To the Editor:
We were greatly interested in the results of a recent observational case series in which Schmidt described an inverse correlation between the admission paracetamol (acetaminophen) plasma concentration and the development of systemic anaphylactoid features, following treatment with a standard regime of intravenous N-acetylcystine (NAC).Citation1 This observation, as the author acknowledges, has previously been describedCitation2 but lacks a comprehensive mechanistic explanation.
We have observed that paracetamol is capable of modifying NAC-induced histamine secretion from both human peripheral blood mononucleocytes (PBMCs) and the non-IgE-expressing human mast cell line 1 (HMC-1) in vitro.Citation3 We suggest that our results both support Schmidt's finding and provide a degree of mechanistic insight.
Declaration of interest
The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References
- Schmidt LE. Identification of patients at risk of anaphylactoid reactions to N-acetylcysteine in the treatment of paracetamol overdose. Clin Toxicol (Philia) 2013; Early online:1–6.
- Waring WS, Stephen AF, Robinson OD, Dow MA, Pettie JM. Lower incidence of anaphylactoid reaction to N-acetylcysteine in patients with high acetaminophen concentrations after overdose. Clin Toxicol (Philia) 2008; 46:496–500.
- Coulson J, Thompson JP. Paracetamol (acetaminophen) attenuates in vitro mast cell and peripheral blood mononucleocyte cell histamine release induced by N-acetylcystine. Clin Toxicol (Philia) 2010; 48: 111–114.