Abstract
A relationship between ocular sarcoidosis (OcSar) and dry eye (DE) has previously been reported. Here we investigated the tear function in OcSar, and the other uveitis, Vogt–Koyanagi–Harada disease (VKH), to elucidate the association between OcSar and DE. This study involved 27 eyes of 27 female OcSar patients [mean age: 67.3 ± 13.5 (SD) years], 18 eyes of 18 female VKH patients (53.1 ± 14.1 years), and 17 eyes of 17 female healthy control subjects (59.7 ± 9.6 years). In all examined eyes, tear meniscus height (TMH, mm), fluorescein breakup time (FBUT, s), scoring of keratoconjunctival epithelial damage (ED), and the Schirmer 1 test (ST1, mm/5 min) were analyzed. In the OcSar patients, VKH patients, and control subjects, the respective TMH, FBUT, ED, and ST1 values (mean ± SD) were 0.26 ± 0.10, 0.24 ± 0.09, and 0.24 ± 0.08, 4.3 ± 2.5, 7.3 ± 2.9, and 6.3 ± 3.1, 1.1 ± 1.1, 0.7 ± 0.8, and 0.1 ± 0.3, and 12.9 ± 10.5, 21.5 ± 12.1, and 24.3 ± 10.5. Statistically, the ST1 values were significantly lower in the OcSar patients than in the VKH patients (P = 0.004) and control subjects (P = 0.001). ST1 findings revealed that the neural reflex arc and lacrimal gland system, which attenuate the vicious cycle between the tear film and ocular surface epithelium in DE, are significantly impaired in OcSar cases, thus indicating a possible association between OcSar and DE.
Highlights
A relationship between OcSar and DE, keratoconjunctivitis sicca, and Sjögren’s syndrome (SS) has previously been r eported[8–10]
No statistically significant difference was found in the comparison of tear meniscus height (TMH) values between the OcSar group (0.26 ± 0.10 mm), Vogt–Koyanagi–Harada disease (VKH) group (0.24 ± 0.09 mm), and normal control (NC) group (0.24 ± 0.08 mm) [P = 0.687 (OcSar vs. VKH), P = 0.670 (OcSar vs. NC), and P = 0.999 (VKH vs. NC)] (Fig. 1a)
The findings in this study revealed that the ST1 values of the OcSar group were significantly less than those of the VKH group and NC group [P = 0.004 (OcSar vs. VKH), P = 0.001 (OcSar vs. NC)]
Summary
A relationship between OcSar (mainly UvSar) and DE, keratoconjunctivitis sicca, and Sjögren’s syndrome (SS) has previously been r eported[8–10]. It is thought that DE in OcSar is primarily related to lacrimal gland inflammation/infiltration of inflammatory cells that results in decreased tear p roduction[11]. According to ADES, in all types of DE, tear film instability plays a central and common role in their pathophysiology[14], and various risk factors can cause instability of the tear film, leading to a vicious cycle between the tear film and the ocular surface epithelium that can result in a variety of symptoms. The previous study showed pathologically the inflammation in the main or accessory lacrimal glands of sarcoidosis patients, the specific tear secretion function in those patients remains unclear. The purpose of this study was to elucidate the possible association between OcSar (UvSar + LaSar) and DE, and DE subtype, by comparing with both Vogt–Koyanagi–Harada disease (VKH) as an uveitis control and healthy subjects as a normal control via the investigation of the tear functions and ocular surface epithelial abnormalities
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