Diabetes and metabolic dysfunction in COPD

J.R.H. Archer, E.H. Baker
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引用次数: 9

Abstract

Diabetes mellitus and metabolic syndrome are common in patients with chronic obstructive pulmonary disease (COPD). Metabolic disorders are associated with worse cardiovascular and pulmonary outcomes in COPD patients. This review will consider the prevalence, detection and management of metabolic disorders in COPD.

Diabetes mellitus is more common in stable COPD patients than in matched controls. COPD may directly increase insulin resistance through effects of chronic inflammation on insulin receptor signalling and through chronic hypoxia and systemic corticosteroid treatment. COPD patients with diabetes have increased risk of pulmonary infection, structural lung damage, hospitalisation and death. Management of diabetes in COPD should follow treatment guidelines for type 2 diabetes. However oral hypoglycaemic treatment may need to be modified in those with respiratory failure, cachexia or heart failure.

Glucose tolerance deteriorates during COPD exacerbations due to physiological stress of acute illness and to increased inflammation, acidosis and corticosteroid dose. Acute hyperglycaemia during COPD exacerbations is associated with prolonged hospital stay, NIV failure and increased risk of death. There is little evidence to guide management of acute hyperglycaemia in COPD, however attention should be given to nutrition and to minimising corticosteroid dose. Intravenous insulin to maintain blood glucose 8–10 mmol.L−1 may also be of therapeutic value.

Insulin resistance commonly occurs with obesity, dyslipidaemia and hypertension. Together these make up the ‘metabolic syndrome’, which is a major determinant of cardiovascular morbidity and mortality. Coordinated management of diverse aspects of the metabolic syndrome is essential to optimise cardiovascular outcomes. Retrospective cohort and population studies have found that use of statins, ACE inhibitors and angiotensin II receptor blocker by COPD patients is associated with improvement in pulmonary function and exercise capacity and reduction in exacerbations and COPD-related mortality. These observations need to be confirmed in large interventional studies.

慢性阻塞性肺病患者的糖尿病和代谢功能障碍
糖尿病和代谢综合征在慢性阻塞性肺疾病(COPD)患者中很常见。在COPD患者中,代谢紊乱与更糟糕的心血管和肺预后相关。这篇综述将考虑慢性阻塞性肺病中代谢紊乱的患病率、检测和管理。糖尿病在稳定的COPD患者中比在匹配的对照组中更常见。慢性阻塞性肺病可能通过慢性炎症对胰岛素受体信号传导的影响以及慢性缺氧和全身皮质类固醇治疗直接增加胰岛素抵抗。慢性阻塞性肺病合并糖尿病患者肺部感染、结构性肺损伤、住院和死亡的风险增加。慢性阻塞性肺病患者的糖尿病管理应遵循2型糖尿病的治疗指南。然而,对于呼吸衰竭、恶病质或心力衰竭的患者,口服降糖治疗可能需要修改。由于急性疾病的生理应激以及炎症、酸中毒和皮质类固醇剂量增加,慢性阻塞性肺病加重期间糖耐量恶化。慢性阻塞性肺病加重期间的急性高血糖与住院时间延长、NIV失效和死亡风险增加有关。很少有证据可以指导慢性阻塞性肺病患者急性高血糖的管理,但应注意营养和尽量减少皮质类固醇剂量。静脉注射胰岛素维持血糖8-10毫摩尔。L−1也可能具有治疗价值。胰岛素抵抗常见于肥胖、血脂异常和高血压。这些共同构成了“代谢综合征”,这是心血管发病率和死亡率的主要决定因素。代谢综合征各方面的协调管理对于优化心血管预后至关重要。回顾性队列和人群研究发现,COPD患者使用他汀类药物、ACE抑制剂和血管紧张素II受体阻滞剂与肺功能和运动能力的改善以及COPD恶化和相关死亡率的降低有关。这些观察结果需要在大型介入性研究中得到证实。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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