Download This Paper
Preprints with The Lancet is a collaboration between The Lancet Group of journals and SSRN to facilitate the open sharing of preprints for early engagement, community comment, and collaboration. Preprints available here are not Lancet publications or necessarily under review with a Lancet journal. These preprints are early-stage research papers that have not been peer-reviewed. The usual SSRN checks and a Lancet-specific check for appropriateness and transparency have been applied. The findings should not be used for clinical or public health decision-making or presented without highlighting these facts. For more information, please see the FAQs.
Heparin-Induced Thrombocytopenia Is a High Risk of Mortality in Critical COVID-19 Patients Receiving Heparin-Involved Treatment
22 Pages Posted: 12 May 2020
More...Abstract
Background: The coronavirus infectious disease 2019 (COVID-19) has developed into a global pandemic. It is essential to investigate the clinical characteristics of COVID-19 and uncover the potential risks of mortality to reduce the overall mortality rate of COVID-19.
Methods: 61 critical COVID-19 patients admitted into intensive care unit (ICU) and 93 severe non-ICU patients in Huoshenshan Hospital (Wuhan, China) were included in this study. The medical records of demographic, platelet counts, heparin-involved treatments, heparin-induced thrombocytopenia (HIT) related laboratory tests, and the fatal outcomes of these patients were analyzed and compared between survivors and non-survivors.
Findings: Among 61 critical ICU patients, including 15 survivors and 46 non-survivors, 41% of them (25/61) had severe thrombocytopenia with platelet count less than 50´109/L, of whom 76% (19/25) had a >50% platelet fall compared to baseline and 96% (24/25) had a fatal outcomes. Among 46 non-survivors, 52·2% (24/46) had severe thrombocytopenia, compared to 6·7% (1/15) in survivor. Moreover, continuous renal replacement therapy (CRRT) could induce significant decrease of platelet count in 81·3% of critical CRRT patients (13/16), resulting in a fatal outcome. Next, high level of anti-Heparin-PF4 antibodies, a marker of heparin-induced thrombocytopenia (HIT), was observed in most of ICU patients. Surprisingly, HIT occurred not only in patients with heparin exposure such as CRRT but also in heparin-naïve patients, suggesting that a spontaneous HIT might occur in COVID-19.
Interpretation: Anti-heparin-PF4 antibodies are induced in critical COVID-19 patients, resulting in a progressive platelet decrease. Exposure to high dose of heparin may trigger further severe thrombocytopenia with a fatal outcome. An alternative anticoagulant other than heparin should be used in the therapy of COVID-19 patients in critical condition.
Funding Statement: This investigation was supported by Grant 2016CB02400 and 2017YFC1201103 from National Major Research and Development Program of China.
Declaration of Interests: Authors declare no potential conflicts of interests.
Ethics Approval Statement: This study was approved by the Ethics Committee of Huoshenshan Hospital (Wuhan, China).
Keywords: COVID-19, platelet, thrombocytopenia, heparin-induced thrombocytopenia, continuous renal replacement therapy
Suggested Citation: Suggested Citation