Correlation of exhaled carbon monoxide level with disease severity in chronic obstruction pulmonary disease.

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.

Right phrenic nerve palsy: a rare presentation of thoracic aortic aneurysm.

Phrenic nerve palsy causing hemidiaphragm paralysis is a very uncommon feature of thoracic aortic aneurysm. In one case, a 45-year-old man complained of chronic chest pain, dysphagia, and hoarseness of voice; posteroanterior view chest radiograph revealed lobular enlargement of the superior mediastinum and elevated right hemidiaphragm. Contrast-enhanced computed tomography (CT) of the thorax revealed a giant partially thrombosed aneurysm originating from the ascending aorta and extending into the aortic arch, causing a widening of the aorta-pulmonary window and a compression of the thoracic esophagus. Right hemidiaphragm elevation was explained by the gross mass effect of the aneurysm on the right hilum, causing right phrenic nerve palsy. The patient was to be operated on for surgical correction of the aneurysm, but died before surgery due to spontaneous rupture.