Finding suggests low-grade inflammation changes gland's structure,,
THURSDAY, Dec. 18 (HealthDay News) -- Childhood obesity may alter the structure and function of the thyroid gland, an organ in the neck that releases hormones crucial to metabolism.
Studies have found that thyroid disorders can lead to obesity, but a new Italian study suggests that obesity may cause thyroid dysfunction in some cases.
"Our study shows that alterations in thyroid function and structure are common in obese children, and we may have uncovered the link," study author Dr. Giorgio Radetti, of the Regional Hospital of Bolzano, said in an Endocrine Society news release. "We found an association between body mass and thyroid hormone levels, which suggests that fat excess may have a role in thyroid tissue modification."
Radetti and his colleagues evaluated 186 overweight and obese children for nearly three years. The children's thyroid hormone levels and thyroid antibodies were measured, and they underwent a thyroid ultrasound. Thyroid antibodies are present in people with Hashimoto's thyroiditis, an autoimmune disease of the thyroid in which immune system T-cells attack the thyroid. Ultrasound results from 73 of the children were suggestive of Hashimoto's disease, but none of them showed thyroid antibodies.
"The ultrasound findings are a bit mysterious," Radetti said. "However, the findings do suggest the existence of a low-grade inflammation state, which has been known to characterize obesity."
The study was published in the December issue of The Journal of Clinical Endocrinology & Metabolism.
Radetti said that thyroid function has been shown to return to normal after weight loss, which means it may be possible to reverse thyroid abnormalities detected on an ultrasound. However, it's not known whether persistent thyroid abnormalities in obese children could progress into chronic thyroid disease in early adulthood. More research is needed to answer these questions, he said.
The American Thyroid Association has more about the thyroid.
-- Robert Preidt
SOURCE: Endocrine Society, news release, Dec. 3, 2008
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