One in 13 patients presenting to an emergency department (ED) with chest pain or symptoms of thrombosis may be at risk for heparin-induced thrombo-cytopenia (HIT), according to a study from the University of Texas School of Medicine at Houston.
The researchers tested admission samples from 324 ED patients for heparin-PF4 antibodies and, if these were positive, for platelet-activating antibodies. Twenty-four patients (7.4%) were found to have the antibodies.
Of the 196 patients hospitalized within the previous six months, 18 (9%) were seropositive, compared with six (5%) of 128 who had not been recently hospitalized. Sixteen of 231 patients with chest pain were seropositive, as were eight of 93 patients with thrombosis.
Although assessment of the platelet count is important for identifying patients with HIT, in this study, it was not generally helpful in determining who might have heparin-PF4 antibodies. The researchers suggested that the patient history is an alternative means of quickly identifying at-risk patients. They reasoned that because heparin is used so commonly in hospital patients, anyone who had been hospitalized in the previous six months (the amount of time during which antibodies are typically circulating) might have a higher risk. Sure enough, of the eight patients with the most reactive (i.e., platelet-activating) antibodies, seven had been hospitalized within the previous six months and one patient had been in the hospital within the previous year.
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It is unlikely that the seropositive patients with symptoms of thrombosis had delayed-onset HIT, because 22 of 24 of them were not thrombocytopenic on admission. However, it was also possible that a relative drop in the platelet count might have occurred.
Heparin-PF4 antibodies, even if they do not induce HIT, are clinically significant. Seropositivity without thrombo-cytopenia is associated with higher rates of myocardial infarction and thrombotic outcomes in at-risk patients. Those patients, they suggest, might benefit from more aggressive antithrombotic therapies. In the meantime, the researchers advise that non-heparin anti-coagulation would be prudent.