From Pregnancy Loss to COVID 19 Cytokine Storm: A Matter of Inflammation and Coagulation

Abstract

Large scientific evidence achieved during the second half of the past century points to a leading role of inflammation in the pathogenic mechanism of the main pregnancy complications, such as abortion, pregnancy loss, premature delivery, infection, fetal encephalopathy, enterocolitis, pulmonary hyaline membrane diseases and death. Thinking about pregnancy inflammation, one must refer today to the umbalance of the normal mediators of organic functions: cytokins, peptides, nucleosides, prostanoids. Indeed, according to the order and quantity of their release, they are involved either in physiology or in pathology of pregnancy. At this regard, it has been shown that Th1-type immunity is incompatible with successful pregnancy. Regulation of the mediators of maternal functions is largely under fetal genetic control. Assessment of the fetal role derives from studies showing an umbalance of cytokines and plasminogen activator system, an increase of endothelin, a downregulation of adenosine receptors, in the fetal compartment, in aneuploid pregnancies. The resulting functional deviations deal with inflammation, imfection, coagulation, impaired utero-placental perfusion, possibly leading to fetal demise and ominus maternal complications. SARS-COV-2 infection, on the other hand, is characterized by a similar umbalance of the inflammatory mediators, leading to hyperactivation of a type-1 lymphobyte T-helper response, which ends in a possibly fatal cytokine storm syndrome. While SARS-COV-2 infection recognizes a viral etiology, the cause of pregnancy inflammation must be recognized in the inability of the fetus to control the maternal immune response. Therefore, the preventive measures are quite different, although both benefit of a similar anti-inflammatory, antibiotic and anti-coagulant therapy.