The presence of
antiphospholipid antibodies was shown to be associated with
thrombosis in
coronavirus disease 2019 (COVID-19) patients. Recently, according to reports from several studies, the
vaccine-induced immune thrombotic
thrombocytopenia is mediated by anti-
platelet factor 4 (PF4)-polyanion complex in adenovirus-vectored
COVID-19 vaccine recipients. It is impendent to explore whether inactivated
COVID-19 vaccine widely used in China influences prothrombotic
autoantibody production and induces
thrombosis. In this prospective study, we recruited 406 healthcare workers who received two doses, 21 days apart, of inactivated severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
vaccine (
BBIBP-CorV, Sinopharm). Paired blood samples taken before vaccination and four weeks after the second vaccination were used in detecting prothrombotic
autoantibodies, including anticardiolipin (aCL), anti-β2
glycoprotein I (aβ2GP1), anti-
phosphatidylserine/
prothrombin (aPS/PT), and anti-PF4-heparin. The seroconversion rate of SARS-CoV-2 specific
antibodies was 95.81% (389/406) four weeks after vaccination. None of the subjects had spontaneous
thrombosis or
thrombocytopenia over a minimum follow-up period of eight weeks. There was no significant difference in the presence of all ten
autoantibodies between samples collected before and after vaccination: for aCL,
IgG (7 vs. 8, P = 0.76),
IgM (41 vs. 44, P = 0.73),
IgA (4 vs. 4, P = 1.00); anti-β2GP1,
IgG (7 vs. 6, P = 0.78),
IgM (6 vs. 5, P = 0.76),
IgA (3 vs. 5, P = 0.72); aPS/PT
IgG (0 vs. 0, P = 1.00),
IgM (6 vs. 5, P = 0.76); aPF4-heparin (2 vs. 7, P = 0.18), and
antinuclear antibody (ANA) (18 vs. 21, P = 0.62). Notably, seven cases presented with anti-PF4-heparin
antibodies (range: 1.18-1.79 U/mL) after vaccination, and none of them exhibited any sign of thrombotic disorder. In conclusion, inactivated
SARS-CoV-2 vaccine does not influence the profile of
antiphospholipid antibody and anti-PF4-heparin antibody nor increase the risk of
thrombosis.