成人桥本甲状腺炎患者的免疫营养指标、炎症标志物及甲状腺相关参数

摘要(中文译文)

桥本甲状腺炎（HT）是一种慢性自身免疫性疾病，其特征不仅包括甲状腺功能障碍，还涉及代谢紊乱、微量营养素不足和低度炎症。因此，由常规实验室参数衍生的复合指标可能有助于反映该疾病更广泛的全身性特征。本研究探讨了免疫营养指标包括预后营养指数（PNI）、营养风险指数（NRI）和控制营养状况（CONUT），以及血细胞计数衍生的炎症标志物包括中性粒细胞与淋巴细胞比值（NLR）、单核细胞与淋巴细胞比值（MLR）、血小板与淋巴细胞比值（PLR）和系统性免疫炎症指数（SII），与桥本甲状腺炎成人患者的甲状腺功能、甲状腺自身免疫、代谢特征、病程及维生素D状态之间的队列内关联。本横断面研究纳入229名确诊为HT的成人。评估了PNI、NRI、CONUT及全血细胞计数衍生的炎症标志物与甲状腺功能、甲状腺自身免疫、病程、代谢特征及维生素D状态的关系。由于大多数变量不服从正态分布，主要分析采用非参数检验。相关性采用Spearman秩相关系数评估。探索性回归模型使用HC3异方差一致性稳健标准误进行估计，并进行了基于CRP的敏感性分析，排除CRP > 10 mg/L的参与者。维生素D缺乏极为普遍，影响70.3%的参与者。在免疫营养指标中，NRI根据BMI分类和HOMA定义的胰岛素抵抗存在显著差异（均 < 0.001），表明其与代谢负担关系更为密切。PNI与病程相关（ = 0.009），而炎症指标在所考察的各临床分组间基本相似。在探索性稳健回归模型中，解释力仍然有限（R = 0.066-0.171）。PLR与TSH的指标相关关联最为一致，而在全样本稳健模型中观察到的CONUT-FT3关联在基于CRP的敏感性分析后未能保留。本研究中HT成人患者普遍存在维生素D缺乏，同时伴有显著的超重和胰岛素抵抗负担。常规免疫营养和炎症指标可能为队列内生化和代谢异质性提供支持性信息，但不应将其解释为独立的诊断或预后标志物。特别是，NRI似乎更多反映代谢和肥胖相关负担而非单纯的营养风险，而PLR与TSH的指标相关关联在内部一致性上最为突出。

Abstract

Hashimoto's thyroiditis (HT) is a chronic autoimmune disorder characterized not only by thyroid dysfunction but also by metabolic disturbances, micronutrient inadequacies, and low-grade inflammation. Composite indices derived from routine laboratory parameters may therefore help capture the broader systemic profile of the disease. This study explored within-cohort associations of immunonutritional indices including the Prognostic Nutritional Index (PNI), Nutritional Risk Index (NRI), and Controlling Nutritional Status (CONUT), and hemogram-derived inflammatory markers including the Neutrophil-to-Lymphocyte Ratio (NLR), Monocyte-to-Lymphocyte Ratio (MLR), Platelet-to-Lymphocyte Ratio (PLR), and Systemic Immune-Inflammation Index (SII), with thyroid function, thyroid autoimmunity, metabolic characteristics, disease duration, and vitamin D status in adults with Hashimoto's thyroiditis. This cross-sectional study included 229 adults diagnosed with HT. PNI, NRI, CONUT, and complete blood count-derived inflammatory markers were evaluated in relation to thyroid function, thyroid autoimmunity, disease duration, metabolic characteristics, and vitamin D status. Because most variables were not normally distributed, the main analyses were conducted using non-parametric tests. Correlations were evaluated using Spearman's rank correlation coefficients. Exploratory regression models were estimated using HC3 heteroscedasticity-consistent robust standard errors, and CRP-based sensitivity analyses were performed by excluding participants with CRP > 10 mg/L. Vitamin D deficiency was highly prevalent and affected 70.3% of the participants. Among the immunonutritional indices, NRI differed significantly according to BMI category and HOMA-defined insulin resistance (both < 0.001), indicating a closer relationship with metabolic burden. PNI was associated with disease duration ( = 0.009), whereas the inflammatory indices were largely similar across the clinical groupings examined. In exploratory robust regression models, the explanatory power remained modest (R = 0.066-0.171). PLR showed the most consistent index-related association with TSH, whereas the CONUT-FT3 association observed in the full-sample robust model was not retained after CRP-based sensitivity analysis. Adults with HT in this study showed frequent vitamin D deficiency together with a substantial burden of excess weight and insulin resistance. Routine immunonutritional and inflammatory indices may provide supportive information on within-cohort biochemical and metabolic heterogeneity, but they should not be interpreted as stand-alone diagnostic or prognostic markers. In particular, NRI appeared to reflect metabolic and adiposity-related burden more than nutritional risk alone, while PLR showed the most internally consistent index-related association with TSH.

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