April 29, 2008

Pituitary Hormone May Boost Women's Heart Risk

TUESDAY, April 29 (HealthDay News) -- Increasing levels of thyrotropin within the normal range may increase the risk of fatal coronary heart disease in women, a Norwegian study finds.

Thyrotropin, a hormone produced by the pituitary gland, is released into the blood and acts on the thyroid gland to stimulate its growth and function.

"Emerging evidence indicates that levels of thyrotropin within the reference [normal] range are positively and linearly associated with systolic [top number] and diastolic [bottom number] blood pressure, body-mass index and serum lipid concentrations with adverse effects on cardiovascular health," according to background information in the study led by Dr. Bjorn O. Asvold, of the Norwegian University of Science and Technology in Trondheim, and colleagues.

They examined the association between thryotropin levels and fatal heart disease in 17,311 women and 8,002 men without known thyroid disease, cardiovascular disease or diabetes at the start of the study.

During follow-up, 228 women (1.3 percent) and 182 men (2.3 percent) died of coronary heart disease.

"Of these, 192 women and 164 men had thyrotropin levels within the clinical reference range of 0.5 milli-international units per liter to 3.5 milli-international units per liter," the researchers wrote. "Overall, thyrotropin levels within the reference range were positively associated with coronary heart disease mortality; the trend was statistically significant in women but not in men."

"This study shows that coronary heart disease mortality increases in women with increasing levels of thyrotropin within the reference range," the researchers concluded. "These results indicate that relatively low but clinically normal thyroid function may increase the risk of fatal coronary heart disease."

The study was published in the April 28 issue of the Archives of Internal Medicine.

More information

The U.S. Food and Drug Administration has more about heart disease in women.

-- Robert Preidt
SOURCE: JAMA/Archives journals, news release, April 28, 2008
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