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Volume 96, Number 8 >
Pp. 402-403
Department of Endocrinology, West Middlesex University Hospital,
Isleworth, London TW7 6AF, UK
1 Department of Dermatology, West Middlesex University Hospital, Isleworth,
London TW7 6AF, UK
Correspondence to: Dr C M B Edwards, Endocrine Unit, St Mary's Hospital, Praed Street, London W2 1NY, UK E-mail: c.m.b.edwards{at}imperial.ac.uk
Chronic urticaria and angio-oedema (CUA) and subacute thyroiditis (SAT) are two conditions in which thyroid autoantibodies are commonly present. Coincidence of CUA and SAT in a single patient seems unusual.
CASE HISTORY
A man of 45 was referred having had four episodes of angio-oedema of the lips over the previous four months. On each occasion the symptoms had resolved over a few hours and at least once had been associated with an area of urticaria. None of the episodes had followed the use of any medications, a particular food, an infection or exposure to heat, cold or sun. He had been treated in the accident and emergency department twice with corticosteroids and antihistamines and once with adrenaline. On the last occasion, the findings had included an area of urticaria on his left upper arm and a fading area on his forearm together with slight angio-oedema of the upper lip; levels of C1-esterase inhibitor had been normal. Regular antihistamines were prescribed for CUA.
On the present occasion the patient said that for the previous month he had been experiencing myalgia, heat intolerance, sweating, palpitations, lassitude and neck pain. On examination he had a tender, firm, smooth goitre, fine tremor, sinus tachycardia of 106/min and lid lag. Plasma thyroxine was 37.8 pmol/L (reference range 10.3-23.2), thyroid stimulating hormone (TSH) < 0.1 mU/L (0.4-5.5), erythrocyte sedimentation rate (ESR) 28 mm/h (1-7), thyroglobulin (Tg) antibodies 7.1 U/mL (<1) and thyroid peroxidase (Tp) antibodies < 0.3 U/mL (<0.3). A thyroid scan revealed no uptake of 99m-pertechnetate. SAT was diagnosed but no treatment was initiated. Two weeks later his thyroxine had dropped to 28.2 pmol/L and he was symptomatically better; the thyroid was no longer palpable or tender and his pulse rate was 80/min, though he still had some action tremor and was heat intolerant. At eight weeks he became subclinically hypothyroid, with thyroxine 11.2 pmol/L and TSH 10.1 mU/L; he was still excessively tired. At five months he had a further episode of angio-oedema, at which time thyroxine was 9.7 pmol/L and TSH 3.1 mU/L; he had no symptoms related to his thyroid. One week later thyroxine was 11.9 pmol/L and TSH 3.5 mU/L. Twelve months after initial presentation he was clinically and biochemically euthyroid, with thyroxine 12 pmol/L, TSH 4.1 mU/L, ESR 2, thyroglobulin antibodies 1.2 U/mL and thyroid peroxidase antibodies < 0.3 U/mL. There had been no further episodes of angio-oedema or urticaria.
COMMENT
CUA is arbitrarily defined as episodes of urticaria and angio-oedema lasting longer than six weeks. Often no cause is found. The presence of thyroid antibodies in 12-29% of patients with CUA compared with 4% of the general population1-3 suggests an autoimmune origin in a subgroup of patients. In one study autoimmune thyroid disease was detected in 6% of these patients—a higher frequency than in controls.2 In addition, 30% of CUA patients have a circulating IgG antibody against the high affinity IgE receptor.4
Subacute thyroiditis typically presents with a brief thyrotoxic illness associated with a tender thyroid gland with no uptake on a thyroid scan. Often a longer hypothyroid phase ensues before resolution to normal thyroid function. The cause of SAT is likewise unknown, although at least 40% of cases seem to be postviral.5 10-20% of patients with SAT have moderately raised thyroglobulin antibodies, which drop when the disease resolves (as in the present case), again suggesting an autoimmune aetiology in a subgroup of patients. As far as we are aware there is no previous case report of CUA and SAT occurring simultaneously.
Thyroxine has been used in patients with CUA and thyroid autoimmunity,3 but this is not widely accepted.7 In the patient presented here, the short-lasting decrease in thyroxine associated with an episode of angio-oedema could represent the sick euthyroid syndrome or an interaction between the two disease processes, though more likely it simply reflects part of the recovery phase of thyroiditis. There is reason to think that the two diseases in this patient are linked by an autoimmune mechanism, but we cannot exclude the possibility that their association was fortuitous.
REFERENCES
-chain of Fc
RI; a selective
marker and pathogenetic factor for a distinct subset of chronic urticaria
patients? J Clin Invest1995; 96:2606
-12
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