Primary prevention aims at keeping the disease from occurring at all by removing risk factors. Secondary prevention is directed at early detection of disease, when the disease is still asymptomatic and when early treatment can stop the disease from progressing. Tertiary prevention refers to those clinical activities that prevent further deterioration or reduce complications after disease has declared itself. When applying the concept of prevention to TED, there is a problem with secondary prevention because there are no good specific serum markers for TED that would allow an early diagnosis of subclinical TED. As a group, such patients have slightly higher proptosis values than healthy subjects, their intraocular pressure on upgaze is abnormally increased in 61%82% and their extraocular eye muscles are found to be enlarged on orbital ultrasound or CT scan in 70%100%. Risk factors for occurrence or progression of TED have been partially identified (non-preventable: genetic, age, sex. Preventable: cigarette smoking, thyroid dysfunction, radioiodine treatment), but the list is probably much longer, and efforts of future research should be aimed at identifying most of them. For non-preventable risk factors obviously little can be done. However, several reports have documented a close association between cigarette smoking and TED. Furthermore, smokers tend to have more severe ocular involvement than non-smokers, although there is no significant association between the degree of tobacco consumption and severity of the ophthalmopathy.
Hyperthyroidism seems to influence the clinical course of eye disease and several studies have shown that careful control of hyperthyroidism may be associated with a more favourable outcome of the ophthalmopathy. Finally, it is widely accepted that radioiodine treatment carries a small but definite risk of causing progression of eye disease. The exacerbation of the ophthalmopathy does not take place in patients with concomitantly treated with glucocorticoids.