- The Washington Times - Tuesday, February 14, 2006


Genes prove it: A rare but devastating esophageal illness that’s on the rise isn’t difficult-to-treat acid reflux as once suspected but a completely different disease — one linked to allergies.

Known by the tongue-twisting name eosinophilic esophagitis, the worst cases of this mysterious disease can force children onto liquid diets and feeding tubes, and leave adults with an esophagus so narrowed that food gets trapped in it.

With no proven treatments, doctors try creative experiments, including an attempt to coat patients’ inflamed throats with a paste made from a popular asthma medicine and the sugar substitute Splenda.

Now scientists have discovered a gene that seems to be the disease’s main trigger, opening a new direction in the therapy hunt — and promising easier diagnosis for patients who can spend years dealing with vomiting, heartburn and stomach pain before doctors figure out what’s wrong.

“They’re suffering a lot,” said Dr. Marc Rothenberg of Cincinnati Children’s Hospital Medical Center, who led the gene research and directs the nation’s leading center for eosinophilic esophagitis, or EE.

The gene discovery, he said, “should give all these people hope.”

First diagnosed in 1977, many doctors initially considered EE to be an especially severe case of the heartburn-causing acid reflux disease; some still do. Symptoms do mimic reflux. But heartburn medicines don’t relieve EE.

Instead, EE occurs when the immune system goes into overdrive: Eosinophils are white blood cells that help the body fight off parasites, among other things. But sometimes too many eosinophils are produced, constantly, in the gastrointestinal tract, causing inflammation that over time damages the delicate tissue. When this eosinophil frenzy targets the esophagus, it’s called EE.

It mostly strikes people prone to allergic diseases, such as asthma or food allergies, in which eosinophils play some role, too.

Like allergies, EE seems to be on the rise, Dr. Rothenberg said. Last summer, he published an analysis estimating that one in 10,000 children — or 22,000 American youngsters — may have some degree of EE.

The new research, published in the Journal of Clinical Investigation this month, raises the possibility of gene testing instead.

Dr. Rothenberg compared healthy people, reflux sufferers and EE patients. The EE patients harbored a unique genetic signature, more than 500 genes that operated differently in them. One gene, called eotaxin-3, was up to 100 times more active.

Eotaxin-3 attracts eosinophils circulating in the body. When Dr. Rothenberg’s team bred mice without an eotaxin cell receptor, the animals were protected from EE. It’s the best evidence yet that eosinophils are the cause, said Dr. Marshall Plaut of the National Institutes of Health, which, with the patient group Campaign Urging Research for Eosinophilic Disease, helped fund the work.

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