The Role of Biological Agents and Immunomodulators in Treatment Strategies for Thyroid Eye Disease: An Evidence-based Review.

Graves' Disease is an autoimmune disease where circulating antibodies bind to the thyrotropin receptors on the thyroid gland. These bound antibodies mimic thyroid stimulating hormone without the normal feedback from the anterior pituitary, causing hyperthyroidism and thyrotoxicosis. These antibodies also interact with orbital tissues and cause the characteristic orbital findings of thyroid eye disease (TED). It is not clearly understood why anatomically and physiologically distinct tissues like the thyroid gland and orbit are affected selectively, or why the orbital disease tends to be self-limited. Identifying and understanding these processes is critical to targeting therapy. In the active phase of the disease patients may experience orbital inflammation, eyelid and conjunctiva edema (chemosis), eyelid retraction, proptosis, ocular motility restriction, and optic nerve compression. Current treatment strategies for the ocular symptoms have been predominantly directed at symptomatic relief. More recently, investigators have concentrated their efforts to better understanding the underlying pathophysiologic processes to direct therapy at these processes. This review examines the current literature exploring a variety of newer therapeutic alternatives, including immunomodulative and suppressive agents, targeted at strategic points of the active-phase TED pathophysiological pathways. Specifically, biological agents including rituximab, adalimumab, intravenous immunoglobulin and others are reviewed with considerations for pathophysiology, extent of literature support, and adverse effects. [Full article available at http://rimed.org/rimedicaljournal-2016-06.asp, free with no login].