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assay, PF4-dependent EIA) both give negative test results, the diagnosis of HIT is virtually excluded (even in a patient with a high pretest probability).

Some investigators advocate routine repeat testing for HIT antibodies by EIA when an initial test result is negative (Refaai et al., 2003). There is a potential pitfall to this approach: the high sensitivity (>98%) of the EIA for HIT means that the clinical events that led to initial testing almost certainly are not due to HIT. Thus, in the absence of progressive or recurrent thrombocytopenia, or subsequent development of thrombosis, a subsequent positive EIA is more likely to represent a seroconversion event involving nonpathogenic anti-PF4/heparin antibodies. When HIT is strongly suspected—despite a negative EIA—there likely is greater utility in performing the complementary platelet activation assay, as it can detect pathologic antibodies against antigens other than the PF4-H complex.

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