Glucocorticoids are the most commonly used immunosuppressive agents for the treatment of active severe thyroid-related ophthalmopathy, and have achieved excellent success rates since their use began in the mid-nineteenth century. Glucocorticoids may suppress the immune response and control inflammation through multiple pathways, including: interference with T and B cell function, reduction in monocyte and macrophage recruitment, inhibition of immune mediator release, and reduction in glycosaminoglycan synthesis and release.
Patients with moderate to severe thyroid-related ophthalmopathy should be given hormonal therapy if acute and severe orbital inflammation and crowding are present. In response to significant congestion and periorbital edema, systemic administration of glucocorticoids often provides dramatic improvement in acute symptoms and health-related life treatment. Glucocorticosteroids have been shown to be effective in improving soft tissue edema, visual acuity, and eye movements, but the therapeutic effect of ocular proptosis is indeed limited.
During the active phase of the extraocular muscle inflammatory response, early suppression of orbital inflammation with glucocorticoids may limit damage to the extraocular muscles and reduce the risk of diplopia due to inflammatory muscle fibrosis. If severe thyroid-related ophthalmopathy presents as a vision threat, glucocorticoids may be used as a first-line treatment option. Glucocorticoid therapy is usually most effective when given early in the disease.
Initial treatment with oral prednisolone is typically 1 mg per kg of body weight per day, which can be tapered over the following weeks based on treatment response and monitored by ophthalmologic examinations at times. The rate of hormone dose reduction depends on the clinical response, and a dose reduction of 5 to 10 mg per week is usually a safe guideline. However, many patients experience relapses during or after the end of hormone tapering and require long-term treatment.
Smoking can reduce the effectiveness of glucocorticoid therapy. In a prospective study of active thyroid-related eye disease, 61 of 65 nonsmokers (93.8%) responded to oral high-dose prednisolone, whereas only 58 of 85 smokers (68.2%) responded to oral high-dose prednisolone.
In any case, patients on systemic glucocorticoids need to be alerted to the possibility of hyperalgesia. Patients will have to be supplemented with glucocorticoids in the event of trauma, surgery, or infection during the several months of high-dose hormone withdrawal. Several complications of systemic glucocorticoid application, including Cushing’s syndrome, diabetes mellitus, hypertension, and osteoporosis, are more likely to limit the use of hormones.
Systemic glucocorticoid users may combine protective agents to avoid osteoporosis and gastric irritation. Vitamin D and calcium can protect bone mass and gastric mucosal protectors can avoid gastric irritation. According to the guidelines, pharmacologic doses of glucocorticoids should be started with bisphosphonates, and atrodronate 70 mg once a week. In addition, potassium supplementation and monitoring of blood pressure, blood glucose and weight are required.