Science topic

Celiac Disease - Science topic

A malabsorption syndrome that is precipitated by the ingestion of foods containing GLUTEN, such as wheat, rye, and barley. It is characterized by INFLAMMATION of the SMALL INTESTINE, loss of MICROVILLI structure, failed INTESTINAL ABSORPTION, and MALNUTRITION.
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I am about to perform a larger mouse experiment in which we collect plasma for different purposes. However, I would like to determine anti-tissue transglutaminase antibodies also - and I have only seen articles that detects the antibodies in serum. Have anybody tried to detect it in plasma?
I know that insulin autoantibodies can be detected in plasma.
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Salman Ajlan thank you very much for your answers.
In the articles that you have listed, they also use serum to detect anti-tTG. I will just have to try detecting it in plasma.
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Dear All,
Greetings from IIPL.
Since the start of COVID-19 pandemic, many research work has been published in the public domain which mainly indicates that patients with celiac disease does not have higher risk of COVID-19 as compared to the general population.
But no research paper has been published which throws some light of impact of COVID-19 on people with diagnosed Celiac Disease. This set of people doen't know that they are already in the celiac zone or atleast in the gluten-intolerant zone. Therefore, they may not be under a gluten-free diet. And when these people contract the COVID-19 infection, how their underlying autoimmune celiac disease interact with the infection by SARS-CoV-2 virus?
If anyone has any understanding, please contact me. Thanks.
Regards
Arnab Guha
+91-9611186720
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Dear Arnab, thank you for asking this interesting technical question. In this context please have a look at the following potentially useful articles which might help you in your analysis:
Risk perception and knowledge of COVID-19 in patients with celiac disease
Risk of Severe Covid-19 in Patients with Celiac Disease: A Population-Based Cohort Study
Risk of COVID-19 in celiac disease patients
The second article has been posted as public full text on RG. Thus it can be freely downloaded as pdf file. I hope it helps.
Good luck with your work and best wishes!
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T1DM is considered an autoimmune disease. However, there are cases having no antibodies.
Q1 How common are these patients in your practice?
Q2 Did they require further investigations (apart from c-peptide)?
Q3 What are the antibodies that you test in your practice?
Q4 Has anyone of them developed thyroid disorder or coeliac disease?
Your contribution is appreciated
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Antibody-negative type 1 diabetes mellitus
About 10% of the patients with Type 1 diabetes are negative for any antibodies (common one being anti-islet cell and anti-GAD antibodies).
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Conventional immunosuppressant Vs biologic treatment(eg: Infliximab) : What are their roles in Celiac sprue?
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Please take a look at this useful RG link.
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to find any significant association between childhood celiac disease and deficiency of vitamin D
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Immune system and Inflammation impact on the Gut-Brain axis !
The Gut/Immune/Nervous (GIN) communication
New insights into how immune system and inflammation play a role in Parkinson's Disease
Nov. 2019
New research indicates that the earliest stages of Parkinson's disease (PD) may occur in the gut with a likely relation to inflammatory bowel disease (IBD).
Parkinsonism is not just a brain disorder, but a group of diseases that may have their onset in the GIT. It is strongly suggested that individuals with an increased tendency for peripheral inflammation have a higher risk to acquire PD. Given the potentially critical role of gut pathology in the pathogenesis of PD, IBD may impact PD risk.
Peripheral immune system alterations may play a role in PD, which has the potential for new therapeutic strategies. Understanding and appreciating the importance of the so-called gut-brain axis, the connection between gut and the brain in PD, has grown rapidly in recent years.
The inflammatory processes have naturally led to discussion of an association between IBD and PD since the two share some basic characteristics. IBD is currently considered an inappropriate immune response to the microbiota in the intestines, characterized by chronic pro-inflammatory immune activity, a trait now also suggested to be a fundamental element of neurodegenerative disorders.
Highlighting the relevance of the immune system, large genome-wide association studies (GWAS) and pathway analyses identified 17 shared loci between PD and seven autoimmune diseases including celiac disease, rheumatoid arthritis (RA), type 1 diabetes, multiple sclerosis, psoriasis, ulcerative colitis and Crohn's disease.
Many epidemiological and genetic studies have found that there seems to be an increased risk of developing PD among people with IBD. The association between IBD and PD may simply be that IBD is just one type of intestinal inflammation, so it is not IBD specifically that increases the PD risk but perhaps intestinal or peripheral inflammation in a broader sense.
