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Auto-antibodies against the angiotensin II type I receptor in women with uteroplacental acute atherosis and preeclampsia at delivery and several years postpartum

Authors

  • A.B. Rieber-Mohn
  • M. Sugulle
  • G. Wallukat
  • P. Alnæs-Katjavivi
  • G. Leite Størvold
  • N. Bolstad
  • C.W. Redman
  • R. Dechend
  • A.C. Staff

Journal

  • Journal of Reproductive Immunology

Citation

  • J Reprod Immunol 128: 23-29

Abstract

  • BACKGROUND: Uteroplacental acute atherosis is a pregnancy-specific lesion resembling early stages of atherosclerosis found frequently in preeclampsia. Preeclampsia is associated with an increased risk for future maternal atherosclerotic cardiovascular disease. The renin-angiotensin-system plays a role both in atherosclerosis and in preeclampsia. Circulating agonistic autoantibodies at the angiotensin-II type 1 receptor (AT(1)-AA) are increased in preeclampsia. We hypothesized an association between AT(1)-AA at delivery and postpartum with acute atherosis in pregnancy. MATERIAL AND METHODS: Maternal serum and decidua basalis tissue was collected at elective cesarean section (n = 41; 24 preeclampsia, 17 normotensive controls). Circulating AT(1)-AA were detected by a bioassay using spontaneously beating rat cardiomyocytes at delivery (n = 41) and 5-8 years postpartum in a subgroup (n = 10). Decidual acute atherosis was assessed by immunohistochemistry. RESULTS: Significantly less normotensive controls (18%; 3/17) than women with preeclampsia (58%; 14/24) were AT(1)-AA positive at delivery, p<0.01. Uteroplacental acute atherosis and circulating AT-AA at delivery were not significantly correlated. Postpartum, 2 prior preeclamptic women had circulating AT(1)-AA, both without acute atherosis in pregnancy. CONCLUSIONS: Our results confirm that circulating AT(1)-AA are present significantly more often in preeclampsia than in normotensive pregnancy, however without association to acute atherosis. Whether circulating maternal AT(1)-AA or acute atherosis target young women at increased long-term cardiovascular risk warrants further investigations.


DOI

doi:10.1016/j.jri.2018.05.008