This study aimed to assess the prevalence of hyperuricemia and the relationship between serum UA concentration and lipid profile parameters in Saudi Arabia. Among the 1206 participants, the prevalence of hyperuricemia at King Abdulaziz University Hospital was 12%. Males were more frequently affected than females (8.13% vs. 3.73%, respectively), which is in agreement with previous studies. The prevalence of hyperuricemia is 21.4% in the USA (6), 18.6% in Bangladesh (10), 11.4% in Korea (11), and 6.4% in China (12). The most likely reasons for variation in the prevalence of hyperuricemia between our study and other studies are cultural differences and differences in eating habits. Saudi Arabia’s cuisine generally includes meat, which is a rich source of UA. Also, populations on the Western Coast often consume seafood. Villegas et al. stated that animal protein and seafood consumption are associated with a high prevalence of hyperuricemia (27). In a cross-sectional study conducted in China, a high intake of fresh meat and fish were quadrated with a high prevalence of hyperuricemia (28). Moreover, a prospective study performed in Riyadh, the capital of Saudi Arabia, showed that high consumption of meat-based foods in the central region of Saudi Arabia is a risk factor for hyperuricemia. Thus, there is strong evidence that hyperuricemia is highly associated with food intake (13).
Our findings reveal that the majority of participants with high serum UA concentrations had high TC and TG concentrations, a low HDL concentration, and a normal LDL concentration. However, there was no significant association between UA concentration and lipid profile parameters. Li et al. claimed no association between serum UA concentration and lipid profile parameters, and an elevated serum UA concentration was identified as a dyslipidemia-independent risk factor for hyperuricemia. Moreover, a high UA concentration significantly affects anti-oxidant reduction rate, whereas UA concentration does not interfere with hyperlipidemia-associated factors (29). Alaqi et al. conducted a study among the adult population of Al-Kharj to assess the association between UA concentration and lipid profile. The study included patients taking anti-hypertensive and anti-diabetic medications in addition to healthy individuals. They found a significant association between serum UA concentration and TG concentration, but no association was observed between UA concentration and TC concentration. However, there was no significant difference between serum UA, TC, or TG concentrations in patients who were taking anti-hypertensive medications compared with those who were not. The study showed a significant difference in TG concentrations among patients using anti-diabetic medications (30). Another study conducted in Al-Kharj found no significant association between serum UA concentration and TG, TC, and HDL concentrations (31). In addition, a study conducted in Sudan on 219 participants, 25% of whom had metabolic syndrome and 24.7% of whom were hypertensive, revealed no significant relationship between serum UA concentration and LDL and HDL concentrations. However, there was a significant relationship between serum UA concentration and TG and TC concentrations (32). In terms of the determinants of blood UA concentration in Arabic patients with dyslipidemia, a study conducted in Kuwait showed a significant relationship between serum UA concentration and TG concentration; however, there was no significant association between UA concentration and TC, LDL, and HDL concentrations (33). In contrast, Cibickova et al. conducted a cross-sectional study that supported the association between serum UA concentration and lipid profile (18). These differences in the association between serum UA concentration and lipid profile parameters may have been influenced by comorbidities and medications. In our study, participants were considered as free from chronic illness; thus, comorbidities and concomitant medications would not have been an influencing factor.
We observed a relationship between serum UA concentration and high BMI, old age, male sex, and nationality, which corroborates other studies. In a cross-sectional study conducted in Japan, serum UA concentration was strongly associated with BMI, and a decrease in BMI contributed to an improvement in serum UA concentration (34). Ismail et al. revealed that a high UA concentration was significantly associated with BMI (32), which supports our result. Furthermore, Zhang et al. stated that hyperuricemia is associated with age and sex (35). Another study showed that UA concentration is strongly related to the male sex (36). This phenomenon is related to the sex hormone estrogen, and the protective effect of estrogen has been addressed in a previous study (37). Estrogen promotes UA excretion by decreasing the tubular reabsorption of urate. Therefore, the age-associated decline in estrogen in females is accompanied by an increase in serum UA. Additionally, aging can result in low physical activity, which leads to visceral fat accumulation, obesity, and insulin resistance. Consequently, urinary excretion of UA is reduced (38). Also, we suggest that high UA concentrations are more frequently observed in males than females because males have a greater muscle mass, which is reflected as a high BMI, whereas the opposite is true for females.
We also observed a significant relationship between serum UA concentration and the Saudi nationality. Specifically, non-Saudis had a higher mean serum UA concentration and a higher prevalence of hyperuricemia compared with Saudis. This outcome is somewhat unexpected, considering that the majority of participants were of Saudi nationality (61.8%). This variation might be due to differences in genetic factors, lifestyle, and eating habits, particularly cultural food traditions, which are highlighted in the Saudi Arabian Society and may contribute to high UA concentrations as described earlier. According to a study conducted in the USA, the non-Hispanic male population demonstrated high UA concentrations (39). In addition, a review of several genetic studies found that hyperuricemia is common in African–American and European populations (40). A study performed in Taiwan found that UA concentrations in Aboriginals were higher compared with non-Aboriginals (41). A population-based study conducted to evaluate the contribution of diet to UA concentration (42) showed that diet accounts for minor variation in UA concentration in contrast to genetics. However, we divided participants in the present study into Saudi and non-Saudi nationalities, and there might be genetic similarities among participants of different nationalities.
In our study, we found no association between serum UA concentration and four factors: ESR, CRP concentration, WBC count, and vitamin D concentration. Liang et al. stated that there is no association between serum UA concentration and ESR (43). Moreover, a study conducted in China demonstrated no association between serum UA concentration and CRP concentration or WBC count (44). Furthermore, an Australian study reported no association between serum UA concentration and vitamin D concentration (45). In contrast, a study performed in Al-Kharj discovered that elevated UA leads to vitamin D deficiency (31); however, UA concentrations in our study were not as high as UA concentrations in their study. We hypothesize that vitamin D deficiency is associated with a significantly high UA concentration, which is not reflected in our findings. We suggest that an elevated UA concentration could elevate WBC counts, inflammatory markers, ESR, and CRP concentration. However, the participants in our study had not reached the concentration of UA that would induce inflammatory markers and elevate WBC counts. This may be due to missing data from electronic health records, as these parameters are not routinely measured with serum UA and lipid profile tests.
Furthermore, an association was observed between sex and mean ESR and mean TG concentration. Males had a higher mean ESR compared with females, while females had a higher mean TG concentration compared with males. Siemens et al. showed that ESR was higher in females compared with males (46). We believe genetic variations and use of different measurements to determine ESR may explain this adverse result. Due to the coronavirus disease 2019 crisis, access to the hospital and hospital healthcare system was restricted. In addition, our study focused on a healthy population; thus, we excluded a large number of patients with comorbidities, which may have affected our findings. Finally, incomplete documentation of patients’ data and inclusion of cases in which not all lipid profile parameters were requested may have influenced the results.