Wednesday, July 18, 2012

Gluten Free Tidbets

Can a positive tTg and negative EMA be Celiac Disease?
A group of researchers at the departments of Gastroenterology, and Immunology at the Northern Deanery of Newcastle upon Tyne, and Freeman Hospital in Newcastle upon Tyne in the UK recently studied cases of positive tissue transglutaminaseantibodies with negative endomysial antibodies to determine whether or not such cases amount to celiac disease.

By way of background, 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. EMA, on the other hand, has extremely high specificity values close to 100% and positive predictive value values approaching 80%. 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. 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.

Source: Family Practice and

Being Gluten-Free 'Is Determined By Evolution', Says Gastroenterologist

According to Professor David Sanders, Consultant Gastroenterologist at the Royal Hallamshire Hospital and University of Sheffield, England, "Only for the past ten thousand years have we had wheat-based foods in our diets, which in evolutionary terms makes wheat almost a novel food. If you put that in context to the 2.5 millions years that mankind has been on earth, it makes sense that our bodies are still adapting to this food, and more specifically, the gluten that it contains."

Sanders' comments were prompted following the recent claim that potentially up to 6% of the population could be suffering from gluten sensitivity, making it by far the most common gluten-related disorder after celiac disease. Celiac disease currently affects around 1% of the population, which is an 80-fold increase in reported cases since the 1950s, when only 1 in 8000 were susceptible, compared with 1 in 100, today.

A recent survey commissioned by the Dr Schär Institute identified that GPs and dietitians frequently see patients with what they believe to be gluten sensitivity but they are uncertain how to manage the condition.

Its gastrointestinal symptoms are general and include abdominal pain and bloating, diarrhea, constipation and generic malaise. Headache, fatigue, limb numbness and anemia make for diagnostic difficulties too. The survey found that 90% of dietitians and 86% of GPs claim to be aware of gluten sensitivity but more than half have a limited or average understanding of it.

Speaking on behalf of the Dr Schär Institute, dietitian Melissa Wilson, said, "The comments from Professor Sanders and the survey results demonstrate that serious confusion exists when experts try to diagnose or manage gluten sensitivity. GPs and dietitians are telling us that they do not feel there is enough information available, despite reporting a large number of patients displaying symptoms associated with the condition."


Gastroenteritis May Trigger Celiac Disease

Food-borne infectious gastroenteritis could be triggering some cases of celiac disease, which might partly explain the rising incidence of the autoimmune condition, a new paper suggests.

The authors of the report - military researchers along with celiac disease expert Dr. Joseph Murray from the Mayo Clinic - focused on active duty personnel in the U.S. armed forces between 1999 and 2008.

Altogether there were more than 13.7 million person-years of follow-up, they reported in The American Journal of Gastroenterology.

The incidence of celiac disease diagnoses increased five-fold from 1.3 per 100,000 in 1999 to 6.5 per 100,000 in 2008. The research team identified a total of 455 cases of incident celiac disease and compared those to 1 820 matched controls.

Overall, 172 subjects had infectious gastroenteritis (IGE) within 24 months before their diagnosis, with the majority (60.5%) of viral etiology. Multivariate analysis showed a significant association between celiac disease and any prior IGE (odds ratio, 2.06), which was stronger when the IGE was non-viral (odds ratio, 3.27) vs viral (odds ratio, 1.44).
Given the apparent association, the researchers suggest that infections may "act as triggers for developing gluten intolerance through molecular mimicry or other immune modulation mechanisms."
Source: (Reuters Health, David Douglas, July 2012)

-Beth Hillson Weekly Newsletter, July 17, 2012