Esper Dema Halasa, Harb Wael A
Horizon Oncology, Lafayette, Indiana, USA.
Nutr Clin Pract. 2005 Aug;20(4):369-76. doi: 10.1177/0115426505020004369.
The progressive deterioration in nutrition status frequently seen in cancer patients is often referred to as cancer cachexia. Unlike starvation, in which fat stores from adipose are depleted and protein is spared from skeletal muscle, neither fat nor protein is spared in cachexia. Cachexia affects nearly half of cancer patients, causing the clinical manifestations of anorexia, muscle wasting, weight loss, early satiety, fatigue, and impaired immune response. Cachexia does not only impede the response to chemotherapy but also is a major cause of morbidity and mortality. According to clinical studies, increasing caloric intake does not necessarily reverse cachexia. The pathophysiology of cachexia involves more complex mechanisms than simply caloric deficiency. The process appears to be mediated by circulating catabolic factors, either secreted by the tumor alone or in concert with host-derived factors, such as tumor necrosis factor-alpha (TNF-alpha), interleukins (IL-1 and IL-6), interferon (IFN-y), and leukemia inhibitory factor (LIF). The successful reversal of this process will require in-depth knowledge of the mechanisms involved, which will then enable the development of effective pharmacologic interventions that may not only improve quality of life, but more importantly, improve survival among cancer patients.
癌症患者中常见的营养状况逐渐恶化通常被称为癌症恶病质。与饥饿不同，饥饿时脂肪组织中的脂肪储备被消耗，骨骼肌中的蛋白质得以保留，而在恶病质中，脂肪和蛋白质都无法保留。恶病质影响近一半的癌症患者，导致厌食、肌肉消瘦、体重减轻、早饱、疲劳和免疫反应受损等临床表现。恶病质不仅会阻碍对化疗的反应，还是发病和死亡的主要原因。根据临床研究，增加热量摄入不一定能逆转恶病质。恶病质的病理生理学涉及比单纯热量缺乏更复杂的机制。这个过程似乎是由循环分解代谢因子介导的，这些因子要么由肿瘤单独分泌，要么与宿主来源的因子共同分泌，如肿瘤坏死因子-α（TNF-α）、白细胞介素（IL-1和IL-6）、干扰素（IFN-γ）和白血病抑制因子（LIF）。要成功逆转这个过程，需要深入了解其中涉及的机制，这将有助于开发有效的药物干预措施，这些措施不仅可以提高生活质量，更重要的是，可以提高癌症患者的生存率。
