Sage Journals: Discover world-class research

Abstract

Purpose:

To investigate changes in anterior scleral thickness (AST) in patients with Posner–Schlossman Syndrome (PSS).

Methods:

Sixty-two patients with PSS were enrolled. AST was measured using swept-source optical coherence tomography at 0 mm (AST0), 1 mm (AST1), 2 mm (AST2), and 3 mm (AST3) from the scleral spur.

Results:

AST0, AST1, AST2, and AST3 were significantly reduced in PSS-affected eyes compared with that in fellow eyes. Furthermore, we divided patients into two subgroups based on the course of PSS: the short-term (PSS course < 1 year) subgroup and the long-term (PSS course ⩾ 1 year) subgroup. In the short-term subgroup, no significant differences in AST parameters (AST0, AST1, AST2, and AST3) were observed in PSS-affected and fellow eyes, while in the long-term subgroup, all the AST parameters (AST0, AST1, AST2, and AST3) were significantly reduced in PSS-affected eyes compared with that in fellow eyes.

Conclusions:

PSS-affected eyes demonstrated significantly reduced AST compared with that in fellow eyes. Moreover, a significant reduction of the AST was observed in long-term PSS-affected eyes, but not in short-term PSS-affected eyes. This indicates that changes in AST in PSS are time-dependent and progressive. Significant reduction of the AST is observed only after a certain period of time.

Keywords

Posner–Schlossman syndrome anterior scleral thickness optical coherence tomography course of disease

Introduction

Posner–Schlossman Syndrome (PSS) is an acute, intermittent, recurrent glaucomatocyclitis characterized by anterior uveitis with markedly elevated intraocular pressure (IOP).^1–6 Repeated attacks of PSS may result in glaucomatous optic nerve damage, and ultimately lead to blindness.^7–10 Research has shown that approximately 26.4% of patients with PSS develop glaucoma, while the exact etiology and pathophysiology of PSS remain unclear.⁹

Our previous studies have revealed iris atrophy, trabecular meshwork (TM) edema, and Schlemm’s canal (SC) enlargement in patients with PSS.^11,12 CMV is considered the leading etiology of PSS,^7,8 with studies reporting that the iris is susceptible to CMV¹³ and may serve as a reservoir for latent CMV.^14,15 The direct viral invasion or vasculitis caused by CMV infection may be the cause of atrophy and thinning of the iris,^11,16 with inflammation also playing an important role in this.^11,17 This kind of anterior uveitis may also have an effect on the anterior scleral thickness (AST). Moreover, the TM and SC are situated in the limbus, which is located right between the cornea and anterior sclera.¹⁷ The scleral spur (SS), which is part of the anterior sclera, is an important factor for maintaining TM and SC morphology.^18,19 Therefore, alterations in AST may influence the morphology and function of the TM and SC. To date, no study has quantitatively assessed AST in PSS. Notably, AST has been reported to be significantly reduced in eyes with primary open-angle glaucoma¹⁸; however, the changes in AST associated with secondary glaucoma, such as PSS, are not characterized. Therefore, the primary objective of this study was to investigate the effects of PSS on the AST.

Methods

Subjects

Sixty-two patients with PSS were enrolled in this cross-sectional study, which was conducted over an 18-month period from January 2021 to June 2022. All the patients underwent ophthalmic examinations (slit-lamp observation, IOP measurement, fundus observation, gonioscopy, corneal endothelial microscopy, axial length (AL) measurement (IOL-Master 500; Carl Zeiss Meditec, Dublin, OH, USA), and cup-to-disc (C/D) ratio assessment with fundus photographs (AFC-210; Nidek Co., Ltd., Gamagori, Aichi, Japan). The diagnostic criteria for PSS were as follows: (1) unilateral and recurrent disease episode; (2) transient elevated IOP with blurred vision; (3) hoar and white suet-shaped keratic precipitates and/or mild inflammation in the anterior chamber; (4) open anterior chamber angle without iris synechiae.¹² Patients/eyes with a history of uveitis, scleritis, ocular laser, ocular surgery, primary glaucoma, secondary glaucoma caused by conditions other than PSS, high myopia, or systemic diseases were excluded.

