Introduction:Amplification of airway inflammation and its destruction due to oxidative stress is a major step in the pathogenesis of chronic obstruction pulmonary disease (COPD). Exhaled carbon monoxide (eCO) may be quantified to evaluate the airway inflammation and oxidative stress in such patients.Objectives:To assess the disease severity of COPD and treatment response by measuring eCO as a biomarker.Materials and Methods:COPD patients diagnosed according to the global initiative for chronic obstructive lung disease guidelines and healthy individuals as controls were selected. One hundred and fifty patients with COPD and 125 controls were included in the study. Participants were further subdivided on the basis of their smoking habits. Clinical examinations and spirometry were done to diagnose COPD by following the standard protocol. eCO was measured using a piCO + Smokerlyzer (Breath CO Monitor, Bedfont Scientific Ltd., Kent, UK). It was a single-center cross-sectional study.Results:Mean (± standard error of mean) CO levels in ex-smokers with COPD were higher (5.21 ± 1.546 ppm; P < 0.05) than in nonsmoking controls (1.52 ± 0.571 ppm) but were lower than in current smokers with COPD (12.55 ± 4.514 ppm; P < 0.05). eCO levels were higher in current smokers with COPD (12.55 ± 4.514 ppm; P < 0.05) compared to healthy smokers (9.71 ± 5.649). There was a negative correlation between eCO and forced expiratory volume in 1 s (FEV1) in COPD (r = −0.28; P < 0.05). The mean eCO level was decreased (6.291–4.332; P < 0.001) with improvement in lung function (FEV1 38.75%–50.65%: P < 0.05) after treatment with inhaled steroid.Conclusion:Our study concludes that quantification of eCO level in COPD varies with different grades of airway obstruction and to measure the treatment response. Measuring the level of eCO can be used to assess the indirect assessment of airway inflammation, oxidative stress, and severity of airway obstruction in COPD patients.
Phrenic nerve palsy causing hemidiaphragm paralysis is a very uncommon feature of thoracic aortic aneurysm. In one case, a 30 year male complained of chronic dull aching chest pain, and hoarseness of voice; posteroanterior view chest radiograph revealed large spherical radiopacity on the left upper lung zone with smooth lobulated margin with elevated left hemidiaphragm. On Colour Doppler sonography, lesion was anechoic on gray scale sonography but on Doppler analysis revealed intense internal vascularity within it with characteristic “Ying Yang” sign. The finding favor the vascular origin of the lesion and a diagnosis of an arterial aneurysm was made Contrast-enhanced computed tomography (CT) of the thorax revealed a large well defined spherical lesion of 8 × 10 cm size with smooth well defined margin arising from the aortic arch and attenuation of impending rupture or dissection were lesion on immediate post contrast and delayed scan was similar to that of aorta. Left hemidiaphragm elevation was explained by the gross mass effect of the aneurysm causing right phrenic nerve palsy.
Background. Chronic obstructive pulmonary disease (COPD) is a general name for the chronic airflow obstruction that develops most commonly due to long term tobacco smoking and other noxious gases. The aim of the present study is to check whether exhaled carbon monoxide (CO) levels had any co-relations with disease severity in various stages of COPD.Methods. The clinical severity of asthma and COPD was determined using the criteria defined in the Global Initiative for Asthma (GINA) and Global Initiative for chronic obstructive pulmonary disease (GOLD) guidelines. Spirometry was used to confirm the presence of airway obstruction. results. We observed that exhaled CO levels increased with increasing severity of airway obstruction. A statistically significant negative correlation was observed between forced expiratory volume in the first second and exhaled CO (p<0.05).conclusions. We found that measuring the level of exhaled CO in patients with COPD along with spirometry forms a new approach for better understanding of the pathophysiology of COPD cases. [indian j chest dis allied sci 2019;61: [83][84][85][86]
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