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Войти в исследования American journal of ophthalmology · 2026
Metabolomic and Lipidomic Profiling Reveals Dysregulated Glycerophospholipid Metabolism in New-Onset Acute Vogt-Koyanagi-Harada Disease.
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Deng Yang, Huang Ziqian, Jiang Xiaoran, Zhang Yinan, Zhang Wanyun, Zhou Qian, Luo Xiang, Su Guannan, Lai Yujie, Huang Changwei, Cao Qingfeng, Yang Peizeng
Аннотация
PURPOSE: Vogt-Koyanagi-Harada (VKH) disease is a sight-threatening autoimmune disorder whose early systemic metabolic alterations remain poorly defined. We aimed to characterize plasma metabolomic and lipidomic signatures in new-onset acute VKH disease and to explore their clinical relevance.
DESIGN: Retrospective case-control study.
PARTICIPANTS: Of 26 patients with new-onset acute VKH disease and 39 healthy controls were included.
METHODS: Untargeted metabolomics and quantitative lipidomics were performed in plasma from treatment-naïve VKH patients and healthy controls. An elastic net model was applied to identify a discriminative glycerophospholipid signature.
MAIN OUTCOME MEASURES: Differential metabolites and lipids and their correlations with cerebrospinal fluid (CSF) white blood cell (WBC) count and subfoveal choroidal thickness (SFCT) were analyzed.
RESULTS: Metabolomics identified 74 significantly altered metabolites, with lipids as the predominate class and glycerophospholipid metabolism as a core perturbed pathway. Lipidomics further revealed 262 significantly altered lipids, with 254 downregulated in the VKH group. Glycerophospholipids predominated among the altered lipids (67.2%), representing a marked enrichment compared with their proportion in the overall lipidome (43.9%, P < .0001). Nine glycerophospholipids correlated negatively with CSF WBC count (all P < .05), with PE (16:0_22:4) showing the strongest association (r = -0.59, P = .003). Three phosphatidylcholine species correlated negatively with SFCT (all P < .05). An elastic net model identified a 25-glycerophospholipid signature that achieved an area under the curve of 0.953 in discriminating VKH patients from healthy controls.
CONCLUSIONS: These findings highlight dysregulated glycerophospholipid metabolism as a key metabolic feature of new-onset acute VKH disease and provide additional insights into disease pathogenesis.
DESIGN: Retrospective case-control study.
PARTICIPANTS: Of 26 patients with new-onset acute VKH disease and 39 healthy controls were included.
METHODS: Untargeted metabolomics and quantitative lipidomics were performed in plasma from treatment-naïve VKH patients and healthy controls. An elastic net model was applied to identify a discriminative glycerophospholipid signature.
MAIN OUTCOME MEASURES: Differential metabolites and lipids and their correlations with cerebrospinal fluid (CSF) white blood cell (WBC) count and subfoveal choroidal thickness (SFCT) were analyzed.
RESULTS: Metabolomics identified 74 significantly altered metabolites, with lipids as the predominate class and glycerophospholipid metabolism as a core perturbed pathway. Lipidomics further revealed 262 significantly altered lipids, with 254 downregulated in the VKH group. Glycerophospholipids predominated among the altered lipids (67.2%), representing a marked enrichment compared with their proportion in the overall lipidome (43.9%, P < .0001). Nine glycerophospholipids correlated negatively with CSF WBC count (all P < .05), with PE (16:0_22:4) showing the strongest association (r = -0.59, P = .003). Three phosphatidylcholine species correlated negatively with SFCT (all P < .05). An elastic net model identified a 25-glycerophospholipid signature that achieved an area under the curve of 0.953 in discriminating VKH patients from healthy controls.
CONCLUSIONS: These findings highlight dysregulated glycerophospholipid metabolism as a key metabolic feature of new-onset acute VKH disease and provide additional insights into disease pathogenesis.