Thyroid function in chronic urticaria and angio-oedema
Authors: L Dunkley, A S M Jawad
Journal: Journal of the Royal Society of Medicine (2003)

In a case report (August 2003, JRSM1) Dr Edwards and colleagues discuss the relation between subacute thyroiditis and chronic urticaria and angio-oedema (CUA).1 Here we describe a case that illustrates the possible role of thyroxine in suppressing CUA, as previously postulated.

A woman of 52 was seen at another department in August 2002 with widespread arthralgia (large joints), shoulder girdle stiffness and early morning stiffness. In September 2002 she also noticed dry eyes and mouth, associated with sweatiness. Her previous history included CUA diagnosed in 1988, and hypothyroidism requiring thyroxine 150 μg daily since the age of 17. Her menstrual periods had stopped eleven months earlier. The relevant findings were: Schirmer's tear test normal (wet); erythrocyte sedimentation rate 22 mm/h, C-reactive protein 11 mg/L, autoimmune screen negative, alkaline phosphatase 136 U/L (normal 39-117), TSH <0.06 mU/L (0.5-4.7), fT4 28.3 pmol/L (9.1-23.9), fT3 1.91 nmol/L (1.20-2.20). She was started on prednisolone 5 mg twice daily and diclofenac/misoprostol 50 mg/200 mg twice daily in October 2002 for a presumed inflammatory musculoskeletal condition. On review in February 2003 her symptoms had not resolved. Thyroid peroxidase antibodies were absent. As the TSH was persistently suppressed (<0.01 mU/L) and fT4 was raised (18-30 pmol/L), the thyroxine dose was reduced from 150 μg to 125 μg daily in February, then to 100 μg in April and 75 μg in May 2003. The prednisolone dose was also reduced every 2-3 weeks by 1 mg/day between March and May to a maintenance dose of 5 mg/day.

In late April, having been urticaria-free for 15 years, the patient developed generalized urticaria and angio-oedema which persisted for 6 weeks and required antihistamine treatment. There was a further episode of CUA in June.

The dose of diclofenac/misoprostol was not changed from October 2002 until May 2003 when it was stopped because of an abnormal liver function test. At the time of writing (September) the patient has had no further episodes of urticaria/angio-oedema and her daily dose of thyroxine has been 75 μg since mid-May. Current TSH is 2.0 mU/L, fT4 16.4 pmol/L.

We propose that this patient's flare of CUA was related to the reduction in thyroxine dose. Previously the condition may have been suppressed by the excessive dosage. However, we cannot exclude the possibility that the reduction of her prednisolone dose was an aetiological factor, though this was very gradual. Furthermore, the treatment with diclofenac, well known to precipitate urticaria, may be relevant—though she took this drug for seven months before the return of CUA and had not taken it for 4 weeks before the second episode.

If we postulate that each reduction in thyroxine dose is followed by a 3-4 week latent period before reactivation of CUA, then the final episode of urticaria in June could be explained by the dosage alteration in May, and the April/May flare by the dosage alteration in mid-March and early April. The possible role of thyroxine in suppressing CUA requires further investigation.