APC resistance during the normal menstrual cycle
2007 (English)In: Thrombosis and Haemostasis, ISSN 0340-6245, Vol. 98, no 6, 1246-1251 p.Article in journal (Refereed) Published
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 affects the individual's sensitivity to APC. Seventy-two women with normal menstrual cycles were included in the study. Blood samples for analysis of estradiol (E2), progesterone (P4) and APC resistance were drawn at two time points of the menstrual cycle (day 3-5 and day 22-25). Two methods of measuringAPC resistance were used: the activated partial thromboplastin time (aPTT)-based assay and the endogenous thrombin potential (ETP)-basedAPC resistance test. Independent of the method used, no changes in APC resistance were found, even though the E2 concentration increased significantly between the two menstrual phases. No correlations between E2 levels andAPC resistance, P4 levels and APC resistance or changes in E2 concentrations and changes in APC resistance were detected. Ten women were carriers of the factor V-Leiden mutation, Their baseline APC resistance was increased, but their response to elevated E2 during the menstrual cycle did not differ from that of non-carriers. In conclusion, our observations suggest that physiological differences in serum levels of estradiol and progesterone between the early follicular and the luteal phase in a normal menstrual cycle do not have any significant impact on the individual's sensitivity to APC.
Place, publisher, year, edition, pages
2007. Vol. 98, no 6, 1246-1251 p.
menstrual cycle, APC resistance, ETP-based, aPTT-based, estradiol, activated protein-c, factor-v gene, hormone replacement therapy, oral-contraceptives, venous thrombosis, acquired-resistance, leiden mutation, women, risk, thromboembolism
IdentifiersURN: urn:nbn:se:kth:diva-17165ISI: 000251687400016OAI: oai:DiVA.org:kth-17165DiVA: diva2:335208
QC 201005252010-08-052010-08-05Bibliographically approved