1 (17%)

Not statedk

3/6 (50%)

Note: Where there was uncertainty over the numbers of patients with HIT, the higher estimated value was indicated in the table, to minimize the bias toward a high frequency of HIT-associated thrombosis (contrast analysis shown in Table 2).

aThe mean platelet count nadir for 127 patients with HIT and platelet count <150x 109/L, and the median platelet count nadir for all 142 patients diagnosed with HIT (including those whose platelet count nadir was >150x 109/L), were both 59x 109/L (Warkentin, 1998a) (see Figure 6 in Chapter 2).

^The cumulative 30-day frequency of new thrombosis in patients with isolated thrombocytopenia following recognition of HIT was 52.8% by Kaplan-Meier analysis.

cOnly deaths in patients who developed thrombosis were reported. Total number of deaths in the HIT cohort was not reported.

dFourteen of the 20 deaths were judged to be caused by HIT-associated thrombosis.

eOf 100 consecutive patients with positive in vitro testing, six were previously known to have heparin-dependent antibodies and were not subsequently reexposed to heparin.

fTwo thromboses of arteriovenous grafts were excluded from classification into arterial or venous thrombosis. gTwo thromboses on the dialysis membrane were excluded from classification into arterial or venous thrombosis.

hIn four of the seven deaths, HIT was judged to be contributory.

Thrombosis of temporary (4) or permanent (10) dialysis access excluded from classification into arterial or venous thrombosis.

jComplete data available on 35 patients.

kType of thrombosis not stated.

Abbreviation: HIT, heparin-induced thrombocytopenia.

uncertain what proportion is related to HIT-associated thrombosis, and to what extent these can be prevented by effective treatment. 2. Most thrombotic events are venous, rather than arterial, although this predominance may not be observed in patient populations at high risk for arterial disease. Pulmonary embolism may be the most frequent life-threatening consequence of HIT.

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