Hypersensitivity reactions from antineoplastic agents

Abstract

Antitumor drugs, like any other therapeutic agent, have the ability to incite hypersensitivity reactions. Certain of such drugs (e.g., L-asparaginase and taxol) cause reactions with great enough frequency to be a major impediment to repetitive use of the drug. Very few antitumor drugs have not had at least one reported instance of causing a hypersensitivity reaction. Most reactions are of the type I category in the Gell and Coombs classification, but there also are instances of types II, III, and IV reactions caused by many of the antineoplastic agents. The mechanisms of such reactions have been poorly evaluated in many reports. In analyzing a hypersensitivity reaction in a patient being treated for cancer, one should document that the antitumor drug is indeed the offender, and not an ancillary drug or a formulation product that is being used. There are many tests that evaluate the source and mechanism of hypersensitivity reactions. This article reviews the current information on hypersensitivity reactions to antineoplastic drugs and provides a logical approach for their assessment.

Sesquiterpenoids from Common Ragweed (Ambrosia artemisiifolia L.), an Invasive Biological Polluter

“…The presence of plant secondary metabolites in pollen has been suggested to explain violent allergic reactions to phytochemicals,36 as exemplified by the sudden death of the very first patient treated with the anticancer drug Taxol 37. Although the scarcity of the material at disposal did not allow the identification of any specific constituents, a pollen extract from A. artemisiifolia showed the presence of a high concentration of compounds having carbonyl conjugated exomethylenes (see Supporting Information).…”

Fatal outcome of a hypersensitivity reaction to paclitaxel: a critical review of premedication regimens

“…The aetiology of paclitaxel-associated HSR is multifactorial and several mechanisms have been postulated: (A) an IgE-mediated mast-cell degranulation induced by paclitaxel (Weiss et al, 1990) or Cremophor EL (Dye and Watkins, 1980;Weiss and Baker, 1987); (B) a non-IgE-mediated idiosyncratic mast-cell degranulation by paclitaxel or by Cremophor EL (Gelderblom et al, 2001) and (C) complement activation (Szebeni et al, 2001). The rapid and overwhelming onset of the HSR as observed in our patient is not compatible with the natural course of an IgE hypersensitivity reaction and points towards one of the two other mechanisms.…”

Drug-Induced Anaphylaxis

“…These are organic structures that require protein binding and multivalence to induce an immunological response [1]. We will also omit anti-neoplastic drugs and direct the readers to reviews in the literature dealing with this problem [13]. Given that over 80 % of anaphylactic drug reactions occur in ambulatory settings [14], we will therefore focus on the most relevant drugs involved: beta-lactam antibiotics (BLs) and non-steroidal anti-inflammatory drugs (NSAIDs).…”