COVID-19 and hemolysis, elevated liver enzymes and thrombocytopenia syndrome in pregnant women - association or causation?

Figure 3 Pathophysiological linkage between coronavirus disease 2019 and Hemolysis, elevated liver enzymes and low platelets syndrome. The binding of severe acute respiratory syndrome coronavirus 2 to angiotensin converting enzyme 2 (ACE2) allows its entry to host cells and, subsequently, downregulation. ACE2 also converts angiotensin II (ATII) to angiotensin 1-7. The downregulation of ACE2 increases the concentration of AT II, which causes activation of the p38 mitogen activated protein kinase (MAPK) pathway. p38 MAPK stimulates the production of inflammatory cytokines, platelet aggregation and thrombosis. Renin-angiotensin-aldosterone system and ATII are also involved in the pathogenesis of pre-eclampsia and hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome. Serum levels of p38 MAPK are elevated in the HELLP syndrome. ACE2: Angiotensin converting enzyme 2; IL: Interleukin; TNF: Tumour necrosis factor; HELLP: Hemolysis, elevated liver enzymes, and low platelet count;ARDS: Acute respiratory distress syndrome. Solid black arrow- stimulation (positive feedback), Dashed black arrow- inhibition (negative feedback), blue arrow: Effects of p38 MAPK overexpression.