title: Hypercoagulability biomarkers in Trypanosoma cruzi -infected patients.
abstract: There is a current controversy over the hypothesis that a number of thromboembolic events could be related to hypercoagulable state in patients with chronic Chagas disease. This study was designed to determine whether a prothrombotic state existed in chronic Trypanosoma cruzi-infected patients and, if so, to describe its evolution after treatment with Benznidazole. Twenty-five patients with chronic Chagas disease and 18 controls were evaluated. The markers used were prothrombin time, activated partial thromboplastin time, fibrinogen, antithrombin, plasminogen, protein C, total protein S, free protein S, factor VIII, D-dimer, activated factor VIIa, tissue-type plasminogen activator inhibitor-1, prothrombin fragment 1+2 (F₁+₂), plasmin-antiplasmin complexes, soluble P-selectin and endogenous thrombin potential (ETP). Despite statistically significant differences between cases and controls in several markers, only ETP (which quantifies the ability of plasma to generate thrombin when activated through tissue factor addition) (p<0.0001) and F₁+₂ (a marker of thrombin generation in vivo) (p<0.0001) showed values outside the normal levels in patients compared with controls. Similar results were obtained in these markers six months after treatment in the cohort of cases (p<0.0008 and p<0.004, respectively). These results may be relevant in clinical practice. Though current treatment for Chagas disease is still controversial, if it were considered as a thromboembolic risk factor the antiparasitic treatment strategy could be reinforced. The results also support further research on haemostasis parameters as candidates for early surrogate biomarkers of cure or progression of Chagas disease.
authors.affiliation: Barcelona Centre for International Health Research (CRESIB), Hospital Clínic/IDIBAPS, Universitat de Barcelona, CIBER Epidemiología y Salud Pública (CIBERESP), Roselló, 132. 4th, 08032 Barcelona, Spain. mpinazo@clinic.ub.es
authors.forename: María-Jesús
authors.initials: MJ
authors.lastname: Pinazo
authors.forename: Dolors
authors.initials: D
authors.lastname: Tàssies
authors.forename: José
authors.initials: J
authors.lastname: Muñoz
authors.forename: Roser
authors.initials: R
authors.lastname: Fisa
authors.forename: Elizabeth de Jesús
authors.initials: Ede J
authors.lastname: Posada
authors.forename: Juan
authors.initials: J
authors.lastname: Monteagudo
authors.forename: Edgar
authors.initials: E
authors.lastname: Ayala
authors.forename: Montserrat
authors.initials: M
authors.lastname: Gállego
authors.forename: Joan-Carles
authors.initials: JC
authors.lastname: Reverter
authors.forename: Joaquim
authors.initials: J
authors.lastname: Gascon
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000378:metabolism*; D054316:Biomarkers, Pharmacological / Q000378:metabolism*; D014355:Chagas Disease / Q000175:diagnosis* / Q000188:drug therapy / Q000503:physiopathology; D002908:Chronic Disease; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D009593:Nitroimidazoles / Q000627:therapeutic use; D011516:Prothrombin / Q000737:chemistry / Q000378:metabolism*; D012306:Risk; D013917:Thrombin / Q000737:chemistry / Q000378:metabolism*; D013923:Thromboembolism; D019851:Thrombophilia; D014349:Trypanosoma cruzi / Q000472:pathogenicity
chemical_list: D015415:Biomarkers; D054316:Biomarkers, Pharmacological; D009593:Nitroimidazoles; D011516:Prothrombin; D013917:Thrombin; C009999:benzonidazole