Bee venom allergy immunotherapy/omalizumab
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Idiopathic non-clonal mast cell activation syndrome, pre-syncopal symptoms and bradycardia: case report A 48-year-old man developed idiopathic non-clonal mast cell activation syndrome (MCAS) during treatment with Bee venom allergy immunotherapy. Additionally, in early 50’s he developed pre-syncopal symptoms and bradycardia during treatment with omalizumab for MCAS. The man presented in January 2011 after a road traffic accident, which occurred after anaphylaxis with complete loss of consciousness while driving 15 minutes after being stung by a bee. On presentation, bee venom specific IgE was found to be 60.5 kU/L. He started receiving treatment with SC injection bee venom allergy immunotherapy [Bee venom allergen immunotherapy] in February 2011. Six months into the bee venom allergy immunotherapy, at a maintenance dose of 100µg, he experienced an allergic reaction. Within few minutes of receiving bee venom allergy immunotherapy injection, symptoms including generalised malaise, lightheadedness, altered vision and the fear of impending collapse were observed. The man’s therapy with bee venom allergy immunotherapy was stopped, and he received treatment with epinephrine [adrenaline], resulting in the resolution of symptoms. The man’s therapy with SC bee venom allergy immunotherapy was restarted in September 2011 and continued at 100 µg/month till the beginning of August 2013. However, he experienced an another episode of allergic reaction. He was pale and unwell with lightheadedness and impending loss of consciousness. His therapy with bee venom allergy immunotherapy was stopped, and he received treatment with epinephrine for anaphylaxis, which resulted in the improvement; however, the reaction continued for 30 minutes despite receiving a second epinephrine injection 20 minutes later. He presented to the emergency department and received further treatment with hydrocortisone and IV fluids. He was discharged after a 5h observation period. After one week, he was admitted to the hospital for persistent symptoms of impeding collapse and light-headedness. He started receiving cetirizine and prednisolone. Dermatological examination ruled out cutaneous mastocytoma. Additionally, he received treatment with montelukast in combination with cetirizine. Fexofenadine was started after discharge in combination with prednisolone. Subsequently, prednisolone was weaned over 6 months and stopped in April 2014. However, his symptoms progressed despite treatment. He further experienced mental clouding, early morning wakening and poor concentration. By July 2014, he reported daily symptoms of impending collapse especially with exercise and a decreased tolerance to caffeine and red wine. He also consulted the clinical psychiatrist for the management of anxiety and depressive symptoms. The combination of these symptoms persistently increased serum mast cell tryptase (MCT). Therefore, a diagnosis of MCAS was made. He was advised to avoid food rich in tyramine and histamine, along with strenuous exercise. Subsequently, minimal symptomatic
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