Torosian M H, Daly J M
Cancer. 1986 Oct 15;58(8 Suppl):1915-29. doi: 10.1002/1097-0142(19861015)58:8+<1915::aid-cncr2820581421>3.0.co;2-n.
Cancer patients have the highest prevalence of malnutrition of any group of hospitalized patients. The potential causes of this malnutrition are numerous, as elements of both starvation and stress are evident in the cancer-bearing host. The presence of the tumor alone may lead to reduced intake of nutrients and treatment modalities of surgery, chemotherapy, and radiation therapy further exacerbate nutritional deficits. It is clear that the tumor requires energy substrates to grow, and that these substrates are exacted from the host. Animal studies identify progressive nutritional depletion concomitant with increasing tumor growth during ingestion of a regular diet. This appears predominantly due to reduced dietary intake in addition to host metabolic alterations. In animal/tumor models deliberate dietary protein depletion results in severe host weight loss, but also causes diminished tumor growth rates. Dietary manipulation in these animal/tumor models have demonstrated methods of improving tumor response to chemotherapy by manipulation of tumor growth rates. In addition, drug-pharmacokinetics have been altered by dietary manipulation. However, data from animal/tumor models are not directly applicable to man since the tumor in animals usually results in the death of the host within six to eight weeks. Nevertheless, controlled laboratory studies in animals provide basic metabolic information which promotes understanding of host/tumor relationships in man. In cancer patients malnutrition has prognostic value, leads to a distortion of body composition with erosion of body protein and fat stores, and compromises the delivery of adequate therapy. There is no direct objective evidence of accelerated tumor growth in humans with cancer who receive nutritional support as part of their treatment regimen. The host benefits to the extent that body composition is at least maintained during the period of nutritional repletion. Thus, nutritional support provides support to the patient during periods of treatment and dietary deprivation. No improvement in the tumor's response to therapy, however, has been demonstrated by this approach.
癌症患者是住院患者中营养不良发生率最高的群体。这种营养不良的潜在原因众多，因为饥饿和应激因素在癌症患者体内都很明显。仅肿瘤的存在就可能导致营养摄入减少，而手术、化疗和放疗等治疗方式会进一步加剧营养缺乏。显然，肿瘤生长需要能量底物，而这些底物是从宿主身上获取的。动物研究表明，在正常饮食摄入期间，随着肿瘤生长的增加，营养会逐渐消耗。这主要是由于饮食摄入量减少以及宿主代谢改变所致。在动物/肿瘤模型中，刻意减少饮食中的蛋白质会导致宿主体重严重下降，但也会使肿瘤生长速度减慢。在这些动物/肿瘤模型中进行饮食调控，已证明可以通过控制肿瘤生长速度来改善肿瘤对化疗的反应。此外，饮食调控还改变了药物的药代动力学。然而，动物/肿瘤模型的数据不能直接应用于人类，因为动物体内的肿瘤通常会在六到八周内导致宿主死亡。尽管如此，动物的对照实验室研究提供了基本的代谢信息，有助于理解人类宿主/肿瘤的关系。在癌症患者中，营养不良具有预后价值，会导致身体成分失衡，身体蛋白质和脂肪储备减少，并影响充分治疗的实施。没有直接客观的证据表明，接受营养支持作为治疗方案一部分的癌症患者肿瘤生长加速。宿主在营养补充期间至少能维持身体成分，从而从中受益。因此，营养支持在治疗和饮食缺乏期间为患者提供支持。然而，这种方法并未证明能改善肿瘤对治疗的反应。
