In inflammatory disease, the levels of high-density lipoprotein cholesterol (HDL-C) decrease, and the composition of HLD-C changes. Data from the “non-inflammatory” general population indicate the presence of the same phenomenon,… Click to show full abstract
In inflammatory disease, the levels of high-density lipoprotein cholesterol (HDL-C) decrease, and the composition of HLD-C changes. Data from the “non-inflammatory” general population indicate the presence of the same phenomenon, albeit to a smaller extent. Levels of uricaemia contribute to the overall inflammatory state of patients. The aim of this study was to analyse the association between inflammatory state, levels of uricaemia, and levels of HLD-C in a hypertensive Spanish population aged 65 or older. This was a retrospective analysis of the FAPRES database. We compared lipid levels [HDL-C, low-density lipoprotein cholesterol (LDL-C), total cholesterol, and triglycerides] in terciles of patients according to their leukocyte counts and uricaemia. When we observed statistically significant differences at a 95% confidence level, we constructed a multivariable linear regression model to adjust for possible confounders. We analysed 860 patients (52.7% women) with a mean age of 72.9 years (±5.8). Participants in the highest tercile for leukocytes or uricaemia presented with significantly lower levels of HDL-C and higher levels of triglycerides, but there was no difference in total cholesterol or LDL-C. The multivariable analysis confirmed an independent and inverse association between HDL-C and both leukocytes (β = −0.001, p = 0.025) and uricaemia (β = −1.054, p = 0037) as well as an independent, direct association between triglycerides and both leukocytes (β = 0.004, p = 0.049), and uricaemia (β = 8.411, p = 0.003). In hypertensive adults aged 65 or older, inflammatory state, and uricaemia independently operate to decrease HDL-C—these findings confirm those described in studies in people with inflammatory disease. This phenomenon could help to define a proatherogenic profile in people without inflammatory disease.
               
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