To further analyze the influence of the disease course of PSS on AST, we divided the patients into two subgroups based on the course of PSS: short-term (PSS course < 1 year) (n = 19) and long-term (PSS course ⩾ 1 year) subgroups (n = 43). In addition, PSS-affected eyes were further stratified into two subgroups based on the presence (n = 17) or absence (n = 45) of secondary glaucoma to investigate whether significant differences in AST existed between the two groups.

Swept-source optical coherence tomography imaging acquisition and processing

Both the PSS-affected and fellow eye of each patient underwent swept-source optical coherence tomography (SS-OCT) (CASIA SS-1000; Tomey Corporation, Nagoya, Japan). The nasal and temporal limbs were measured separately by an experienced examiner (XY) after adjusting the fixture to the corresponding scan areas.

The AST was measured as the distance from the episcleral blood vessels (thin hyporeflective area in the anterior part of the sclera) to the posterior boundary of the sclera (the line separating the hyperreflective sclera from the hyporeflective ciliary muscle).^18,19 The AST was measured at 0 mm (AST0), 1 mm (AST1), 2 mm (AST2), and 3 mm (AST3) from the SS (Figure 1). The pupil diameter (PD) was measured as the distance between the two opposite sides of the pupillary margin of the iris.²⁰ All the measurements were conducted using the ImageJ software (National Institutes of Health, Bethesda, MD, USA) by an experienced observer (ML) blinded to the study information.

Figure 1.

The measurements of AST. AST0, AST1, AST2, and AST3 are measured at 0 mm, 1 mm, 2 mm, and 3 mm from the scleral spur, respectively. AST, anterior scleral thickness.

Statistical analysis

Data are shown as mean ± standard deviation, where applicable. The normality of interocular differences was assessed using the Shapiro–Wilk test, and the Wilcoxon signed-rank test was used to compare measurements in the PSS-affected eyes with that of the fellow eyes, as the differences did not follow a normal distribution. Parameters with nasal and temporal values were compared with generalized estimating equations (GEEs) because GEEs take the correlation between the nasal and temporal measurements of one eye into account.^11,12,18,21 Linear regression was used to determine the associations between AST and corneal endothelium (CE) density and the C/D ratio in eyes with PSS. Adjusted β coefficients for the associations between independent and dependent variables were assessed using GEEs. To test the reproducibility of AST measurements, the AST (including both nasal and temporal AST in PSS-affected and fellow eyes) was re-measured by the same observer. Intraobserver reproducibility was assessed using the intraclass correlation coefficient (ICC). All the analyses were performed using R-software version 3.4.3 (http://www.r-project.org) and EmpowerStats software (www.empowerstats.com; X&Y Solutions, Inc., Boston, MA, USA). All the tests were two-tailed, and p < 0.05 was defined as statistically significant.

Results

As shown in Table 1, no significant differences in AL or PD were observed between the PSS-affected and fellow eyes (both p > 0.05). The CE density was significantly lower, and the C/D ratio and IOP were significantly greater in the PSS-affected eyes compared with that in the fellow eyes (all p < 0.05).

Table 1.

Study subject characteristics.

	Affected eye	Fellow eye	p
Age (years)	37.29 ± 11.48	37.29 ± 11.48	—
Sex (Male/Female)	35/27	35/27	—
Axial length (mm)	23.90 ± 1.01	23.88 ± 0.93	0.644
Corneal endothelium density (/mm²)	2427.03±425.83	2700.61±301.02	<0.001*
C/D ratio	0.51 ± 0.19	0.37 ± 0.09	<0.001*
Intraocular pressure (mmHg)	23.60 ± 11.51	17.40 ± 3.70	0.001*
Pupil diameter (mm)	4.62 ± 0.86	4.51 ± 0.85	0.271

C/D, cup-to-disc.

Wilcoxon signed-rank test.

Comparison of AST in PSS-affected and fellow eyes

AST0, AST1, AST2, and AST3 were significantly reduced in PSS-affected eyes compared with that in fellow eyes (all p < 0.05) (Table 2).

