Nurhayat Yildirim

Pulmonary function in multiple sclerosis without any respiratory complaints

OBJECTIVES Pulmonary complications in severe multiple sclerosis (MS) are often seen secondary to respiratory muscle dysfunction. The development of respiratory muscle dysfunction and its association with disability during the course of MS is unknown. In our study, we investigated the predictive value of respiratory muscle functions and the change in forced vital capacity (Delta forced vital capacity [FVC]; FVC upright-FVC supine) to detect deterioration of respiratory muscle functions in the early phase of MS. PATIENTS AND METHODS Twenty-one MS patients with a median age of 34.5+/-9.45 years were enrolled. Fourteen cases were relapsing-remitting, six were secondary progressive, one was primary progressive type. The mean duration of disease was 10.76+/-6.6 years. Seventeen healthy subjects with a median age of 40.7+/-7.6 years were chosen as a control group. Smoking habit was similar in both groups. Pulmonary function tests (PFT), lung volumes, diffusion, respiratory muscle function ( P(Imax) , P(Emax)), mouth occlusion pressure, and indirect sign of respiratory center function (P(0.1)) tests were performed. PFT were repeated in supine and upright positions. RESULTS Our results in the MS group and the control group, respectively, were: diffusion (DL(CO): 18.8+/-4.2 vs. 26.4+/-7.3 mL/mmHg/min), P(I(max) (82.1+/-26.3 vs. 109.1+/-23.3 cm H(2)O), P(E(max) (119.2+/-42 vs. 171.8+/-50.2 cm H(2)O), P(0.1) (2.6+/-0.7 vs. 4.2+/-0.7). All parameters were lower in the MS group compared with the control group (p<0.05). In the MS group, FVC values in the upright position were higher than FVC values in the supine position. The difference in FVC values in MS patients between the upright and supine positions (Delta FVC) was also found to be significantly higher than in the control group (Delta FVC 262.3+/-247.6 (MS), 98.8+/-179.1 mL (CONTROL)) (p<0.01). CONCLUSION Our results indicate the presence of pulmonary dysfunction in MS even in the absence of any respiratory symptoms.

Iron, nitric oxide, and myeloperoxidase in asthmatic patients.

Plasma nitric oxide (NO), myeloperoxidase (MPO), and iron (Fe) levels were determined in bronchial asthma. The relations among these parameters in different stages of asthma were interpreted. Their association with airway inflammation observed in patients with bronchial asthma as well as the roles and the contributions to the pathological processes were evaluated. A total of 62 individuals, 32 asthmatics and 30 controls, were included into the scope of this study. Plasma nitric oxide metabolites (NOx) and MPO and Fe levels were determined by the Griess reaction, ELISA, and the automated TPTZ (2,4,6-tri[2-pyridyl]-5-triazine) method, respectively. In the asthmatic individuals, plasma NOx, MPO, and Fe concentrations were 133 ± 13 μM, 95 ± 20 ng/ml, and 159 ± 20 μg/dl, respectively; in the control group these values were 82 ± 11 μM, 62 ± 11 ng/ml, and 96 ± 9 μg/dl. Increased values were detected for plasma MPO (p > 0.05), NOx (p < 0.01), and Fe (p < 0.01) concentrations in asthmatic individuals. Considering the facts that NO modulates the catalytic activity of MPO and induces the expression of heme oxygenase as important contributors to the mechanisms causing free Fe release, it is concluded that elevated NOx, MPO, and Fe levels observed in the asthmatic group act in a concerted manner and appear to be involved in the pathogenesis of asthma.

Plasma paraoxonase activities, lipoprotein oxidation, and trace element interaction in asthmatic patients.

Paraoxonase (PON1) protects low and high-density lipoproteins (LDL and HDL) against oxidation induced by reactive oxygen species formation facilitated by iron (Fe) and copper (Cu) ions. Plasma PON1, arylesterase, oxidized LDL (Ox-LDL), Cu, Fe, thiobarbituric acid-reactive substances (TBARS), lipid, lipoprotein, and apolipoprotein profile in bronchial asthma were determined and the relations among these parameters in different steps of asthma were interpreted. A total of 58 individuals, 30 asthmatics and 28 controls, were included into the scope of this study. Plasma PON1, arylesterase, and TBARS levels were measured spectrophotometrically. Determination of plasma oxidized LDL, Cu, and Fe levels were performed by enzyme-linked immunosorbent assay, atomic absorption spectrophotometry, and the automated TPTZ method, respectively. Apo-A-1 and Apo-B levels were determined immunoturbidometrically. Plasma total cholesterol, triglyceride, and HDL cholesterol levels were enzymatically determined. Plasma LDL levels were estimated using the Fridewald formula. The average plasma PON1 and arylesterase activities in the group of patients were lower than those of the individuals in the control group, but there was no statistically significant difference found between them (p>0.05). No significant difference was found in plasma Apo-A-1, Apo-B, total cholesterol, triglyceride, HDL, and LDL concentrations between the control and patient groups (p>0.05). Plasma oxidized LDL (p<0.05), Cu (p<0.01), Fe (p<0.01), and TBARS (p<0.001) levels in patients with asthma were found to be significantly higher than for the control group. Increases in Cu, Fe, lipid peroxidation, and oxidized LDL levels supported by relative decreases in PON1 activities observed in asthmatic patients might be introduced as the striking findings as well as the possible potential indicators of this airway disease, the prevalence of which has increased dramatically over recent decades.

