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Hypercoagulability biomarkers in Trypanosoma cruzi -infected patients
María-Jesús Pinazo1, Dolors Tàssies, José Muñoz
1Barcelona 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
Insights
Chronic Chagas disease patients exhibit a prothrombotic state, indicated by elevated thrombin generation markers. Treatment with Benznidazole did not significantly alter these markers, suggesting ongoing thromboembolic risk.
Area of Science:
- Hematology
- Infectious Diseases
- Cardiovascular Medicine
Background:
- Chronic Chagas disease is linked to a controversial hypothesis of hypercoagulable states.
- Thromboembolic events are a concern in patients with chronic Trypanosoma cruzi infection.
Purpose of the Study:
- To investigate the existence of a prothrombotic state in chronic Chagas disease patients.
- To evaluate the evolution of this prothrombotic state after Benznidazole treatment.
Main Methods:
- Evaluated 25 chronic Chagas disease patients and 18 controls.
- Assessed multiple hemostasis markers, including endogenous thrombin potential (ETP) and prothrombin fragment 1+2 (F₁+₂).
Main Results:
- Patients showed significantly higher ETP and F₁+₂ levels compared to controls.
- These elevated markers persisted six months post-Benznidazole treatment.
- Several other coagulation markers did not show significant differences between groups.
Conclusions:
- Chronic Chagas disease is associated with a persistent prothrombotic state.
- Benznidazole treatment did not resolve the observed hypercoagulability.
- Hemostasis parameters may serve as biomarkers for Chagas disease progression or treatment efficacy.
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.
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