Abstract
AimThe aim of this study is to investigate the prevalence of asymptomatic hyperuricemia in Qatar and to examine its association with changes in markers of dyslipidemia, prediabetes and subclinical inflammation.MethodsA cross-sectional study of young adult participants aged 18 - 40 years old devoid of comorbidities collected between 2012 and 2017. Exposure was defined as uric acid level, and outcomes were defined as levels of different blood markers. De-identified data were collected from Qatar Biobank. T-tests, correlation tests and multiple linear regression were all used to investigate the effects of hyperuricemia on blood markers. Statistical analyses were conducted using STATA 16.ResultsThe prevalence of asymptomatic hyperuricemia is 21.2% among young adults in Qatar. Differences between hyperuricemic and normouricemic groups were observed using multiple linear regression analysis and found to be statistically and clinically significant after adjusting for age, gender, BMI, smoking and exercise. Significant associations were found between uric acid level and HDL-c p = 0.019 (correlation coefficient -0.07 (95% CI [-0.14, -0.01]); c-peptide p = 0.018 (correlation coefficient 0.38 (95% CI [0.06, 0.69]) and monocyte to HDL ratio (MHR) p = 0.026 (correlation coefficient 0.47 (95% CI [0.06, 0.89]).ConclusionsAsymptomatic hyperuricemia is prevalent among young adults and associated with markers of prediabetes, dyslipidemia, and subclinical inflammation.
Highlights
Hyperuricemia is a pathophysiological condition observed in association with chronic inflammatory diseases such as rheumatoid arthritis, diabetes, and cardiovascular and kidney diseases [1, 2]
Participants’ blood levels of uric acid, Triglycerides, LDL, HDL, glucose, c-peptide, HbA1c and ferritin were measured at Hamad Medical Corporation (HMC) laboratories, Department of Laboratory Medicine and Pathology (DLMP) that holds College of American Pathologist (CAP) accreditation
The associations we report between uric acid, and markers of prediabetes and dyslipidemia, further support this notion
Summary
Hyperuricemia is a pathophysiological condition observed in association with chronic inflammatory diseases such as rheumatoid arthritis, diabetes, and cardiovascular and kidney diseases [1, 2]. Hyperuricemia results from the overproduction of uric acid, the end product of purine catabolism. Accumulation of uric acid is due to increased production of uric acid in the body coupled with the paucity of the degradative enzyme, uricase [3]. Humans lack the uricase enzyme, which converts uric acid to a more soluble and excretable product, allantoin [4]. Uric acid is released from the cells in the soluble form; after exceeding 404 μmol/L (6.8 mg/dL) concentration in a solution, monosodium urate crystals (MSU) begin to precipitate, especially in the settings of other potentiating factors such as low temperatures and acidic environments [5,6,7]. Uric acid has paradoxical effect and appears to be pro-inflammatory at higher concentrations [8]. Uric acid is mostly excreted through the kidneys by tubular secretion and through the intestines (to a lesser extent); elevated uric acid is implicated in kidney stone formation [9]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
