunity to heal and I will gain some foods back, but never Gluten. If I am incorrect and never get these foods back -- at least I am out of bed, feeling great (most days) and have a life once again.

     

    PS All three of my children and two grandchildren had negative celiac panels, but have all had greatly improved health on a gluten free diet. Two children had to remove a few other foods through elimination...and are also now healthier than ever before. I am certain they were on the same path as me and would have only got sicker as the decades passed.

    I would like a list of the foods you eat because I have been eliminating the same foods over the past decade and am feeling frustrated and hunger about what to eat. Thanks.

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  • About Me

    I am a retired Doctor of Optometry after practicing for 20 years. I have monoclonal gammopathy (paraproteinemia), limited systemic scleroderma, Hashimoto's thyroiditis, obstructive sleep apnea, beginning neuropathy, and have just been found to have the celiac HLA type: DQ8.

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    Jefferson Adams
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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.
    For their review, the team searched Medline, PubMed, and EMBASE for the keywords ‘celiac disease,’ ‘celiac,’ ‘tissue transglutaminase antibody,’ ‘anti-endomysium antibody,’ ‘endomysial antibody,’ and ‘prevalence’ for studies published from January 1991 through March 2016. 
    The team cross-referenced each article with the words ‘Asia,’ ‘Europe,’ ‘Africa,’ ‘South America,’ ‘North America,’ and ‘Australia.’ They defined celiac diagnosis based on European Society of Pediatric Gastroenterology, Hepatology, and Nutrition guidelines. The team used 96 articles of 3,843 articles in their final analysis.
    Overall global prevalence of celiac disease was 1.4% in 275,818 individuals, based on positive blood tests for anti-tissue transglutaminase and/or anti-endomysial antibodies. The pooled global prevalence of biopsy-confirmed celiac disease was 0.7% in 138,792 individuals. That means that numerous people with celiac disease potentially remain undiagnosed.
    Rates of celiac disease were 0.4% in South America, 0.5% in Africa and North America, 0.6% in Asia, and 0.8% in Europe and Oceania; the prevalence was 0.6% in female vs 0.4% males. Celiac disease was significantly more common in children than adults.
    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. 
    This review demonstrates a need for more comprehensive population-based studies of celiac disease in numerous countries.  The 1.4% rate indicates that there are 91.2 million people worldwide with celiac disease, and 3.9 million are in the U.S.A.
    Source:
    Clin Gastroenterol Hepatol. 2018 Jun;16(6):823-836.e2. doi: 10.1016/j.cgh.2017.06.037.