A case of eperisone hydrochloride-induced anaphylaxis: A true type I reaction?

Centrally acting muscle relaxants (CMRs) are often used to alleviate musculoskeletal pain. Among them, eperisone hydrochloride is the most popular in Japan.1 Although it is a welltolerated drug,2 allergic reactions to eperisone have been reported, most of which are anaphylactic or urticarial reactions.1 Acute generalized exanthematous pustulosis3 and fixed drug eruption4 are reported rare manifestations of eperisone-induced drug eruption. Tolperisone hydrochloride, an analog of eperisone hydrochloride, is another CMR often used in European countries. Ribi et al. reviewed the adverse effects of tolperisone hydrochloride; almost half of the adverse effects were immediate-type hypersensitivity reactions.5 To date, reported CMR-related drug eruptions have mainly been immediate-type hypersensitivity reactions. However, it is not clear whether this hypersensitivity is IgE mediated, a so-called “true” type I allergic reaction. Here, we report a case of eperisone-induced anaphylaxis in which skin prick test (SPT) and basophil activation test (BAT) showed negative results. An oral challenge test was the most reliable procedure for diagnosing eperisone-induced immediate-type hypersensitivity. A 64-year-old woman was referred to our dermatology department to determine potential allergens causing anaphylaxis. She had taken eperisone hydrochloride and loxoprofen sodium, which resulted in urticaria, throat swelling, and loss of consciousness. She was taken to the emergency room, where she responded well to administration of corticosteroids. The patient had a history of low-back pain for which she was prescribed eperisone hydrochloride and loxoprofen sodium. She also had a history of bronchial asthma but not food allergy. SPT was negative for all tested drugs, including eperisone hydrochloride and loxoprofen sodium. Oral challenge test was negative for non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin (up to 500 mg), loxoprofen sodium (up to 60 mg), and paracetamol (up to 400 mg), indicating that the patient did not have aspirin-sensitive urticaria. Oral administration of 0.5e5 mg of eperisone induced slight itchiness on the palms. About 90 min after oral administration of 16 mg of eperisone, the patient developed general pruritus and swelling of the face, tongue, and palms (Fig. 1). Thus, she was diagnosed with eperisone hydrochloride-induced anaphylaxis. To investigate whether eperisone hydrochloride itself directly induced basophil activation, we performed a BAT.6 Contrary to