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Hypercoagulability biomarkers in Trypanosoma cruzi -infected patients

Journal: Thrombosis and Haemostasis
ISSN: 0340-6245
Issue: 2011: 106/4 (Oct) pp. 567–752
Pages: 617-623
Ahead of Print: ###MANUSCRIPT_aheadofprint###

Hypercoagulability biomarkers in Trypanosoma cruzi -infected patients

M.-J. Pinazo (1), D. Tàssies (2), J. Muñoz (1), R. Fisa (3), E. de Jesús Posada (1), J. Monteagudo (2), E. Ayala (4), M. Gállego (3), J.-C. Reverter (2), J. Gascon (1)

(1) Barcelona Centre for International Health Research (CRESIB), Hospital Clínic / IDIBAPS, Universitat de Barcelona, CIBER Epidemiología y Salud Pública (CIBERESP), Barcelona, Spain; (2) Hemotherapy and Hemostasis Department. Hospital Clínic, Barcelona, Spain; (3) Laboratori de Parasitologia, Facultat de Farmàcia, Universitat de Barcelona, Barcelona, Spain; (4) Health Biostatistics, Centre for International Health Research (CRESIB), Barcelona, Spain


prothrombin fragment 1+2, hypercoagulability, biomarkers, endogenous thrombin potential, Chagas Disease


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-selectinand 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.

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