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[Acquired resistance to activated protein C in pregnancy]
D M Schneider1, G F von Tempelhoff, D Hoppenstaedt
1Abteilung für Geburtshilfe und Frauenheilkunde, Stadtkrankenhaus Rüsselsheim.
Abstract:
A recently identified mechanism for familial thrombophilia--the poor anticoagulant response to activated protein C (APC-resistance)--is said to be one of the leading risk factors for thrombosis. This has been demonstrated by a large number of studies. But there is still a need for data concerning the prevalence of APC-resistance in pregnancy. Therefore we performed the study with 50 pregnant women and 10 non-pregnant controls to evaluate this question with the blood samples drawn at trimester 1., 2., 3. and at term. A progressive shortening of the APC-ratio (APCR) and normalised APCR (nAPCR) was noted in our population. In comparison to the first (APCR 2.32 +/- 0.39; nAPCR 0.99 +/- 0.17) significant differences were noticed at 2. (APCR 2.12 +/- 0.34; nAPCR 0.92 +/- 0.14) (p = 0.001) and 3. trimester (APCR 1.98 +/- 0.26; nAPCR 0.87 +/- 0.13) and at term (APCR 1.98 +/- 0.26; nAPCR 0.92 +/- 0.19) (p = 0.001). In addition to the APC-resistance we determined protein C and factor VIII:C. Whereas factor VIII:C showed an increasing trend which achieved statistical significance (1. trimester: 109%; 2.: 115%; 3.: 128%) (p = 0.005) protein C remained unchanged. Physiological changes during pregnancy lead to an acquired APC-resistance. Our study suggests that e.g. an increase in factor VIII contributes to this phenomenon.