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Showing results for tags 'endomysial'.
Found 7 results
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Hello I was diagnosed years ago with celiac disease, With positive blood test and positive biopsy. Recently had to have an endoscopy for h pylori and ulcers. The doctor noted that normal mucosa was seen at the entrance to the duodenum. No villi atrophy seen, even under the microscope. So Dr ordered anti tissue transglutaminase antibody blood test (ttg). It came back 15 U/ml. So i think only slightly positive. So a weak positive ttg test a negative biopsy test. So she ordered an Endomysial (EMA) test. It came back negative. How can i be diagnosed years ago as positive, +ttg and + biopsy. Now only weak positve ttg? So confusing. Could it be another autoimmune disease? -
My 14-year-old daughter has Type 1 diabetes and Hashimotos. She is tested for celiac every year due to these other autoimmune issues. In the spring, her ttg was 4, a weak positive, after years of being normal. Her GI doctor retested it in late August, and at our request, also tested the endomysial antibody and the genes. This time, the ttg was a 3 (normal) but endomysial was positive (1:5 titer) and she had both genes and was considered high risk genetically. We did more bloodwork a month later to follow up - ttg still a 3, endomysial positive with no mention of the titer, gliadin antibody normal, metabolic blood panel normal, and a bunch of vitamins normal such as calcium, zinc, b6, and ferritin. Vitamin D was a 33 - normal but I’d say it is low considering she was taking 2000 in supplements a day. We have an appointment with a celiac doctor at a children’s hospital in early December, and in the meantime, I have been reorganizing the kitchen and pantry, researching food brands and restaurants, getting gluten-free recipe books, and keeping her on a gluten diet while also having her try different gluten-free foods and making a list of what she likes and doesn’t like. Everything I’ve read indicates that if the endomysial is positive it is definitely celiac. With the gene test and her two autoimmune diseases, I am wondering if they will still want to do a scope to give the official diagnosis, and if we did one, what happens if it comes back negative? Am I correct in interpreting these results as full blown celiac or potentially early stage celiac and a need to go gluten free and avoid cross contamination regardless of what a scope and biopsy would indicate? Deep down, I feel like she is celiac, but with all this waiting, I keep second guessing myself and wondering if I should be waiting till the doctor’s appt. to make all these preparations. Our current GI says a scope is the best way to diagnose but that it is unlikely to have false positives on the endomysial test. She is asymptomatic though has had a chronic sluggish digestive system for years despite being on fiber supplements. She also can have a very short fuse, and I know irritability can be a symptom. Sometimes she gets tingling in her feet or soreness in her calves at night though her pediatrician and endo think it is just growing pains. I’d value any thoughts. My daughter is very anxious about doing a scope. I feel like we have to do it if it’s the only way to get the official diagnosis, but I’m hoping we have enough evidence. She doesn’t meet the European guidelines of ttg 10 times over the upper limit. -
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Celiac.com 06/29/2012 - A group of researchers recently set out to study cases of positive tissue transglutaminase antibodies with negative endomysial antibodies to determine whether or not such cases amount to celiac disease. The team included Thomas Hornung; Pavel Gordins; Clare Parker; and Nicholas Thompson. They are variously affiliated with the departments of Gastroenterology, and Immunology at the Northern Deanery of Newcastle upon Tyne, and with the department of Gastroenterology at Freeman Hospital in Newcastle upon Tyne in the UK. The most sensitive and specific blood tests for diagnosing celiac disease are those that detect immunoglobulin A (IgA) antibodies against human tissue transglutaminase (tTGA) enzyme, and those that measure aspects of connective tissue covering individual smooth muscle fibers, endomysial antibodies (EMA). Because of the high sensitivity (up to 98%) and high specificity (around 96%) reported for the tTGA assay, detection of tTGA is currently the primary blood test used in screening for celiac disease. The tTGA test also has a high negative predictive value approaching 100%, which makes it an excellent test for excluding celiac disease in both high and low risk groups. In contrast, positive predictive value of the tTGA test is rather poor with values between 28.6% and 60.2% being reported in several studies. EMA, on the other hand, has extremely high specificity values close to 100% and positive predictive value values approaching 80%.[5 10] However, compared with tTGA, EMA has lower sensitivity, usually under 90%. This being the case, the present standard celiac disease screening strategy is to first use tTGA, and then confirm positive results using EMA. However, doing it this way, doctors often end up with a group of patients who show divergent test results. For their study, the researchers wanted to gauge the percentage of patients with positive tTGA and negative EMA, but who were confirmed with celiac disease upon biopsy, and to identify factors in these patients that may help to increase diagnostic accuracy in such patients. The research team identified 125 consecutive patients with positive tTGA and negative EMA, who subsequently underwent endoscopy with at least two biopsies from the second part of the duodenum. The team charted any tTGA result over 15 U/ml as positive. They excluded any patients with known celiac disease at the time of testing. They then reviewed patient notes to assess