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High sensitive C-reactive protein as a systemic inflammatory marker and LDH-3 isoenzyme in chronic obstructive pulmonary disease.

BACKGROUND AND OBJECTIVES: Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease, mainly due to tobacco smoke. Pulmonary function tests (PFTs) are mandatory to diagnose COPD which shows irreversible airway obstruction. This study was aimed at understanding the behavior of biochemical parameters such as high sensitive C-reactive protein (hs-CRP) and lactate dehydrogenase (LDH) isoenzymes in COPD. Cytoplasmic cellular enzymes, such as LDH in the extracellular space, although of no further metabolic function in this space, are of benefit because they serve as indicators suggestive of disturbances of the cellular integrity induced by pathological conditions. The lung pattern is characterized by proportional increases in isoenzymes 3, 4, and 5. Hs-CRP indicates low grade of systemic inflammation.

MATERIALS AND METHODS: Total (n = 45) patients of COPD (diagnosed on PFTs) were included. We followed the guidelines laid by the institute ethical committee. Investigations performed on the serum were the serum for hs-CRP, LDH isoenzymes on agarose gel electrophoresis.

RESULTS: The results obtained showed that the value of hs-CRP was 4.6 ± 0.42 mg/L. The isoenzymes pattern was characterized by an increase in LDH-3 and LDH-4 fractions. This is evident even in those patients with normal LDH (n = 13) levels.

INTERPRETATION AND CONCLUSION: This study states that there is a moderate positive correlation in between CRP and LDH-3 (r = 0.33; P = 0.01). Raised LDH-3 levels do not correlate with FEV(1) % (forced expiratory volume in first second) predicted. Moreover, it associates positively with hs-CRP and smoking status and negatively with body mass index. This underlines the potential of these parameters to complement the present system of staging which is solely based upon FEV(1) % predicted.

The Reality of an Intermediate Type Between Asthma and COPD in Practice.

BACKGROUND: Asthma and chronic obstructive pulmonary disease (COPD) are obstructive airway diseases related to chronic airway inflammation. However, it is known that the overlapped syndrome of the two diseases exists in real practice.

OBJECTIVES: The purpose of this study was to investigate the reality of an intermediate type between asthma and COPD when diagnosed by physicians in Korea.

METHODS: The study involved 633 Korean patients with asthma, 157 with COPD, and 41 with an intermediate type. The latter group consisted of patients with clinically mixed or overlapping characteristics of asthma and COPD. The diagnoses were dependent on physicians' clinical decision. We analyzed the clinical differences among those three groups.

RESULTS: There were differences among the three groups in age, gender, atopy, and BMI. Differences in smoking status, including percentages of current smokers, duration of smoking, and number of cigarettes smoked per day, were also observed. Prebronchodilator FEV₁ (%), FVC (%), and FEV₁/FVC ratio (%) gradually decreased from the asthma group to the intermediate type group to the COPD group. Positivity of postbronchodilator response, increase of FEV₁ (%) and postbronchodilator FEV₁/FVC ratio also showed gradual patterns. For emergency room visits and hospital admissions, frequencies were lowest in the asthma group, higher in the intermediate type group, and highest in COPD patients. All p-values were statistically significant (<0.001).

CONCLUSIONS: We have identified and characterized an intermediate type, lying between asthma and COPD in clinical characteristics. Further investigations are required to determine whether these three conditions are part of the chronic obstructive airway diseases spectrum or are rather distinct clinical entities.

Antioxidant pharmacological therapies for COPD.

Increased oxidative stress occurs in the lungs and systemically in COPD, which plays a role in many of the pathogenic mechanisms in COPD. Hence, targeting local lung and systemic oxidative stress with agents that modulate the antioxidants/redox system or boost endogenous antioxidants would be a useful therapeutic approach in COPD.

