Entangling COVID-19 associated thrombosis into a secondary antiphospholipid antibody syndrome: Diagnostic and therapeutic perspectives (Review)

Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) is a novel β coronavirus that is the etiological agent of the pandemic coronavirus disease 2019 (COVID‑19) that at the time of writing (June 16, 2020) has infected almost 6 million people with some 450,000 deaths. These numbers are still rising daily. Most (some 80%) cases of COVID‑19 infection are asymptomatic, a substantial number of cases (15%) require hospitalization and an additional fraction of patients (5%) need recovery in intensive care units. Mortality for COVID‑19 infection appears to occur globally between 0.1 and 0.5% of infected patients although the frequency of lethality is significantly augmented in the elderly and in patients with other comorbidities. The development of acute respiratory distress syndrome and episodes of thromboembolism that may lead to disseminated intravascular coagulation (DIC) represent the primary causes of lethality during COVID‑19 infection. Increasing evidence suggests that thrombotic diathesis is due to multiple derangements of the coagulation system including marked elevation of D‑dimer that correlate negatively with survival. We propose here that the thromboembolic events and eventually the development of DIC provoked by SARS‑CoV‑2 infection may represent a secondary anti‑phospholipid antibody syndrome (APS). We will apply both Baconian inductivism and Cartesian deductivism to prove that secondary APS is likely responsible for coagulopathy during the course of COVID‑19 infection. Diagnostic and therapeutic implications of this are also discussed.

Figure 1

Similarities in the etiopathogenic mechanisms underlying APS and COVID-19. APS, anti-phospholipid antibody syndrome.

Figure 2

Cartesio deductivism and Baconian inductivism lead to the same hypothesis. APS, anti-phospholipid antibody syndrome.