Figure 1.
Treatment in anti-F4 antibody disorders. A summary of the pathway associated with anti-PF4 disorders. In cHIT, stopping heparin and initiating an alternative anticoagulant is associated with an increment in platelet count and halting of the thrombotic risk. In aHIT, related to heparin-dependent antibodies, the pathway would be comparable to cHIT. But in those developing non–heparin-dependent antibodies, further therapy is required. It is related to progression in the immune response, requiring IVIg or occasionally additional immunomodulation, such as PEX for platelet count increase and prevention of further thrombosis. In VITT and VITT-like disorder, there is no heparin exposure. Heparin can be used, but there are alternative anticoagulants. The prompt initiation of IVIg and/or plasma exchange or alternate immunosuppressive therapy is required. *Alternative, non–heparin-based anticoagulation must be started. PEX, plasma exchange.

Treatment in anti-F4 antibody disorders. A summary of the pathway associated with anti-PF4 disorders. In cHIT, stopping heparin and initiating an alternative anticoagulant is associated with an increment in platelet count and halting of the thrombotic risk. In aHIT, related to heparin-dependent antibodies, the pathway would be comparable to cHIT. But in those developing non–heparin-dependent antibodies, further therapy is required. It is related to progression in the immune response, requiring IVIg or occasionally additional immunomodulation, such as PEX for platelet count increase and prevention of further thrombosis. In VITT and VITT-like disorder, there is no heparin exposure. Heparin can be used, but there are alternative anticoagulants. The prompt initiation of IVIg and/or plasma exchange or alternate immunosuppressive therapy is required. *Alternative, non–heparin-based anticoagulation must be started. PEX, plasma exchange.

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