Skipworth Richard J E, Fearon Kenneth C H
Clinical and Surgical Sciences (Surgery), School of Clinical Sciences and Community Health, The University of Edinburgh, Royal Infirmary, Edinburgh, UK.
Eur J Gastroenterol Hepatol. 2007 May;19(5):371-7. doi: 10.1097/MEG.0b013e3280bdbf87.
Cancer patients lose weight as a result of the anorexia-cachexia syndrome, and this weight loss is associated with significant morbidity and mortality. Thus, nutritional support to arrest or reverse weight loss is of paramount importance in the management of Cachexia cancer patients. Persistent tumour-induced metabolic changes result, however, in a suboptimal response to such support, making nutritional maintenance or improvement difficult targets to achieve. Mechanisms involved in the blockade to anabolism in cancer cachexia include alterations in skeletal muscle and hepatic protein metabolism, and reduced physical activity. Mediators underlying these mechanisms of weight loss include proinflammatory cytokines, tumour-specific cachectic factors, and neuroendocrine mediators of muscle catabolism. The complex mix of different mediators renders unimodal nutritional intervention a strategy that is unlikely to succeed completely. Therefore, clinical trials using combination therapies or immunonutrition are required for future success.
癌症患者因厌食-恶病质综合征而体重减轻，这种体重减轻与显著的发病率和死亡率相关。因此，在恶病质癌症患者的管理中，阻止或逆转体重减轻的营养支持至关重要。然而，持续的肿瘤诱导的代谢变化导致对这种支持的反应不理想，使得营养维持或改善难以实现。癌症恶病质中合成代谢受阻所涉及的机制包括骨骼肌和肝脏蛋白质代谢的改变以及身体活动的减少。这些体重减轻机制的潜在介质包括促炎细胞因子、肿瘤特异性恶病质因子和肌肉分解代谢的神经内分泌介质。不同介质的复杂组合使得单一模式的营养干预不太可能完全成功。因此，未来的成功需要使用联合疗法或免疫营养的临床试验。
