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Etiology
APL does not have a known etiology. There are several hypotheses to explain the probable cause
which are:
Passive transfer of maternal antibodies mediate autoimmune disorders in the fetus and
newborn.
Familial occurrence of APL has been reported, and suggested genetic associations include
HLA-DR4, DR7, DRw53 and C4 null allele .
Phospholipid molecules are ubiquitous in nature and are present in the inner surface of
the cell and in microorganisms. Therefore, during infectious disease processes, including
viral (eg, HIV,EBV and CMV), bacterial , spirochetal and parasitic ; the disruption of
cellular membranes may occur during cell damage. Phospholipids release and stimulate
APL antibodies.
Pathophysiology
Biologic effects mediated by the human APL antibodies include the following:
APL activate endothelial cells and these express adhesion molecules (such as intercellular
cell adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin) and upregulates
the production of tissue factor .
APL activate monocytes and induce their increased tissue factor expression .
APL activate platelets that increase expression of glycoprotein 2b-3a and synthesis of
thromboxane A2.The activation of endothelial cells, monocytes, and platelets by
antiphospholipid antibodies, conducting to the increased synthesis of tissue factor and
thromboxane A2, this further induces a procoagulant state.
Complications of APL:
Reference:
Fosca. A.etc.(2011). Antiphospholipid Syndrome during pregnancy: the state of the art. Journal
of prenatal medicine.
Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279165/[Accessed on 14th
February 2017]