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[A case of hookworm infestation with dissociation values between FDP-E and FDP-D dimer].

R Nakagoshi1, H Oguchi, E Ishii

  • 1Division of Clinical Pathology, Nagano Children's Hospital, Minami-azumi-gun, Nagano-pref. 399-8288.

Rinsho Byori. the Japanese Journal of Clinical Pathology
|February 24, 2001
PubMed
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A rare case of accelerated fibrinogenolysis and fibrinolysis linked to hookworm (Necator Americanus) infestation in a child is detailed. This bleeding disorder involved unusual FDP-E and D-dimer assay discrepancies, suggesting a novel parasitic mechanism.

Area of Science:

  • Hematology
  • Parasitology
  • Biochemistry

Background:

  • Hookworm (Necator Americanus) infestation can cause bleeding disorders.
  • Platelet abnormalities, including morphological and functional changes, have been observed in parasitic infections.
  • Fibrinogenolysis and fibrinolysis are crucial components of the coagulation cascade, and their dysregulation can lead to bleeding.

Observation:

  • A five-year-old girl presented with bleeding tendency and transient platelet abnormalities.
  • The patient exhibited significantly accelerated fibrinogenolysis and/or fibrinolysis, evidenced by a marked discrepancy between FDP-E and D-dimer assay results.
  • D-dimer values were substantially lower than expected based on FDP-E levels during hospitalization.

Findings:

  • Accelerated fibrinogenolysis/fibrinolysis was likely induced by circulating protease(-like) agents produced by the hookworm.

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  • Limited involvement of plasmin and granulocyte elastase was suggested by enzyme-inhibitor complex analysis.
  • Other causes, such as blast- or tumor-associated proteases, were ruled out based on clinical presentation.

    • Implications:

    • This case highlights a rare complication of hookworm infestation, emphasizing the need for thorough parasitic evaluation in bleeding disorders.
    • The findings suggest a unique mechanism of coagulation system dysregulation by parasitic factors.
    • Further research into the specific parasitic agents and their mechanisms is warranted to understand the pathogenesis of bleeding and platelet abnormalities.