ONCOLOGY Vol 23 No 2_Suppl_1

In recent years, both the cost and efficiency of medical care have emerged as important considerations and areas of research. These considerations are of particular importance in the outpatient community oncology setting, where the demands for clinical productivity and evidence for quality and effectiveness are increasing amidst an evolving reimbursement system.

Oncology clinicians administer monoclonal antibodies (MoAbs) as part of the armamentarium against cancer. Nurses are skilled in the management of general treatment-related symptoms and are knowledgeable regarding the care of patients receiving these therapies. New therapies require expanded knowledge bases regarding unique and selective side effects, such as those seen with targeted therapy agents.

Infusion reactions are a well-known phenomenon in cancer treatment, occurring with both cytotoxic and biologic agents. The severity, symptomatology, and time course of these hypersensitivity events differ significantly among agents, ranging from simple cutaneous manifestations and urticaria to life-threatening hypotension, bronchospasm, and vascular collapse. They can occur despite adequate preparation and premedication.

The use of engineered monoclonal antibodies as antineoplastic therapy has been a significant advance within the past 15 years. These agents target various receptors and ligands required for the proliferation, survival, or maintenance of angiogenesis of tumors. Currently there are several agents approved by the US Food and Drug Administration for clinical use in solid tumors. Bevacizumab (Avastin) is a humanized monoclonal antibody that targets the vascular endothelial growth factor (VEGF) and inhibits angiogenesis, and is currently approved for the treatment of colorectal, lung, and breast cancer (Avastin package insert, 2008). Trastuzumab (Herceptin) inhibits the HER2/neu receptor, and is utilized in both the adjuvant and palliative settings in breast cancer (Herceptin package insert, 2008).

Infusion reactions (IRs) can be broadly categorized by their immunologic mechanism. Anaphylaxis is a systemic, immediate hypersensitivity reaction mediated by factors released from interactions between immunoglobulin E (IgE) and mast cells that produce an antigen-antibody reaction.[1] Anaphylactoid reactions can be differentiated from anaphlaxis by the fact that they are not IgE-mediated but rather cytokine-mediated.

The phenomenon of anaphylaxis was discovered by Portier and Richet in 1903.[1,2] They injected dogs with toxins from sea anemone with the intent of generating protective antibodies. Unexpectedly, they found that certain dogs became ill with a rapid heartbeat and collapse. Because this syndrome was the precise opposite of protection or prophylaxis, they termed it anaphylaxis.