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.
Disturbed sleep is common in chronic obstructive pulmonary disease (COPD). Conventional hypnotics worsen nocturnal hypoxemia and, in severe cases, can lead to respiratory failure. Exogenous melatonin has somnogenic properties in normal subjects and can improve sleep in several clinical conditions. This randomized, double-blind, placebo-controlled study was carried out to determine the effects of melatonin on sleep in COPD. Thirty consecutive patients with moderate to very severe COPD were initially recruited for the study. None of the participants had a history of disease exacerbation 4 weeks prior to the study, obstructive sleep apnea, mental disorders, current use of oral steroids, methylxanthines or hypnotic-sedative medication, nocturnal oxygen therapy, and shift work. Patients received 3 mg melatonin (N = 12) or placebo (N = 13), orally in a single dose, 1 h before bedtime for 21 consecutive days. Sleep quality was assessed by the Pittsburgh Sleep Quality Index (PSQI) and daytime sleepiness was measured by the Epworth Sleepiness Scale. Pulmonary function and functional exercise level were assessed by spirometry and the 6-min walk test, respectively. Twenty-five patients completed the study protocol and were included in the final analysis. Melatonin treatment significantly improved global PSQI scores (P = 0.012), particularly sleep latency (P = 0.008) and sleep duration (P = 0.046). No differences in daytime sleepiness, lung function and functional exercise level were observed. We conclude that melatonin can improve sleep in COPD. Further long-term studies involving larger number of patients are needed before melatonin can be safely recommended for the management of sleep disturbances in these patients.
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.
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.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.