超越摄入减少：肿瘤代谢与免疫失调驱动头颈部鳞状细胞癌（HNSCC）的癌症相关营养不良

文献信息

中文摘要

癌症相关营养不良在头颈部鳞状细胞癌（HNSCC）患者中高度普遍，并且是治疗耐受性、生活质量和生存的主要决定因素。尽管传统上将其归因于吞咽困难、黏膜炎和治疗相关毒性导致的口腔摄入减少，但越来越多的证据表明，HNSCC中的营养不良在很大程度上是由肿瘤诱导的代谢和炎症改变所驱动的。增强的有氧糖酵解、全身性炎症和肿瘤衍生因子促进高代谢、底物重新分布和进行性骨骼肌耗竭。在这一免疫代谢框架内，肿瘤表现为一个代谢汇，将葡萄糖、脂质和氨基酸从宿主组织重新导向以维持其生长，从而独立于热量摄入导致能量消耗和肌肉减少症。近期临床数据支持该模型的转化相关性。第三颈椎（C3）水平的基于影像的身体成分评估以及总病灶糖酵解（TLG）等代谢成像参数，提供了肿瘤代谢负荷及其与骨骼肌丢失和营养风险关联的可测量指标。整合代谢成像、炎症生物标志物和身体成分分析可能有助于更早识别营养不良和治疗相关毒性高风险患者。本综述将这些互补的生物学和影像学领域整合为一个统一的免疫代谢框架，用于HNSCC的营养风险分层。将HNSCC中的癌症相关营养不良视为一种肿瘤驱动的免疫代谢综合征具有重要的治疗意义。早期免疫代谢营养策略，而非仅反应性热量补充，可能成为旨在保留瘦体重和改善临床结局的综合肿瘤治疗的关键组成部分。

英文摘要

Cancer-related malnutrition is highly prevalent in patients with head and neck squamous cell carcinoma (HNSCC) and represents a major determinant of treatment tolerance, quality of life, and survival. Although traditionally attributed to reduced oral intake caused by dysphagia, mucositis, and treatment-related toxicity, increasing evidence indicates that malnutrition in HNSCC is largely driven by tumor-induced metabolic and inflammatory alterations. Enhanced aerobic glycolysis, systemic inflammation, and tumor-derived factors promote hypermetabolism, substrate redistribution, and progressive skeletal muscle depletion. Within this immune-metabolic framework, the tumor behaves as a metabolic sink, redirecting glucose, lipids, and amino acids from host tissues to sustain its growth, thereby contributing to energy wasting and sarcopenia independently of caloric intake. Recent clinical data support the translational relevance of this model. Imaging-based assessment of body composition at the third cervical vertebra (C3) and metabolic imaging parameters such as total lesion glycolysis (TLG) provide measurable indicators of tumor metabolic burden and its association with skeletal muscle loss and nutritional risk. Integrating metabolic imaging, inflammatory biomarkers, and body composition analysis may enable earlier identification of patients at high risk of malnutrition and treatment-related toxicity. This review integrates these complementary biological and imaging domains into a unified immune-metabolic framework for nutritional risk stratification in HNSCC. Recognizing cancer-related malnutrition in HNSCC as a tumor-driven immune-metabolic syndrome has important therapeutic implications. Early immune-metabolic nutritional strategies, rather than reactive caloric supplementation alone, may represent a key component of integrated oncologic care aimed at preserving lean body mass and improving clinical outcomes.