Re: Solution to Celiac - Oral Tolerance: from on 2005-03-03
Below are articles concerning the safety of Oral Tolerance therapy:
The Role of Immune Tolerance in Preventing and Treating Arthritis
Current Rheumatology Reports 2004, 6:434-441
Another potentially interesting approach is based on induction of oral
tolerance to putative antigenic triggers.Mucosal tolerance induction
was first described in 1911 and refers to the observation that mucosal
administration of an antigen induces systemic hypo-responsiveness to
the fed protein . The underlying mechanisms that induce this state
of hypo-responsiveness are largely dependent on the very nature of
the mucosal immune system, a preeminently tolerogenic microenvironment
where T cells circulate. Mucosal tolerance can be induced through the
oral(Oral Tolerance) and nasal route.
Autoimmune diseases are all about loss of tolerance, and therapy
should be all about regaining it. Conventional therapies induce tolerance
already nonspecific and with undesirable side effects. A far more
delicate way of inducing tolerance and balancing the immune system
is doing so in an antigen-specific fashion. Immune therapy has
shown to be SAFE and beneficial for patients with autoimmune disease
in several clinical trials. Future research will be directed to new
targets to deviate immune responses in an epitope specific fashion.
Indian Journal of Clinical Biochemistry, 2003, 18(2) 216-222
Oral Tolerance is a SAFE and simple treatment strategy, which has been used to suppress Experimental autoimmune encephalomyelitis, AIA and diabetes. This new strategy has
also been used for treating diseases like multiple sclerosis, Rheumatoid Arthritis and uveitis.
View this article at:
Induction of Immune Tolerance to Human Type I Collagen in Patients with Systemic Sclerosis by Oral Administration of Bovine Type I Collagen
Kevin M. McKown, et. al
This report describes the use of oral type I collagen in patients with systemic sclerosis to induce tolerance to type I collagen, an autoantigen in systemic sclerosis. The induction of oral tolerance is of great interest to clinicians because of the potential specificity and SAFETY of this form of therapy. This interest would be especially keen in the case of systemic sclerosis, for which there is currently no effective, safe therapy.
View this article at:
Ref. # 1054
Re Gluten sensitivity without celiacs disease: from s) Saadah OI ; Zacharin M ; O'Callaghan A ; Oliver MR on 2005-03-31
There are several points here.
If you stop eating gluten, and the intestine has time to heal, the symptoms won't show up on an endosopy. A few days eating gluten is certainly not long enough for the endosopy to be positive!
Your display of symptoms to the challenge are a sign of a strong response to gluten.
You would be advised to follow a completely gluten-free diet for the rest of your life. Don't restart the diet just because symptoms are now not so apparent. You are putting your health at risk.
There is an accepted medical risk that relates the coeliac condition to diabetes.
2005 Jan; 164(1) 9-12
Additional Info Germany
Standard No ISSN 0340-6199; NLM Unique Journal Identifier 7603873
Abstract Coeliac disease has been shown to occur more frequently among first-degree relatives of diabetic patients than in the general population. Our objective was to assess the prevalence of endomysium antibodies (EMA) in non-diabetic siblings of Czech diabetic children and to evaluate the effects of HLA-DQ polymorphisms in determining the genetic susceptibility to coeliac disease (CD) in these subjects. We investigated 240 siblings of diabetic children from 213 families (125 males and 115 females, aged 12.6+/-4.9 years, mean +/- SD). All subjects were tested for the total IgA level to exclude IgA deficiency, and for endomysium IgA to disclose CD. In five IgA-deficient subjects, anti-gliadin IgG was used instead. Small bowel biopsy was offered to subjects with confirmed positive EMA. The HLA-DQA1, -DQB1 genotypes were determined using PCR-SSP. Positive EMA were found in 9/240 (3.8\%) subjects (three males, six females). The biopsy confirmed CD in six children, two had a normal mucosal finding and one refused the biopsy. The HLA-DQ2 polymorphism was more frequent among siblings with EMA (seven of nine) than in siblings without EMA (33\%), corrected P = 0.031. CONCLUSION The 3.8\% frequency of coeliac disease found in siblings of diabetic children is close to the 4.3\% found previously in Czech children with type 1 diabetes mellitus and is substantially higher than the rate in the healthy children population.
