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已有文献报道,体重减轻是COPD患者死亡率增加的原因之一,但COPD患者体重减轻的机制尚不清楚。已往的研究工作着重于能量平衡和潜在的代谢亢进因素。然而,这咎假设不能真正解释这类患者出现恶病质的原因,因为代谢所需能量很容易通过增加饮食来补充,所以本文试图从另一个角度来探讨COPD患者体重减轻的机制。 已知肿瘤坏死因子(TNF-α)在动物模型中可产生恶病质综合征,研究表明TNF-α在癌症、慢性心力衰竭、囊性纤维变、神经性厌食等严重疾病中充当恶病质的介质。给正常人体注入TNF-α,可导致代谢率和代谢底物的变化。但在大部分临床实验中,血清TNF-α和
It has been reported in the literature that weight loss is one of the causes of mortality in COPD patients, but the mechanism of weight loss in COPD patients is not yet clear. Past research efforts have focused on energy balance and potential metabolic hyperfunction. However, this hypothesis does not really explain the causes of cachexia in this group of patients, since the energy required for metabolism can easily be supplemented by an increased diet, this article attempts to explore the mechanism of weight loss in COPD patients from another perspective. It is known that tumor necrosis factor (TNF-α) can produce cachexia syndrome in animal models and studies have shown that TNF-α acts as a cachectic mediator in severe diseases such as cancer, chronic heart failure, cystic fibrosis and anorexia nervosa. Injecting TNF-alpha into normal humans can lead to changes in metabolic rate and metabolic substrates. However, in most clinical trials, serum TNF-α and