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Published on: May 25, 2022
Inflammatory response and ACE2's potential role in acute primary angle-closure glaucoma during the Omicron epidemic
Bei Zeng1, Yuning Zhang1, Yufan Jiang1
1State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangdong Provincial Clinical Research Center for Ocular Diseases, Guangzhou, China.
Purpose:
To investigate the potential relationship between COVID-19 infection and the increased incidence of acute primary angle-closure glaucoma (APACG) observed during the pandemic.
Methods:
This study enrolled 91 APACG patients and 40 cataract patients who needed surgery as controls during the COVID-19 pandemic. Levels of 27 cytokines and angiotensin-converting enzyme 2 (ACE2) in aqueous humor and plasma were measured using multiplex bead immunoassay. Cytokine levels and ocular characteristics were compared between groups. Correlations between cytokine levels and the interval from COVID infection to APACG attack were assessed.
Results:
APACG patients were younger and predominantly female (P < 0.05). They also exhibited higher intraocular pressure, greater coefficient of variation of corneal endothelial cell, higher lens thickness, but shorter axial length and lower corneal endothelial cell density (all P < 0.05). Aqueous humor in APACG showed significantly elevated ACE2 (P < 0.001) and 19 cytokines (including IL-1ra, IL-6, IL-8; all P < 0.05). While the concentrations of ACE2 in plasma and other cytokines, only MCP-1 and IP-10 showed significant differences between groups (all P < 0.05). ACE2 levels in aqueous humor were positively correlated with 17 cytokines in APACG patients but not in the control group. In addition, 53 APACG patients (58 %) reported the APACG attack within 3 days of confirmed COVID-19 infection. Their ACE2 and MIP-1 in aqueous humor showed a negative correlation with the time interval between COVID-19 onset and APACG occurrence.
Conclusions:
Increased aqueous ACE2 and inflammatory cytokines were prominent in APACG during COVID-19 pandemic, which indicated a potential inflammatory mechanism linking COVID-19 infection to APACG onset.
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