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Related Concept Videos

Hypersensitivity Reactions: Cytolytic Reactions01:01

Hypersensitivity Reactions: Cytolytic Reactions

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Type II hypersensitivity involves IgG and IgM antibodies targeting cell surface antigens, leading to cell destruction. This can occur through complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), or acting as opsonins for phagocytosis. When excessive, these reactions cause significant tissue damage.Drug-induced hemolytic anemia is a common example, where drugs like penicillin or cephalosporins bind to red blood cells, forming drug-protein complexes. These complexes...
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Hypersensitivity Reactions: Immune-Complex Reactions01:19

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Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum...
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Continuous Manual Exchange Transfusion for Patients with Sickle Cell Disease: An Efficient Method to Avoid Iron Overload
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Hyperhemolysis Syndrome without Underlying Hematologic Disease.

Lauren Anne Eberly1, Diaa Osman1, Nathaniel Perryman Collins1

  • 1Department of Internal Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.

Case Reports in Hematology
|March 19, 2015
PubMed
Summary
This summary is machine-generated.

Hyperhemolysis, a severe transfusion reaction, can occur in patients without sickle cell disease. This case highlights delayed hemolytic transfusion reactions (DHTR) causing severe drops in hemoglobin and hematocrit after red blood cell transfusions.

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Area of Science:

  • Transfusion Medicine
  • Hematology
  • Immunology

Background:

  • Hyperhemolysis is a rare, life-threatening hemolytic transfusion reaction.
  • It is typically observed in patients with sickle cell disease.
  • This phenomenon is uncommon in patients without hemoglobinopathies.

Purpose of the Study:

  • To report a case of hyperhemolysis in a patient without hemoglobinopathy.
  • To investigate the underlying mechanism of hyperhemolysis in this context.
  • To highlight the potential for delayed hemolytic transfusion reactions (DHTR) to cause hyperhemolysis.

Main Methods:

  • A case report of a 55-year-old male trauma patient requiring multiple red blood cell transfusions.
  • Laboratory investigations including direct and indirect antiglobulin tests, antibody identification, and assessment of hemolysis markers.
  • Clinical monitoring of hemoglobin and hematocrit levels following transfusions.

Main Results:

  • The patient developed a positive direct antiglobulin test (DAT) for IgG and complement, and indirect antiglobulin test (IAT) for anti-Jka alloantibodies.
  • The patient's red blood cells (RBCs) were Jka negative, while transfused blood contained the Jka antigen, consistent with DHTR.
  • Subsequent transfusions precipitated further drops in hemoglobin and hematocrit, indicating hyperhemolysis, which resolved upon cessation of transfusions.

Conclusions:

  • Hyperhemolysis can occur in the setting of a delayed hemolytic transfusion reaction (DHTR).
  • This case demonstrates that hyperhemolysis is not exclusive to patients with hemoglobinopathies.
  • Careful monitoring and management are crucial for patients experiencing severe hemolytic reactions post-transfusion.