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Prevalence of metabolic syndrome in patients with chronic obstructive pulmonary disease: An observational study in South Indians.
Priyadharshini, N, Renusha, RC, Reshma, S, Sindhuri Sai, M, Koushik Muthu, RM, Rajanandh, MG
Diabetes & metabolic syndrome. 2020;(4):503-507
Abstract
BACKGROUND AND AIMS Metabolic syndrome (MetS) has a significant association with airflow obstruction and physical inactivity, which are the relevant extra-pulmonary markers of chronic obstructive respiratory disease (COPD). This study aimed to estimate the prevalence of MetS and its correlation with comorbidities and health related quality of life (HRQoL) in South Indian patients with COPD. METHODS A cross-sectional study was conducted among the 76 COPD patients. Pulmonary function test (PFT) and parameters for MetS such as waist circumference, blood pressure, fasting blood glucose, triglycerides (TGs) and high density lipoprotein cholesterol (HDL-C) levels of COPD patients were measured. HRQoL was calculated using Saint George Respiratory Questionnaire (SGRQ). RESULTS 54% of COPD patients were presented with MetS especially in stage II and III. TGs and HDL-C were significantly associated with the severity of COPD (p < 0.05), while waist circumference, TGs and HDL-C were significantly (p < 0.05) correlated with PFT. Symptom, activity, impact and total scores of SGRQ was increased statistically (p < 0.05) in COPD patients with MetS than without MetS. CONCLUSION According to our findings, screening the grade II and III COPD patients for the presence of MetS is a reasonable option. The results of this study should be confirmed with a larger sample of population.
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2.
Iron and Sphingolipids as Common Players of (Mal)Adaptation to Hypoxia in Pulmonary Diseases.
Ottolenghi, S, Zulueta, A, Caretti, A
International journal of molecular sciences. 2020;(1)
Abstract
Hypoxia, or lack of oxygen, can occur in both physiological (high altitude) and pathological conditions (respiratory diseases). In this narrative review, we introduce high altitude pulmonary edema (HAPE), acute respiratory distress syndrome (ARDS), Chronic Obstructive Pulmonary Disease (COPD), and Cystic Fibrosis (CF) as examples of maladaptation to hypoxia, and highlight some of the potential mechanisms influencing the prognosis of the affected patients. Among the specific pathways modulated in response to hypoxia, iron metabolism has been widely explored in recent years. Recent evidence emphasizes hepcidin as highly involved in the compensatory response to hypoxia in healthy subjects. A less investigated field in the adaptation to hypoxia is the sphingolipid (SPL) metabolism, especially through Ceramide and sphingosine 1 phosphate. Both individually and in concert, iron and SPL are active players of the (mal)adaptation to physiological hypoxia, which can result in the pathological HAPE. Our aim is to identify some pathways and/or markers involved in the physiological adaptation to low atmospheric pressures (high altitudes) that could be involved in pathological adaptation to hypoxia as it occurs in pulmonary inflammatory diseases. Hepcidin, Cer, S1P, and their interplay in hypoxia are raising growing interest both as prognostic factors and therapeutical targets.
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3.
Association between chronic obstructive pulmonary disease and serum lipid levels: a meta-analysis.
Xuan, L, Han, F, Gong, L, Lv, Y, Wan, Z, Liu, H, Zhang, D, Jia, Y, Yang, S, Ren, L, et al
Lipids in health and disease. 2018;(1):263
Abstract
BACKGROUND Metabolic syndrome is a common extrapulmonary comorbidity in patients with chronic obstructive pulmonary disease (COPD). However, the reported relationship of COPD with dyslipidemia, an important component of metabolic syndrome, is ambiguous. The aim of this meta-analysis is to investigate the association between COPD and the serum levels of high-density lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol (LDL), total cholesterol (TC), and triglyceride (TG). METHODS The PubMed and Embase databases were searched to find potential studies using the search terms of ("dyslipidemia" or "HDL" or "LDL" or "cholesterol" or "triglyceride") and COPD. We also performed subgroup analysis enrolling patients who were not receiving treatment for dyslipidemia. Mean differences (MD) with 95% confidence intervals (CI) were estimated with random effects models. RESULTS A total of 11 studies comprising 615 cases and 471 controls were included in the study. No significant differences were found in the HDL (MD = -2.55, 95% CI [-6.03, 0.93], P = 0.15), LDL (MD = -2.25, 95% CI [-13.36, 8.86], P = 0.69), TC (MD = -2.69, 95% CI [-13.30, 7.92], P = 0.62), and TG (MD = 6.90, 95% CI [-2.81, 16.60], P = 0.16) levels of the 2 groups. However, subgroup analysis enrolling patients who were not receiving treatment for dyslipidemia showed that TG levels were higher in patients with stable COPD than in healthy individuals (MD = 16.35, 95% CI [5.90, 26.80], P = 0.002). CONCLUSIONS Excluding the impact of hypolipidemic treatment on serum lipid profile, TG levels were higher in patients with COPD than in healthy individuals. This meta-analysis suggested that physicians should screen COPD patients for elevated TG levels to reduce the risk of cardiovascular morbidity and mortality.
