Evidence that long-term COX-treatment improves energy homeostasis and body composition in cancer patients with progressive cachexia.
Evidence that long-term COX-treatment improves energy homeostasis and body composition in cancer patients with progressive cachexia.
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DOI：
10.3892/ijo.24.3.505
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发表时间：
2004-03
影响因子：
5.2
通讯作者：
K. Lundholm;P. Daneryd;U. Körner;A. Hyltander;I. Bosaeus
中科院分区：
文献类型：
--
作者：
K. Lundholm;P. Daneryd;U. Körner;A. Hyltander;I. Bosaeus
癌症患者因食欲不足和不适当的高能量消耗而导致能量负平衡，从而导致体重减轻。宿主和肿瘤衍生的细胞因子和最近的类二十烷酸已被认为是负责介质。因此，在选定的癌症患者组中的动物实验和短期临床试验中的观察结果表明，环加氧酶（考克斯）阻断可以改善宿主代谢和健康，并且COX治疗组的长期COX治疗意味着改善的存活率。本研究的目的是寻找长期COX治疗改善非肥胖减肥癌症患者能量和心血管稳态的证据。对连续收集的数据库材料进行回顾性病例对照分析。与营养不良的非癌症患者相比，体重减轻的未经治疗的癌症患者的静息能量消耗升高（23.3+/-0.1，n=702 vs 20.9+/-0.3千卡/千克/天，n=132，p<0.001）。长期消炎痛治疗后，这种差异显著降低（p<0.003）。吲哚美辛治疗后心率相应减慢，收缩压升高（P<0.006-0.008）。癌症患者全身脂肪保存更多（p<0.005），而瘦体重不受长期吲哚美辛的影响。所有这些有益的效果与癌症患者服用吲哚美辛时全身炎症（C反应蛋白，红细胞沉降率）的降低平行（p<0.0004）。全身炎症和静息能量代谢预测进展性癌症的体重减轻（p<0.0001）。我们的数据支持这样的概念，即COX治疗可能通过减弱静息代谢和改善食欲（由于全身炎症减少）为减肥癌症患者提供有益的代谢作用。
Cancer patients lose weight due to negative energy balance because of insufficient appetite and inappropriately high energy expenditure. Host and tumor derived cytokines and more recently eicosanoids have been held responsible as mediators. Accordingly, observations in animal experiments and short-term clinical trials in selected groups of cancer patients, have implied that cyclo-oxygenase (COX) blockade can improve host metabolism and well-being, and long-term COX-treatment of unselected groups have implied improved survival. The aim of this study was to search for evidence that long-term COX-treatment improves energy and cardiovascular homeostasis in unselected weight-losing cancer patients. A retrospective case control analysis was performed on a data-base material collected consecutively. Weight-losing untreated cancer patients had elevated resting energy expenditure compared to undernourished non-cancer patients (23.3+/-0.1, n=702 vs 20.9+/-0.3 kcal/kg/day, n=132, p<0.001). This difference became significantly reduced by long-term indomethacin treatment (p<0.003). Heart rate was correspondingly decreased, while systolic blood pressure increased following indomethacin treatment of cancer patients (p<0.006-0.008). Total body fat was more preserved (p<0.005), while lean body mass was uninfluenced by long-term indomethacin to cancer patients. All these beneficial effects were parallel to a decrease in systemic inflammation (C-reactive protein, erythrocyte sedimentation rate) in cancer patients on indomethacin (p<0.0004). Systemic inflammation and resting energy metabolism predicted weight loss in progressive cancer (p<0.0001). Our data support the concept that COX-treatment may offer beneficial metabolic effects to weight-losing cancer patients by attenuation of resting metabolism and improved appetite due to decreased systemic inflammation.