scholarly journals Serum Vitamin A and Inflammatory Markers in Individuals with and without Chronic Obstructive Pulmonary Disease

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
L. M. O. Caram ◽  
R. A. F. Amaral ◽  
R. Ferrari ◽  
S. E. Tanni ◽  
C. R. Correa ◽  
...  

Background.Vitamin A is essential for the preservation and integrity of the lung epithelium and exerts anti-inflammatory effects.Objective.Evaluating vitamin A in the serum and sputum and testing its correlation with inflammatory markers in individuals with or without COPD.Methods.We evaluated dietary intake, serum and sputum vitamin A, tumor necrosis factor alpha, interleukin- (IL-) 6, IL-8, and C-reactive protein in 50 COPD patients (age = 64.0 ± 8.8 y; FEV1(forced expiratory volume in the first second) (%) = 49.8 ± 16.8) and 50 controls (age = 48.5 ± 7.4 y; FEV1(%) = 110.0 ± 15.7).Results.COPD exhibited lower serum vitamin A (1.8 (1.2–2.1) versus 2.1 (1.8–2.4)μmol/L,P<0.001) and lower vitamin A intake (636.9 (339.6–1349.6) versus 918.0 (592.1–1654.6) RAE,P=0.05) when compared with controls. Sputum concentration of vitamin A was not different between groups. Sputum vitamin A and neutrophils were negatively correlated (R2=-0.26;P=0.03). Smoking (0.197,P=0.042) exhibited positive association with serum vitamin A. COPD was associated with lower serum concentrations of vitamin A without relationship with the systemic inflammation.Conclusions.Serum concentration of vitamin A is negatively associated with the presence of COPD and positively associated with smoking status. Sputum retinol is quantifiable and is negatively influenced by neutrophils. Although COPD patients exhibited increased inflammation it was not associated with serum retinol.

Author(s):  
Laxma Reddy S. ◽  
Ravicharan Avala ◽  
Rajshekar Varma ◽  
Narendrakumar Narahari ◽  
Bhaskar K. ◽  
...  

Background: Vitamin D deficiency is common all over the Indian subcontinent, with a prevalence of 70-100% in the general population. Vitamin D deficiency has a role in several diseases of the respiratory system including chronic obstructive pulmonary disease (COPD). Studies have shown that vitamin D deficient COPD patients have lower lung function measured by FEV1. We conducted a study to see prevalence of Vitamin D deficiency in COPD patients and it’s correlation with Forced Expiratory Volume in 1 second.Methods: A cross sectional observational study was performed in a tertiary care hospital in Hyderabad, Telangana during the period of one and half year. This included 104 COPD cases attending outpatient department of pulmonary medicine. Serum vitamin D levels were measured, and spirometry was done in all patients and data was analyzed accordingly.Results: Among 104 patients, 87 were males and 17 were females. Most of the study population (44.2%) was aged between 60-70 years. Mean BMI was 26.40 (±5.77) kg/m2. Majority of study populations (66.34%) were in GOLD stage 1 and 2. The mean Vitamin D value of the study population was 20.77±11.74ng/ml. Majority of the COPD patients were vitamin D deficient (69.2%). 25.0 % was severely deficient of vitamin D. The mean FEV1 volume (%) was 83.15±11.53, 60.97±17.47, 30.71±7.96 in sufficient, deficient and severe deficient patients.Conclusions: Vitamin D deficiency is common in COPD patients. Serum vitamin D deficiency increases with increased severity of COPD. There is positive correlation between serum vitamin D levels and post bronchodilator FEV1 (%). 


2021 ◽  
Author(s):  
Wenjia Chen ◽  
Mohsen Sadatsafavi ◽  
J Mark FitzGerald ◽  
Larry Lynd ◽  
Don Sin

Abstract Background: Low body weight is associated with poor prognosis in patients with chronic obstructive pulmonary disease (COPD). However, it is not known whether gender modifies this relationship. Methods: We pooled data of 8,686 COPD patients from 7 studies with a median length of 36-months of follow up. Using a longitudinal natural cubic spline regression model, we examined the dose-response relationship between body mass index (BMI) and the rate of decline in forced expiratory volume in one second (FEV1) in patients with GOLD 1 and 2 disease, stratified by gender and adjusted for age, smoking status, and cohort effects. Results: There was an inverse linear relationship between BMI and the rate of FEV1 decline in GOLD Grades 1 and 2, which was modified by gender (p<0.001). In male patients, an increase of BMI by 1 kg/m2 reduced FEV1 decline by 1.05mL/year (95% CI: 0.96, 1.14). However, in female patients, BMI status did not have a clinically meaningful impact on FEV1 decline: an increase of baseline BMI by 1 kg/m2 reduced FEV1 decline by 0.16 ml/year (95% CI: 0.11, 0.21). These gender-modified relationships were similar between GOLD 1 and 2 patients, and between current and former smokers. Conclusion: In mild to moderate COPD, higher BMI was associated with a less rapid decline of FEV1 in male patients whereas this association was minimal in females patients. This gender-specific BMI effect was independent of COPD severity and smoking status.


