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Acute pre‐tibial myxoedema following radioiodine therapy for thyrotoxic Graves' disease
Author(s) -
Harvey R. D.,
Metcalfe R. A.,
Morteo C.,
Furmaniak W.,
Weetman A. P.,
Bevan J. S.
Publication year - 1995
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1995.tb02695.x
Subject(s) - medicine , trab , graves' disease , endocrinology , thyroglobulin , autoantibody , thyrotropin receptor , thyroid , thyroiditis , prednisolone , antibody , immunology
Summary A 54‐year‐old woman was treated with an oral dose of S55MBq of 131 I radioiodine for thyrotoxicosis. She had no clinically detectable extrathyroidal manifestations of Graves' disease at the time, but within two months developed moderately severe ophthalmopathy and very extensive thyroid dermopathy affecting her face, arms, hands and feet, in addition to the classic pre‐tlblal area. Although she developed mild post radioiodine hypothyroidism, this was detected at an early stage and its treatment had no effect on the extrathyroldal signs. Thyrotrophin receptor antibodies (TRAb) were positive before treatment (22% Inhibition of T S H binding in neat serum), rose to very high levels following radioiodine (97.6% Inhibition), and fell progressively over the following year during treatment with prednisolone. Thyroglobulln autoantibodies became detectable following radioiodine but thyroid peroxidase antibodies were undetectable throughout. Serum and purified IgG from blood samples obtained prior to steroid therapy and over the subsequent year were tested on a dermal fibroblast cell line in vitro for the stimulation of synthesis of glycosamlnoglycans, protein and DNA, but no increase in radiolabel incorporation was apparent for any sample when compared to controls. The temporal relation between the radioiodine and the acute onset of dermopathy and ophthalmopathy, together with the abrupt rise in TRAbs, indicates a probable causal association. However, the absence of In‐vitro fibroblast stimulation would suggest that the pathogenesis of Graves' dermopathy is not dependent solely on any simple humoral factor.