**1. Introduction**

Graves' ophthalmopathy (GO) is a periocular and orbital inflammatory manifestation that is caused by autoimmune thyroid disease [1]. The pathogenesis of GO involves autoantibodies against thyroid-stimulating hormone (TSH) receptors, which lead to excess production of thyroid hormone. This, in turn, induces an inflammatory response against the periocular and orbital tissues [2–4]. Dry eye disease (DED) is a frequent complaint among patients with GO [2,5], and a high proportion of patients with GO reportedly exhibit dry eye symptoms [5,6]. However, although numerous studies have investigated the pathogenesis of GO, few have o ffered detailed insight into the association and interaction between GO and DED [2–9]. Moreover, in clinical settings, DED in GO tends to remain neglected.

Regarding the DED mechanism in GO, previous studies have suggested (1) a decrease in tear volume, because the lacrimal gland is one of the target tissues of TSH [2–4], and (2) an increase in palpebral fissure height, leading to accelerated evaporation of tears [10]. Recent studies have suggested

that GO pathogenesis is mediated not only by morphological changes but also by immunological causes, including T-cell-mediated inflammation [3] and TSH-receptor expression in the acinar cells of impaired lacrimal glands [2].

Meibomian glands secrete the lipid component of tears, which prevents excessive tear evaporation. Meibomian gland dysfunction (MGD) is considered to be a major cause of evaporative dry eye [11–13]. However, few reports have investigated the relationship between GO and the ocular surface, including both MGD and DED. Therefore, here we investigated the relationship between GO and MGD in patients with GO and dry eye symptoms, using detailed GO information obtained using various modalities, such as magnetic resonance imaging (MRI).

#### **2. Experimental Section**
