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Platelet dysfunction-eosinophilia syndrome in parasitized Venezuelan children
Arlette Ruiz-Sáez1, Luz Núñez Sifontes, Rosa Feijoo
1Banco Municipal de Sangre del Distrito Capital, Caracas, Venezuela.
Insights
Intestinal parasites and eosinophilia caused platelet dysfunction and bleeding in children. Anti-parasite treatment resolved these hematologic and bleeding issues.
Area of Science:
- Pediatric Hematology
- Parasitology
- Immunology
Background:
- Platelet dysfunction can manifest with bleeding symptoms.
- Eosinophilia and intestinal parasites are common in certain pediatric populations.
- The interplay between parasitic infections, eosinophilia, and platelet function is not well understood.
Purpose of the Study:
- To investigate platelet function in children presenting with purpura and eosinophilia.
- To identify potential underlying causes, such as intestinal parasites.
- To evaluate the efficacy of anti-parasite therapy on hematologic parameters and bleeding manifestations.
Main Methods:
- Clinical evaluations and comprehensive hematologic testing were performed.
- Platelet function assays included aggregation studies with various agonists.
- Clotting studies, antibody assays, and stool parasite examinations were conducted.
Main Results:
- Six children presented with purpura, eosinophilia, and transient bleeding phenomena.
- All children harbored intestinal parasites and exhibited marked eosinophilia.
- Prolonged bleeding times and defective platelet aggregation were observed; anti-parasite therapy normalized these abnormalities.
Conclusions:
- Intestinal parasitism and associated eosinophilia can lead to acquired platelet dysfunction and bleeding in children.
- Anti-parasite therapy is effective in reversing these hematologic alterations.
- This study highlights a unique clinicopathologic combination in Latin American children.
Abstract:
Platelet dysfunction was detected in six children with purpura and eosinophilia. We conducted clinical evaluations, hematologic and platelet function tests, clotting studies (bleeding time, prothrombin time, partial thromboplastin time, thrombin time, factor XIII, factor VIII, and von Willebrand factor), assays for IgG and IgM antibodies to platelets, and a search for stool parasites. Mild bleeding phenomena (ecchymoses, petechiae, epistaxis, and gingival) were transient. All children showed intestinal parasites and marked eosinophilia (mean count = 2,615.2 cells/muL, 95% confidence interval = 1,259.6-5,429.8). Main abnormalities included prolonged bleeding times (50%) and defective aggregation with collagen (100%) adrenaline (66%), or ADP (66%). Antibodies to platelets were not detected. Anti-parasite therapy reversed the hemorrhagic manifestations and normalized eosinophil counts and platelet alterations. No relationship could be established between excess eosinophils, intensity of bleeding, or type and degree of platelet abnormalities. Thrombocytopathic features mimicked the intrinsic defect of storage pool disease. The possible pathogenic roles of eosinophilia and parasitism are reviewed. This is the first report of this pathologic combination in Latin American children.
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