Correlation of serum estrogen levels with uterine and carotid arteries flow in postmenopausal women on hormone replacement therapy.

Autor:	Predanic M; Department of Obstetrics and Gynecology, The New York Flushing Hospital Medical Center, 4500 Parsons Boulevard, Flushing, New York, NY 11355, USA. amfromsa@aol.com, Ujevic B, Aleem F, Pennisi J
Jazyk:	angličtina
Zdroj:	Croatian medical journal [Croat Med J] 1998 Jun; Vol. 39 (2), pp. 181-4.
Abstrakt:	Objective: To determine the pattern of blood flow in the patients compliant and non-compliant to hormone replacement therapy. Methods: In the period of 12 months, 106 postmenopausal women were examined by the color and pulsed Doppler ultrasonography of the blood flow through uterine, common, and internal carotid arteries (Resistance Index, RI). The study was retrospective-descriptive. Patients were divided into three groups: (1) 38 patients compliant with hormone replacement therapy and daily using Premarin/Provera, (2) 27 patients non-compliant with the treatment because of discontinuation of the therapy and/or irregular use of medicine, and (3) control group of 41 women who never used hormone replacement therapy. Results were compared with serum estrogen (E2) drawn on the day of the blood flow assessment. Results: Mean E2 serum concentration in the hormone replacement therapy-compliant group was 90.1 pg/mL, 45.5 pg/mL in the non-compliant group, and 26.6 pg/mL in the control group (p<0.01). Serum E2 concentration correlated with the decrease in resistance to blood flow in the uterine artery (p=0.001), but did not in the common carotid (p=0.34) and internal carotid arteries (p=0.66). The compliant group and control group differed in the uterine artery blood flow (RI 0.78 vs. 0.87, respectively). Conclusion: Differences in E2 serum concentration between the groups are related to the hormone replacement therapy and the patients' compliance to the therapy. Small peripheral arteries readily respond to the serum E2 levels, whereas large peripheral arteries (common and internal carotid) are too "rigid" to respond to E2-induced vasodilatation.
Databáze:	MEDLINE
Externí odkaz:	Zobrazit plný text záznamu