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4.
Effects of early administration of acetazolamide on the duration of mechanical ventilation in patients with chronic obstructive pulmonary disease or obesity-hypoventilation syndrome with metabolic alkalosis. A randomized trial.
Rialp Cervera, G, Raurich Puigdevall, JM, Morán Chorro, I, Martín Delgado, MC, Heras la Calle, G, Mas Serra, A, Vallverdú Perapoch, I
Pulmonary pharmacology & therapeutics. 2017;:30-37
Abstract
BACKGROUND Metabolic alkalosis (MA) inhibits respiratory drive and may delay weaning from mechanical ventilation (MV). MA is common in CO2-retainer patients that need MV. Acetazolamide (ACTZ) decreases serum bicarbonate concentration and stimulates respiratory drive. This study evaluated the effects of ACTZ on the duration of MV in patients with MA and COPD or obesity hypoventilation syndrome (OHS) intubated with acute respiratory failure. METHODS Multicenter, randomized, controlled, double-blind study, with COPD or OHS patients with MV < 72 h and initial bicarbonate >28 mmol/L and pH > 7.35. Test-treatment, ACTZ 500 mg or placebo, was daily administered if pH > 7.35 and bicarbonate >26 mmol/L. Clinical, respiratory and laboratory parameters were recorded. RESULTS 47 patients (36 men) were randomized. There were no significant differences between groups in comorbidities, baseline characteristics or arterial blood gases at inclusion. The mean difference in the duration of MV between placebo and ACTZ group was 1.3 days (95%CI, -2.1-4.8; p = 0.44). Kaplan-Meier curves showed no differences in the duration of MV (Log-Rank p = 0.41). Between-group comparison of estimated marginal means (CI 95%) during MV were, respectively: PaCO2 55 (51-59) vs 48 (47-50) mm Hg, p = 0.002; bicarbonate concentration 34 (32-35) vs 29 (28-30) mmol/L, p < 0.0001; and minute volume 9.7 (8.9-10.4) vs 10.6 (9.2-12.0) L/min, p = 0.26. There were no severe adverse effects with ACTZ administration. CONCLUSIONS Among patients with MA and COPD or OHS, early treatment with ACTZ did not shorten significantly the duration of MV compared with placebo. TRIAL REGISTRY clinical.trials.gov; NCT01499485; URL:.www.clinicaltrials.gov.
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5.
The pathophysiology of cachexia in chronic obstructive pulmonary disease.
Schols, AM, Gosker, HR
Current opinion in supportive and palliative care. 2009;(4):282-7
Abstract
PURPOSE OF REVIEW The focus of this review is on translation of putative mechanisms of altered energy metabolism and muscle maintenance in cachexia to clinical comparative and intervention studies on chronic obstructive pulmonary disease (COPD). RECENT FINDINGS Pulmonary cachexia is a well recognized feature of COPD, but its cause is poorly understood. Recent studies have shed new light on the molecular mechanisms that underlie cachexia in this disorder. In addition to muscle wasting, COPD patients also suffer from so-called loss of peripheral 'muscle oxidative phenotype', rendering these muscles less energy efficient and more prone to oxidative stress, which may in turn augment loss of muscle mass. SUMMARY Recent translational approaches have clearly advanced our understanding of the pathophysiology of cachexia in COPD. Although this complex clinical syndrome may clearly benefit from multidimensional interventions, for a tailored therapeutic approach based on distinct wasting and pulmonary phenotypes, more mechanistic knowledge on abnormal regulation of energy balance and muscle maintenance in COPD cachexia is needed.