Russell D M, Shike M, Marliss E B, Detsky A S, Shepherd F A, Feld R, Evans W K, Jeejeebhoy K N
Cancer Res. 1984 Apr;44(4):1706-11.
Changes in energy metabolism, substrate use, and hormone profiles were prospectively studied in 31 patients with small cell lung cancer receiving chemotherapy. Patients were randomized to receive either 4 weeks of total parenteral nutrition (n = 15) or to continue self-regulated p.o. diet (control group; n = 16). The initial actual resting energy expenditure measured by indirect calorimetry was 31% higher than the predicted resting energy expenditure determined by the Harris-Benedict formula. The p.o. calorie intake was inappropriately low for these hypermetabolic patients. Total parenteral nutrition resulted in a significant positive net energy balance, but in follow-up was associated with prolonged anorexia and a negative energy balance. Complete response to therapy reduced resting energy expenditure and increased calorie intake, whereas the contrary was true in nonresponders. Elevated plasma-free fatty acids (800 +/- 62 microM; S.E.) and a low respiratory quotient (0.74 +/- 0.02) indicate that the dominant energy source in patients with small cell lung cancer is fat, and that increased fat oxidation continues despite tumor response. Elevated fasting plasma catecholamines and insulin resistance may contribute to continued fat mobilization. Initially, there was a significant increase in blood lactate (1118 +/- 95 microM) suggesting either increased tumor or tumor-mediated glycolytic activity. Response to therapy was associated with a fall in blood lactate levels. The most effective way of improving the metabolic derangements in patients with small cell lung cancer was to achieve tumor response to therapy.
对31例接受化疗的小细胞肺癌患者的能量代谢、底物利用和激素谱变化进行了前瞻性研究。患者被随机分为两组,一组接受4周的全胃肠外营养(n = 15),另一组继续自行调节的口服饮食(对照组;n = 16)。通过间接测热法测得的初始实际静息能量消耗比根据哈里斯-本尼迪克特公式确定的预测静息能量消耗高31%。对于这些高代谢患者,口服热量摄入过低。全胃肠外营养导致显著的正净能量平衡,但在随访中与长期厌食和负能量平衡相关。对治疗的完全缓解降低了静息能量消耗并增加了热量摄入,而无反应者则相反。血浆游离脂肪酸升高(800±62μM;标准误)和低呼吸商(0.74±0.02)表明小细胞肺癌患者的主要能量来源是脂肪,并且尽管肿瘤有反应,但脂肪氧化增加仍在继续。空腹血浆儿茶酚胺升高和胰岛素抵抗可能导致脂肪持续动员。最初,血乳酸显著升高(1118±95μM),提示肿瘤或肿瘤介导的糖酵解活性增加。对治疗的反应与血乳酸水平下降相关。改善小细胞肺癌患者代谢紊乱的最有效方法是使肿瘤对治疗产生反应。