Urotensin-II levels in chronic obstructive pulmonary disease

Chronic Obstructive Pulmonary Disease is a preventable disease characterised by both alveolar abnormalities and airway stenosis caused by persistent respiratory symptoms and/or exposure to harmful particles or gases. Exacerbations affect disease progression and mortality. A new approach to predict the severity and outcome of COPD exacerbations is the use of biomarkers. COPD is characterised by chronic inflammation of the airways, lung parenchyma and pulmonary vascular structures. In addition to inflammation, endothelial dysfunction affecting the pulmonary vascular bed has been shown to play an important role in the pathogenesis of COPD and markers of endothelial dysfunction are increased in patients with COPD. Urotensin-II, a cyclic petide, is the most potent endogenous vasoconstrictor molecule known today and its effects on the cardiovascular system are still under investigation. The aim of our study was to determine serum urotensin-II levels in COPD patients, to evaluate the relationship between serum urotensin-II levels and right ventricular dysfunction, to determine the optimal cut-off value of serum urotensin-II in predicting right ventricular dysfunction in COPD patients and to evaluate the relationship between urotensin-II and other clinical and laboratory parameters. A total of 110 patients, 92 (83.6%) males and 18 (16.4%) females, aged between 35 and 93 years, were included in the study. The mean age was 67.57±11.97 years. The patients were divided into two groups as 'Study' (n=80) and 'Control' (n=30). The ages of the subjects in the study group ranged between 37 and 93 years, 69 (86.3%) were male and 11 (13.7%) were female. The mean age was 68.90±11.39 years. There was no statistically significant difference between the groups in terms of mean age and gender distribution (p>0.05). While 92.5% of the patients were alive, 7.5% were deceased. There was no statistically significant difference in urotensin-II levels between living and deceased patients (p>0.05). 81.3% of the patients had comorbidities, and there was no statistically significant difference in urotensin-II levels between patients with and without comorbidities (p>0.05). According to SFT, 10% had stage 2, 65% had stage 3 and 25% had stage 4 COPD. There was no statistically significant difference in urotensin-II levels between SFT stages (p>0.05). There was an inverse, moderate (31.9%) and statistically significant relationship between urotensin-II level and urea (p:0.004; p<0.05). There was no statistically significant relationship between urotensin-II level and other biochemical parameters (p>0.05). The urotensin-II level of the study group was statistically significantly higher than the control group (p:0.001; p<0.05). A peak gradient value of 20 mmHg and above on bedside ECHO was considered positive. PG level was positive in 48.8% and negative in 51.2% of the study group. There was no statistically significant difference in urotensin-II levels between patients with positive and negative PG levels (p>0.05). When urotensin-II level was evaluated with the ROC curve in the diagnosis of Chronic Obstructive Pulmonary Disease, the area under the curve was 0.797 and the standard error was 0.05. The area under the ROC curve was significantly higher than 0.5 (p:0.001; p<0.05). The cut-off point for urotensin level in the diagnosis of Chronic Obstructive Pulmonary Disease was >4.21 with a sensitivity and specificity of 66.2% and 86.7%, respectively. COPD is a chronic, inflammatory process and endothelial dysfunction and related right ventricular failure findings may develop in this process. Elevated serum urotensin-II levels in COPD patients may be a useful parameter in predicting the development of airway obstruction. However, more detailed studies on this subject are needed. Keywords: COPD, urotensin-II, right ventricular dysfunction