Inflammation of the gut is only one of many symptoms on the list of changes in the gut and is associated with neural structures in PD patients. Thus, IBD might be just one of many sources of intestinal inflammation.
While IBD patients are more likely to get PD, the risk is still very small. Yet, for a given IBD patient, the probability of not getting the diagnosis is 95%-97%.
Future pharmacological therapies aiming at slowing or stopping PD progression should not only target patients well into the course of the disease, but also be administered to patients in the very early phases of the disease or at risk for developing PD.
Clinicians should be aware of early Parkinsonian symptoms in IBD patients but also in patients with chronic inflammatory disorders.
A focus on the potential role of the immune system and of systemic inflammation these neurological diseases is encouraged.
A clear knowledge of the mechanisms implicated in Gut/Immune/Nervous communication could help improve the prognostic and therapeutic tools leading to better quality of life for patients, reducing the exacerbation of PD symptoms, and delaying the progression of the disease.
Parkinson's disease is a slowly progressive disorder that affects movement, muscle control and balance. It is the second most common age-related neurodegenerative disorder affecting about 3% of the population by the age of 65 and up to 5% of individuals over 85 years of age. During the 20th century, PD was thought to be primarily a brain disorder, however, research has shown that it may actually begin in the enteric nervous system, the part of the autonomic nervous system that controls the gastrointestinal organs.
Source: Brudek, T. et al. (2019) Inflammatory Bowel Diseases and Parkinson’s Disease. Journal of Parkinson's Disease. doi.org/10.3233/JPD-191729
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I suggest reading this article-
Dinan TG, Cryan JF.The Microbiome-Gut-Brain Axis in Health and Disease. Gastroenterol Clin North Am. 2017 Mar;46(1):77-89. doi: 10.1016/j.gtc.2016.09.007. Epub 2017 Jan 4
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Theoretically, yes! However, even a gluten-free diet has very tiny amounts of gluten and probably these small amounts are not overtly harmful in most patients. A few patients might be very sensitive
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Yes, even small amounts of gluten can be harmful to a patient with coeliac disease.
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We are looking for a good antibody for plasma/serum zonulin (haptoglobin 2). There are few antibodies in the market but the problem most of them don´t have any citation. Some of them are not correctly mapped. We want to see all of the possible bands (alpha chains, or intact peptide  seq). We are planning to do western blot. 
Thanks!
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Quite old question, but it may still be interesting to someone else. Unfortunately, there are only predatory ELISA kits commercially available (for instance Immundiagnostik and Cusabio as the most common, but there are many others) for "zonulin", to understanding of zonulin being the same protein as pre-haptoglobin 2 has to be carefully taken, as a quick BLAST search will give that sequence to be gamma immunoglobulin heavy chain.
This considered, one should look at these papers on Immunodiagnostik kit ( )and on CusaBio kit ( )
Zonulin as shown in the original publication is definitely not pre-haptoglobin 2. However, this paper ( ) suggests that it is, even if the sequence of zonulin has still not been described whatsoever. There is a good pre-haptoglobin 2 antibody, but it is not commercially available ( ), but this one fits genotyping of Hp genes. Have fun!
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I need the velocity in runner and sprue zones at uphill ingot casting
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I think this is not just a number, With the help of simulation, we can obtain the graph of velocity changes. This is shown for a hollow cylinder in parts of the attached paper.
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I have conducted a systematic literature review collecting data on the prevalence of coeliac disease. I now need to analyse the data in a meta analysis. Any recommendations? My tutor has recommended Revman but I can’t seem to get along with it. Also I will need some step by step guidence.
Thank you
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Revman, R, Stata
Check this link
Statistical methods in the meta-analysis of prevalence of human diseases ...
by KS Wang · 2016
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Gluten sensitive enteropathy, also known as celiac disease, is an autoimmune inflammatory disease affecting the small intestine, so I think it is organ specific autoimmune disease; however, the clinical features are diverse. I searched in internet to know if it is organ specific or non-organ specific disease but I could not find an answer.
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Very clear the answer. It is a Systemic Autoimmune Disease because can be affected several organs simultaneously or later in the evolution.
It is the only systemic autoimmune disease whose etiology is very well defined only by the gluten
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Hello.I would like to have your input on a matter.
Patient: BMI of 21. Daily fatty feces, headaches, tiredness and swelling in left foot over the last year and a half (arthritis has been discarded as an option). Strict gluten and dairy free diet for over a year.