A Simple Measure to Assess Hyperinflation and Air Trapping: 1-Forced Expiratory Volume in Three Second / Forced Vital Capacity

Background: Several recent studies have suggested that 1 minus-forced expiratory volume expired in 3 seconds / forced vital capacity (1-FEV3/FVC) may be an indicator of distal airway obstruction and a promising measure to evaluate small airways dysfunction. Aims: To investigate the associations of 1-FEV3/FVC with the spirometric measures and lung volumes that assess small airways dysfunction and reflects hyperinflation and air trapping. Study Design: Retrospective cross-sectional study. Methods: Retrospective assessment of a total of 1110 cases who underwent body plethysmographic lung volume estimations between a time span from 2005 to 2012. Patients were assigned into two groups: firstly by FEV1/FVC (FEV1/FVC <70% vs. FEV1/FVC ≥70%); secondly by FEV3/FVC < lower limits of normal (LLN) (FEV3/FVC < LLN vs. FEV3/FVC ≥ LLN). Spirometric indices and lung volumes measured by whole-body plethysmography were compared in groups. Also the correlation of spirometric indices with measured lung volumes were assessed in the whole-study population and in subgroups stratified according to FEV1/FVC and FEV3/FVC. Results: Six hundred seven (54.7%) were male and 503 (45.3%) were female, with a mean age of 52.5±15.6 years. Mean FEV3/FVC and 1-FEV3/FVC were 87.05%, 12.95%, respectively. The mean 1-FEV3/FVC was 4.9% in the FEV1/FVC ≥70% group (n=644) vs. 24.1% in the FEV1/FVC <70% group (n=466). A positive correlation was found between 1-FEV3/FVC and residual volume (r=0.70; p<0.0001), functional residual capacity-pleth (r=0.61; p<0.0001), and total lung capacity (r=0.47; p<0.0001). 1-FEV3/FVC was negatively correlated with forced expiratory flow25-75 (r=−0.84; p<0.0001). The upper limit of 95% confidence interval for 1-FEV3/FVC was 13.7%. 1-FEV3/FVC showed significant correlations with parameters of air trapping and hyperinflation measured by whole-body plethysmography. Importantly, these correlations were higher in study participants with FEV1/FVC <70% or FEV3/FVC < LLN compared to those with FEV1/FVC ≥70% or FEV3/FVC ≥ LLN, respectively. Conclusion: 1-FEV3/FVC can be easily calculated from routine spirometric measurements. 1-FEV3/FVC is a promising marker of air trapping and hyperinflation. We suggest that 1-FEV3/FVC is complementary to FEV1/FVC and recommend clinicians to routinely report and evaluate together with FEV1/FVC during spirometry.

Updates in Chronic Obstructive Pulmonary Disease for the Year 2014

Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality in the world. Research conducted over the past decade has contributed much to our current knowledge of the pathogenesis and treatment of COPD. Additionally, an evolving literature has recently accumulated information about the management of COPD and also about exacerbations. This article reviews a concise summary on the updates in COPD including 1) new pathogenic mechanisms and therapeutic targets, 2) management of patients in Group B, C and D according to GOLD 2014 report; 3) prevention and management of exacerbation; 4) monitoring of natural history; and 5) essential but usually forgotten parts of the management.

[Effects of inhaled corticosteroids/long-acting beta-2 agonist fix combinations in COPD].

Chronic obstructive pulmonary disease (COPD) is an inflammatory disease characterized with progressive air flow limitation, and is expected to be the third leading cause of death until 2030 worldwide. The clinical trials in the last 10 years revealed that fix combinations (inhaled corticosteroids/long-acting beta-2 agonist; ICS/LABA) improve lung functions and quality of life, and reduced symptoms and exacerbation rates in patients with severe and very severe COPD.