Restless legs syndrome, sleep impairment, and fatigue in chronic obstructive pulmonary disease.

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.

Melatonin reduces lung oxidative stress in patients with chronic obstructive pulmonary disease: a randomized, double-blind, placebo-controlled study.

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.