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.
Questions related to Celiac Disease
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.
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.
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
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
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
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
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.
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.
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.
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.
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 ?,
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?
Please can you inform of the real prevalence of ANAs positivity in the Celiac Disease and their evolution with a Gluten-free-diet?
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?
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!
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.
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 !!
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.
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?
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.
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.
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.
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.
The risk of celiac disease is associated with HLA haplotypes, but if we determine these haplotypes could we estimate the degree of mucosal damages?
Conference Paper Correlation between distribution of HLA haplotypes and sever...
We experienced this association recently, and noted very interesting and peculiar aspects of the disorder.
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.
Article Celiac Disease