Vancomycin-induced release of histamine from rat peritoneal mast cells and a rat basophil cell line (RBL-1)

Williams, Patricia D.; Laska, D. A.; Shetler, T; McGrath, John P.; White, Steve; Hoover, D. M.

doi:10.1007/bf01980877

Cited by 24 publications

(13 citation statements)

References 16 publications

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“…The underlying mechanism of red man syndrome has been found to be IgE-independent degranulation of mast cells brought about by vancomycin, with mast cell-derived histamine being a significant mediator of the observed adverse effect (11). As a re-sult, the established effectiveness of antihistamines in the prevention and treatment of red man syndrome (7), as observed in our patient, is not surprising.…”

supporting

confidence: 71%

Red Man Syndrome Adverse Reaction following Intravenous Infusion of Cefepime

Panos

Watson

Σαργιάνου

et al. 2012

Antimicrob Agents Chemother

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bWe report the first case of cefepime-induced "red-man syndrome," which appeared 30 min following drug infusion and was confirmed with a rechallenge test. This syndrome is classically associated with vancomycin infusion and is the result of non-IgE mediated mast cell degranulation. While this adverse effect can be easily managed with drug withdrawal and antihistamine administration, it is unknown whether it can be prevented with slower cefepime infusion and preinfusion antihistamines, as is the case with vancomycin.

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supporting

confidence: 71%

Red Man Syndrome Adverse Reaction following Intravenous Infusion of Cefepime

Panos

Watson

Σαργιάνου

et al. 2012

Antimicrob Agents Chemother

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“…This notion is based on the following experimental evidence: (1) VCM caused the syndrome in the majority (80%-90%) of healthy vol- unteers [19], (2) its severity depended on the plasma histamine concentration which was determined by the dose and infusion rate of VCM [8,[20][21][22], (3) VCM released histamine from isolated mast cells in vitro [23,24]. Thus, it seems important to investigate how VCM releases histamine from mast cells.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of vancomycin-induced histamine release from rat peritoneal mast cells

et al. 1993

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The mechanisms of vancomycin (VCM)-induced histamine release were studied with rat peritoneal mast cells. VCM (> 1 x 10(-3) M) released histamine from the isolated mast cells in a dose-dependent and noncytotoxic manner. In the absence of extracellular Ca2+, the histamine release was reduced markedly. When the intracellular Ca2+ was depleted, it was further decreased. The Fura-2-loaded single mast cells showed a biphasic increase in the intracellular Ca2+ concentration ([Ca2+]i) by VCM: the first transient and the second sustained components. In the absence of extracellular Ca2+, the transient component was unchanged, while the sustained component was eliminated completely. The IP3 content in the mast cells increased within 10 s after the application of VCM. These results suggest that VCM release histamine from rat peritoneal mast cells via an IP3 production and increase in [Ca2+]i.

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“…In rats vancomycin has been shown to directly degranulate mast cells [77,78]. Several studies have shown an increase in serum histamine levels associated with red man syndrome [79,80].…”

Section: Vancomycinmentioning

confidence: 99%

Nonallergic Drug Hypersensitivity Reactions

Farnam

Chang

Teuber

et al. 2012

Int Arch Allergy Immunol

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Background: Nonallergic drug hypersensitivities, also referred to as pseudoallergic or anaphylactoid reactions, have clinical manifestations that are often indistinguishable from allergic reactions. Methods: We performed a PubMed search using the terms ‘drug allergy, drug hypersensitivity, pseudoallergies, anaphylaxis and nonallergic drug reactions’ and reviewed 511 publications dated between 1970 and 2012. A total of 160 papers that were relevant to the most common nonallergic drug hypersensitivity reactions were selected for discussion. Results: Nonallergic drug hypersensitivities do not involve either IgE-mediated (type 1) or delayed (type 4) hypersensitivity. Nonallergic hypersensitivities are commonly referred to as pseudoallergic or idiosyncratic reactions. The common nonallergic drug hypersensitivities are secondary to chemotherapeutic drugs, radiocontrast agents, vancomycin, nonsteroidal anti-inflammatory agents, local anesthetic reactions and opiates. Protocols for skin testing of radiocontrast, nonsteroidal anti-inflammatory agents, local anesthetics and chemotherapeutic agents have been developed, though most have not been validated or standardized. Other diagnostic tests include in vitro-specific IgE tests, and the current ‘gold’ standard is usually an oral challenge or bronchoprovocation test. In the case of aspirin, even though it is not believed to be IgE-mediated, a ‘desensitization’ protocol has been developed and utilized successfully, although the mechanism of this desensitization is unclear. Conclusions: Diagnostic methods exist to distinguish allergic from nonallergic drug hypersensitivity reactions. The best option in nonallergic drug hypersensitivity is avoidance. If that is not possible, premedication protocols have been developed, although the success of premedication varies amongst drugs and patients.

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Vancomycin-induced release of histamine from rat peritoneal mast cells and a rat basophil cell line (RBL-1)

Cited by 24 publications

References 16 publications

Red Man Syndrome Adverse Reaction following Intravenous Infusion of Cefepime

Red Man Syndrome Adverse Reaction following Intravenous Infusion of Cefepime

Mechanisms of vancomycin-induced histamine release from rat peritoneal mast cells

Nonallergic Drug Hypersensitivity Reactions

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