First ATA lgA test was positive. Duodenum biopsy (3 samples) within normal bounds apparently, H pylori wasnt found
Biopsy of large intestine show slight lymphocytic inflammation. Test Van de Kamer is positive. White blood cells in stool. HLA DQ2 positive. Stool elastase test and alpha-1 antitrypsin test normal. No parasites found. MRI and CAT scans show mildly inflamed mesenteric lymph nodes. Anti lkm, ASMA, AMA, Anti dna negatives. Anti VIH,HVC,HBS ag Negatives.
Albumin is normal. SIBO has been discarted. Calprotectin test is Ok.
H pylori wasnt found.
Has not responded to mesalamine, antispasmodic, or digestive enzymes.
How could you help this patient? What do you think this patient has?Thank you in advance.
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I think this patient has celiac disease. He has positive genetic markers and serum serology. The duodenal biopsies must be reviewed by an expert pathologist. the first question is if the patient follow an strict gluten-free diet and if the response is positive it would be recommended to repeat the duodenal biopsies in order to discard a refractory celiac disease and in this case to treat with oral steroids
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Whats is the most common genotypes for celiac disease ?-
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Celiac disease is a systemic multifactorial disorder resulting from the interaction of  genes (e.g. HLA-DQA1 and HLA-DQB1 ), gliadin, and other environmental and/or host factors (e.g. intestinal microbiota)
Genetic Risk is correlated to HLA-DQ2 and/or DQ8 Genotype  (From Megiorni et al [2009] for all genotypes included, except DQ8+DQ8: From Pietzak et al [2009])
DQ2+DQ8 Risk = 1:7 (14.3%)
DQ2+DQ2 OR DQ2 Homozygous DQB1*02 = 1:10 (10%)
DQ8+DQ8 2 = 1:12 (8.4%) 2
DQ8+DQB1*02 = 1:24 (4.2%)
Homozygous DQB1*02 = 1:26 (3.8%)
DQ2 alone = 1:35 (2.9%)
DQ8 alone = 1:89 (1.1%)
General Population risk = 1:100 (1%)
½ DQ2: DQB1*02 = 1:210 (0.5%)
½ DQ2: DQA1*05 = 1:1842 (0.05%)
No HLA-DQA/DQB celiac susceptibility alleles = 1:2518 (<0.04%)
Read:
- The Interaction among Microbiota, Immunity, and Genetic and Dietary Factors Is the Condicio Sine Qua Non Celiac Disease Can Develop. Pagliari D et al. J Immunol Res. 2015;2015:123653. doi: 10.1155/2015/123653.
- Taylor AK, Lebwohl B, Snyder CL, et al. Celiac Disease. 2008 Jul 3 [Updated 2015 Sep 17]. In: Pagon RA, Adam MP, Ardinger HH, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2017.
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 A man now 80 years old presents progressive ataxia amb pendular nystagmus wich began at age 75. A extensive study was negative. He doesn't present malabsorption and diarrhea, Two month ago vomited freqüently  and ataxia got worse . Transglutaminase and endomisium antibodies were negative, Recent duodenal biopsy is compatible with celiac disease (MARSH 3), amb HLA-DQ2 is positive. Slight improvement with gluten free diet. 
This case, a silent seronegative celiac disease with clinical neuroloy over age 75,is a exception, or is not a true celiac disease, or instead, may be a possible cause of some idiophatic ataxias ?, 
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Indeed well established, well known - refer to Hajdivassalou's work from Sheffield. AV
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The pathogenesis of celiac disease involves interplay of genetic, host microbiome and environmental factors like IBD. These include dynamic changes and exposure times starting from neonatal period. Recently there is rise in incidence of both celiac disease and IBD in India. Can anybody say whether this is result of similar changes in microbiome and environmental factors like diet, use of antibiotics?
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These papers that may be of interest to you. The rise of obesity and the use of anti-biotics and proton-pump inhibitors have greatly reduced the diversity of the microbiome. The use of emulsifiers in the food supply compromises the gut barrier. 
  1. Mar Rodríguez M, Pérez D, Javier Chaves F, et al. Obesity changes the human gut mycobiome. Scientific Reports. 2015;5:14600. doi:10.1038/srep14600.
  1. Corouge M, Loridant S, Fradin C, et al. Humoral Immunity Links Candida albicans Infection and Celiac Disease. Naglik JR, ed. PLoS ONE. 2015;10(3):e0121776. doi:10.1371/journal.pone.0121776.
  1. Serena G, Yan S, Camhi S, et al. Proinflammatory cytokine interferon-gamma and microbiome-derived metabolites dictate epigenetic switch between forkhead box protein 3 isoforms in coeliac disease. Clinical and experimental immunology. 2017:n/a-n/a. Manuscript available from author on ResearchGate.
