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SAT0093 High triglycerides and low hdl lipid profile as a surrogate marker of hdl dysfunction in ra: potential links with inflammation and oxidative status
  1. J Rodríguez-Carrio1,
  2. M Alperi-Lόpez2,
  3. P Lόpez1,
  4. R Lόpez-Mejías3,
  5. S Alonso-Castro4,
  6. F Abal5,
  7. FJ Ballina-García2,
  8. MΆ González-Gay3,6,7,
  9. A Suárez1
  1. 1Area of Immunology, University of Oviedo
  2. 2Department of Rheumatology, Hospital Universitario Central de Asturias, Oviedo
  3. 3Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Hospital Universitario Marqués de Valdecilla, IDIVAL, Santander
  4. 4Department of Rheumatology, Hospital de Cabueñes, Gijόn
  5. 5Centro de Salud Sariego, SESPA, Pola de Siero
  6. 6Department of Medicine, University of Cantabria, Santander, Spain
  7. 7Cardiovascular Pathophysiology and Genomics Research Unit, University of the Witwatersrand, Witwatersrand, South Africa


Background the interactions between inflammation and lipid profile in RA are poorly understood. The study of lipid profiles in RA has been biased towards lipoprotein levels, whereas those of triglycerides (TG) and lipoprotein functionality have been neglected.

Objectives since recent findings point to an emerging role for TG and TG-rich lipoproteins (TRL) on inflammation, we aimed to evaluate a combined lipid profile characterized by high TG and low HDL levels (TGhighHDLlow) in RA.

Methods lipid profiles were analyzed in 113 RA patients, 113 healthy controls (HC) and 27 dyslipemic subjects (DL). A group of 13 biological-naïve RA patients was prospectively followed for 3 months upon TNFα-blockade. Serum levels of inflammatory mediators were assessed by immunoassays. PON1 activity and Total Antioxidant Capacity (TAC) were quantified in serum. PON1 rs662 status was evaluated by RT-PCR

Results the prevalence of the TGhighHDLlow profile was similar among RA patients (29/113), HC (30/113) and DL (11/27), linked to higher TRL levels in all groups. However, this profile was associated with increased CRP (p=0.012), TNFα (p=0.004), MCP-1 (p=0.004), IP-10 (p=0.018) and leptin (p<0.001) serum levels in RA, where decreased PON1 activity and TAC were found (both p<0.001). TRL serum levels were positively correlated to inflammatory mediators, whereas a negative association was found for PON1 activity (r=-0.203, p=0.036). These findings remain after excluding patients with previous CV events or those under statins. No associations were observed in the HC and DL groups. When RA patients were stratified by PON1 rs662 status, these associations were restricted to the low activity genotype (QQ) (TNFα: p=0.002, MCP-1: p=0.013, EGF: p=0.047, IP-10: p=0.018 and leptin: p=0.002), whereas no effect of the lipid profile was observed in those harboring the QR or RR genotypes (all p>0.050). As expected, QQ-patients exhibited a lower PON1 activity compared to the other genetic variants (both p<0.010). The TGhighHDLlow prevalence was related to a decreased anti-TNFα usage in the cross-sectional sample (p=0.004). A poor clinical response upon TNFα-blockade was related to an increasing prevalence of the TGhighHDLlow profile over treatment (p=0.021) and elevated baseline TRL levels (p=0.042).

Conclusions the TGhighHDLlow profile is associated with systemic inflammation, increased TRL levels, decreased PON1 activity and a poor clinical outcome upon TNFα-blockade in RA. Overall, these findings support the link between inflammation and lipid profile, oxidative status and TRL having a pivotal role. The TGhighHDLlow profile can be proposed as a surrogate marker of HDL dysfunction in RA.

Disclosure of Interest None declared

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