First-pass extracted concept

Heparin-induced thrombocytopenia

Candidate: concept label1 source documents9 linked claims
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Aliases

HIT

Evidence Snippets

Heparin-induced thrombocytopenia (HIT) is a transient prothrombotic disorder initiated by heparin.
Evidence 1Source 1DOIPubMedprovenance

Supporting Sources

Linked Claims

Claim 1clinical frequency summarysupports2003Source 1DOIPubMed

Thrombocytopenia is the most common event in HIT and occurs in at least 90% of patients depending on the definition used.

Claim 2diagnostic definitionsupports2003Source 1DOIPubMed

The diagnosis of HIT should be based on both HIT-associated clinical events and detection of HIT antibodies in patient serum or plasma.

Claim 3diagnostic exclusionsupports2003Source 1DOIPubMed

A patient who appears clinically to have HIT but has negative sensitive HIT antibody tests does not have HIT according to the review's clinicopathological definition.

Claim 4diagnostic exclusionsupports2003Source 1DOIPubMed

A patient with HIT antibody seroconversion alone but no thrombocytopenia or other adverse events does not meet the review's definition of HIT.

Claim 5disease associationsupports2003Source 1DOIPubMed

HIT is associated with increased thrombin generation in vivo and increased risk for arterial and especially venous thrombosis.

Claim 6mechanism summarysupports2003Source 1DOIPubMed

Pathogenic HIT antibodies are directed against neoepitopes on PF4 that are expressed when PF4 is bound to heparin or certain other polyanions.

Claim 7mechanism summarysupports2003Source 1DOIPubMed

The review describes a central role for thrombin generation in HIT pathogenesis, with platelet, endothelial-cell, and monocyte activation contributing to the prothrombotic state.

Claim 8pathogenesis summarysupports2003Source 1DOIPubMed

HIT is a transient prothrombotic disorder initiated by heparin in which thrombocytopenia is caused by antibody-mediated platelet activation.

Claim 9treatment summarysupports2003Source 1DOIPubMed

Alternative non-heparin anticoagulant therapy reduces the risk of subsequent thrombosis in HIT.