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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Acknowledgements
We thank José Sánchez Payá, MD for his statistical support and Mrs. Meggan Harris for the English edition of the manuscript.
The FAPRES register research group members are: Juan Alberola, Vicente Javier; Maestre Amat, Luis; Mateo Limiñana, José Manuel; Monleón Gómez, José; Montagud Moncho, Miguel; Guinot Martínez, Enrique; Gamón Pastor, José Blas; Salanova Penalba, Alejandro; Sanchis Domenech, Carlos; Pallares Carratala, Vicente; Palacios Del Cerro, Antonio; Pérez Martínez, Rafael; Baudet Dejean, Chantal; Pérez Alonso, Manuel; Fácila Rubio, Lorenzo; Sipan Sarrión, Yolanda; Saro Pérez, Eugenia; Villaro Gumpert, Juan; Cabrera Ferriols, M. Ángeles; Fraile Fraile, Belén; Carbonell Franco, Francisco; Cornejo Mari, Francisco Javier; Barberá Comes, Javier; Quiles Añon, Fernando; Llisterri Caro, José Luis; Almenar Cubells, Enrique; Casado González, Joaquín; Godoy Rocati, Diego; Martínez Guerola, Carmen; Bonet García, Jorge Alejo; Blázquez Encinar, Julio César; Botella Estrada, Carlos; Saen Alcoy, Montepio; Almarcha Pérez, Natividad; Salanova Chilet, Lorena; Torres Ferrando, Miquel; Debon Belda, Manuel; Fluixa Carrascosa, Carlos; Aznar Baset, Lucía; Vivancos Aparicio, Diego; Pineda Cuenca, Manuel; Obarrio Moreno, Alicia; Núñez Jorge, Carlos; Matoses Nacher, Daniel; Baño Aracil, Manuel; Balanza Garzón, Alicia; García Palomar, Carlos; Peña Forcada, Enrique; Raga Casasus, José; Martínez Lahuerta, Juan; Mendizábal Núñez, Andrea; Santos Alonso, Eufrosina; Corbí Pascual, Miguel; Lillo Sánchez, Antonio; Martorell Adsuara, Vicente; Sánchez Ruiz, Tomás; Ortiz Díaz, Francisco; Llinares Orts, José Francisco; Lahoz Ferrer, Julio; Morillas Blasco, Pedro; Pertusa Martínez, Salvador; Manclus Montoya, Carlos; Adriá Mico, José Manuel; Llaudes Soler, Ricardo; Castillo Castillo, Jesús; Llopis Martínez, Francisco; Ruiz De La Prada Abarzuza, Ignacio; Nebot Rico, Lidia.
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The authors acknowledge the unconditional support of Lácer laboratories in the performance in this study. No company representatives participated in the data collection or interpretation or in the drafting of this report.
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Authors MA and EP have received speaking fees from Menarini labs. The other authors declare no conflict of interest.
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All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.
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MAQ and MA share the first authorship for this paper.
The members of the FAPRES Research Group have been listed in the “Acknowledgements” section.
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Quintanilla, M.A., Andrés, M., Pascual, E. et al. Inflammatory status and uricaemia determine HDL-cholesterol levels in hypertensive adults over 65: an analysis of the FAPRES register. Rheumatol Int 37, 941–948 (2017). https://doi.org/10.1007/s00296-017-3683-8
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DOI: https://doi.org/10.1007/s00296-017-3683-8