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Advances Aid Treatment, Diagnosis of Celiac Disease

Disorder triggered by gluten in common foods, such as bread, pasta, often goes unnoticed

MONDAY, May 19 (HealthDay News) -- New research could lead to improved diagnosis and treatment of celiac disease, according to studies presented at the Digestive Disease Week meeting in San Diego.

Celiac disease, which affects an estimated one in every 100 Americans, is an autoimmune disorder in the small intestine triggered by a protein called gluten, found in bread, pasta and many other common foods. Celiac disease often goes undiagnosed.

"At this time, the only effective treatment for celiac disease is a lifelong gluten-free diet, a lifestyle that is difficult for many patients to manage," Dr. Peter H. Green, of the Columbia University Medical School, said in a prepared statement.

"Unfortunately, many people are unaware that they have celiac disease, and if left untreated, it can be life threatening. These studies ... will hopefully lead to improved diagnosis, prevention, treatment and quality of life for this disease," Green said.

In one study, researchers found that an investigational medicine called AT-1001 may protect celiac disease patients from exposure to gluten. The drug does this by preventing gluten from crossing the intestinal mucosa.

While most people with celiac disease do well on a gluten-free diet, inadvertent exposure to gluten is the leading cause of persistent symptoms in adults with celiac disease.

The study of 86 patients found that those who were given gluten and AT-1001 had fewer symptoms of gluten toxicity than those who were given gluten and a placebo. The researchers are now conducting a larger, longer trial.

"Even allowing for the fact that people in clinical trials may practice healthier habits, the fact that all of the groups showed improvement in the first week of the study is significant and helps us to plan better celiac studies," study author Dr. Daniel Leffler, clinical research director at the Celiac Disease Center at Beth Israel Deaconess Medical Center in Boston, said in a prepared statement.

"This work offers great promise for patients who, in the near future, may have a treatment that improves upon dietary restrictions alone," Leffler added.

A second study concluded that the criteria for diagnosing celiac disease may be too stringent, meaning some patients go undiagnosed and, therefore, untreated. Current diagnostic criteria for celiac disease include small intestinal muscosal membrane villus atrophy and inflammation.

This study included 145 people suspected of having celiac disease. Of those, 71 were found to be endomysial antibody positive. Of those 71, 48 met the current criteria for celiac disease diagnosis. The other 23 patients were randomly divided into two groups -- one group ate a regular diet, while the other ate a gluten-free diet. They were re-assessed after one year.

The patients on the gluten-free diet were asymptomatic and had no endomysial antibodies or small intestine mucosal inflammation. The patients on the regular diet continued to have symptoms, were endomysial antibody positive, and had further deterioration of the small intestine membrane, inflammation and gluten-induced lesions in the bowel.

The patients on the regular diet decided to eliminate gluten from their diet and, over time, became symptom-free, endomysial antibody-free, and showed healing of the mucosal membrane.

Some people who are endomysial antibody positive may develop the intestinal damage that makes up the current criteria for diagnosing celiac disease, the researchers said.

"By redefining the criteria for celiac disease, we can treat patients before they begin to experience the most severe symptoms and signs of the disease," study author Dr. Markku Maki, professor of pediatrics at the University of Tampere, Celiac Disease Study Group, in Tampere, Finland, said in a prepared statement.

More information

The American Academy of Family Physicians has more about celiac disease.

-- Robert Preidt

SOURCE: Digestive Disease Week, news release, May 19, 2008

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