Association between serum cytokines and timeframe for conversion from clinical high‐risk to psychosis

精神病 分位数回归 内科学 医学 细胞因子 分位数 肿瘤坏死因子α 血管内皮生长因子 白细胞介素6 相关性 肿瘤科 内分泌学 胃肠病学 血管内皮生长因子受体 精神科 计量经济学 几何学 数学 经济
作者
Tianhong Zhang,YanYan Wei,Lihua Xu,XiaoChen Tang,YeGang Hu,HaiChun Liu,Zixuan Wang,Tao Chen,Chunbo Li,Jijun Wang
出处
期刊:Psychiatry and Clinical Neurosciences [Wiley]
卷期号:78 (7): 385-392 被引量:3
标识
DOI:10.1111/pcn.13670
摘要

Aim Although many studies have explored the link between inflammatory markers and psychosis, there is a paucity of research investigating the temporal progression in individuals at clinical high‐risk (CHR) who eventually develop full psychosis. To address this gap, we investigated the correlation between serum cytokine levels and Timeframe for Conversion to Psychosis (TCP) in individuals with CHR. Methods We enrolled 53 individuals with CHR who completed a 5‐year follow‐up with a confirmed conversion to psychosis. Granulocyte macrophage‐colony stimulating factor (GM‐CSF), interleukin (IL)‐1β, 2, 6, 8, 10, tumor necrosis factor‐α (TNF‐α), and vascular endothelial growth factor (VEGF) levels were measured at baseline and 1‐year. Correlation and quantile regression analyses were performed. Results The median TCP duration was 14 months. A significantly shorter TCP was associated with higher levels of TNF‐α ( P = 0.022) and VEGF ( P = 0.016). A negative correlation was observed between TCP and TNF‐α level ( P = 0.006) and VEGF level ( P = 0.04). Quantile regression indicated negative associations between TCP and GM‐CSF levels below the 0.5 quantile, IL‐10 levels below the 0.3 quantile, IL‐2 levels below the 0.25 quantile, IL‐6 levels between the 0.65 and 0.75 quantiles, TNF‐α levels below the 0.8 quantile, and VEGF levels below the 0.7 quantile. A mixed linear effects model identified significant time effects for IL‐10 and IL‐2, and significant group effects for changes in IL‐2 and TNF‐α. Conclusions Our findings underscore that a more pronounced baseline inflammatory state is associated with faster progression of psychosis in individuals with CHR. This highlights the importance of considering individual inflammatory profiles during early intervention and of tailoring preventive measures for risk profiles.

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