Thiol antioxidants (N-acetyl-l-cysteine [NAC] and N-acystelyn, carbocysteine, erdosteine, and fudosteine) have been used to increase lung thiol content. Modulation of cigarette smoke (CS) induced oxidative stress and its consequent cellular changes have also been reported to be effected by synthetic molecules, such as spin traps (α-phenyl-N-tert-butyl nitrone), catalytic antioxidants (superoxide dismutase [ECSOD] mimetics), porphyrins, and lipid peroxidation and protein carbonylation blockers/inhibitors (edaravone and lazaroids/tirilazad). Preclinical and clinical trials have shown that these antioxidants can reduce oxidative stress, affect redox and glutathione biosynthesis genes, and proinflammatory gene expression.

In this review the approaches to enhance lung antioxidants in COPD and the potential beneficial effects of antioxidant therapy on the course of the disease are discussed.

Effects of Extra-Fine Inhaled and Oral Corticosteroids on Alveolar Nitric Oxide in COPD.

PURPOSE: Alveolar nitric oxide (CA(NO)) has been suggested as a surrogate marker of distal airway inflammation in COPD. Coarse particle-inhaled corticosteroids (ICS) have been shown not to suppress CA(NO). We evaluated whether extra-fine particle size ICS (HFA-BDP) or systemic oral corticosteroids could suppress CA(NO) in COPD.

METHODS: Chronic obstructive pulmonary disease (COPD) patients with a FEV1/FVC ratio <0.7, FEV1 <80% predicted with CA(NO) > 2 ppb underwent a double-blind randomized, controlled, crossover trial with an open-label systemic steroid comparator. After a 2 week steroid washout period, participants were randomized to 3 weeks of 100 mcg of HFA-BDP twice daily and then 3 weeks of 400 mcg of HFA-BDP twice daily, or matched placebos with subsequent crossover. All patients then received 1 week open-label, 25 mg/day of prednisolone. Exhaled nitric oxide, plasma cortisol, and lung function were recorded. CA(NO) was corrected for axial diffusion.

RESULTS: In 16 participants, there were no significant differences seen with either dose of HFA-BDP compared with placebo. Oral prednisolone significantly reduced FE(NO) and J'aw(NO) but not CA(NO). Plasma cortisol was significantly suppressed by oral prednisolone only.

CONCLUSIONS: Whilst CA(NO) remains a biomarker of interest in COPD, it is not suppressed by systemic or extra-fine particle ICS. CA(NO) is not a useful marker for monitoring response of small airway disease to therapies in COPD. The study was approved by the local Committee on Medical Research Ethics and registered on ClinicalTrials.Gov (NCT 00921921).

Actigraphic assessment of sleep in chronic obstructive pulmonary disease.

PURPOSE: Previously, sleep in chronic obstructive pulmonary disease (COPD) has been objectively investigated only by lab-based polysomnography. The main purpose of this study was to evaluate sleep quality in COPD patients in their home environment using actigraphy. We also investigated the factors associated with sleep impairment and the relationship between objective and subjective sleep quality and daytime somnolence in these patients.

METHODS: Twenty-six patients with moderate to very severe COPD and 15 controls were studied by actigraphy for at least 5 days. Subjective sleep quality was evaluated by the Pittsburgh Sleep Quality Index and daytime sleepiness by the Epworth Sleepiness Scale (ESS). Dyspnea was quantified by the modified Medical Research Council (MMRC) scale.

RESULTS: COPD patients showed increased sleep latency (p = 0.003), mean activity (p = 0.003), and wake after sleep onset (p = 0.003) and reduced total sleep time (TST; p = 0.024) and sleep efficiency (p = 0.001), as compared to controls. In patients, severity of dyspnea was correlated with sleep activity (r = 0.41; p = 0.04) and TST (r = -0.46; p = 0.02) and multiple regression analysis showed that MMRC score was the best predictor of TST (p = 0.02) and sleep efficiency (p = 0.03). Actigraphy measures during daytime were not significantly different between patients and controls. Subjective sleep quality was poorer in patients than controls (p = 0.043). ESS scores were not significantly different between the two groups. Actigraphy measures were not correlated with subjective sleep quality or daytime somnolence in both groups.

CONCLUSIONS: 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.

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