Abstract
Imagine this scenario: a 14-year-old Native American boy is being treated with vancomycin for osteomyelitis caused by methicillin-resistant Staphylococcus aureus . During the first infusion, he develops diffuse flushing, which resolves with a slower infusion rate and administration of diphenhydramine. During bedside rounds the next morning, the medical student managing the patient reports that overnight the patient developed red man syndrome. An uncomfortable pause follows as the medical team recognizes the awkwardness of the phrase and as the patient and his family try to understand what message is being conveyed by “red man syndrome”: a term that would seem, erroneously, to invoke race as a key component to its pathophysiology. Providing some historical context is important. In 1959, an article entitled “An anaphylactoid reaction to vancomycin” was published in the Journal of the American Medical Association .1 The pathophysiology of this reaction was hypothesized to involve vancomycin-induced release of histamine from mast cells. Because of this and other untoward effects (eg, oto- and renal toxicity), vancomycin (a name derived from the word vanquish), was not extensively used until the proliferation of methicillin-resistant S aureus occurred in the 1970s and 80s.2 Sometime during this …
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