Comparison of the Arterial PaCO 2 Values and ETCO 2 Values Measured with Sidestream Capnography in Patients with a Prediagnosis of COPD Exacerbation.

Background Aim of this study is to investigate whether end-tidal carbon dioxide (ETCO 2 ) values can be used instead of partial pressure of carbon dioxide (PaCO 2 ) values in guiding treatment, and determining treatment benefits in patients that received a pre-diagnosis of chronic obstructive pulmonary disease (COPD) exacerbation at the emergency department. Methods This observational prospective study was conducted with patients who presented to the emergency department with the complaint of shortness of breath and were diagnosed with COPD exacerbation. ETCO 2 was measured with the sidestream method during blood gas analysis in patients with indications for this analysis. Measurements were repeated at hour 1 after treatment. Results The study included a total of 121 cases. There was a positive correlation between the PaCO 2 and ETCO 2 values measured before and after treatment ( r = 0.736, p < 0.01 and r = 0.883, p < 0.01, respectively). High ETCO 2 values were accompanied by high PaCO 2 values. When the measurements before and after treatment were evaluated using the Bland-Altman method, most of the result were within the limits of agreement (-4.9 and +31.4/- 2.6 and +9.4), with mean differences being calculated as 13.2 and 8.4, respectively. Conclusions Although ETCO 2 and PaCO 2 were statistically consistent according to the results of our study, due to the high averages of differences between these two parameters, the ETCO 2 value has limited clinical use in COPD cases compared to PaCO 2 . However, high ETCO 2 values may indicate that noninvasive mechanical ventilation should be included in the treatment of COPD cases without waiting for the results of blood gas analysis, and they can also be when needed for inpatient treatment.

Relationships between Obstructive Sleep Apnea Syndrome, Continuous Positive Airway Pressure Treatment, and Inflammatory Cytokines.

The cardiovascular complications that frequently accompany obstructive sleep apnea syndrome (OSAS) are thought to develop as a result of inflammatory stress associated with cytokines such as IL-6 and TNF- α . We conducted the current study to compare levels of these cytokines in OSAS patients (n = 33) and nonapneic controls (n = 24). Furthermore, we investigated the impact of a three-month regime of continuous positive airway pressure (CPAP) on serum levels of IL-6 and TNF- α only in the OSAS patients. There were no significant differences in serum levels of either IL-6 (P = 0.782) or TNF- α (P = 0.722) or TNF- α (P = 0.722) between OSAS patients and nonapneic controls. Serum IL-6 levels correlated significantly with neck circumference in OSAS patients (P = 0.006). In OSAS patients, reduced levels of TNF- α and IL-6 correlated with increases in mean SaO2 after CPAP treatment (P = 0.020 and P = 0.051, resp.). However, neither of cytokine levels was significantly impacted by CPAP therapy (both P > 0.137). We have demonstrated that plasma cytokine levels are similar in both otherwise healthy subjects with OSAS and in nonapneic control, and we conclude that OSAS-related parameters and CPAP treatment do not play a significant role in altering cytokine levels.

Matrix Metalloproteinase-9 Level and Gene Polymorphism in Sleep Disordered Breathing Patients with or without Cardiovascular Disorders.

OBJECTIVE: Obstructive sleep apnea syndrome (OSAS) is associated with increased cardiovascular morbidity and mortality. We aimed to investigate the matrix metalloproteinase-9 (MMP-9) level and MMP-9 gene polymorphism in sleep apnea patients with or without cardiovascular disease. STUDY DESIGN: Case-control study. MATERIAL AND METHODS: Two hundred nine patients [Mean age (±SD), 47 (±12) yrs; M/F, 170/39] diagnosed with sleep-disordered breathing were included in the study. Serum MMP-9 level was performed using enzyme-linked immunosorbant assay (ELISA) and MMP-9 gene polymorphism with polymerase chain reaction-restriction fragment length polymorphism. We divided the patient group into two subgroups: (1) patients with confirmed cardiovascular disease, i.e. CV-P Group and (2) patients without cardiovascular disease, CV-N Group. We compared all parameters between the two groups. RESULTS: There were 56 OSAS patients with cardiovascular disorder (CV-positive group) and 153 OSAS patients without cardiovascular disorder (CV-negative group). CC, CT and TT genotype distributions between groups were similar [31 (55%), 25 (45%), 0 (0%) vs 88 (57%), 61 (40%), 4 (3%); respectively, p>0.05]. MMP-9 level was significantly higher in CV-P patients (442.7±139.3 pg/mL) than in CV-N patients (364.4±165.0 pg/mL; p=0.0018). CONCLUSION: Our results showed that the presence of MMP-9 polymorphism was not associated with cardiovascular disease. MMP-9 level was higher in OSAS patients with cardiovascular disorders than without cardiovascular disorders. Finally, MMP-9 genotype was not associated with serum MMP-9 levels.

A case of endobronchial inflammatory pseudotumor invading the mediastinum.

A 50-year-old-male was admitted to our hospital in March 2007, complaining of cough and hemoptysis for 3 months. Postero-anterior chest X-ray showed an opacity on right upper zone. Computed tomography of the thorax showed a mass lesion occupying the right upper lobe and superior segment of the lower lobe and invading the mediastinum. Fiberoptic bronchoscopy showed total occlusion of the right upper lobe bronchus by the mass and infiltration of the bronchus intermedius. Bronchoscopic biopsies were nondiagnostic. PET-CT revealed SUVmax of 18.8. Right thoracotomy was performed. Vena cava superior and right pulmonary artery was invaded by the mass. Biopsies were performed. Histopathologic examination demonstrated an inflammatory pseudotumor. Corticosteroid treatment was started. The tumor was clinically and radiologically unresponsive to corticosteroids. He was referred to oncology department for radiotherapy. The patient died on November 2007.