Editor,—The pathogenesis of thyroid eye disease is believed to derive from fibroblast stimulation by cytokines released by activated T lymphocytes. There is evidence of abnormal cell mediated autoimmunity and humoral autoimmunity resulting in infiltration of lymphocytes and adipocytes into the extraocular muscles.1 The success of therapeutic immunosuppressants (steroids/azathioprine/radiotherapy) strengthens this hypothesis. A single definitive cross reacting (thyroid/retro-orbital) autoantibody has not been identified. Zhang et alfound that sera from 50% of patients with thyroid eye disease reacted with an eye muscle specific protein of 55 kDa relative molecular weight.2 Pittsburgh data showed 67% patients with active Graves' ophthalmopathy have antibodies against a 67 kDa mitochondrial flavoprotein subunit although it has been subsequently found in 20% of controls.3 They also identified a 220 kDa cell membrane specific protein known as G2S specific to eye muscle and thyroid tissue, but antibodies to this have been demonstrated in both thyroid eye disease patients and normal people.4 No autoantibody has been demonstrated in every case and all lack specificity. Our case …