title: Inflammatory and prothrombotic activation with conserved endothelial function in patients with chronic, asymptomatic Chagas disease.
abstract: Previously, our group showed a prothrombotic state in asymptomatic patients with chronic Chagas disease. The current paper studies the inflammatory status and endothelial function in these patients.
  
  
  METHODS
  In 40 patients and 40 healthy volunteers, we evaluated prothrombotic state, blood parasitemia (molecular biology: polymerized chain reaction [PCR]-amplification), tissue factor pathway inhibitor antibodies (aTFPI), interleukin 6 (IL-6), and vascular cell adhesion molecule-1 (VCAM-1). Endothelial function was determined by reactive hyperemia (pulse plethysmography).
  
  
  RESULTS
  In patients, prothrombin fragment 1 + 2, d-dimer, PAI-1, and fibrinogen were higher. Amplification of 121/122 primers (Trypanosoma cruzi) was positive in 45% of the patients. Patients presented higher values of aTFPI- immunoglobulin G (IgG; P < .05), aTFPI-IgM (P < .001), IL-6 (P = .004), and VCAM-1 (P = .00001). In both groups, endothelial function was preserved.
  
  
  CONCLUSIONS
  We found that asymptomatic patients with chronic Chagas disease presented a prothrombotic/inflammatory status. The fact that endothelial function is still preserved suggests that prothrombosis and inflammation are primarily implicated in the beginning of cardiovascular damage.
authors.affiliation: Haemostasis and Thrombosis Department, Zenón J. Santillán Hospital Health Center, Facultad de Medicina, Universidad Nacional de Tucumán, Tucumán, Argentina.
authors.forename: Ramón N
authors.initials: RN
authors.lastname: Herrera
authors.forename: Elba I
authors.initials: EI
authors.lastname: Díaz de Amaya
authors.forename: Rossana C
authors.initials: RC
authors.lastname: Pérez Aguilar
authors.forename: Claudio
authors.initials: C
authors.lastname: Joo Turoni
authors.forename: Rodrigo
authors.initials: R
authors.lastname: Marañón
authors.forename: Sofía G
authors.initials: SG
authors.lastname: Berman
authors.forename: Héctor L
authors.initials: HL
authors.lastname: Luciardi
authors.forename: Alfredo
authors.initials: A
authors.lastname: Coviello
authors.forename: María
authors.initials: M
authors.lastname: Peral de Bruno
mesh_terms: D000328:Adult; D001323:Autoantibodies / Q000097:blood; D014355:Chagas Disease / Q000097:blood* / Q000150:complications / Q000469:parasitology; D002908:Chronic Disease; D004730:Endothelium, Vascular / Q000378:metabolism / Q000469:parasitology; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism*; D006801:Humans; D006940:Hyperemia / Q000097:blood* / Q000469:parasitology; D007249:Inflammation / Q000097:blood / Q000469:parasitology; D015850:Interleukin-6 / Q000097:blood; D008074:Lipoproteins / Q000097:blood; D008297:Male; D018512:Parasitemia; D010446:Peptide Fragments / Q000097:blood*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D011516:Prothrombin; D013927:Thrombosis / Q000097:blood / Q000209:etiology / Q000469:parasitology; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D001323:Autoantibodies; D005338:Fibrin Fibrinogen Degradation Products; C508600:IL6 protein, human; D015850:Interleukin-6; D008074:Lipoproteins; D010446:Peptide Fragments; D017395:Plasminogen Activator Inhibitor 1; C051321:SERPINE1 protein, human; D019010:Vascular Cell Adhesion Molecule-1; C036309:fibrin fragment D; C051928:lipoprotein-associated coagulation inhibitor; C045879:prothrombin fragment 1.2; D011516:Prothrombin