title: Markers of platelet, endothelial cell and blood coagulation activation in leprosy patients with antiphospholipid antibodies.
abstract: OBJECTIVE
  To evaluate plasma levels of markers of platelet, endothelial cell and blood coagulation activation in leprosy patients with or without antiphospholipid antibodies (aPL) and to compare them to those found in patients with antiphospholipid syndrome (APS).
  
  
  METHODS
  42 patients with leprosy (35 lepromatous and 7 borderline): 29 aPL(+) and 13 aPL(-), as well as 26 healthy subjects as normal controls (NC) and 79 control aPL patients without leprosy (59 with and 20 without APS) were included in the study. Plasma soluble P and E selectin (sPsel and sEsel), and VCAM-1 (sVCAM-1), prothrombin F1 + 2 fragment (F1 + 2), thrombin-antithrombin complexes (TAT) and D dimer (DD) were measured by ELISA. The protein C pathway was assessed by the ProC global test.
  
  
  RESULTS
  Leprosy patients with aPL presented increased median levels of sPsel [ng/ml (82.0 vs 36.0, p < 0.001)] and sVCAM-1 [ng/ml (495 vs 335, p < 0.001)] compared to NC, as observed in control aPL patients without leprosy. Levels of sPsel in aPL(+) patients with leprosy were significantly higher than in aPL(-) ones (52.5 ng/ml), p = 0.005. However, plasma markers of thrombin generation were increased in control aPL patients without leprosy but not in those with leprosy. ProcC global test was abnormal in 24.1% of leprosy patients with aPL compared to 4.4% of NC (p < 0.024), and to 57.2% of control patients with aPL without leprosy (p = 0.005).
  
  
  CONCLUSIONS
  We demonstrated that although patients with leprosy present a high prevalence of aPL, and platelet and endothelial cell activation in vivo to the same extent than patients with APS, they do not show a procoagulant state.
authors.affiliation: Division of Haematology, Favaloro University, Favaloro Foundation, Buenos Aires, Argentina.
authors.forename: M E
authors.initials: ME
authors.lastname: Martinuzzo
authors.forename: G F
authors.initials: GF
authors.lastname: de Larrañaga
authors.forename: R R
authors.initials: RR
authors.lastname: Forastiero
authors.forename: Y
authors.initials: Y
authors.lastname: Pelegri
authors.forename: M H
authors.initials: MH
authors.lastname: Fariña
authors.forename: B S
authors.initials: BS
authors.lastname: Alonso
authors.forename: L C
authors.initials: LC
authors.lastname: Kordich
authors.forename: L O
authors.initials: LO
authors.lastname: Carreras
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D017152:Antibodies, Antiphospholipid / Q000097:blood*; D000990:Antithrombin III; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation / Q000502:physiology*; D001792:Blood Platelets / Q000502:physiology*; D015815:Cell Adhesion Molecules / Q000097:blood; D004730:Endothelium, Vascular / Q000502:physiology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D006023:Glycoproteins / Q000276:immunology; D006801:Humans; D007074:Immunoglobulin G / Q000032:analysis; D007075:Immunoglobulin M / Q000032:analysis; D015439:Leprosy, Borderline / Q000097:blood*; D015440:Leprosy, Lepromatous / Q000097:blood*; D016682:Lupus Coagulation Inhibitor / Q000097:blood; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000097:blood; D010447:Peptide Hydrolases / Q000097:blood; D011486:Protein C / Q000032:analysis; D011516:Prothrombin; D053482:beta 2-Glycoprotein I
chemical_list: D017152:Antibodies, Antiphospholipid; D015415:Biomarkers; D015815:Cell Adhesion Molecules; D005338:Fibrin Fibrinogen Degradation Products; D006023:Glycoproteins; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D016682:Lupus Coagulation Inhibitor; D010446:Peptide Fragments; D011486:Protein C; C046193:antithrombin III-protease complex; D053482:beta 2-Glycoprotein I; C036309:fibrin fragment D; C045879:prothrombin fragment 1.2; D000990:Antithrombin III; D011516:Prothrombin; D010447:Peptide Hydrolases