The effect of hormone replacement therapy on cardiovascular hemodynamics in women with Turner's syndrome

Citation
M. Elsheikh et al., The effect of hormone replacement therapy on cardiovascular hemodynamics in women with Turner's syndrome, J CLIN END, 85(2), 2000, pp. 614-618
Citations number
42
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
ISSN journal
0021972X → ACNP
Volume
85
Issue
2
Year of publication
2000
Pages
614 - 618
Database
ISI
SICI code
0021-972X(200002)85:2<614:TEOHRT>2.0.ZU;2-8
Abstract
Women with Turner's syndrome, the majority of whom are estrogen deficient, have an increased incidence of coronary artery disease. The aim of this stu dy was to assess the effects of hormone replacement therapy (HRT) on centra l arterial hemodynamics, insulin sensitivity, and lipids in adults with Tur ner's syndrome. Twenty-one women with Turner's syndrome were studied prospe ctively, on and off 3 months of estradiol valerate in combination with levo norgestrel. The following measurements were made: body mass index, waist/hi p ratio, serum lipids, fasting insulin and glucose, and mean arterial blood pressure. Aortic root pressure and waveforms were estimated noninvasively and the augmentation index (AI), a measure of aortic stiffness, was calcula ted. The AT was significantly lower during estrogen therapy (22% vs. 15%; P = 0.008), suggesting a reduction in central arterial stiffness. Fasting in sulin and glucose concentrations were also significantly lower during HRT ( P = 0.01 and P = 0.0004, respectively). There was no difference in body mas s index, serum Lipids, or brachial and aortic blood pressures on and off tr eatment. Total cholesterol was correlated with the AI (r = 0.4; P = 0.03). These results suggest that HRT in women with Turner's syndrome has a favora ble effect on central arterial hemodynamics and insulin sensitivity. The la ck of effect on serum lipids suggests that the effects of HRT on aortic com pliance may be mediated by an improvement in endothelial function.