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Biomedical subjects

G Richard-Davis

Publications and source records attributed to G Richard-Davis.

2 recordsLinked to original sources

In vitro platelet function in controlled ovarian hyperstimulation cycles.

OBJECTIVE: To determine the effects of elevated endogenous E2 levels on in vitro platelet function in patients undergoing controlled ovarian hyperstimulation (COH). DESIGN: Women with normal ovulatory cycles and patients undergoing COH on cycle day 3 and near ovulation (preovulatory follicles were at least 16 mm in diameter) were studied. Serum E2, Thrombostat 4000, (V. d. Goltz, Seeon, Germany), von Willebrand factor antigen (vWF-Ag), and platelet aggregation and adenosine triphosphate (ATP) release to adenosine diphosphate (ADP), collagen (COL), and arachidonic acid (AA) were measured. SETTING: University-based outpatient infertility clinic. PATIENT(S): Twenty-two consenting infertile women undergoing COH cycles and 14 women with documented ovulatory cycles. MAIN OUTCOME MEASURE(S): Whole blood platelet aggregation with ADP, COL, AA, and Thrombostat 4000. RESULTS(S): Estradiol levels rose significantly at peak times (P = 0.011). No changes were noted in in vitro platelet function measured by the Thrombostat 4000 and by whole blood platelet aggregation with ADP and AA and in ATP release with ADP, COL, or AA. Aggregation with collagen was increased because of likely elevations in vWF-Ag levels. CONCLUSION(S): No significant changes in in vitro platelet function were noted in 19 women undergoing COH with E2 levels two to three times that observed in oral contraceptive or hormone replacement therapy users, suggesting no increased risk for arterial thromboembolism.

Adenosine Diphosphate↗

Fibrinolytic parameters in women undergoing ovulation induction.

OBJECTIVE: The purpose of this study was to evaluate the effect of elevated levels of circulating estradiol on the clotting and fibrinolytic system in patients undergoing controlled ovarian hyperstimulation. STUDY DESIGN: Fifty-two patients undergoing controlled ovarian hyperstimulation with human menopausal gonadotropins or urofollotropin were asked to participate. Blood for hemostasis parameters was obtained on the days that patients returned for estradiol sampling. Sample days were identified as cycle days 1 to 5 (baseline), 6 to 9, and 10 to 14. Each factor was analyzed by repeated-measures analysis of variance and correlation analysis. RESULTS: A significant decline was observed for tissue plasminogen activator antigen and plasminogen activator inhibitor type 1 activity from baseline to cycle days 10 to 14. As serum estradiol levels increased throughout each phase (maximum mean estradiol 739.8 pg/ml), a significant linear decrease was observed for both tissue plasminogen activator antigen and plasminogen activator inhibitor type 1 activity, whereas thrombin-antithrombin III complexes did not change significantly. A significant positive correlation was also observed for plasminogen activator inhibitor activity and tissue plasminogen activator antigen level over all cycle days examined. CONCLUSION: Down-regulation of the fibrinolytic system was observed as estradiol levels increased. However, thrombin formation did not change, thus suggesting that elevated circulating estradiol alone does not predispose to a thromboembolic event.

Adult↗