Kern K A, Norton J A
Surgery Branch, National Cancer Institute, Bethesda, MD 20892.
JPEN J Parenter Enteral Nutr. 1988 May-Jun;12(3):286-98. doi: 10.1177/0148607188012003286.
Cancer cachexia describes a syndrome of progressive weight loss, anorexia, and persistent erosion of host body cell mass in response to a malignant growth. Although often associated with preterminal patients bearing disseminated disease, cachexia may be present in the early stages of tumor growth before any signs or symptoms of malignancy. A decline in food intake relative to energy expenditure (which may be increased, normal, or decreased) is the fundamental physiologic derangement leading to cancer-associated weight loss. In addition, abnormalities of host carbohydrate, protein, and fat metabolism lead to continued mobilization and ineffective repletion of host tissue, despite adequate nutritional support. Mediators of cancer anorexia and associated abnormalities are unknown. Cachectin/TNF or other host-derived cytokines (produced as a defense against malignancy) have been implicated as signal molecules in cachexia, based upon similar metabolic derangements produced by these cytokines in other chronic wasting illnesses. Nutritional support is effective in maintaining body weight of cachectic cancer patients, but ineffective in maintaining lean body mass. Although in one study parenteral nutritional support has improved operative morbidity and mortality in cancer patients, it has not yet improved response to chemotherapy or radiation therapy. Because of metabolic derangements seen in cancer cachexia, effective nutritional treatment regimens will probably require manipulation of host intermediary metabolism in addition to feeding. Insulin therapy or exercise are two such methods which appear to preserve host composition by preferential feeding of the host at the expense of the tumor. Future studies which more clearly define the role of signal molecules in producing cancer cachexia syndrome may lead to new treatment strategies, possibly involving modulation of the effects of such molecules on host metabolism.
癌症恶病质是指机体因恶性肿瘤生长而出现的进行性体重减轻、厌食以及机体细胞群持续消耗的一种综合征。尽管恶病质常与患有播散性疾病的终末期患者相关，但在肿瘤生长的早期阶段，在出现任何恶性肿瘤的体征或症状之前，恶病质就可能已经存在。相对于能量消耗（能量消耗可能增加、正常或减少）而言，食物摄入量的下降是导致癌症相关性体重减轻的根本生理紊乱。此外，尽管给予了充足的营养支持，但机体碳水化合物、蛋白质和脂肪代谢的异常仍会导致机体组织持续动员和补充无效。癌症厌食及相关异常的介质尚不清楚。基于这些细胞因子在其他慢性消耗性疾病中产生的类似代谢紊乱，恶病质素/肿瘤坏死因子或其他宿主源性细胞因子（作为对抗恶性肿瘤的防御机制而产生）被认为是恶病质中的信号分子。营养支持对维持恶病质癌症患者的体重有效，但对维持瘦体重无效。尽管在一项研究中，肠外营养支持改善了癌症患者的手术发病率和死亡率，但尚未改善化疗或放疗的反应。由于在癌症恶病质中观察到代谢紊乱，有效的营养治疗方案可能除了喂食外还需要对机体中间代谢进行调控。胰岛素治疗或运动是两种这样的方法，它们似乎通过优先为机体提供营养而牺牲肿瘤来维持机体组成。未来更明确界定信号分子在产生癌症恶病质综合征中作用的研究可能会带来新的治疗策略，可能涉及调节这些分子对机体代谢的影响。
