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      Therapeutics and Clinical Risk Management (submit here)

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      Predictive value of serum uric acid in hospitalized adolescents and adults with acute asthma


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          High serum uric acid (sUA) is an indicator of oxidative stress and is linked to tissue hypoxia in asthma. The objective of this case series was to investigate the prognostic role of sUA in patients with acute asthma exacerbations and the link between sUA and spirometric lung tests.

          Patients and methods

          This cross-sectional observational study included 120 patients with acute asthma exacerbations and 120 controls, categorized according to peak expiratory flow rate into moderate, and severe and life-threatening asthma. On admission, a detailed history was obtained and investigations were carried out regarding oxygen saturation (SaO 2), arterial blood gas, spirometry, sUA, number of asthma exacerbations, smoking status, history of previous hospitalization, intensive care unit admission, and mechanical ventilation.


          The current study revealed higher sUA in asthmatic patients compared with healthy subjects and in severe asthma patients compared with moderate asthma patients ( P<0.001). A positive correlation of sUA with asthma severity, number of asthma exacerbations and smoking index ( r=0.6, 0.42 and 0.29, respectively, P<0.001) and a negative correlation of sUA with SaO 2, partial pressure of arterial oxygen (PaO 2), percent predicted forced vital capacity, percent predicted forced expiratory volume (FEV%) and peak expiratory flow rate percent of predicted (PEFR%; r=−0.48, −0.29, −0.44, −0.44 and −0.66, respectively, P<0.001) were observed. Degree of asthma severity, number of asthma exacerbations, and smoking index were significant predictors of high sUA ( R 2=0.43, P<0.001) in multiple linear regression model 1. SaO 2 and PEFR% were significant predictors of high uric acid ( R 2=0.50, P<0.001) in model 2. The sensitivity and specificity of sUA in predicting severity of asthma at the cutoff point of 6.3 mg/dL were 80% and 90%, respectively. The odds ratios of sUA, number of asthma exacerbations, and asthma duration were 5.4, 1.95 and 1.3, respectively.


          sUA may be a useful marker of predictive value of severity of asthma exacerbations.

          Most cited references31

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          Uric acid is a danger signal activating NALP3 inflammasome in lung injury inflammation and fibrosis.

          Lung injury leads to pulmonary inflammation and fibrosis through myeloid differentiation primary response gene 88 (MyD88) and the IL-1 receptor 1 (IL-1R1) signaling pathway. The molecular mechanisms by which lung injury triggers IL-1beta production, inflammation, and fibrosis remain poorly understood. To determine if lung injury depends on the NALP3 inflammasome and if bleomycin (BLM)-induced lung injury triggers local production of uric acid, thereby activating the NALP3 inflammasome in the lung. Inflammation upon BLM administration was evaluated in vivo in inflammasome-deficient mice. Pulmonary uric acid accumulation, inflammation, and fibrosis were analyzed in mice treated with the inhibitor of uric acid synthesis or with uricase, which degrades uric acid. Lung injury depends on the NALP3 inflammasome, which is triggered by uric acid locally produced in the lung upon BLM-induced DNA damage and degradation. Reduction of uric acid levels using the inhibitor of uric acid synthesis allopurinol or uricase leads to a decrease in BLM-induced IL-1beta production, lung inflammation, repair, and fibrosis. Local administration of exogenous uric acid crystals recapitulates lung inflammation and repair, which depend on the NALP3 inflammasome, MyD88, and IL-1R1 pathways and Toll-like receptor (TLR)2 and TLR4 for optimal inflammation but are independent of the IL-18 receptor. Uric acid released from injured cells constitutes a major endogenous danger signal that activates the NALP3 inflammasome, leading to IL-1beta production. Reducing uric acid tissue levels represents a novel therapeutic approach to control IL-1beta production and chronic inflammatory lung pathology.
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            Uric acid and oxidative stress.

            Uric acid is the final product of purine metabolism in humans. The final two reactions of its production catalyzing the conversion of hypoxanthine to xanthine and the latter to uric acid are catalysed by the enzyme xanthine oxidoreductase, which may attain two inter-convertible forms, namely xanthine dehydrogenase or xanthine oxidase. The latter uses molecular oxygen as electron acceptor and generates superoxide anion and other reactive oxygen products. The role of uric acid in conditions associated with oxidative stress is not entirely clear. Evidence mainly based on epidemiological studies suggests that increased serum levels of uric acid are a risk factor for cardiovascular disease where oxidative stress plays an important pathophysiological role. Also, allopurinol, a xanthine oxidoreductase inhibitor that lowers serum levels of uric acid exerts protective effects in situations associated with oxidative stress (e.g. ischaemia-reperfusion injury, cardiovascular disease). However, there is increasing experimental and clinical evidence showing that uric acid has an important role in vivo as an antioxidant. This review presents the current evidence regarding the antioxidant role of uric acid and suggests that it has an important role as an oxidative stress marker and a potential therapeutic role as an antioxidant. Further well designed clinical studies are needed to clarify the potential use of uric acid (or uric acid precursors) in diseases associated with oxidative stress.
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              An unexpected role for uric acid as an inducer of T helper 2 cell immunity to inhaled antigens and inflammatory mediator of allergic asthma.

              Although deposition of uric acid (UA) crystals is known as the cause of gout, it is unclear whether UA plays a role in other inflammatory diseases. We here have shown that UA is released in the airways of allergen-challenged asthmatic patients and mice, where it was necessary for mounting T helper 2 (Th2) cell immunity, airway eosinophilia, and bronchial hyperreactivity to inhaled harmless proteins and clinically relevant house dust mite allergen. Conversely, administration of UA crystals together with protein antigen was sufficient to promote Th2 cell immunity and features of asthma. The adjuvant effects of UA did not require the inflammasome (Nlrp3, Pycard) or the interleukin-1 (Myd88, IL-1r) axis. UA crystals promoted Th2 cell immunity by activating dendritic cells through spleen tyrosine kinase and PI3-kinase δ signaling. These findings provide further molecular insight into Th2 cell development and identify UA as an essential initiator and amplifier of allergic inflammation. Copyright © 2011 Elsevier Inc. All rights reserved.

                Author and article information

                Ther Clin Risk Manag
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                14 November 2016
                : 12
                : 1701-1708
                [1 ]Chest Diseases and Tuberculosis Department, Faculty of Medicine, Cairo University, Cairo
                [2 ]Department of Pediatrics, Children and Women’s University Hospital, Minia University, El-Minya
                [3 ]Department of Pediatrics, Mansoura University Children’s Hospital, Faculty of Medicine, Mansoura University, Mansoura, Egypt
                Author notes
                Correspondence: Nehad Mohamed Shalaby, Department of Pediatrics, Mansoura University Children’s Hospital, Faculty of Medicine, Mansoura University, Algomhoriah Street, Mansoura, Postal Code 35511, Egypt, Tel +20 10 9398 8813, Email amahalawy2002@ 123456yahoo.com
                © 2016 Abdulnaby et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Original Research

                asthma,uric acid,exacerbation,spirometery
                asthma, uric acid, exacerbation, spirometery


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