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To the Editor: The increased prevalence of coronary heart disease (CHD) in women with monosomy X (Turner syndrome) has been attributed to their premature ovarian failure, which causes loss of estrogen effect and excess adiposity.^1-2 However, the longstanding view of estrogen as a cardioprotective agent responsible for the relative protection from CHD enjoyed by women compared with men has recently been challenged.³ To investigate the possibility that haploinsufficiency for X-chromosome genes, rather than gonadal insufficiency, contributes to the increased CHD risk in monosomy X, we compared fasting lipid profile, glucose and insulin levels, and body composition in young, nonobese women with Turner syndrome and in 46,XX women with premature ovarian failure.

Methods

Women were recruited mainly through notices on the National Institute of Child Health Web site. The criteria for inclusion in our institutional review board–approved studies on premature ovarian failure and Turner syndrome have been described previously.^4-5 Participants were 33 . . . [Full Text of this Article]

Margaret Cooley, BA; Vladimir Bakalov, MD; Carolyn A. Bondy, MD
National Institute of Child Health and Human Development
National Institutes of Health
Bethesda, Md

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