  2. Lerner A, Matthias T. Changes in intestinal tight junction permeability associated with industrial food additives explain the rising incidence of autoimmune disease. Autoimmunity reviews. 2015;14(6):479-489. http://www.sciencedirect.com/science/article/pii/S1568997215000245
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Please can you inform of the real prevalence of ANAs positivity in the Celiac Disease and their evolution with a Gluten-free-diet?
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Dear Anthony : 
Thanks so much for your interesting information
My best regards
Luis
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A 30-year-old male patient _known to have celiac disease and not compliant with gluten-free diet_ has been accidentally discovered to have hypertension (150/90). 
What are the possible causes?
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A young hypertensive must be investigated for certain conditions e.g. medical renal disease and renal artery stenosis (USG kidneys, renal function tests, DTPA scan), vascular diseases (coarctation of aorta, Takayasu disease manifested by unequal pulses in extremities and detected by angiography), endocrine disease (Conn's disease i.e. primary hyperaldosteronism, thyroid disorders, pheochromocytoma). Other factors like obesity, Drug abuse and family history of hypertension. Celiac disease as a direct cause of hypertension is rare but not unknown. The vascular endothelium maintains a relatively vasodilated state via the release of nitric oxide, a process that could be disrupted by hyperhomocysteinaemia due to Vitamin B 12 malabsorption in celiac disease (Vit B12 and other cofactors are involved in homocysteine metabolism). This cause systemic vasoconstriction and endothelial dysfunction resulting in hypertension. In such cases treatment with multivitamins can help
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DPP-4 is a" digestive enzyme" commonly found as the active ingredient in OTC "digestive-supplements" whose benefits are quite dubious but nonetheless often used by those with celiac disease or non-celiac gluten sensitivity. Januvia is a DPP-4 inhibitor used to treat type2 diabetes---presumably it inhibits systemic or pancreatic DPP-4 from degrading incretin hormones permitting their sustained action in stimulating insulin and blocking glucagon---so if a patient with type2 Diabetes had taken Januvia and then later took a digestive supplement with DDP-4, could that DPP-4 degrade any incretins negating the effects of the previous DPP-4 inhibitor---the Januvia.   My suspicion is NO, since the digestive supplement would only work locally---intraluminally in small intestine whereas  Januvia and the incretin hormones are systemic in function or probably at pancreatic receptors ----but I  have been unable to verify---anyone have any thoughts or better yet FACTS! 
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Tausif---thanks for your reply---that was my belief just unable to verify that Januvia works entirely systemically---no conflict
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Since undigested gliadin is the mechanism of the autoimmune reaction in Celiac Disease, I was wondering if anyone was investigating the degradation of gliadin and would appreciate any discussion on the topic.
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Dear Anthony,
With all due respect, while it is true that researchers and clinicians choose to measure the TTg antibody response as a convenience, and claim that this is a valid autoimmune response (rather than a result of a collateral reaction associated with a primary reaction against an exogenous antigen), this in no way proves or even infers that the primary inflammatory reaction is not directed at the gliadin and glutelin peptides resulting from the digestion of the gluten found in wheat and related species.
To support that observation I submit the fact that when the exogenous antigen is withdrawn from the diet, the TTg reaction ceases.  Obviously it is not an independent reaction.  So how could the TTg antibody response actually be a valid autoimmune response?  The answer is, "It cannot be a true AI response".  If the reaction were truly autoimmune, then it would continue, independent of the status (presence or absence) of any exogenous antigens in the diet.
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celiac disease
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this interaction is mediated thru IL-15 whose production is induced by gliadin from intestinal cells and which in turn upregulates the proliferation of IELS=intraepithelial lymphocytes-and their NKG2D molecules inducing cytotoxicity while also upregulating stress receptors on the intestinal epithelial cells such as MICA,HLE,and FAS-Lwhich are then targeted by the NKG2D+IELS resulting in apoptosis---this innate response may then trigger an adaptive response thru the activation of TTG and increase in intestinal permeability eventually activating gluten specific T-cells and perpetuating the inflammatory reaction---there is a great deal of info on this in celiac literature----particularly from investigators like-Bana Jabri, N. Cerf-Benussen, Fris Koning , and L. Sollid among others 
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It means if a child has a Celiac disease has a  diabetes type I?
Is exists a link between celiac disease and type 1 diabetes mellitus ?. Are they share some of the same genes and have increased risk for associated autoimmune diseases and include symptoms that mimic other diseases?
