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2.3 Circulating Microparticles and Arterial Stiffness Index – a Measure of Vascular Endothelial Dysfunction in Pregnancy and Systemic Lupus Erythematosus
  1. S Mathen1,
  2. O Kiss1,
  3. A Allibone1,
  4. R Pietralska1,
  5. I Bruce2,
  6. I Crocker1,
  7. C Tower1
  1. 1Maternal and Fetal Health Research Center, St Mary’s Hospital, Manchester, UK
  2. 2Kellgren Centre for Rheumatology, Central Manchester Foundation Hospitals, Manchester, UK


Introduction Microparticles (MPs) are circulatory vesicles with pro-thrombotic and inflammatory characteristics. Systemic lupus erythematosus (SLE) is an autoimmune condition with increased pregnancy morbidity. We investigated the role of MPs in pregnancy and SLE by longitudinal assessment, and correlated these with arterial stiffness index (SI), as a marker of vascular dysfunction.

Methods Plasma was obtained from pregnant (n = 20) and non-pregnant healthy women (n = 19), and pregnant (n = 15) and non-pregnant SLE patients (n = 30). MPs were quantified by flow cytometry. Arterial SI was measured by digital Pulse Contour Analysis (dPCA) (Micro Medical Ltd).

Results Platelet and endothelial MPs were significantly higher in non-pregnant women with SLE compared to healthy women (p < 0.05). In healthy pregnancy, platelet MPs declined at 12 wks gestation from non-pregnant controls (p ≤ 0.01), but thereafter returned. This pattern was not observed in SLE pregnancy, which remained higher throughout gestation. Outside pregnancy, a positive correlation was recorded in SLE patients between SI and platelet, endothelial and total MPs (p ≤ 0.05, p ≤ 0.05 and p = 0.05; respectively). This relationship was lost in the SLE pregnant group. Placental MPs were unchanged in SLE and healthy pregnancies.

Conclusions SLE is associated with increased circulating MPs. These MPs may contribute or reflect vascular dysfunction as determined by arterial SI. A loss of this association implies alternative vascular and MP regulation in pregnancy. A lack of decline in platelet MPs in early pregnancy may predispose SLE patients to pregnancy complications, but the mechanism remains unclear.

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