indications for celiac disease serological screening, including the presence of iron deficiency anaemia, and symptoms such as diarrhea or weight loss, and family history of celiac disease. They defined diarrhea as a bowel frequency of more than three times a day. They then assessed histological evidence of celiac disease based on subsequent duodenal biopsies, plus Marsh grading. In cases where patient histology was unclear, they relied on the clinical assessment of a consulting gastroenterologist. Unclear histology included minimal/mild increase in intraepithelial lymphocytes of not more than 30 per 100 enterocytes and without villous atrophy, plus mild villous blunting with no increase in intraepithelial lymphocytes. They then categorized patients as either celiac disease negative, or celiac disease positive. Patients with no histological evidence of celiac disease on duodenal biopsies or equivocal histology plus overall clinical impression of celiac disease absence were categorized as celiac disease negative. Patients with histological evidence of celiac disease on duodenal biopsies or equivocal histology plus overall clinical impression of celiac disease presence were categorized as celiac disease positive. To measure IgA anti-tTGA antibody the team used a commercially available enzyme linked immunosorbent assay called Aeskulisa, manufactured by Aesku Diagnostics GmbH in Wendelsheim, Germany. To detect IgA anti-EMA with the standard immunofluorescent method, they used commercial slides of monkey oesophagus sections (Euroimmun, Euroimmun AG, Lübeck, Germany). They used conjugated sheep antihuman IgA as a secondary antibody, relying on a test manufactured by Instrumentation Laboratory UK Ltd., in Warrington, UK. Overall, the team categorized 113 patients (90.4%) as celiac disease negative. Of these, 102 patients had no histological features of celiac disease, while 11 patients had unclear histology plus an overall clinical impression of not having celiac disease. They categorized twelve patients (9.6%) as celiac disease positive. Of these, 10 patients had positive histology, and two patients had unclear histology plus an overall clinical impression of having celiac disease. Of those with positive histology, 17% were Marsh grade I, 8% were Marsh grade II, 33% were Marsh grade IIIa, 17% were Marsh grade IIIb and 25% were Marsh grade IIIc. Those with celiac disease were more likely to be older and to have a higher tTGA level. The groups showed no difference in any clinical parameter. Source: Frontline Gastroenterol. 2012;3(2):81-83. -
Celiac.com 01/11/2007 – Researchers in Finland have determined that many patients with untreated celiac disease show the presence of intestinal endomysial autoantibodies (EmA), even in the 10-20% of cases where their serum EmA is negative. The researchers also believe that the negative serum EmA test in these cases is an indication of more advanced and long-standing celiac disease. Normally positive serum EmA is close to 100% accurate, however there is a subset of around 10-20% of patients where the test is negative even though they do have the disease. Dr. Katri Kaukinen and colleagues at the University of Tampere looked at 177 celiac disease patients and found that 22 were serum EmA-negative. A common theme among the 22 serum EmA-negative patients was that they were older and had more abdominal symptoms and other complications that indicated a more advanced stage of celiac disease than their serum EmA-positive counterparts. The research team found that even though the EmA antibodies could not be detected in the blood of these 22 patients, they could be detected in the small bowel mucosa in all of them, and none were detected in 20 control patients. Dr. Kaukinen and colleagues believe that the use of intestinal EmA antibody detection should be used in seronegative individuals who are suspected to have celiac disease. This study further supports Dr. Kenneth Fines use of IgA antigliadin antibodies in the stool to detect gluten sensitivity, and one has to wonder if the EmA antibodies, if detectable in the small bowel mucosa, would not also be detectable in the patient’s stool, and if so would that not be a much better and more cost-effective way to perform such a screening? Gut 2006;55:1746-1753. -
The following abstract was submitted to celiac.com directly by William Dickey, Ph.D., a leading celiac disease researcher and gastroenterologist who practices at Altnagelvin Hospital, Londonderry, Northern Ireland. Scandinavian Journal of Gastroenterology 2005; 40: 1240-3. Dickey W, Hughes DF, McMillan SA. Celiac.com 09/27/2005 - What does a positive endomysial antibody (EmA) test mean if the biopsy does not show villous atrophy? The authors studied 35 patients where this was the case. In the authors practice, these patients account for 10% of all EmA positives. Firstly, the lack of villous atrophy did not necessarily mean a normal biopsy: 14 patients had excess inflammatory cells (lymphocytes) consistent with a mild abnormality of gluten sensitivity. Secondly, many of these patients had typical celiac features: twelve had a family history of celiac, five had dermatitis herpetiformis and thirteen had osteopenia or osteoporosis on DEXA scan. After discussion, 27 patients opted to take a gluten-free diet from the first biopsy: 26 of these had clinical improvement. Seven of eight patients who persisted with a normal diet developed villous atrophy on follow-up biopsies. The authors conclude that a positive EmA result indicates gluten sensitivity even if biopsies do not show villous atrophy. While a biopsy remains important as a baseline reference, these patients should be offered a gluten-free diet to allow clinical improvement and prevent the development of villous atrophy. There may be no such thing as a "false positive" EmA, although the authors emphasise that the same conclusion cannot yet be applied to tissue transglutaminase antibody results.
