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Dr Dunkley and Dr Jawad1 propose that a patient's flare of chronic urticaria and angio-oedema (CUA) was related to a reduction in thyroxine dosage. We have seen a patient in whom CUA was apparently exacerbated by treatment of hyperthyroidism with carbimazole. The patient, a woman of 50, first consulted us after three weeks of generalized urticaria. She had no obvious precipitating factors and was taking no medications. Thirteen months previously an episode of acute urticaria had been precipitated by a viral illness. With a short course of prednisolone this had resolved completely within three weeks. Autoimmune serology and thyroid function tests had been normal at that time. The present episode of urticaria was controlled with cyproheptadine 4 mg four times a day and cimetidine 400 mg four times a day. A routine blood test revealed FT4 27.1 pmol/L (normal range 9.0-26.0), TSH < 0.02 m IU/L (0.3-5.5), T3 28.8 nmol/L (0.8-2.5); thyroid autoantibodies were within normal range. For this biochemical hyperthyroidism she was started on carbimazole 20 mg twice daily. After three weeks she returned with generalized urticaria and angio-oedema. Sulfasalazine 1 g twice daily was added to the treatment and her rash resolved completely within days; four months later she is still in remission, taking low doses of cyproheptadine and cimetidine daily. She has stopped taking sulfasalazine. With thyroid function approaching normal, carbimazole has been reduced to 15 mg daily. We postulate that the flare of CUA was due to reduction of endogenous thyroxine by carbimazole. The possible role of endogenous thyroxine in suppressing urticaria deserves further investigation.