P-selectin and antibodies against heparin-platelet factor 4 in patients with venous or arterial diseases after a 7-day heparin treatment.

BACKGROUND

We investigated heparin influence on P-selectin (platelet adhesion molecule), and the association of P-selectin with antibodies against heparin-platelet factor 4, known mediators of heparin induced thrombocytopenia (HIT) occurring in about 5% of vascular patients.

STUDY DESIGN

This cohort study included 78 patients, 22 to 90 years old (mean age +/- SD, 66.5 +/- 12.2 years), suffering from arterial thromboembolism (n = 43), deep vein thrombosis (n = 21), and peripheral arterial occlusive disease (PAOD) (n = 14). Plasma P-selectin was tested by ELISA before heparin administration (day 1), and under heparin treatment (day 7). HIT antibodies on day 7 were assayed using a sandwich-type ELISA. Platelets and fibrinogen were measured on days 1 and 7. P-selectin was also examined in 30 healthy controls, 22 to 81 years old (49.8 +/- 16.4 years).

RESULTS

On day 7, patients with PAOD had increased P-selectin and HIT antibodies, and decreased platelets compared with patients with arterial thromboembolism or deep vein thrombosis, in whom P-selectin decreased, and HIT antibodies were mostly negative. Fibrinogen increased in all patients. HIT antibody titers and P-selectin were positively associated and were increased in nine patients who developed lower limb artery occlusion or bypass thrombosis, stroke, or myocardial infarction during hospitalization (days 5 to 24). Five of these patients suffered from PAOD and the majority had taken heparin in the past.

CONCLUSIONS

P-selectin and HIT antibodies could be useful markers of HIT syndrome-associated thromboses during hospitalization of vascular patients receiving heparin. In arterial thromboembolism or deep vein thrombosis, P-selectin decreases without HIT antibody development. In PAOD, their concomitant increase may alert the surgeon to forthcoming life-threatening complications.