Record Type Index Medicus
Article Type Journal Article
Citation Status In-Process Owner NLM
Date of Entry 20041207
Accession No PMID 15480779
2004 Sep; 89(9) 871-6
Additional Info England
Standard No ISSN 1468-2044; NLM Unique Journal Identifier 0372434
Abstract AIMS To study the effect of gluten-free diet on growth and diabetic control of children with type 1 diabetes mellitus and coeliac disease. METHODS Twenty one children (mean age 7.5 years, range 1.6-12.9) with type 1 diabetes, primarily initially identified on the basis of symptoms and consecutively diagnosed with coeliac disease by biopsy over a 10 year period, were matched by sex, age at onset, and duration of diabetes with two diabetic controls without coeliac disease. Weight, height, haemoglobin A1c, and insulin requirements were measured before and for 12 months after the diagnosis and treatment of coeliac disease. Dietary awareness and adherence were assessed by structured questionnaire. RESULTS A gluten-free diet resulted in a significant increase in weight-for-age z scores at 12 months after diagnosis (mean increase in z score 0.33) and in BMI (mean increase in z score 0.32). Increases in height did not achieve statistical significance. Controls showed no significant changes in weight, height, or BMI over the same period. Insulin dosage at diagnosis was less in coeliacs than in controls (mean difference 0.16 units/kg/day), but was similar to controls once a gluten-free diet had been established. Questionnaires were obtained in 20 patients. There appeared to be a relation between dietary awareness/adherence and growth parameters, but the small number of patients with "poor/fair" dietary adherence prevented meaningful analysis of this group. CONCLUSION Identification and dietary treatment of coeliac disease in children with diabetes improved growth and influenced diabetic control. Evaluation of the outcome of treatment of coeliac disease in diabetics should include assessments of gluten intake.
Re DH as a celiac symptom: from Peter on 2005-03-31
Persistant skin rashes are often misdiagnosed as psoriasis.
If the rash persists, a gluten allergy / dermatitis herpetiformis should always be considered.
Re Immune System and Celiac: from Lori on 2005-04-13
I am an american and have used information from the uk often RE gluten Interalance. Your information regarding type I diabetes should also include type II it is associated with microscopic colitis (a gluten interalance as distructive as celiacs). My extended family has many autoimmunes and my children have had problems since birth and were breastfeed for their first year of life.
After the blood tests for IgA. Test for genes, ie. HLA many in the HLA-D chain are tested to be autoimmune. (HLA -DQ2 and HLA -DQ8 are the 95\% celiac) HLA-DQ3, HLA-DQ1 and HLA-DR? are not going to meet the 'gold standard" because microscopic colitis damages the large intestines. Entrolab.com and Dr. Fine are doing research and finding answers for the orphans even celiac has left behind.
Re Immune System and Celiac: from Peter on 2005-04-15
High prevalence of celiac sprue-like HLA-DQ genes and enteropathy in patients with the microscopic colitis syndrome.
Source Am J Gastroenterol (The American journal of gastroenterology.) 2000 Aug; 95(8) 1974-82
Additional Info UNITED STATES
Standard No ISSN 0002-9270; NLM Unique Journal Identifier 0421030
Abstract OBJECTIVE Celiac sprue is associated with specific HLA-DQ genes (mainly DQ2). Because there are epidemiological and histopathological similarities between celiac sprue and microscopic colitis, we hypothesized that these syndrome may share an HLA genetic predisposition and pathogenesis. METHODS The HLA-DQ genes of 25 patients with celiac sprue, 53 patients with the microscopic colitis syndrome, and 429 normal controls were typed and compared. Serum was analyzed for antigliadin and antiendomysial antibodies. Small intestinal biopsies were analyzed for signs of histopathology. RESULTS HLA-DQ2 or DQ1,3 (the latter as DQ1,7,DQ1,8, or DQ1,9) were seen more frequently in both patient groups relative to controls. In patients with the microscopic colitis syndrome, serological tests for celiac sprue were weakly positive in 17\%; mild inflammation of the small intestine without villous atrophy was present in 43\%, and inflammation plus partial or subtotal villous atrophy was present in 27\%. CONCLUSIONS A shared set of predisposing HLA-DQ genes account for the epidemiological overlap of celiac sprue and microscopic colitis. Mild to moderate mononuclear cell inflammation of the small intestine, often accompanied by partial or subtotal villous atrophy, is frequent in patients with the microscopic colitis syndrome. Although further studies will be necessary to determine if this enteropathy is induced by dietary gluten, we speculate that the small intestinal but not colonic histopathology in patients with microscopic colitis is caused by immunological gluten sensitivity.
