Purpose of review: The purpose of the present review is to describe recent insights into the pathomechanism of ocular surface impairment in the course of thyroid dysfunctions. The review focuses in particular on Graves' ophthalmopathy as the majority of the literature is published on this topic.
Recent findings: Mechanical factors were thought, until now, to be the indirect causes of ocular surface function failure. In particular, eyeglobe bulging and upper eyelid retraction with consequent eyelid fissure width increase were mainly considered responsible for increased exposed area and ocular surface impairment. Recent evidence demonstrated that ocular surface tissues are direct targets for autoantibodies in either hypothyroid or hyperthyroid states. A set of tear protein biomarkers were identified and shown to have high diagnostic performance.
Summary: New horizons can be displayed on the basis of these new findings, in particular, as referred earlier, Graves' ophthalmopathy diagnosis. A detailed slit-lamp examination and a careful medical history by validated questionnaires in patients with ocular surface discomfort symptoms are now recommended to investigate early manifestations of an underlying thyroid dysfunction. Ocular surface signs should also be included in professional guidelines. Autoantibody assays in tears and proteomic analysis of tear protein expression could be important further steps in early diagnosis and posttherapy control of thyroid dysfunction.