Table 2.

Comparisons of AST between PSS-affected and fellow eyes.

	Affected eye	Fellow eye	p
AST0 (μm)	637.69 ± 66.94	651.61 ± 72.80	0.016*
AST1 (μm)	476.02 ± 53.89	494.71 ± 50.90	<0.001*
AST2 (μm)	492.06 ± 59.15	508.46 ± 57.36	0.001*
AST3 (μm)	492.47 ± 69.65	518.67 ± 64.87	<0.001*

AST, anterior scleral thickness; AL, axial length.

The influence factors such as age, sex, and AL have been adjusted.

Generalized estimating equations.

Comparisons of AST between PSS-affected and fellow eyes in short-term (PSS course <1 year) and long-term (PSS course ⩾ 1 year) subgroups

In the short-term subgroup, no significant differences were observed between the PSS-affected and fellow eyes for all the AST parameters (AST0, AST1, AST2, and AST3) (all p > 0.05). In the long-term subgroup, all the AST parameters (AST0, AST1, AST2, and AST3) were significantly reduced in PSS-affected eyes compared with that in fellow eyes (all p < 0.05) (Table 3).

Table 3.

Comparisons of AST between PSS-affected and fellow eyes in short-term (course of PSS < 1 year) and long-term (course of PSS ⩾1 year) subgroups.

Short-term subgroup (Course of PSS <1 year)
	Affected eye	Fellow eye	p
AST0 (μm)	639.32 ± 78.50	641.58 ± 70.84	0.858
AST1 (μm)	485.43 ± 68.87	493.19 ± 51.36	0.373
AST2 (μm)	497.68 ± 65.37	507.19 ± 52.20	0.281
AST3 (μm)	503.51 ± 79.60	513.03 ± 63.82	0.387
Long-term subgroup (Course of PSS ⩾ 1 year)
	Affected eye	Fellow eye	p
AST0 (μm)	636.99 ± 61.87	655.81 ± 73.60	0.010*
AST1 (μm)	472.01 ± 45.97	495.35 ± 50.99	<0.001*
AST2 (μm)	489.67 ± 56.54	508.99 ± 59.68	0.001*
AST3 (μm)	487.77 ± 64.90	521.03 ± 65.53	<0.001*

AST, anterior scleral thickness; AL, axial length; PSS, Posner–Schlossman syndrome.

The influence factors such as age, sex, and AL have been adjusted.

Generalized estimating equations.

Comparison of AST between PSS-affected eyes with and without secondary glaucoma

After adjusting for potential confounding factors, including age, sex, and AL, no statistically significant differences were observed between the two subgroups (with and without secondary glaucoma) for any of the measured AST parameters (Table 4).

Table 4.

Comparisons of AST between PSS-affected eyes with and without secondary glaucoma.

PSS-affected eyes
	Without secondary glaucoma	With secondary glaucoma	p
AST0 (μm)	635.31 ± 66.93	643.97 ± 67.56	0.855
AST1 (μm)	470.78 ± 49.45	489.88 ± 62.89	0.672
AST2 (μm)	485.68 ± 56.98	508.94 ± 62.30	0.686
AST3 (μm)	484.93 ± 67.53	512.41 ± 72.24	0.353

AST, anterior scleral thickness; AL, axial length; PSS, Posner–Schlossman syndrome.

The influence factors such as age, sex, and AL have been adjusted by GEEs.

Comparison of nasal and temporal AST between PSS-affected and fellow eyes

In the nasal subgroup, AST1 and AST3 were significantly different in PSS-affected and fellow eyes (both p < 0.05), whereas AST0 and AST2 showed no significant differences (both p > 0.05). In the temporal subgroup, AST0, AST1, AST2, and AST3 were significantly lower in PSS-affected eyes than that in fellow eyes (all p < 0.05) (Supplemental Table S1).

Comparison of nasal and temporal AST between PSS-affected and fellow eyes in short-term and long-term PSS subgroups

In the short-term subgroup, a significant difference between the PSS-affected and fellow eyes was observed only for nasal AST3 (p = 0.049). In contrast, in the long-term subgroup, significant differences were observed for all the AST measurements, except for nasal AST0 and AST2 (all p < 0.05) (Supplemental Table S2).

