Anti-PF4/heparin antibodies are increased in hospitalized patients with bacterial sepsis

Abstract Heparin-induced thrombocytopenia (HIT) is caused by antibodies targeting platelet factor 4 (PF4)/heparin complexes. The immune response leading to HIT remains perplexing with many paradoxes. Unlike other drug induced reactions, anti-PF4/heparin antibody generation does not follow the classic immunologic response. Research in murine models suggests that that there is close interplay among infection, PF4 and the immune system. We hypothesized there would be a relatively higher prevalence of anti-PF4/heparin antibodies in patients hospitalized for sepsis. We retrospectively examined anti-PF4/heparin antibody testing in 200 such patients. This included patients who had sepsis with bacteremia (n = 57), sepsis with fungemia (n = 7) and sepsis without bacteremia or fungemia (n = 136). For comparison, data from 50 patients without sepsis during the same time period was used. Results confirmed that patients hospitalized with sepsis have higher anti-PF4/heparin antibody levels. The groups of patients having sepsis with bacteremia, and sepsis without bacteremia, had significantly higher OD than the control group without sepsis (p