Immunologic causes and thrombophilia in recurrent pregnancy loss

Successful maternal adaptation to the semi-allogenic fetus occurs in the uterus at the site of placentation with maternal–fetal immune tolerance. Impairments of these mechanisms are involved in certain cases of RPL. The role of thrombophilia and imunologic causes in RPL is discussed.
Immunologic causes and thrombophilia in recurrent pregnancy loss

VOLUME 115, ISSUE 3, P561-566, MARCH 01, 2021


Diana Alecsandru, M.D., Ph.D., Amber M. Klimczak, M.D., Juan A. Garcia Velasco, M.D., Paul Pirtea, M.D., Jason M. Franasiak, M.D.


Certain miscarriages result from immunologic factors, but there is no clear identification of the precise causes of recurrent pregnancy loss (RPL). Miscarriages and RPL can arise from a disruption of maternal–fetal immune homeostasis. Remodeling of the maternal uterine spiral arteries is one of the key steps for normal growth and development of the fetus. An adequate oxygen supply is necessary for correct placentation, and it is accomplished by proper vascular changes. The development of fetal tissues creates a potential immunologic problem since the fetus can express paternal antigens and, in some cases, antigens of a gamete donor. The maternal immune system actively responds to fetal antigens, and dysregulation of this crosstalk could partly explain pregnancy complications such as miscarriages and RPL. RPL resulting from thrombophilia is primarily due to acquired thrombophilia, and therefore screening and treatment should be focused on antiphospholipid antibody syndrome.

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