Vaccine-induced immune thrombotic thrombocytopenia
The exact incidence of this syndrome is unknown; however, by the spring of 2021 within the United States, approximately 15 cases had been identified among 8 million individuals vaccinated with As26.COV2.S (incidence of 1 in 533 333). In Norway, the incidence is higher (approximately 1 in 26 000). Initial studies showed a female predominance; however, a later study from the United Kingdom showed no sex predilection. Regardless, the incidence is felt to be extremely low, and the risk of death and serious outcomes of COVID-19, including thrombosis, far outweigh the risk of TTS possibly associated with these highly efficacious vaccines.
VITT is distinct from HIT in that the antibodies are not heparin dependent in VITT. Triggers other than heparin previously have been described as causing a HIT-like syndrome. These include pentosan polysulfate, antiangiogenic agent PI-88, and hypersulfated chondroitin sulfate. Other known triggers include bacterial and viral infection as well as joint replacement surgery. Such cases with no exposure to heparin are known as "spontaneous HIT."
IgG antibodies in the serum of patients with VITT strongly activate platelets via PF4, both in the presence and absence of heparin. These antibodies may also cause widespread activation of coagulation, endothelial cells, and neutrophils, leading to higher risk of thrombosis.
Related topics: cutaneous reactions after COVID-19 vaccination, COVID-19
D69.59 – Other secondary thrombocytopenia
1156746003 – Vaccine-induced prothrombotic immune thrombocytopenia
Differential Diagnosis & Pitfalls