Univariate linear regression analysis of the association between AST and CE density in PSS-affected eyes

No significant associations between AST and CE density were observed in PSS-affected eyes (all p > 0.05) (Supplemental Table S3).

Univariate linear regression analysis of the association between AST and C/D ratio in PSS-affected eyes

No significant associations between AST and the C/D ratio were observed in PSS-affected eyes (all p > 0.05) (Supplemental Table S4).

Reproducibility of AST measurements

The results indicated that the reproducibility of the measurements was good. The ICC of the measurements ranged from 0.855 to 0.929 (Table 5).

Table 5.

Reproducibility of AST measurements.

	ICC value	Lower 95% CI	Upper 95% CI
Nasal AST of PSS-affected eye
AST0	0.873	0.733	0.942
AST1	0.908	0.803	0.958
AST2	0.887	0.761	0.949
AST3	0.929	0.847	0.968
Temporal AST of PSS-affected eye
AST0	0.887	0.761	0.949
AST1	0.905	0.796	0.957
AST2	0.901	0.788	0.955
AST3	0.918	0.824	0.963
Nasal AST of PSS-fellow eye
AST0	0.858	0.700	0.936
AST1	0.902	0.788	0.957
AST2	0.874	0.732	0.944
AST3	0.866	0.716	0.940
Temporal AST of PSS-fellow eye
AST0	0.893	0.770	0.952
AST1	0.896	0.775	0.954
AST2	0.855	0.695	0.935
AST3	0.904	0.791	0.957

AST, anterior scleral thickness; AL, axial length; ICC, intraclass correlation coefficient; PSS, Posner–Schlossman Syndrome.

Discussion

To date, no clinical observations of changes in AST in patients with PSS have been reported. In this study, we conducted quantitative AST measurements at different distances (0/1/2/3 mm) from the SS using SS-OCT and observed that all the AST parameters (AST0, AST1, AST2, and AST3) were significantly reduced in PSS-affected eyes compared with that in fellow eyes. Furthermore, when patients were divided into short-term and long-term PSS subgroups, the result pattern was significantly different. In patients with short-term PSS, none of the AST parameters (AST0, AST1, AST2, AST3) were significantly different to that of the fellow eyes; however, in patients with long-term PSS, all the AST parameters (AST0, AST1, AST2, AST3) were significantly different to that of the fellow eyes, with reduced AST in PSS-affected eyes. Previous studies have reported significant TM edema, CE loss, iris atrophy, and C/D enlargement in PSS-affected eyes.^8–12 In addition to these findings, we also identified significantly reduced AST in PSS-affected eyes compared with that in fellow eyes in the current study. To the best of our knowledge, this is the first study to report changes in AST in patients with PSS.

As previously mentioned, PSS is associated with CMV infection,^7,8 which leads to both iris atrophy¹⁶ and CE loss.^8,22,23 PSS is also associated with significantly elevated levels of inflammation proteins and cytokines in the anterior chamber.^3,6,24 Therefore, anterior segmental inflammation may also contribute to iris atrophy and CE loss in PSS-affected eyes.¹¹ Aketa et al. suggested that iris injury is associated with increases in inflammation cytokines (e.g., TNF-α IL-1, IL-4, IL-6, IL-8, and MCP-1) in the aqueous humor,¹⁷ and Alfawaz et al. indicated that anterior uveitis/inflammation has a negative effect on CE count.²⁵ Moreover, given that the anterior sclera is located right next to the CE and iris, CMV infection and anterior inflammation may also have negative effects on the anterior sclera, leading to its atrophy and reduction of the AST, similar to the changes in the iris and CE in PSS-affected eyes.

