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Related Concept Videos

Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

266
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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Drug Toxicity: Allergic Reactions01:30

Drug Toxicity: Allergic Reactions

206
Drug-related allergies are immune-mediated responses triggered by the administration of pharmacological agents. These hypersensitivity reactions are classified based on the immune mechanisms involved. The four primary types—Type I, II, III, and IV—are mediated by different immunological pathways and exhibit distinct clinical manifestations.Type I Hypersensitivity/ IgE-Mediated Reactions: Immunoglobulin E (IgE) immediately mediates Type I hypersensitivity reactions. Upon initial...
206

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Desensitization protocol for rituximab-induced serum sickness.

Merritt L Fajt, Andrej A Petrov1

  • 1UPMC Montefiore Hospital - NW628, 3459 Fifth Ave Pittsburgh, PA 15213, USA. petrovaa@upmc.edu.

Current Drug Safety
|May 28, 2014
PubMed
Summary

Successful rituximab desensitization is reported for a patient experiencing serum sickness, a delayed hypersensitivity reaction. This approach allowed for continued treatment and remission of gastric lymphoma.

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Area of Science:

  • Rheumatology
  • Oncology
  • Clinical Immunology

Background:

  • Rituximab, an anti-CD20 monoclonal antibody, treats rheumatologic and hematologic conditions.
  • Serum sickness, a Type III hypersensitivity reaction, is a known adverse effect of rituximab.
  • Traditional drug desensitization targets Type I IgE-mediated reactions.

Observation:

  • A patient with Sjogren's syndrome and gastric MALT lymphoma developed serum sickness 72 hours post-rituximab infusion.
  • The patient's MALT progressed after rituximab discontinuation.
  • A rapid 12-step intravenous rituximab desensitization protocol was administered.

Findings:

  • The rituximab desensitization was successful, with no recurrence of serum sickness.
  • Following four desensitization treatments, the patient achieved gastric MALT remission.
  • The patient received 25 subsequent maintenance rituximab doses quarterly without complications.

Implications:

  • This is the first documented case of successful rituximab desensitization for a delayed hypersensitivity reaction (serum sickness).
  • Rituximab desensitization may offer a viable treatment option for patients developing delayed hypersensitivity reactions to rituximab.
  • This protocol enables continued rituximab therapy for conditions like MALT lymphoma, even in the presence of hypersensitivity.