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Purpose: Previously, sleep in chronic obstructive pulmonary disease (COPD) has been objectively investigated only by lab-based polysomnography. The main purpose of this study was to evaluate sleep quality in COPD patients in their home environment using actigraphy. We also investigated the factors associated with sleep impairment and the relationship between objective and subjective sleep quality and daytime somnolence in these patients., Methods: Twenty-six patients with moderate to very severe COPD and 15 controls were studied by actigraphy for at least 5 days. Subjective sleep quality was evaluated by the Pittsburgh Sleep Quality Index and daytime sleepiness by the Epworth Sleepiness Scale (ESS). Dyspnea was quantified by the modified Medical Research Council (MMRC) scale., Results: COPD patients showed increased sleep latency (p = 0.003), mean activity (p = 0.003), and wake after sleep onset (p = 0.003) and reduced total sleep time (TST; p = 0.024) and sleep efficiency (p = 0.001), as compared to controls. In patients, severity of dyspnea was correlated with sleep activity (r = 0.41; p = 0.04) and TST (r = -0.46; p = 0.02) and multiple regression analysis showed that MMRC score was the best predictor of TST (p = 0.02) and sleep efficiency (p = 0.03). Actigraphy measures during daytime were not significantly different between patients and controls. Subjective sleep quality was poorer in patients than controls (p = 0.043). ESS scores were not significantly different between the two groups. Actigraphy measures were not correlated with subjective sleep quality or daytime somnolence in both groups., Conclusions: Nocturnal sleep is markedly impaired in stable COPD patients studied by actigraphy in their home environment and this impairment is related to severity of dyspnea.

Chronic obstructive pulmonary disease (COPD), a major cause of death and disability, is attributed to an abnormal inflammatory response by the lungs to noxious substances, primarily from cigarette smoke. Although oxidative stress is regarded as central to the pathogenesis of COPD, very few studies have examined the effects of antioxidants in this condition. This was a randomized, double-blind, placebo-controlled study on the effects of melatonin in COPD. Thirty-six consecutive patients with clinically stable moderate to very severe COPD (30 men; mean±S.D.=66.6±7.8yr) were randomized to receive 3mg melatonin (N=18) or placebo for 3 months. Oxidative stress was evaluated by 8-isoprostane levels in exhaled breath condensate at baseline (T0) and after one (T1), two (T2), and three months (T3) of treatment. Additionally, exhaled breath condensate levels of IL-8, dyspnea severity (Medical Research Council scale), lung function (spirometry), and functional exercise capacity (six min walk test) were compared at baseline and after treatment. Patients receiving melatonin showed a decrease in 8-isoprostane (T0: mean±S.E.M.=20.41±2.92pg/mL; T1: 18.56±2.68pg/mL; T2: 12.68±2.04pg/mL; T3: 12.70±2.18pg/mL; P=0.04; repeated measures ANOVA) with significant differences from baseline after 2 (P=0.03) and 3months (P=0.01). Dyspnea was improved by melatonin (P=0.01), despite no significant changes in lung function or exercise capacity. Placebo-treated patients, but not those who were given melatonin, showed an increase in IL-8 (P=0.03). In summary, melatonin administration reduced oxidative stress and improved dyspnea in COPD. Further studies are necessary to determine the potential role for melatonin in the long-term management of these patients., (© 2012 John Wiley & Sons A/S.)

Objective: To investigate the frequency of factors associated with restless legs syndrome (RLS) in patients with chronic obstructive pulmonary disease (COPD)., Methods: RLS diagnosis was investigated (International RLS Study Group, IRLSSG) and severity was assessed (IRLS rating scale) in 104 consecutive COPD patients (age 69.1±8). Other measures were dyspnea severity (Modified Medical Research Council, MMRC), sleep quality (Pittsburgh Sleep Quality Index, PSQI), daytime somnolence (Epworth Sleepiness Scale, ESS), depressive symptoms (Beck Depression Inventory, BDI-II), and fatigue (Fatigue Severity Scale, FSS). Laboratory values included hemoglobin, ferritin, creatinine, and fibrinogen., Results: Thirty-two patients (30.8%) were diagnosed with RLS (65.6% women), which was moderate/severe (IRLS >11) in 26 (81.3%). RLS symptoms started after age 40 in most patients (93.3%). RLS patients had poorer sleep quality (PSQI >5=59.6%; p=0.002), worse fatigue (FSS >27=51%; p=0.005), and more depressive symptoms (BDI-II >10=14.4%; p=0.005). Patients with RLS also presented more severe dyspnea (p=0.009) and lower creatinine levels (p=0.005). Overall, fatigue severity was correlated with older age (p=0.001); level of dyspnea was positively correlated with PSQI and FSS (p<0.005) and negatively correlated with ferritin (p=0.03) and creatinine (p=0.005), and PSQI scores correlated positively with FSS (p<0.005) and negatively with ferritin (p=0.005) and creatinine (p=0.02). Quality of sleep was independently predicted by dyspnea severity and creatinine and fatigue by age and depression., Conclusion: RLS is common in COPD. Patients with RLS have low creatinine, poorer quality of sleep, and more fatigue and depressive symptoms. RLS symptom severity is correlated to lower ferritin and severity of dyspnea., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Worldwide, COPD is a major cause of morbidity and mortality. The clinical and functional manifestations of COPD result from lung injury occurring through various mechanisms, including oxidative stress, inflammation, protease-antiprotease imbalance and apoptosis. Oxidative stress is central to the pathogenesis of COPD, since it can directly damage lung structures and exacerbate the other mechanisms involved. The cellular and molecular events involved in such lung injury are believed to occur long before the clinical and functional expression of COPD. Although the use of bronchodilators is currently the principal treatment for COPD, bronchodilators have little or no effect on disease progression. A better understanding of the pathogenesis of COPD, together with renewed efforts in basic and clinical research, will allow the diagnosis of COPD at a pre-clinical stage and provide more appropriate monitoring of disease activity, as well as leading to the development of novel therapeutic agents that will effectively prevent the progression of the disease.

Disturbed sleep is reportedly common in chronic obstructive pulmonary disease (COPD), but the impact of quality of sleep on health-related quality of life (HRQL) has not been previously investigated in these individuals. The purpose of this study was to assess the impact of quality of sleep on HRQL in patients with COPD. In 30 clinically stable patients with moderate to very severe COPD, we evaluated subjective sleep quality using the Pittsburgh Sleep Quality Index (PSQI) and HRQL using the Saint George's Respiratory Questionnaire. Additionally, lung function was assessed by spirometry, severity of dyspnea by the Modified Medical Research Council scale, and functional exercise capacity by the Six-Minute Walk Test. Twenty-one (70%) patients showed poor quality of sleep (PSQI > 5). HRQL was significantly correlated with quality of sleep (P = 0.02), post-bronchodilator FEV1 (P = 0.04), and severity of dyspnea (P < 0.01). Multiple regression analysis showed that quality of sleep was the best predictor of quality of life in our subjects. Our data suggest that quality of sleep is major determinant of HRQL in COPD. Increased efforts to diagnose and treat sleep problems, including measures to improve factors that adversely affect sleep should receive great attention in the daily management of these patients.