Although PSS has been reported as self-limited and benign,¹ glaucomatous optic nerve damage has also been reported in PSS-affected eyes.^8–10 The potential reasons could be the acute elevation of IOP and subsequent decrease in ocular perfusion (determined by both local arterial blood pressure and IOP) during PSS attack.^11,26 In addition to optic nerve damage, this could also contribute to iris atrophy in PSS-affected eyes.¹¹ Thus, the injurious effect of acute elevation of IOP and the subsequent decrease in ocular perfusion could be observed in both the anterior (iris atrophy) and posterior (glaucomatous optic nerve damage) segments of PSS-affected eyes, indicating that the whole eyeball/ocular tissue could be affected. Accordingly, we speculated that in addition to the iris and optic nerve, the mechanical pressure and ischemia caused by high IOP in PSS-affected eyes may also act on the anterior sclera, resulting in anterior sclera atrophy and AST reduction. Thus, acute elevation in IOP could be an additional reason for the reduction of the AST in PSS-affected eyes.

Another interesting phenomenon observed in the current study was significant reduction of the AST in long-term PSS-affected eyes, but not in short-term PSS-affected eyes. Accordingly, we speculated that the atrophy of the anterior sclera and reduction of the AST in PSS might be time-dependent and progressive. Therefore, in the short-term period after PSS onset, the sclera was able to withstand the negative influences of PSS (CMV infection, anterior inflammation, mechanical pressure, and ischemia caused by high IOP); thus, no significant changes in the anterior sclera and AST occurred. However, when the course of PSS reached 1 year or longer, pathological changes in the anterior sclera and AST gradually became significant. Considering the close relationship between AST reduction and the course of PSS, we also speculated that reduction of the AST in PSS-affected eyes might also be a clinical indicator for long-term PSS.

This study had certain limitations. First, this was a clinical observational study in which only morphological data derived from SS-OCT were collected and analyzed. CMV load testing was not performed. Therefore, the potential influence of the CMV status on AST was not evaluated in the present study. Second, we only observed the anterior sclera and not the posterior sclera in this study. Third, this was a cross-sectional observational study and not a longitudinal follow-up study. Therefore, dynamic changes in AST were not recorded. Fourth, during the PSS attack, short-term applications of IOP-lowering medications were chosen, and IOP-lowering medications may have affected AST.²⁷ However, all the administration of IOP-lowering treatment was short-term and temporary. Only a small subset of study patients (3 of 62, less than 5%) received prostaglandin analog treatment. Thus, the potential effect of IOP-lowering medications on AST in patients with PSS may be limited in this study. Fifth, the number of episodes per patient was not recorded in this study. Sixth, a sample size calculation was not performed prior to the initiation of this study. Seventh, this study was conducted in China. Considering that the prevalence of CMV infection varies across geographic regions and countries,^28,29,30 our results may therefore only be specifically applicable to a Chinese/Asian population.

Conclusion

This is the first study to report that PSS-affected eyes have significantly reduced ASTs compared with that in fellow eyes. Moreover, significant reduction in AST was observed in long-term PSS-affected eyes, but not in short-term PSS-affected eyes. Thus, changes in AST in PSS are time-dependent and progressive and significant reduction of AST occurs only after a certain period of time after PSS onset.

Supplemental Material

sj-docx-1-smo-10.1177_20503121251379680 – Supplemental material for Quantification of anterior scleral thickness in Posner–Schlossman syndrome

Supplemental material, sj-docx-1-smo-10.1177_20503121251379680 for Quantification of anterior scleral thickness in Posner–Schlossman syndrome by Mu Li, Dan Zhao, Xiaoqin Yan and Zhiqi Chen in SAGE Open Medicine

Supplemental Material

sj-docx-2-smo-10.1177_20503121251379680 – Supplemental material for Quantification of anterior scleral thickness in Posner–Schlossman syndrome

Supplemental material, sj-docx-2-smo-10.1177_20503121251379680 for Quantification of anterior scleral thickness in Posner–Schlossman syndrome by Mu Li, Dan Zhao, Xiaoqin Yan and Zhiqi Chen in SAGE Open Medicine

Supplemental Material

sj-docx-3-smo-10.1177_20503121251379680 – Supplemental material for Quantification of anterior scleral thickness in Posner–Schlossman syndrome

