Abstract

We prospectively evaluated the relationship between meibomian gland dysfunction (MGD) and Graves’ ophthalmopathy (GO) in 19 patients (38 eyes) with subjective dry eye symptoms, compared to 14 age-matched normal participants (14 eyes). Extraocular muscle and lacrimal gland enlargement were evaluated by magnetic resonance imaging (MRI). Ocular surface examinations included fluorescein staining for keratoconjunctival epithelial damage, tear breakup time (TBUT) evaluation, and Schirmer’s test. Dry eye symptoms were evaluated with the Dry Eye-related Quality-of-Life Score (DEQS) questionnaire. Lid-margin abnormalities, meibum grade, and meiboscores were assessed using meibography. Clinical activity scores and T2 signal intensity ratios were used to define GO activity. All GO patients had obstructive MGD and 79% exhibited levator muscle enlargement. Ocular surface parameters of TBUT (p = 0.000), meibum score (p = 0.000), eyelid vasculitis (p = 0.000), meiboscore of the upper lid (p = 0.002), total meiboscores (p = 0.001), and DEQS (p = 0.000) significantly differed between GO patients and normal subjects. In addition, GO patients had significantly more abnormalities of the central region of the upper eyelid than normal subjects (p = 0.000). Thus, MGD might be related to eye discomfort and deterioration of the ocular surface in GO patients. Inflammation and morphological meibomian gland changes might be characteristic of GO.

Highlights

  • Graves’ ophthalmopathy (GO) is a periocular and orbital inflammatory manifestation that is caused by autoimmune thyroid disease [1]

  • Our findings revealed that patients presented with clinical features of vascular engorgement and inflammation of eyelid margins, levator muscle thickening, and in some patients, meibomian gland changes in the central region of the eyelids, based on meibography

  • Kim et al reported that patients with GO exhibited morphological changes in the meibomian glands, which correlated with proptosis and palpebral fissure height [24]

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Summary

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 [2,3,4]. 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]. Numerous studies have investigated the pathogenesis of GO, few have offered detailed insight into the association and interaction between GO and DED [2,3,4,5,6,7,8,9]. In clinical settings, DED in GO tends to remain neglected

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