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0 2 4 6 8 10 12 14 16 18 20 22 24 Days after starting heparin

FIGURE 3 A 49-yr-old patient exhibiting both typical- and rapid-onset HIT: The platelet count began to fall on day 6 of sc UFH injections given for antithrombotic prophylaxis following neurosurgery (typical HIT). An abrupt fall in platelet count occurred twice on day 18, each after a 5000 U iv UFH bolus (rapid HIT). Symptoms and signs of acute systemic reaction occurred 10 mins after each bolus (dyspnea, tachypnea, hypertension, chest tightness, restlessness). Note that the patient's platelet count never fell below 150 x 109/L, even though her serum tested strongly positive for HIT antibodies by serotonin release assay. She developed proximal DVT shortly after developing HIT. Abbreviations: ASR, acute systemic reaction; DVT, deep venous thrombosis; HIT, heparin-induced thrombocytopenia; iv, intravenous; sc, subcutaneous; UFH, unfractionated heparin.

0 2 4 6 8 10 12 14 16 18 20 22 24 Days after starting heparin

FIGURE 3 A 49-yr-old patient exhibiting both typical- and rapid-onset HIT: The platelet count began to fall on day 6 of sc UFH injections given for antithrombotic prophylaxis following neurosurgery (typical HIT). An abrupt fall in platelet count occurred twice on day 18, each after a 5000 U iv UFH bolus (rapid HIT). Symptoms and signs of acute systemic reaction occurred 10 mins after each bolus (dyspnea, tachypnea, hypertension, chest tightness, restlessness). Note that the patient's platelet count never fell below 150 x 109/L, even though her serum tested strongly positive for HIT antibodies by serotonin release assay. She developed proximal DVT shortly after developing HIT. Abbreviations: ASR, acute systemic reaction; DVT, deep venous thrombosis; HIT, heparin-induced thrombocytopenia; iv, intravenous; sc, subcutaneous; UFH, unfractionated heparin.

there truly been an anamnestic immune response more rapid than the usual 5- to 10-day period, one might have expected to identify such a group of patients. Third, patients reexposed to heparin following disappearance of HIT antibodies do not necessarily form HIT antibodies again; those who do appear to form antibodies after day 5 (Gruel et al., 1990; Warkentin and Kelton, 2001a). Indeed, several patients with well-documented previous HIT have received full treatment courses of heparin several months or years later without incident (Warkentin and Kelton, 2001a; Lindhoff-Last et al., 2002).

HIT Antibodies Are Transient

There is a plausible biological basis to explain why patients who develop rapid-onset HIT have received heparin in the recent, rather than in the remote, past: HIT antibodies are transient and become undetectable at a median of 50 days (95% CI, 32-64 days) after first testing positive, using the platelet serotonin release assay. The median time to a negative test is somewhat longer (85 days; 95% CI, 64-124 days) using a commercial antigen assay (Fig. 4). At 100-day follow-up, the probability of the activation and antigen assays being negative is approximately 90% and 60%, respectively (Warkentin and Kelton, 2001a).

Rule 2

A rapid fall in the platelet count that began soon after starting heparin therapy is unlikely to represent HIT unless the patient has received heparin in the recent past, usually within the past 30, and latest, 100 days.

To summarize, the rapid fall in platelet count appears to be caused by the repeat administration of heparin to a patient with residual circulating HIT antibodies, rather than resulting from a rapid regeneration of HIT antibodies.

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