European journal of anaesthesiology · 2025
MRGPRX2 Triggers rocuronium bromide-induced peri-operative phase allergic shock: A case report with case control study.
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Gao Zijun, Gong Ling, Li Lu, Song Lei, Xiao JianBo, Zhuang Jian, Wang Fang
Аннотация
BACKGROUND: Activation of mast cells and systemic histamine release are major side effects of intravenously administered neuromuscular blocking agents (NMBAs). Mas-related G protein-coupled receptor-X2 (MRGPRX2) plays a key role in mediating anaphylactoid reactions.
OBJECTIVE: To explore the mechanism of acute anaphylactic shock induced by muscle relaxants through the typical shock cases.
DESIGN: Case report and case control study.
PATIENTS: A 68-year-old male patient (80 kg) underwent surgical treatment in September 2023 and developed anaphylactic shock during anaesthesia induction.
METHODS: A trial was conducted to evaluate the patient who experienced anaphylactic shock during the peri-operative period in comparison to control patients. The levels of MRGPRX2 and total immunoglobulin E (IgE) were measured in patient plasma, along with allergic mediators such as histamine and tryptase. Mast cell activation assay was performed to assess degranulation effectiveness by measuring β-hexosaminidase, histamine release, and calcium influx. Additionally, mast cell activation by peri-operative drugs was investigated. Local inflammatory experiments were conducted in a mouse model to evaluate rocuronium bromide-induced allergic reactions. Finally, MRGPRB2-CKO mice and siRNA silencing were used to elucidate the mechanism of rocuronium-induced anaphylactic shock.
RESULTS: Plasma analysis of the patient experiencing anaphylaxis revealed normal total IgE levels (38.4 IU ml -1 ) but significantly elevated histamine concentration (53.78 ng ml -1 ). The MRGPRX2 concentration (52.22 ng ml -1 ) in this patient was markedly higher than the negative control group (16.40 ng ml -1 ). Serum-activated mast cell assays demonstrated that the anaphylaxis patient's plasma induced a significant release of β-hexosaminidase, calcium, and histamine from mast cells (significantly higher than the histamine levels naturally present in the plasma). Drug-activated mast cell experiments confirmed that rocuronium bromide triggered dose-dependent mast cell activation, leading to MCP-1, histamine, and calcium release. Local paw oedema experiments in mice further validated that rocuronium bromide induced local allergic reactions. Using MRGPRB2-CKO mice and siRNA silencing, we determined that rocuronium bromide-induced anaphylactic shock was mediated through MRGPRX2 activation, resulting in mast cell degranulation.
CONCLUSION: This study highlights the critical role of MRGPRX2 in rocuronium bromide-induced anaphylactic shock. In vitro diagnosis of MRGPRX2 levels may provide new criteria for reducing intra-operative risks.
TRIAL REGISTRATION: The clinical trial was registered at the China Clinical Trial Registration Center (Registration Number: ChiCTR2300077364).
OBJECTIVE: To explore the mechanism of acute anaphylactic shock induced by muscle relaxants through the typical shock cases.
DESIGN: Case report and case control study.
PATIENTS: A 68-year-old male patient (80 kg) underwent surgical treatment in September 2023 and developed anaphylactic shock during anaesthesia induction.
METHODS: A trial was conducted to evaluate the patient who experienced anaphylactic shock during the peri-operative period in comparison to control patients. The levels of MRGPRX2 and total immunoglobulin E (IgE) were measured in patient plasma, along with allergic mediators such as histamine and tryptase. Mast cell activation assay was performed to assess degranulation effectiveness by measuring β-hexosaminidase, histamine release, and calcium influx. Additionally, mast cell activation by peri-operative drugs was investigated. Local inflammatory experiments were conducted in a mouse model to evaluate rocuronium bromide-induced allergic reactions. Finally, MRGPRB2-CKO mice and siRNA silencing were used to elucidate the mechanism of rocuronium-induced anaphylactic shock.
RESULTS: Plasma analysis of the patient experiencing anaphylaxis revealed normal total IgE levels (38.4 IU ml -1 ) but significantly elevated histamine concentration (53.78 ng ml -1 ). The MRGPRX2 concentration (52.22 ng ml -1 ) in this patient was markedly higher than the negative control group (16.40 ng ml -1 ). Serum-activated mast cell assays demonstrated that the anaphylaxis patient's plasma induced a significant release of β-hexosaminidase, calcium, and histamine from mast cells (significantly higher than the histamine levels naturally present in the plasma). Drug-activated mast cell experiments confirmed that rocuronium bromide triggered dose-dependent mast cell activation, leading to MCP-1, histamine, and calcium release. Local paw oedema experiments in mice further validated that rocuronium bromide induced local allergic reactions. Using MRGPRB2-CKO mice and siRNA silencing, we determined that rocuronium bromide-induced anaphylactic shock was mediated through MRGPRX2 activation, resulting in mast cell degranulation.
CONCLUSION: This study highlights the critical role of MRGPRX2 in rocuronium bromide-induced anaphylactic shock. In vitro diagnosis of MRGPRX2 levels may provide new criteria for reducing intra-operative risks.
TRIAL REGISTRATION: The clinical trial was registered at the China Clinical Trial Registration Center (Registration Number: ChiCTR2300077364).