Abstract and Introduction
Purpose of review The present review summarizes the body of literature concerning the medical and surgical treatment of thyroid eye disease (TED) from 1 January 2014 through 30 March 2015.
Recent findings Corticosteroids continue to be the primary medical therapy for TED. Recent research has offered insight into potential differences between oral corticosteroid and intravenous corticosteroid treatment regimens in terms of efficacy and side-effect profiles. Steroid-sparing medications, for example, rituximab and others, are an area of active study. There has been renewed interest in the role of radiation therapy as a nonmedical treatment for TED with some promising data. The use of balanced orbital decompression techniques have become popular, although the data regarding postoperative diplopia are mixed, and 'fat decompression' offers an alternative or an augmentation to bony decompression. Stereotactic image guidance is a useful adjunct to orbital decompression surgery.
Summary TED continues to be a difficult condition for the patient to cope with and for the clinician to treat, and recent research builds on the present foundation of knowledge and treatments, but unfortunately does not offer paradigm-shifting information at the present time.
Thyroid eye disease (TED) is a form of lymphocytic orbital inflammation most commonly associated with Graves hyperthyroidism, but can also be noted in hypothyroid and euthyroid states. Due to shared antigens and cross-reactivity of orbital and thyroid tissue, circulating thyroid antibodies stimulate proteins of the extraocular muscles and orbital fat, resulting in a proliferation of fibroblasts and production of glycosaminoglycans. This leads to orbital congestion and exophthalmos, often with the consequences of ocular dysmotility, diplopia, and more rarely compressive optic neuropathy. These changes progress during the active phase of disease, typically lasting 6–24 months, followed by a stable plateau of inactive disease. Reactivation following this course is fortunately uncommon.
One goal of TED treatment is to maintain a euthyroid state. Among the strongest modifiable risk factors for disease progression is tobacco smoking: it carries an odds ratio (OR) of at least 7.7 for developing TED compared to not smoking, as well as up-regulates inflammatory cytokines in severe active TED.[1–3] For active TED of sufficient severity (i.e. with vision threat or corneal exposure), the mainstay of treatment has been corticosteroid therapy and/or orbital decompression surgery. Modern research is investigating the efficacy of a variety of steroid-sparing agents, nutritional supplements, orbital radiation therapy, and various surgical interventions. This review provides an update on the treatment of TED as based on the literature from 1 January 2014 to 30 March 2015.
Curr Opin Ophthalmol. 2015;26(6):484-490. © 2015 Lippincott Williams & Wilkins