Heparin-induced thrombocytopenia: An illustrated review

Heparin-induced thrombocytopenia (and autoimmune heparin-induced thrombocytopenia): an illustrious review

“…May et al. [ 2 ] have prepared such a review of the complex and counterintuitive adverse drug reaction, entitled “Heparin-induced thrombocytopenia: an illustrated review.” Their work is beautiful, comprehensive, grounded in both established and new scientific concepts in heparin-induced thrombocytopenia (HIT), and deserving of the appellation, an “illustrious” illustrated review. The authors tackle major HIT issues, such as incidence, pathophysiology, diagnosis (divided into clinical and laboratory evaluation and their integration), HIT management (from the perspective of the sequential phases of HIT), and selection of nonheparin anticoagulation, as well as specialized topics, such as performing heart surgery during acute or previous HIT and so-called “autoimmune HIT” (aHIT).…”

“…Capsule 1 —adapted from the work of May et al. [ 2 ]—lists 6 aHIT disorders and presents pathogenesis. The definition of aHIT remains in flux, and some classifications of anti-platelet factor 4 (PF4) disorders [ 4 ] define aHIT as requiring a triggering exposure to heparin (or low-molecular-weight heparin or fondaparinux); thus, in my slightly altered version of the May et al.…”

“…The definition of aHIT remains in flux, and some classifications of anti-platelet factor 4 (PF4) disorders [ 4 ] define aHIT as requiring a triggering exposure to heparin (or low-molecular-weight heparin or fondaparinux); thus, in my slightly altered version of the May et al. [ 2 ] capsule, I have separated out “spontaneous HIT” (SpHIT), which by definition has a nonheparin trigger [ 5 ], such as knee replacement surgery or infection (sometimes, no precipitant is identified).

Capsule 1 Autoimmune heparin-induced thrombocytopenia (aHIT): definition and pathogenesis.

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“…In the corresponding version of Capsule 1 found in the article by May et al. [ 2 ] is the statement, “functional assay may show platelet activation in the absence of heparin, but a non-heparin control is not performed in all laboratories.” Indeed, performing a functional test such as the serotonin-release assay only in the presence of differing heparin concentrations, but not at 0-U/mL heparin (“buffer control”), helps explain the widespread underrecognition of aHIT [ 6 ].…”

“…As, due to space constraints, May et al. [ 2 ] included only a single page discussing aHIT, I have taken this opportunity to pen an editorial commentary that in itself is an illustrated commentary of an illustrated review. In Capsule 2 , I summarize the distinction between “classic” HIT—featuring predominantly heparin-dependent antibodies—vis-à-vis aHIT, along with 3 other anti-PF4 disorders that also feature heparin-independent platelet-activating antibodies: the aforementioned SpHIT, vaccine-induced immune thrombotic thrombocytopenia (VITT), and a more recently described nonvaccine-induced VITT-mimicking disorder, “spontaneous VITT” [ 7 ].…”