Persistent villous atrophy not associated with heart disease

Reuters Health Information: Persistent villous atrophy not associated with heart disease

Persistent villous atrophy not associated with heart disease

Last Updated: 2015-02-09

By Will Boggs MD

NEW YORK (Reuters Health) - Persistent villous atrophy in patients with celiac disease is not associated with the risk of ischemic heart disease or atrial fibrillation, researchers from Sweden report.

Patients with celiac disease face an increased risk of death from cardiovascular causes, but persistent villous atrophy resulting from gluten exposure does not appear to affect overall or cardiovascular mortality, they say.

Dr. Jonas F. Ludvigsson from Karolinska University Hospital in Stockholm studied 7,440 celiac disease patients (43% with persistent villous atrophy) who had follow-up biopsies, along with up to five controls each, matched for age, gender, county, and calendar year.

Overall, the risk of ischemic heart disease was not significantly higher in the patients with celiac disease, they reported January 30 online in the open access journal PLoS ONE.

After adjusting for age at follow-up biopsy, gender, duration of celiac disease, and other factors, there was no significant difference in the risk of ischemic heart disease risk between patients with villous atrophy and those with mucosal healing.

Similarly, there was no significant difference in the risk of atrial fibrillation between patients with villous atrophy and those with mucosal healing.

Factors associated with ischemic heart disease risk included male sex, increased age, and lower degree of educational attainment. Factors associated with atrial fibrillation risk included male sex and increased age.

"These negative findings suggest that follow-up histology does not risk-stratify patients for the development of ischemic heart disease or atrial fibrillation," the researchers say, "with the caveat that a small positive association cannot be ruled out in certain subgroups due to limited statistical power."

They have two potential explanations for their findings: first, that villous atrophy might not be an adequate marker for immune activation in celiac disease, and second, that patients who had follow-up biopsies may be a healthier subset.

"Our results also suggest that even patients with mucosal healing require surveillance for ischemic heart disease, coronary risk factor modification, and preventive measures such as aspirin in select patients," the investigators conclude. "Future studies should investigate novel biomarkers of inflammation in celiac disease that may impact the risk of ischemic heart disease and atrial fibrillation."

Dr. Francesco Valitutti from Umberto I Hospital Rome, Sapienza University, Rome, Italy, has published extensively on celiac disease. He told Reuters Health by email, "This is theoretically in contrast with the assumption that chronic inflammation (related to the continuous gluten ingestion and thus to villous atrophy) enhances atherosclerosis, and in contrast with previous clinical data; however, this should remind us that chronic inflammation due to intestinal immune activation might not be among the major risk factors, such as smoking, diabetes, cholesterol, hypertension, and obesity, which we should always be aware of."

"Patients with celiac disease should adhere strictly to gluten-free diet to physically and mentally function at their 100%," Dr. Valitutti said. "This means to ensure the best possible growth pattern among children, to provide the best care for the offspring of pregnant women, to prevent micronutrient deficiency, to avoid the development of other autoimmune disease and other complications such as rare malignancies, like T-cell intestinal lymphoma."

Dr. Valitutti added, "It would be advisable for countries other than Sweden to develop (a) similar National Database. This is an excellent tool to unveil risk factors for specific disease subgroups and the whole population."

Dr. Ludvigsson did not respond to a request for comments.

SOURCE: http://bit.ly/16Ikvsn

PLoS ONE 2015.

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