Heparin-Induced Thrombocytopenia in COVID-19

Abstract

COVID-19 (coronavirus disease-2019) infection is a highly prothrombotic state, resulting from a dysregulation of the coagulation cascade. Therefore, thromboprophylaxis is strongly recommended in these patients, with some experts even advocating for therapeutic dosing to prevent thromboembolic events. Heparin-induced thrombocytopenia (HIT) is a well-known complication of heparin therapy. In this article, we report a case of HIT in a patient with COVID-19. A 63-year-old male presented with 1 week of dry cough and diarrhea. He had a positive nasopharyngeal COVID-19 reverse-transcriptase–polymerase chain reaction. On admission, the platelet count and liver function tests were within normal limits. During his hospitalization, he developed a right femoral deep venous thrombosis and was started on therapeutic anticoagulation. Due to worsening respiratory failure, he was intubated and mechanically ventilated. Between days 11 and 12 of hospitalization, platelet count dropped from 304 000 to 96 000 cells/µL. He had a high pretest probability for HIT with a 4T score of 6 and a positive anti-PF4/heparin antibody. Heparin drip was discontinued and was switched to argatroban. The serotonin release assay eventually returned positive, which confirmed the diagnosis of HIT. We also discuss potential overdiagnosis of HIT in COVID-19 through 4 cases with false-positive HIT antibodies.

COVID-19 and Cardiovascular Disease

“…Curiously, several patients with COVID-19, meeting clinical diagnostic criteria for heparin-induced thrombocytopenia, subsequently tested positive for anti-PF4 antibodies, but in heparin-induced platelet aggregation assays were negative using the heparin-induced thrombocytopenia confirmatory test platelet serotonin release assay. 172 , 173 Most recently, it was revealed that circulating blood IgG in patients with COVID-19 promotes a procoagulant phenotype and thrombocytopenia through platelet apoptosis by stimulating platelet Fc gamma receptor IIA. 174 Overall, a pattern of autoantibody production in COVID-19 that simultaneously activates neutrophils and promotes thrombosis seems clear and may account for the morbidity and mortality benefit shown in the CoDEX and Recovery trials, respectively, when patients were randomized to immune suppression with dexamethasone.…”

Heparin in COVID-19 Patients Is Associated with Reduced In-Hospital Mortality: The Multicenter Italian CORIST Study

“…Paradoxically, HIT is characterized by both thrombocytopenia and a prothrombotic state. Recently, some reports presented the occurrence of HIT in COVID-19 patients [36,37]. However, larger investigations are warranted to confirm this increased incidence of HIT and to understand its physiopathology [36].…”

Should we avoid heparin based anticoagulants in “COVID-19 infection-vaccination related thrombosis”? Insights from the HIT like syndrome observed with infected cases. 

“…Several reports of HIT were reported (a total of 9 reports/series including 18 cases) before the current vaccine rollout; these were reviewed and summarized in table 1 (4)(5)(6)(7)(8)(9)(10)(11)(12). All the reports incriminated heparin in the development of the observed prothrombotic state.…”