title: P-selectin and antibodies against heparin-platelet factor 4 in patients with venous or arterial diseases after a 7-day heparin treatment.
abstract: 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.
  
  
  METHODS
  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.
authors.affiliation: First Department of Surgery, Laiko Hospital, University of Athens Medical School, Athens, Greece.
authors.forename: Efstathios
authors.initials: E
authors.lastname: Papalambros
authors.forename: Fragiska
authors.initials: F
authors.lastname: Sigala
authors.forename: Anthi
authors.initials: A
authors.lastname: Travlou
authors.forename: Elias
authors.initials: E
authors.lastname: Bastounis
authors.forename: Petros
authors.initials: P
authors.lastname: Mirilas
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000925:Anticoagulants / Q000009:adverse effects / Q000276:immunology*; D001157:Arterial Occlusive Diseases / Q000188:drug therapy; D001792:Blood Platelets / Q000276:immunology; D015331:Cohort Studies; D005260:Female; D005340:Fibrinogen / Q000276:immunology; D006493:Heparin / Q000009:adverse effects / Q000276:immunology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000096:biosynthesis / Q000276:immunology*; D010978:Platelet Factor 4 / Q000276:immunology*; D011446:Prospective Studies; D013921:Thrombocytopenia / Q000209:etiology / Q000276:immunology; D013923:Thromboembolism / Q000188:drug therapy; D014652:Vascular Diseases / Q000188:drug therapy*; D020246:Venous Thrombosis / Q000188:drug therapy
chemical_list: D000925:Anticoagulants; D019007:P-Selectin; D010978:Platelet Factor 4; D005340:Fibrinogen; D006493:Heparin