Heparin-Induced Thrombocytopenia In A Patient After Covid-19 And Proven Thrombophilia

Abstract

Heparin-induced thrombocytopenia (HIT) is an immune response provoked by treatment with unfractionated heparin and, in rare cases, low molecular weight heparin. The condition is associated with the formation of an antigen-antibody complex responsible for platelet aggregation and a potent hypercoagulable state, , leading to both thrombocytopenia on the one hand and severe thrombosis on the other, further dictated by endothelial dysfunction. The condition is associated with increased mortality if not identified in time and the necessary measures are not implemented (1). Recurrent vascular events, especially at a young age, should direct the clinician to genetic preexposure and rejection of thrombophilia. Severe thromocytopenia, on the other hand, is part of the pathogenesis of severe fatal COVID-19. The three conditions: HIT, Thrombophilia and COVID-19 are related to the still incompletely understood platelet cascade and thrombosis factors. At this stage, there are no clear guidelines to determine behavior in such situations. We present a clinical case of a patient in critical condition with another recurrence of massive pulmonary thromboembolism (PE) and deep vein thrombosis (DVT), in which heparin-induced thrombocytopenia was detected and thrombophilia was demonstrated after genetic testing. The condition had occurred in the early phase of the recovery period after COVID 19 infection complicated by bilateral pneumonia.

Key words: Heparin induced thrombocytopenia; Pulmonary thromboembolism; Thrombophilia; Deep venous thrombosis, COVID-19.