activated protein c resistance/прогестерон

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Activated protein C resistance during in vitro fertilization treatment.

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Acquired resistance to the anticoagulant action of activated protein C (APC) has been proposed to explain the increased risk of venous thrombosis associated with pregnancy, hormone replacement therapy and the use of oral contraceptives. In this study, we have investigated whether the hormonal

APC resistance during the normal menstrual cycle.

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Increased serum levels of endogenous as well as exogenous estrogen are regarded to be responsible for acquired activated protein C (APC) resistance. It was the objective of this study to evaluate whether the physiological increase in serum estradiol concentration during the normal menstrual cycle

Differential effects of oral and transdermal estrogen/progesterone regimens on sensitivity to activated protein C among postmenopausal women: a randomized trial.

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OBJECTIVE Activated protein C (APC) resistance not related to the factor V Leiden mutation is a risk factor for venous thrombosis. Oral estrogen replacement therapy (ERT) has been reported to induce APC resistance. Little is known about the effect of transdermal estrogen. RESULTS We enrolled 196

Activated protein C resistance among postmenopausal women using transdermal estrogens: importance of progestogen.

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OBJECTIVE Although the route of estrogen administration is known to be an important determinant of the thrombotic risk among postmenopausal women using hormone therapy, recent data have shown that norpregnane derivatives but not micronized progesterone increase venous thromboembolism risk among

Measurement of activated protein C resistance during menstrual cycle in women with and without the Leiden mutation.

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Variations in the APC ratio during the menstrual cycle were assessed in 25 women without the Leiden mutation, and 10 women who were carrier of the mutation. Blood samples were collected at four occasions during one menstrual cycle. APC ratios were measured with two APTT based plasma methods with and

Increased coagulation activity and genetic polymorphisms in the F5, F10 and EPCR genes are associated with breast cancer: a case-control study.

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BACKGROUND The procoagulant state in cancer increases the thrombotic risk, but also supports tumor progression. To investigate the molecular mechanisms controlling cancer and hemostasis, we conducted a case-control study of genotypic and phenotypic variables of the tissue factor (TF) pathway of

Effect of in vitro fertilization treatment and subsequent pregnancy on the protein C pathway.

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Thirty-three women who were planned for an in vitro fertilization (IVF) cycle donated blood at four time points during treatment: at baseline, after downregulation, hyperstimulation and luteal support. Levels of progesterone, 17beta-oestradiol and indicators of the protein C pathway, i.e. activated

Effects of hormone replacement on hemostasis in spontaneous menopause.

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OBJECTIVE To examine the effects of continuous combined estrogen-progesterone replacement therapy on coagulation and natural anticoagulant systems in spontaneous menopause. METHODS A randomized, double-blind, placebo-controlled study was conducted during a 6-month period to examine the effect of

Sensitivity to activated protein C during the menstrual cycle in women with and without factor VLeiden.

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BACKGROUND Activated protein C (APC) resistance is associated with an increased risk of venous thrombosis. High levels of estradiol and progesterone, e.g. during ovarian stimulation and pregnancy, as well as exogenously administered estrogens and progestagens during oral contraceptive use, induce an

Low risk of venous thrombosis in two families with combined type I plasminogen deficiency and factor V R506Q mutation.

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Two families with type I plasminogen deficiency and APC resistance are reported. The proposita of family A suffered from ischemic stroke when taking estrogen-progesterone-containing oral contraceptive. Several hemostatic challenges in the past (ovariectomy, appendectomy, and two pregnancies) were

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