Antioxidant and gouty arthritis in chronic obstructive pulmonary disease: the perplexing uric acid molecule

• Main Authors: Nourane Azab, Rana El-Helbawy, Gehan Abd-Elaal, Eglal El-Naggar
• Format: Article
• Language: English
• Published: Wolters Kluwer Medknow Publications 2020-01-01
• Series: Egyptian Journal of Chest Disease and Tuberculosis
• Subjects: chronic obstructive airway disease; serum uric acid; smoking
• Online Access: http://www.ejcdt.eg.net/article.asp?issn=0422-7638;year=2020;volume=69;issue=2;spage=331;epage=338;aulast=
• ISSN: 0422-7638; 2090-9950

Background Uric acid (UA) contributes to beneficial extracellular antioxidant defense activities in the airways. However, pro-oxidant powers of UA can be a potential risk factor for gouty arthritis in chronic obstructive airway disease (COPD). Objectives To investigate the proper causation (antioxidant/pro-oxidant) and correlation between UA indices and COPD and whether the associations were modified by smoking. Is serum uric acid (SUA) concentration a reliable biomarker to predict COPD severity? Patients and methods A prospective cohort study enrolled 45 male patients, who were divided into COPD smoker group I, cigarette smoker group II, and apparently healthy participants, serving as a control group III. SUA concentration and creatinine (Cr) level, arterial blood gases, radiographic imaging, and postbronchodilator spirometric measurements were performed. Results SUA was significantly elevated in COPD smoker and cigarette smoker groups than control one. SUA/Cr ratios were significantly increased in COPD smoker than in other groups. Overall, 8/20 (40%) patients were diagnosed with gouty arthritis in COPD smoker group, 1/15 (6.7%) in non-COPD cigarette smoker group, and none in control group. There were statistical significant differences among three groups (P=0.010). There were significantly higher number of patients with severe to very severe COPD (6/8) than patients with mild to moderate COPD (2/8) (P=0.028). There were significant positive correlations between SUA and smoking index (P=0.033), COPD grading (P=0.011), and partial arterial carbon dioxide tension (P=0.028) and also negative correlations with forced expiratory volume in the first second (FEV1)/forced vital capacity (FVC) (P=0.029), partial arterial oxygen tension (P=0.001), and O2 saturation (P=0.001) in COPD smoker group I. In cigarette smoker group II, there were statistically significant positive correlations between SUA level and FVC% (P=0.033), FEV1 (P=0.017), and FEV1/FVC (P=0.010). Receiver operating characteristic curves for the evaluation of performance of serum uric acid/serum creatinine ratio in the diagnosis of severity of chronic obstructive airway disease. Conclusion SUA had pivotal antioxidant and pro-oxidant inflammatory effects (gouty arthritis) in COPD. Cigarette smoking is an independent risk factor that influences SUA in COPD. SUA and SUA/Cr ratio increase with rising severity of COPD. UA/Cr ratio is the proper biomarker in the assessment of COPD grading, with higher sensitivity and specificity.