LETTERS TO THE EDITOR

eye disease associated with athyria 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 lym-phocytes and adipocytes into the extraocular muscles.1 The success of therapeutic immuno-suppressants (steroids/azathioprine/radiothe-rapy) strengthens this hypothesis. A single definitive cross reacting (thyroid/retro-orbital) autoantibody has not been identified. Zhang et al found 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 anti-bodies against a 67 kDa mitochondrial flavo-protein subunit although it has been subse-quently 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 demonstrates that whatever the autoimmune process may be, the presence of normal thyroid tissue or autoim-mune disease aZicted thyroid is not essential at the time of onset and development of clinical disease. CASE REPORT At age 30, this woman underwent partial thy-roidectomy for papillary thyroid cancer. At 36 years she underwent radioactive ablation (2.2 GBq iodine-131) of the residuum for sus-pected recurrence. At this time there was no evidence of orbital disease. At 70 years, she presented with 6 months’ diplopia and “puVy, gritty ” eyes. She was clinically euthyroid on thyroxine, with bilateral proptosis (worse on the left) with conjunctival congestion, periorbital oedema, a divergent strabismus (Fig 1) and limitation of upward gaze. A clinical diagnosis of thyroid eye disease was made, which was confirmed by orbital computed tomography (Fig 2). Both her sister and paternal grandmother had goitres without thyroid eye disease. Her sister had thyroid microsomal antibodies