2020 ◽  
Author(s):  
Wenjia Chen ◽  
Mohsen Sadatsafavi ◽  
J Mark FitzGerald ◽  
Larry Lynd ◽  
Don Sin

Abstract Background: Body weight is a poor prognostic risk factor in patients with chronic obstructive pulmonary disease (COPD). However, it is not known whether gender modifies this relationship.Methods: We pooled data of 8,686 COPD patients from 7 studies. Using a longitudinal natural cubic spline regression model, we examined the dose-response relationship between body mass index (BMI) and the rate of decline in forced expiratory volume in one second (FEV1) in patients with GOLD 1 and 2 disease, stratified by gender and adjusted for smoking status and cohort effects. Results: There was an inverse, nearly relationship between BMI and the rate of FEV1 decline in GOLD Grades 1 and 2, which was modified by gender (p<0.001). In male patients, an increase of BMI by 1 kg/m2 reduced FEV1 decline by 1.05mL/year (95% CI: 0.96, 1.14). However, in female patients, BMI status barely clinically affected FEV1 decline: an increase of baseline BMI by 1 kg/m2 reduced FEV1 decline by 0.16 ml/year (95% CI: 0.11, 0.21). These gender-modified relationships were generally similar between GOLD 1 and 2 patients, and between current smokers and former smokers.Conclusion: In mild to moderate COPD, higher BMI was associated with a less rapid decline of FEV1 in male patients whereas it hardly affected females patients. This gender-specific BMI effect was independent of COPD severity and smoking status.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Wenjia Chen ◽  
Mohsen Sadatsafavi ◽  
J. Mark FitzGerald ◽  
Larry D. Lynd ◽  
Don D. Sin

Abstract Background Low body weight is associated with poor prognosis in patients with chronic obstructive pulmonary disease (COPD). However, it is not known whether gender modifies this relationship. Methods We pooled data of 8686 COPD patients from 7 studies with a median length of 36-months of follow up. Using a longitudinal natural cubic spline regression model, we examined the dose–response relationship between body mass index (BMI) and the rate of decline in forced expiratory volume in one second (FEV1) in patients with GOLD 1 and 2 disease, stratified by gender and adjusted for age, smoking status, and cohort effects. Results There was an inverse linear relationship between BMI and the rate of FEV1 decline in GOLD Grades 1 and 2, which was modified by gender (p < 0.001). In male patients, an increase of BMI by 1 kg/m2 reduced FEV1 decline by 1.05 mL/year (95% CI 0.96, 1.14). However, in female patients, BMI status did not have a clinically meaningful impact on FEV1 decline: an increase of baseline BMI by 1 kg/m2 reduced FEV1 decline by 0.16 ml/year (95% CI 0.11, 0.21). These gender-modified relationships were similar between GOLD 1 and 2 patients, and between current and former smokers. Conclusion In mild to moderate COPD, higher BMI was associated with a less rapid decline of FEV1 in male patients whereas this association was minimal in females patients. This gender-specific BMI effect was independent of COPD severity and smoking status.


2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Wen-Jun Wang ◽  
Shi-Fang Yang ◽  
Zhi-Rui Gao ◽  
Ze-Ru Luo ◽  
Yuan-Ling Liu ◽  
...  

Introduction. Some studies have found that cilia were shorter in COPD smokers than in nonsmokers or healthy smokers. However, the structural abnormalities of cilia and the cause of such abnormalities in COPD patients still remain unknown. Tumor necrosis factor alpha receptor 3 interacting protein 1 (MIP-T3) may play an important role in the progress of ciliary protein transporting. Objectives. This study aimed at exploring the dominated structural abnormalities of cilia and the involvement of MIP-T3 in the pathogenesis of cilia of COPD patients. Methods. Patients who accepted pulmonary lobectomy were divided into 3 groups: the chronic obstructive pulmonary disease (COPD) smoker group, the healthy smoker group, and the nonsmoker group, according to smoking history and pulmonary function. The ultrastructure of cilia and the percentage of abnormal cilia were analyzed using a transmission electron microscope. Real-time PCR, immunohistochemical staining, and western blotting in bronchial epithelium were used to determine MIP-T3 mRNA and protein expression. The relationship between the percentage of abnormal cilia and lung function and MIP-T3 protein expression was analyzed. Results. Patients in the COPD smoker group had increased percentage of abnormal cilia comparing to both the healthy smoker group and the nonsmoker group (both P values <0.05). MIP-T3 expression was significantly declined in the COPD smoker group (P value <0.05). Moreover, the percentage of abnormal cilia was negatively correlated with FEV1, FEV1/FVC ratio, and FEV1%pred (all P values <0.05). Moreover, the MIP-T3 protein expression was positively correlated with the percentage of abnormal cilia (P value <0.05). Conclusions. Our results suggested that the abnormal ciliary ultrastructure, which was common in COPD patients, might be due to MIP-T3 downregulation.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Junghyun Kim ◽  
Bom Kim ◽  
So Hyeon Bak ◽  
Yeon-Mok Oh ◽  
Woo Jin Kim