Supplemental material, sj-docx-3-smo-10.1177_20503121251379680 for Quantification of anterior scleral thickness in Posner–Schlossman syndrome by Mu Li, Dan Zhao, Xiaoqin Yan and Zhiqi Chen in SAGE Open Medicine

Supplemental Material

sj-docx-4-smo-10.1177_20503121251379680 – Supplemental material for Quantification of anterior scleral thickness in Posner–Schlossman syndrome

Supplemental material, sj-docx-4-smo-10.1177_20503121251379680 for Quantification of anterior scleral thickness in Posner–Schlossman syndrome by Mu Li, Dan Zhao, Xiaoqin Yan and Zhiqi Chen in SAGE Open Medicine

Footnotes

ORCID iD

Mu Li

Ethical considerations

This study was approved by the ethical committee of Tongji Hospital, Huazhong University of Science and Technology (TJ-IRB20201024).

Consent to participate

Written informed consent was obtained from the study subjects.

Consent for publication

Written informed consent was obtained from the study subjects.

Author Contributions

Conceptualization: ML, DZ, XY, and ZC; Methodology: ML, DZ, XY, and ZC; Software: ML; Validation: ML, DZ, XY, and ZC; Formal Analysis: ML, DZ, and XY; Investigation: ML, DZ, XY, and ZC; Resources: XY and ZC; Data Curation: ML and DZ; Writing – Original Draft Preparation: ML and DZ; Writing – Review & Editing: XY and ZC; Visualization: ML, DZ, XY, and ZC; Supervision: ZC; Project Administration: ZC; Funding Acquisition: ML, XY, and ZC.

Funding

The authors disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This work was supported by the National Natural Science Foundation of China (Grant No. 82000893, 81800821) and Natural science foundation of Hainan Province (Grant No. 823MS175).

Declaration of conflicting interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Data availability statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

Supplemental material

Supplemental material for this article is available online

References

Posner

Schlossman

Syndrome of unilateral recurrent attacks of glaucoma with cyclitic symptoms. Arch Ophthal 1948; 39: 517–535.

Posner

Schlossman

Further observations on the syndrome of glaucomatocyclitic crises. Trans Am Acad Ophthalmol Otolaryngol 1953; 57: 531–536.

Igarashi

Honjo

Kaburaki

, et al. Effects of ROCK inhibitors on apoptosis of corneal endothelial cells in CMV-positive Posner–Schlossman syndrome patients. Invest Ophthalmol Vis Sci 2020; 61: 5.

Joseph

Lim

Samalia

, et al. Long term outcome and prognostic indicators in Posner Schlossman syndrome. Clin Exp Ophthalmol 2023; 51: 781–789.

Shen

, et al. Peripheral vascular endothelial dysfunction in glaucomatocyclitic crisis: a preliminary study. Invest Ophthalmol Vis Sci 2010; 51: 272–276.

Ang

Cheung

CMG

, et al. Aqueous cytokine changes associated with Posner–Schlossman syndrome with and without human cytomegalovirus. PLoS One 2012; 7: e44453.

Lee

, et al. Prevalence and clinical manifestations of cytomegalovirus infection in patients with Posner–Schlossman syndrome: a systematic review and meta-analysis. Surv Ophthalmol 2025; 70(6): 1252–1260.

Wang

, et al. Clinical outcomes in cytomegalovirus-positive Posner–Schlossman syndrome patients treated with topical ganciclovir therapy. Am J Ophthalmol 2014; 158: 1024–1031.e2

Jap

Sivakumar

Chee

SP.

Is Posner Schlossman syndrome benign?

Ophthalmology 2001; 108: 913–918.

10.

Liu

Tseng

Huang

, et al. Glaucomatocyclitic crises may occur in patients with narrow or closed angles. J Ophthalmol 2017; 2017: 4074912.

11.

Yan

Chen

, et al. Quantification of iris atrophy by swept-source optical coherence tomography in Posner–Schlossman syndrome. J Clin Med 2022; 11: 6484.

12.

Yan

Wang

, et al. Morphology of the trabecular meshwork and Schlemm's canal in Posner–Schlossman syndrome. Invest Ophthalmol Vis Sci 2022; 63: 1.

