Medical Journal of Dr. D.Y. Patil Vidyapeeth

COMMENTARY
Year
: 2020  |  Volume : 13  |  Issue : 6  |  Page : 665--666

Role of uric acid in chronic obstructive pulmonary disease exacerbations: Current concepts and perspectives


Rajlaxmi Sarangi 
 Department of Biochemistry, Kalinga Institute of Medical Sciences, Bhubaneswar, Odisha, India

Correspondence Address:
Rajlaxmi Sarangi
Associate Professor, Department of Biochemistry, Kalinga Institute of Medical Sciences, Bhubaneswar, Odisha
India




How to cite this article:
Sarangi R. Role of uric acid in chronic obstructive pulmonary disease exacerbations: Current concepts and perspectives.Med J DY Patil Vidyapeeth 2020;13:665-666


How to cite this URL:
Sarangi R. Role of uric acid in chronic obstructive pulmonary disease exacerbations: Current concepts and perspectives. Med J DY Patil Vidyapeeth [serial online] 2020 [cited 2021 Jan 20 ];13:665-666
Available from: https://www.mjdrdypv.org/text.asp?2020/13/6/665/300154


Full Text



Chronic obstructive pulmonary disease (COPD) and its exacerbations are the leading cause of mortality and morbidity worldwide among all respiratory disorders. As per the WHO estimate, nearly 65 million people are suffering from COPD, which contributes to 5% of all death globally.[1] It will occupy the fifth rank in terms of burden of disease and third in terms of mortality by 2030.[2] In developing country, COPD-related mortality is more in comparison to developed one. Localized airway inflammation and cytokine production, generations of reactive oxygen and nitrogen species (ROS and RNS) play a major role in the pathogenesis of the disease process. Acute exacerbations (AEs) of COPD compromise quality of life in an individual, compromise progressive decline in lung function, and increase hospitalization, higher economic burden, and mortality.[3] Serum uric acid (sUA) is a major extracellular antioxidant present in the respiratory tract along with ascorbic acid, α-tocopherol, and ferritin, which counteracts against the oxidative stress generated in the respiratory tract epithelium due to cigarette smoking, biomass fuel, industrial pollution.[4] UA has both beneficial effects as antioxidant or free radical scavenger and deleterious effects if present at an elevated level. The powerful antioxidant properties of UA are at serum level of 5 mg/dl.[5] As the level increases, antioxidant properties mainly diminish. Hypoxia during the time of AE results in increased purine and adenosine catabolism and in turn leads to increased UA. So higher UA as a marker of oxidative stress and increases when exposed to triggering factors such as different types of viral, bacterial infections or noninfectious causes such as air pollution.[6] Hyperuricemia is seen in various respiratory diseases such as obstructive sleep apnea, pulmonary arterial hypertension, and many more systemic diseases. However, controversies still persist about the altered UA level with severity of COPD.

UA level can be influenced by many factors such as weight of individuals, age, male gender, food intake, alcohol consumption, and genetic disorder of purine metabolism. Since UA excretion may be affected in subjects who have concealed renal impairment, sUA-to-creatinine ratio (sUA/Cr) is a better indicator than sUA level in COPD patients as it normalizes the effect of derangement of kidney function. Hence, corrected UA (UA/Cr) level can be used for grading of the disease process. Studies done by AbdelHalim and AboEINaga[7] and Sato et al.[8] show a positive correlation between UA level and UA/Cr ratio with the frequency of exacerbations and hospitalization per year. They also show a positive correlation between UA and UA/Cr with inflammatory markers such as C-reactive protein. However, inverse association was found out between UA and UA/Cr ratio with oxygen saturation, forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), FEV1/FVC, maximum midexpiratory flow, and peak expiratory flow.

Oxidative stress (both local and systemic) is the important feature of COPD. This effect can be modulated by low-molecular-weight water-soluble, most abundant extracellular antioxidant (UA) which can protect lungs from oxidative stress by inhibiting lipid peroxidation and scavenging free radicals. With increasing severity of the disease (Stage III and IV of COPD), antioxidant capacity of UA may be inadequate. Smoking, air pollution, gastroesophageal reflux disease, and exposure to biomass fuel cause oxidant and antioxidant imbalance, which in turn increases severity of the disease. More than two-third of never-smokers are most commonly women, who are exposed to biomass fuel during cooking, indoor air pollution, and passive smoking are suffering from COPD. Confounding factors such as healthier lifestyle, exercise, less calorie intake, vitamin supplementation, and quality of food with high antioxidants can affect the level of sUA. Hence, lower level of UA can be obtained in patients suffering from severe COPD. Since future studies should be undertaken to keep all these in view as UA/Cr ratio and sUA can be used as a useful biomarker of severity of COPD, as it plays a central role in the disease process and associated with prognosis and exacerbations. More attention should be given for measuring these easily affordable, readily available, noninvasive parameters not only in COPD subjects but also in healthy subjects who are coming for routine health check-up.

References

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