Endocrine Abstracts

Graves’ orbitopathy or thyroid-associated orbitopathy is the most frequent extrathyreoidal manifestation of Graves’ disease with autoimmun mechanism which is still incompletely understood. The epidemiologic data provided evidence that sever, infiltrative orbitopathy is in 3–5% of patients, the quality of life is impaired even in individuals with mild form of this disease. The anti-TSH receptor and anti-eye muscle autoantibodies have been proved to be involved into pathomechanism of orbitopathy. The accumulation of glucose-aminoglycan and proinflammatory cytokines in retroorbital fibroblasts are responsible for enlargement of eye muscle and the retroorbital tissues resulting in inflammation of periorbital tissues and proptosis. Management of orbitopathy can be either medical and surgical. The medical therapy relies on the use of high dose systemic glucocorticoids or retroorbital irradiation, either alone or in combination. Recent randomized clinical trials have confirmed that glucocorticoids are more effective in intravenous than oral use. Retroorbital radiotherapy is an effective and safe therapy for orbitopathy and the side effects are avoidable. Somatostatin analogs are not so effective as it has been waited in previous studies. The high dose intravenous immunoglobulins and pentoxifylline therapy are favourable, however, prospective randomized trials have been not yet made. The manifestation of orbitopathy includes both unavoidable (genetic background) and avoidable (smoking, cytokine therapy, iodine exposure, radioiodine therapy) risk factors. The cigarette smoking must be given up for all patients with Graves’disease. Pentoxifylline therapy is advisable for all patients with Graves’ patients, especially for those who have genetic susceptibility to autoimmune disorders and not able to give up cigarette smoking.

The ocular symptoms of GO comprise signs of inflammation, diplopia and restricted eye movements, eyelid swelling and retraction and exophthalmos. Several treatment modalities are available. Inflammatory symptoms can be treated with steroids and/or retrobulbar irradiation, diplopia can be treated with extraocular muscle surgery, exophthalmos with orbital decompression and eyelid abnormalities with eyelid surgery.

Our current opinion regarding timing and choice of treatment will be presented. Basically, retrobulbar irradiation may be indicated in patients with severe inflammatory signs or severe eye motility restrictions. We find high-dose steroids only indicated when signs of “malignant” GO are present: either a decreased visual acuity, or keratitis. Orbital decompression is considered to be indicated either when steroids do not improve “malignant” GO, or when cosmetically disturbing exophthalmos is still present in a quiescent phase of the disease. Diplopia as well as eyelid abnormalities are treated in a quiescent phase, as final treatment modalities.