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The pathogenesis of bromoderma is still under debate. Some authors have proposed that halogenodermas belong to the group of hypersensitivity reactions. 1,3,5 However, accumulation of the halogenide seems to play a pivotal role leading to a rather toxic inflammatory reaction provoked by the elimination of bromine through the eccrine and sebaceous glands. 1,3,5 Indeed, bromides show slow elimination rates and both bromoderma and bromism may persist for weeks after drug withdrawal. 9 Diagnosis of bromoderma is primarily based on the clinical features and history of bromine intake. 1,2,5 Histology is rather unspecific but helpful in excluding other differential diagnoses. However, pseudo-hyperchloraemia is a typical laboratory finding, which is due to the method used for serum chloride assessment. Since the electric charge of chloride and bromide is the same, enhanced serum bromide is detected by an increase in chloride. 5 Treatment mainly relies on the withdrawal of the offending drug. 2,4,6 In addition, diuretics, such as furosemide and ethacrynic acid, could be administered because of their activity in accelerating bromide excretion through the kidneys. 9,10 Local therapies include topical corticosteroids and antiseptic measurements. 2,4,6 Our case highlights that bromoderma has still to be considered as a side effect of therapeutic interventions utilizing bromide-containing agents. Funding sources: None.