13.

Markomichelakis

Canakis

Zafirakis

, et al. Cytomegalovirus as a cause of anterior uveitis with sectoral iris atrophy. Ophthalmology 2002; 109: 879–882.

14.

Voigt

Andoniou

Schuster

, et al. Cytomegalovirus establishes a latent reservoir and triggers long-lasting inflammation in the eye. PLoS Pathog 2018; 14: e1007040.

15.

Rocher

Duchesne

Andouard

, et al. Cytomegalovirus detected by qPCR in iris and ciliary body of immunocompetent corneal donors. J Clin Virol 2024; 171: 105636.

16.

Woo

Lim

, et al. Characteristics of cytomegalovirus uveitis in immunocompetent patients. Ocul Immunol Inflamm 2015; 23: 378–383.

17.

Aketa

Yamaguchi

Suzuki

, et al. Iris damage is associated with elevated cytokine levels in aqueous humor. Invest Ophthalmol Vis Sci 2017; 58: BIO42–BIO51.

18.

Yan

Chen

, et al. The anterior scleral thickness in eyes with primary open-angle glaucoma. Graefes Arch Clin Exp Ophthalmol 2022; 260: 1601–1610.

19.

Luo

Yan

, et al. The anterior segment biometrics in high myopia eyes. Ophthalmic Res 2023; 66: 75–85.

20.

Song

Zhao

, et al. Influence of exercise on the structure of the anterior chamber of the eye. Acta Ophthalmol 2018; 96: e247–e253.

21.

Liu

Zhu

Yan

, et al. The effect of repeated low-level red-light therapy on Myopia control and choroid. Transl Vis Sci Technol 2024; 13: 29.

22.

Ang

Sng

Chee

, et al. Outcomes of corneal transplantation for irreversible corneal decompensation secondary to corneal endotheliitis in Asian eyes. Am J Ophthalmol 2013; 156: 260–266.e2.

23.

Koizumi

Inatomi

Suzuki

, et al. Clinical features and management of cytomegalovirus corneal endotheliitis: analysis of 106 cases from the Japan corneal endotheliitis study. Br J Ophthalmol 2015; 99: 54–58.

24.

Pohlmann

Schilickeiser

Metzner

, et al. Different composition of intraocular immune mediators in Posner–Schlossman syndrome and Fuchs' uveitis. PLoS One 2018; 13: e0199301.

25.

Alfawaz

Holland

, et al. Corneal endothelium in patients with anterior uveitis. Ophthalmology 2016; 123: 1637–1645.

26.

Chen

Yao

, et al. Optical coherence tomography angiography in Posner–Schlossman syndrome – a preliminary study. Ocul Immunol Inflamm 2023; 31: 891–899.

27.

Park

Yoo

Chung

Kim

YY.

Effect of prostaglandin analogues on anterior scleral thickness and corneal thickness in patients with primary open–angle glaucoma. Sci Rep 2021; 11: 11098.

28.

Fowler

Ross

Shimamura

, et al. Racial and ethnic differences in the prevalence of congenital cytomegalovirus infection. J Pediatr 2018; 200: 196–201.e1.

29.

Fowler

Mucha

Neumann

, et al. A systematic literature review of the global seroprevalence of cytomegalovirus: possible implications for treatment, screening, and vaccine development. BMC Public Health 2022; 22: 1659.

30.

Ssentongo

Hehnly

Birungi

, et al. Congenital cytomegalovirus infection burden and epidemiologic risk factors in countries with universal screening: a systematic review and meta-analysis. JAMA Netw Open 2021; 4: e2120736.

Supplementary Material

Please find the following supplemental material available below.

For Open Access articles published under a Creative Commons License, all supplemental material carries the same license as the article it is associated with.

For non-Open Access articles published, all supplemental material carries a non-exclusive license, and permission requests for re-use of supplemental material or any part of supplemental material shall be sent directly to the copyright owner as specified in the copyright notice associated with the article.

0.00 MB

0.01 MB

0.02 MB

0.01 MB