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Karoly Horvath, M.D., Ph.D., Associate Professor of Pediatrics; Director, Peds GI & Nutrition Laboratory; University of Maryland at Baltimore: Serological tests are performed at the time of diagnosis of celiac disease and they are repeated later to estimate the efficacy of the gluten-free diet. It is recommended to perform a full serological test-panel in patients with suspected celiac disease. These tests measure antibodies belonging to both the IgA and IgG classes of immunoglobulins. The incidence of selective IgA deficiency is much higher in celiac patients than in the general population. In patients with selective IgA deficiency only the IgG antigliadin antibody may be present, however, this antibody is less specific. It means that the IgG-type antigliadin antibody may be present in otherwise normal individuals. If somebody had a positive endomysial antibody test at the time of diagnosis he/she may choose to use only this antibody test to monitor the effect of the diet. There are individual differences in the disappearance of serum antibodies.
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The following is an abstract of an article which was recently published in Clinical and Diagnostic Immunology (1996; 3:143-146), and was sent to me by Kevin Lawson. If you have any questions about it you can e-mail him at: IMMTEST@AOL.COM Vijay Kumar (1,2), J.E. Valeski (1,2) and Jacobo Wortsman (3) IMMCO Diagnostics, Inc.,1 Departments of Microbiology and Dermatology, State University of New York at Buffalo,2 Buffalo, New York, and Department of Internal Medicine, School of Medicine, Southern Illinois University, Springfield, Illinois. Celiac disease (celiac disease) is a gluten-sensitive enteropathy characterized by the presence of serum antibodies to endomysial reticulin and gliadin antigens. celiac disease has been associated with various autoimmune endocrine disorders, such as diabetes. We report a rare case of idiopathic hypoparathyroidism with coexistent celiac disease characterized by the presence of serum autoantibodies. Studies were conducted to determine the specificities of these autoantibodies and to localize the antibody binding sites by indirect immunofluorescence and immunoelectron microscopy. Sera from a patient with idiopathic hypoparathyroidism and celiac disease and from two patients with celiac disease alone were tested by indirect immunofluorescence for autoantibodies to parathyroid and endomysial antigens. The specificities of the antibody reactions were determined by testing the sera before and after absorption with monkey stomach tissue. In addition, immunoelectron microscopic studies were performed to determine the localization of the endomysial antigen. Indirect-immunofluorescence studies on the patients serum were positive with a parathyroid as well as the endomysial substrate. Similar reactions were also observed with the sera of endomysial antibody-positive patients with celiac disease. Absorption of the sera with monkey stomach powder, which is known to have the endomysial antigen, abolished the antibody activities on both the endomysial substrate and the parathyroid tissue. Immunoelectron microscopic studies showed that endomysial antibody activity was associated with antigens localized on the myocyte plasma membrane and in the intercellular spaces. Thus, reactions of the patient s serum with the parathyroid tissue were due to endomysial antibodies and were not parathyroid specific as in patients with idiopathic hypoparathyroidism who did not have coexistent celiac disease. In conclusion, indirect-immunofluorescence tests on parathyroid tissue detect not only tissue-specific antibodies but also cross-reactive antibodies, and this should be taken into consideration when these tests are performed.
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