Dear Colleague: Your contribution will be much appreciated. Thanks in advance !!
Regads
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There are some published studies looking into the prevalence of other autoimmune diseases/pathological findings in T1DM. For example:
The celiac iceberg: from the clinical spectrum to serology and histopathology in children and adolescents with type 1 diabetes mellitus and Down syndrome.
Scand J Gastroenterol. 2016;51(2):178-85. doi: 10.3109/00365521.2015.1079645. Epub 2015 Sep 4.
ATPase4A Autoreactivity and Its Association With Autoimmune Phenotypes in the Type 1 Diabetes Genetics Consortium Study.
Diabetes Care. 2015 Oct;38 Suppl 2:S29-36. doi: 10.2337/dcs15-2006.
The increased sensitivity of method of detection (presence of autoantibodies) can yield positive findings, but they do not always translate into clinical presentation of disease, which makes the determination of link difficult... especially when even within the T1DM genetic predisposition is far from being able to predict that a certain person will be diagnosed with the disease.
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Celiac plexus neurolysis is an established indication. There have been some clinical studies in therapy of locally advanced pancreatic cancer using gemcitabine and some another agents. Pancreatic cyst by paclitaxel or alcohol ablation was another idea.
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I wanted to make ELISA kit to quantify antibodies anti-deamidated gliadin in human serum. 
Where I can get deamidated gliadin for coat microtiter plate?
Thaks!
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Their description is a little ambiguous, but your might try biorbyt:
and see if they can clarify whether it is deamidated or not.
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I wanted to develop a 3D model for Celiac disease (an autoimmune disease of small intestinal villi, gluten toxicity). As Celiac disease become the major challenge for us. Its been very difficult to survive without gluten as it is present in almost every diet. Gluten free means-wheat, barley, rye etc.
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Thank yoU all....
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I am currently working on a hypothesis regarding the pathogenesis of demyelinating mechanisms in individuals with concomitant celiac disease and multiple sclerosis. Some literature suggests that NCGS is more closely associated with gluten ataxia and other neurological problems than is CD. I am wondering if possession of alleles for both CD and NCGS could contribute to the manifestation of autoimmune disorders with a demyelinating component.
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Probably, you are aware of this review. It might help.
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For celiac disease
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Grains gluten is a cereal proteins, more specifically wheat proteins, are
initially characterized by their solubility. These socalled Osborne fractions—water-soluble albumins, saltsoluble globulins, alcohol-soluble prolamins, and insoluble
glutelins—are complex mixtures of different polypeptides, especially in the case of wheat. The nomenclature and classification systems for the most important cereals (e.g.,wheat, barley, rye, maize, rice, and sorghum) are based on Osborne fractionation, while in the case of other cereals (e.g., pseudocereals—amaranth, quinoa, buckwheat, and millet) trivial names are in use for their protein fractions.  All gluten-containing cereals are rich in glutamine and proline and poor in basic amino acids. Water-soluble albumins and salt-soluble globulins represent the small size proteins of gluten-containing cereals and are present at relatively low levels of
total protein content. The bulk of these proteins are enzymes and related proteins, though some can have an immunotoxic effect. Prolamins are the alcohol-soluble
protein fractions of cereal grains. The cereal prolamins,  namely glutenins and gliadins in wheat, secalins in rye,and hordeins in barley, are the major storage proteins found
in the endosperm of cereal grains. Gliadins and glutenins together form the gluten protein family with a size range of 30 to millions kDa (26). The ratio of gliadin to glutenin is approximately 65 to 35 and can vary depending on genetic and environmental influences.Osborne fractionation scheme is applied for separation.Oat proteins might not belong to the celiac-harmful protein family, because their prolamin composition and amino acid sequence differ from those found in wheat, rye, and barley 
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Dermatitis herpetiformis (DH) is an autoimmune blistering disorder of known antibody IgA and unknown antigen associated with a gluten-sensitive enteropathy (GSE), and is generally accepted as a cutaneous manifestation of celiac disease and is characterized by grouped excoriations; erythematous, urticarial plaques; and papules with vesicles.
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Dear Adil ,salam ,see the reference 
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I am designing a bone density intervention which will include a gluten-free diet, but am finding very little intervention evidence of what physical activity works best. Most studies are cross-sectional or involve pediatric or healthy populations.