Abstract Background The clinical and radiological presentation of chronic obstructive pulmonary disease (COPD) is heterogenous depending on the characterized sources of inflammation. This study aimed to evaluate COPD phenotypes associated with specific dust exposure. Methods This study was designed to compare the characteristics, clinical outcomes and radiological findings between two prospective COPD cohorts representing two distinguishing regions in the Republic of Korea; COPD in Dusty Area (CODA) and the Korean Obstructive Lung Disease (KOLD) cohort. A total of 733 participants (n = 186 for CODA, and n = 547 for KOLD) were included finally. A multivariate analysis to compare lung function and computed tomography (CT) measurements of both cohort studies after adjusting for age, sex, education, body mass index, smoking status, and pack-year, Charlson comorbidity index, and frequency of exacerbation were performed by entering the level of FEV1(%), biomass exposure and COPD medication into the model in stepwise. Results The mean wall area (MWA, %) became significantly lower in COPD patients in KOLD from urban and metropolitan area than those in CODA cohort from cement dust area (mean ± standard deviation [SD]; 70.2 ± 1.21% in CODA vs. 66.8 ± 0.88% in KOLD, p = 0.028) after including FEV1 in the model. COPD subjects in KOLD cohort had higher CT-emphysema index (EI, 6.07 ± 3.06 in CODA vs. 20.0 ± 2.21 in KOLD, p < 0.001, respectively). The difference in the EI (%) was consistently significant even after further adjustment of FEV1 (6.12 ± 2.88% in CODA vs. 17.3 ± 2.10% in KOLD, p = 0.002, respectively). However, there was no difference in the ratio of mean lung density (MLD) between the two cohorts (p = 0.077). Additional adjustment for biomass parameters and medication for COPD did not alter the statistical significance after entering into the analysis with COPD medication. Conclusions Higher MWA and lower EI were observed in COPD patients from the region with dust exposure. These results suggest that the imaging phenotype of COPD is influenced by specific environmental exposure.


2021 ◽  
Vol 10 (2) ◽  
pp. 269
Author(s):  
Elisabetta Zinellu ◽  
Alessandro G. Fois ◽  
Elisabetta Sotgiu ◽  
Sabrina Mellino ◽  
Arduino A. Mangoni ◽  
...  

Background: Chronic obstructive pulmonary disease (COPD) is a progressive condition characterized by chronic airway inflammation and lung parenchyma damage. Systemic inflammation and oxidative stress also play a role in the pathogenesis of COPD. Serum albumin is a negative acute-phase protein with antioxidant effects and an important marker of malnutrition. The aim of this meta-analysis was to investigate differences in serum albumin concentrations between patients with stable COPD and non-COPD subjects. Methods: A systematic search was conducted, using the terms “albumin” and “chronic obstructive pulmonary disease” or “COPD”, in the electronic databases PubMed and Web of Science, from inception to May 2020. Results: Twenty-six studies were identified on a total of 2554 COPD patients and 2055 non-COPD controls. Pooled results showed that serum albumin concentrations were significantly lower in COPD patients (standard mean difference, SMD = −0.50, 95% CI −0.67 to −0.32; p < 0.001). No significant differences were observed in SMD of serum albumin concentrations between COPD patients with forced expiratory volume in the 1st second (FEV1) < 50% and those with FEV1 > 50%. Conclusions: Our systematic review and meta-analysis showed that serum albumin concentrations are significantly lower in patients with stable COPD compared to non-COPD controls. This supports the presence of a deficit in systemic anti-inflammatory and antioxidant defense mechanisms in COPD.


2021 ◽  
Vol 31 (1) ◽  
Author(s):  
Sandeep Bansal ◽  
Martin Anderson ◽  
Antonio Anzueto ◽  
Nicola Brown ◽  
Chris Compton ◽  
...  