Re Solution to Celiac - Oral Tolerance: from Prateek on 2005-04-18
Please send me the details of o.t. As i am also facing the same problem.
Re Anti-tTG blood test shows 1 in 80 celiac in population: from Arline Chambers on 2005-05-10
Simple question - what is the range of test scores fo Ttg? What is the "normal" range for Ttg? I have a number "88". What does it really mean? Many thanks.
Re Anti-tTG blood test shows 1 in 80 celiac in population: from Mari on 2005-06-22
do you have to do a gluten challenge before having the Anti-Tissue Transglutaminase (tTG) IgA test?
Re Anti-tTG blood test shows 1 in 80 celiac in population: from Peter on 2005-06-23
The following paper highlights the need for a gluten challenge. Note the results for group 2 - children on a gluten-free diet, compared with the results for group 3 - children on a gluten challenge. This very sensitive test detected less than half of known celiacs on a gluten-free diet without a challenge.
Title Radioimmunoassay to detect antitransglutaminase autoantibodies is the most sensitive and specific screening method for celiac disease.
Source Am J Gastroenterol (The American journal of gastroenterology.) 2001 May; 96(5) 1536-40
Additional Info United States
Standard No ISSN 0002-9270; NLM Unique Journal Identifier 0421030
Abstract OBJECTIVE The aim of this study was to establish the most sensitive and specific screening method for celiac disease. We tested three methods based on different principles, which all detect autoantibodies against the same antigen (tissue transglutaminase). METHODS Sixty-two celiac children at the first biopsy (group 1), 78 celiac children on a gluten-free diet (group 2), 14 celiac children on a gluten-challenge (group 3), and 56 controls with a normal duodenal mucosa (group 4) were studied. The methods used were 1) radioimmunoprecipitation assay using recombinant tissue transglutaminase (RIA); 2) commercial enzyme immunoassay using guinea pig tissue transglutaminase (ELISA); and 3) indirect immunofluorescence method for detection of antiendomysium antibodies (IF-EMA). RESULTS RIA antitransglutaminase autoantibodies were detected in 100\% of group 1, 43.6\% of group 2, 100\% of group 3, and none of the control subjects. ELISA antitransglutaminase autoantibodies were detected in 90.3\% of group 1, 9\% of group 2, 78.6\% of group 3, and in none of the control subjects. IF-EMA were detected in 95.2\% of group 1, 11.5\% of group 2, 92.3\% of group 3, and 1.8\% of the controls. CONCLUSIONS Our results demonstrate a very high sensitivity and specificity of the RIA method to detect antitransglutaminase autoantibodies in comparison to ELISA and IF-EMA assays. We can explain this finding with the use of human recombinant antigen and the increased capacity of the RIA method to detect low titers of autoantibodies. If our data are confirmed by studies on larger series, tissue transglutaminase RIA could be proposed as the best screening method for celiac patients.
Re Gluten sensitivity without celiacs disease: from Cara on 2005-07-07
I am just searching through the net and found ur post interesting
I have just had all the blood tests done for celiacs, but they come back negative, i believe that i would benifit from a gluten free diet due to many of the symptoms that i get
I am trying to search if there are any "bad"things from going on a gluten free diet?
i have found many articles on people finding benefits from going on the diet and no one saying anything bad except maybe a lack of fibre?
Anyone with any info i would love to hear from
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