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In the US only recently have high risk individuals been screened for celiac disease. So many of the adults who are diagnosed have had the disease many years before diagnosis and treatment. In the US the physical activity levels of adults are much lower than in the EU. A significant number of people with CD have hypercalciuria which responds to a balanced diet and bisphosphonates. Rarely is physical activity mentioned as part of treatment in the literature and it is well known that disuse atrophy is an important factor. Individuals with osteoporosis are ten times more likely than others to have CD. Besides the malabsorption theory, there is a growing support for chronic inflammation being an important factor in bone mineral loss. Exercise reduces inflammation. It is difficult to determine how much and what frequency impact or non-impact exercise should be recommended. Marques,Mota & Carvalho (Age, 2012) review of studies on older adults show a benefit of exercise on BMD. Yet, a subject with CD would have been eliminated from these trials.
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Has anybody done this research in Isfahan city?
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Dear Dr.Masjedi,
According to our knowledge the prevalence of CD in Isfahan is similar to Shiraz and something like 0.5% in general population, If we exclude the immigrated people from Khozestan province and other provinces.
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The risk of celiac disease is associated with HLA haplotypes, but if we determine these haplotypes could we estimate the degree of mucosal damages?
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Celiac disease is associated with HLA DQ2 and DQ8 haplotypes. However, these haplotypes are found in about 30% of the worldwide population and not all of them develop the disease (mucosal damage). The HLA- DQ2 confers a higher risk for CD and therefore it is expected that patients with CD have a positive association with its alleles. Thus, to determine the degree of mucosal damage, intestinal biopsy is required (gold standard). Whether a patient has CD associated symptoms, besides HLA DQ2 or DQ8 haplotype with anti-tissue transglutaminase, antigliadins or antiendomysium antibodies suggests the diagnosis of CD, but it must be confirmed by biopsy finding the mucosal damage. The degree of mucosal damage is in association with uncontrolled disease. Patients in remission by dietary treatment may not have mucosal damage despite being HLA-DQ2.
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I am a Celiac. Could anyone help me to find out which of these products I can and cannot eat? If the products contain the following ingredients:
- Prague
- Phosphate
- Salt
- MSG
- Sodium Erythobate
- Sugar
- Sodium Benzoate
- Carrageenan
- Smoke Flavour
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As a person with Celiac and a Registered Dietitian, I am always suspicious of ingredients like "Smoke Flavour." Liquid smoke depends on the type of tree used to produce the liquid smoke. In general, the concentration of Poly Aromatic Hydrocarbons found in the liquid smoke samples decreases from: poplar, vine shoot, oak, cherry tree and beech woods. Whether there are enough PAH's to cause cancer is not yet known. Personally, I don't need another risk for colon cancer.
The toxicity of carrageenan controversy is not supported in the latest 2014 review (http://www.ncbi.nlm.nih.gov/pubmed/24467586). But, Joanne Tobacman's work at the University of Illinois has demonstrated colitis in lab animals from carrageenan. The red seaweed from which it is made is pro-inflammatory. Many cultures eat seaweed but each variety has very different biologic effects. Brown seaweed, on the other hand, has been shown to be anti-inflammatory. What I always tell my students is that the farther away from the real food you get, the more the "concert effect" of the many bioactive compounds in food's natural state is disrupted. Much of the processed foods on the shelf for celiac sufferers is of very low nutrient density. What gastroenterologists must start telling their celiac patients is that they are at very high risk of heart disease and should follow a whole foods Mediterranean or plant-based diet.
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Celiac disease.
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corn flour, Rice, legumes, Starch and their combination
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We experienced this association recently, and noted very interesting and peculiar aspects of the disorder.
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Ierardi,
Thanks!
I think the lack of funding on the issue of gluten sensitivityis one of the key reasons there are more researchers interested in this Area. However, the number of patients I have who are dramatically healthier by being gluten free and eating fermenting foods gives me encouragement to continue researching this topic for the rest of my life.
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Recent studies have shown that there is a high percentage of people who are overweight or obese at the time of diagnosis. Celiac patients have a higher risk of autoimmune diseases, including diabetes.
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In my clients I have seen both weight gain and weight loss. The loss is what is usually expected and attributed to 'failure to thrive' syndrome. I had one client that gained weight and could not lose it until she gave up wheat.
Many of the gluten sensitive people that I have known socially or professionally want to be able to eat all of the same junk food only without wheat. There is an entire food industry dedicated to selling gluten free junk food. This is where the weight gain comes from. A gluten free diet, as I follow because I am gluten sensitive, should be fruits, vegetables and meat. This is not what people want. People want the cakes, cookies, breads and other nutrition devoid foods.