Observational study found elevated uric acid relates to disease severity in patients with COPD exacerbations, suggesting potential clinical implications.
Background: Tissue hypoxia triggers the degradation of purine and Uric Acid (UA) is an end product of this metabolic pathway, and therefore may reflect the severity of hypoxia. Only a few studies have focused on the role of uric acid in patients hospitalized for exacerbations of COPD (ECOPD). Objectives: To evaluate the associations of UA and Uric acid/Creatinine ratio (UA/Cr) with clinical parameters related to disease severity for patients hospitalized for ECOPD. Methods: UA and UA/Cr and parameters related to the severity of ECOPD, including PaO 2 /FiO 2 ratio, MRC dyspnea scale, and Saint George's Respiratory Questionnaire (SGRQ) were measured on admission. Patients underwent spirometry and 6-minute walking test (6MWT) on stable condition and were followed-up for 1 year. Results: We included 153 consecutive patients (92.8% male, mean age 73.1 years). UA levels were higher in more severe disease according to GOLD stages (6.38±9.1 vs 6.59±0.6 vs 7.45±0.8 vs 8.90±1.2 mg/dL respectively; p<0.001), with similar classification of UA/Cr levels (p<0.001). On admission, UA presented significant correlations with PaO2/FiO2 (r=-0.163, p=0.44), MRC (r=0.630, p<0.001) and SGRQ total score (r=0.485, p<0.001). UA/Cr presented similar associations. Baseline levels of UA and UA/Cr presented significant negative correlations with 6MWD (r=-0/756 and r=-0.734, p<0.001) and all SGRQ domains on stable condition. Patients in the higher quartiles of UA and UA/Cr presented more ECOPD and hospitalizations in the year of follow-up, but did not present differences in mortality. Conclusions: UA and UA/Cr levels present significant correlations with important variables expressing COPD severity both on exacerbation and on stable condition.
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Papadopoulos et al. (2011) studied this question.
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