I. Hotea 1, T. O. Crisan 2, C. Pamfil 1, M. Badii 2, O. Gall 2, L. Peca², A. Mirea², R. Popp 2, S. Rednic 1,3, L. Ab Joosten 2,4.
1 Department of Rheumatology “Iuliu Hatieganu” University Of Medicine And Pharmacy Cluj-Napoca, Romania ² Department of Medical Genetics “Iuliu Hatieganu” University Of Medicine And Pharmacy Cluj-Napoca, Romania ³ Department of Rheumatology Emergency County Hospital Cluj-Napoca, Romania 4 Department of Internal Medicine, Radboud University Medical Centre, Nijmegen, The Netherlands
Introduction: Alpha-1-antitrypsine (AAT) is an important serine protease inhibitor. Previous studies assessed the role of AAT as an inflammatory modulator due to the effects on neutrophil mediated inflammation in gout. Gout is an inflammatory form of arthritis with acute episodes highly dependent on neutrophil involvement. In this study we assessed the association between the AAT, serum urate levels (SUA) and inflammatory parameters in patients with gout, asymptomatic hyperuricaemia and a control group of healthy subjects.
Materials and methods: We included 114 patients with gout based on the ACR/EULAR 2015 classification criteria, with minimum of 8 points, 100 asymptomatic hyperuricaemic patients with SUA level >7 mg/dl, and 89 normouricaemic controls matched in age. The inflammatory markers, erythrocytes sedimentation rate (ESR), C reactive protein, and SUA levels were determined by routine laboratory test. AAT was determined by ELISA assay (Hycult Biotech The Netherlands) using EDTA plasma samples. Statistical analyzed was perform using Spearman correlation test.
Results: A significant negative correlation was found between circulating AAT and SUA concentration in the control group. This result was not observed in gout and asymptomatic hyperuricaemic group, where a tendency for positive correlation between AAT and SUA or ESR was observed. There was also a significant positive correlation between AAT and ESR in patients with gout, consistent with the role of AAT as an acute phase reactant.
Conclusion: We were able to validate previous reported findings in which a negative correlation between SUA levels and AAT was observed, possibly due to the role of uric acid to inhibit the production of AAT. This was not confirmed in the gout and hyperuricaemic patients, in the line with the fact that hyperuricaemic patients often present inflammation which positively correlates with AAT. The results obtained in this study reinforce the dual role that AAT could play in inflammation and further studies are needed to assess the effects of uric acid in AAT production.