AbstractChronic obstructive pulmonary disease (COPD) treatment guidelines do not currently include recommendations for escalation directly from monotherapy to triple therapy. This 12-week, double-blind, double-dummy study randomized 800 symptomatic moderate-to-very-severe COPD patients receiving tiotropium (TIO) for ≥3 months to once-daily fluticasone furoate/umeclidinium/vilanterol (FF/UMEC/VI) 100/62.5/25 mcg via ELLIPTA (n = 400) or TIO 18 mcg via HandiHaler (n = 400) plus matched placebo. Study endpoints included change from baseline in trough forced expiratory volume in 1 s (FEV1) at Days 85 (primary), 28 and 84 (secondary), health status (St George’s Respiratory Questionnaire [SGRQ] and COPD Assessment Test [CAT]) and safety. FF/UMEC/VI significantly improved trough FEV1 at all timepoints (Day 85 treatment difference [95% CI] 95 mL [62–128]; P < 0.001), and significantly improved SGRQ and CAT versus TIO. Treatment safety profiles were similar. Once-daily single-inhaler FF/UMEC/VI significantly improved lung function and health status versus once-daily TIO in symptomatic moderate-to-very-severe COPD patients, with a similar safety profile.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Jinyuan Zhu ◽  
Faxuan Wang ◽  
Xueyan Feng ◽  
Beibei Li ◽  
Liqiong Ma ◽  
...  

Abstract Background To explore the role of family with sequence similarity 13 member A (FAM13A) in TGF-β1-induced EMT in the small airway epithelium of patients with chronic obstructive pulmonary disease (COPD). Methods Small airway wall thickness and protein levels of airway remodeling markers, EMT markers, TGF-β1, and FAM13A were measured in lung tissue samples from COPD and non-COPD patients. The correlations of FAM13A expression with COPD severity and EMT marker expression were evaluated. Gain- and loss-of-function assays were performed to explore the functions of FAM13A in cell proliferation, motility, and TGF-β1-induced EMT marker alterations in human bronchial epithelial cell line BEAS-2B. Results Independent of smoking status, lung tissue samples from COPD patients exhibited significantly increased small airway thickness and collagen fiber deposition, along with enhanced protein levels of remodeling markers (collagen I, fibronectin, and MMP-9), mesenchymal markers (α-SMA, vimentin, and N-cadherin), TGF-β1, and FAM13A, compared with those from non-COPD patients. FAM13A expression negatively correlated with FEV1% and PO2 in COPD patients. In small airway epithelium, FAM13A expression negatively correlated with E-cadherin protein levels and positively correlated with vimentin protein levels. In BEAS-2B cells, TGF-β1 dose-dependently upregulated FAM13A protein levels. FAM13A overexpression significantly promoted cell proliferation and motility in BEAS-2B cells, whereas FAM13A silencing showed contrasting results. Furthermore, FAM13A knockdown partially reversed TGF-β1-induced EMT marker protein alterations in BEAS-2B cells. Conclusions FAM13A upregulation is associated with TGF-β1-induced EMT in the small airway epithelium of COPD patients independent of smoking status, serving as a potential therapeutic target for anti-EMT therapy in COPD.


2013 ◽  
Vol 114 (9) ◽  
pp. 1309-1318 ◽  
Author(s):  
Mahroo Mofarrahi ◽  
Ioanna Sigala ◽  
Theodoros Vassilokopoulos ◽  
Sharon Harel ◽  
Yeting Guo ◽  
...  

The role of angiogenesis factors in skeletal muscle dysfunction in patients with chronic obstructive pulmonary disease (COPD) is unknown. The first objective of this study was to assess various pro- and antiangiogenic factor and receptor expressions in the vastus lateralis muscles of control subjects and COPD patients. Preliminary inquiries revealed that angiopoietin-2 (ANGPT2) is overexpressed in limb muscles of COPD patients. ANGPT2 promotes skeletal satellite cell survival and differentiation. Factors that are involved in regulating muscle ANGPT2 production are unknown. The second objective of this study was to evaluate how oxidants and proinflammatory cytokines influence muscle-derived ANGPT2 expression. Angiogenic gene expressions in human vastus lateralis biopsies were quantified with low-density real-time PCR arrays. ANGPT2 mRNA expressions in cultured skeletal myoblasts were quantified in response to proinflammatory cytokine and H2O2 exposure. Ten proangiogenesis genes, including ANGPT2, were significantly upregulated in the vastus lateralis muscles of COPD patients. ANGPT2 mRNA levels correlated negatively with forced expiratory volume in 1 s and positively with muscle wasting. Immunoblotting confirmed that ANGPT2 protein levels were significantly greater in muscles of COPD patients compared with control subjects. ANGPT2 expression was induced by interferon-γ and -β and by hydrogen peroxide, but not by tumor necrosis factor. We conclude that upregulation of ANGPT2 expression in vastus lateralis muscles of COPD patients is likely due to oxidative stress and represents a positive adaptive response aimed at facilitating myogenesis and angiogenesis.


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