Abstract Objectives While lipid metabolism disorder is widely acknowledged as a contributing factor to inflammation, the association between remnant cholesterol (RC), which indicates lipid metabolism, and rheumatoid arthritis (RA) has not been investigated. Accordingly, this study evaluated whether RC is associated with RA disease events. Methods Data were collected and specifically extracted from the National Health and Nutrition Examination Survey (NHANES) 1999–2008 database. The RC value was derived by subtracting the combined amount of low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) from the total cholesterol (TC). The association between RC and RA was evaluated using multivariate regression analysis and subgroup analysis. Results The study analyzed 7777 patients, of which 581 patients (7.47%) were diagnosed with RA. After accounting for different covariates, the multivariate logistic regression analysis revealed a notable correlation between increased RC levels and an increased likelihood of RA (odds ratio OR = 1.54; 95% confidence interval CI: 1.11–2.13; P = 0.0092). The interaction test did not yield statistically significant effects on this association. The linear correlation between RC and RA was observed within restricted cubic spline regression model limitations. Conclusion The results suggest that higher RC levels are associated with increased odds of RA, indicating that RC can serve as a novel and convenient index for forecasting the likelihood of RA in the United States. Additionally, these findings offer insights into early intervention strategies for susceptible populations at risk of developing RA. 

The association between remnant cholesterol and rheumatoid arthritis: insights from a large population study

Dyslipidemia has been implicated in various musculoskeletal diseases, including rheumatoid arthritis (RA). Evidence is emerging that there might be a pathogenic interaction among inflammation, dyslipidemia, and adipokines. We prospectively investigated the association of cumulative lipid levels with radiographic progression of RA. RA patients (n = 242) underwent plasma cholesterol assessment at four visits. Disease activity parameters and X-rays of the hands and feet were also serially monitored in these patients. The cumulative inflammatory burden and lipid levels were estimated by time-integrated values. Serum leptin and adiponectin concentrations were determined by ELISA. When patients were divided into three groups according to time-integrated lipid levels, as expected, patients with LDL cholesterol and/or triglyceride levels in the third tertile had persistently higher ESR and CRP levels. In parallel, a more rapid radiographic progression over two years was observed in patients with higher LDL cholesterol and/or triglyceride levels. In multivariate analysis, time-integrated LDL cholesterol was independently associated with radiographic progression. Particularly, the risk of radiographic progression was 5.6-fold in a subgroup with both LDL cholesterol and triglyceride levels in the third tertile. Moreover, LDL cholesterol synergistically increased the adjusted probability of radiographic progression in patients with high serum leptin levels but not in those without. These results demonstrate that LDL cholesterolemia is a novel serum marker that can be used to predict radiographic progression of RA, which seems to be related to circulatory leptin levels. We suggest that personalized and more aggressive anti-rheumatic therapy is required for dyslipidemic subgroups in RA patients.

/pdf/ldl-cholesterolemia-as-a-novel-risk-factor-for-radiographic-2bysk78ikz.pdf

LDL Cholesterolemia as a Novel Risk Factor for Radiographic Progression of Rheumatoid Arthritis: A Single-Center Prospective Study

LDL-cholesterol concentrations : a genome-wide association study. Commentary

Abstract We aimed to explore whether the rs2073618 variant (G1181C) of the osteoprotegerin (OPG) gene and the methylenetetrahydrofolate reductase (MTHFR) rs1801131 (A1298AC) and rs1801133 (C677T) gene polymorphisms contribute to rheumatoid arthritis (RA) susceptibility and RA related subclinical atherosclerosis. Overall 283 RA patients and 595 healthy controls (HC) were genotyped for common variants of the OPG and MTHFR genes using PCR based assays. Clinical and laboratory parameters were recorded following thorough chart review. Surrogate markers of subclinical atherosclerosis (Carotid/Femoral intima media thickness/plaque formation) along with traditional risk factors for atherosclerosis were assessed in all RA patients and 280HC. Increased prevalence of the CC genotype of the rs2073618 variant was detected in RA patients vs HC (42.4% vs. 33%, p-value: 0.04). RA patients with high serum titers of rheumatoid factor (RF) or anti-cyclic citrullinated peptide (CCP) antibodies displayed increased prevalence of the CC genotype of the rs2073618 variant of the OPG gene compared to HC (48.6% and 47.5 vs 33.3%, p-values: 0.0029and 0.0077 respectively). Of interest, this genotype turned to be associated with higher carotid IMT scores (0.872 ± 0.264 vs 0.816 ± 0.284, p-value: 0.01) and marginally with higher rates of carotid plaque formation (66% vs 54.1%, p = 0.06). The MTHFR 1298CC genotype was more prevalent only in the anti-CCP positive group compared to HC, with no associations detected with markers of subclinical atherosclerosis, following adjustment for traditional cardiovascular (CVD) risk factors. Reduced rates of carotid/femoral plaque formation were detected among RA patients harboring the MTHFR TT genotype (52.4 vs 72.7, p-value: 0.009, respectively). This association remained significant following adjustment for classical CVD risk factors (OR [95% CI 0.364 [0.173–0.765], p-value: 0.008). Genetic variations of the osteoprotegerin and MTHFR genes seem to increase susceptibility for seropositive RA and potentially contribute to subclinical atherosclerosis linked to RA. Larger studies are needed to confirm these findings. 

/pdf/osteoprotegerin-and-mthfr-gene-variations-in-rheumatoid-3eir3av7.pdf

Osteoprotegerin and MTHFR gene variations in rheumatoid arthritis: association with disease susceptibility and markers of subclinical atherosclerosis

Objective: To identify risk factors for cardiovascular disease in patients with Rheumatoid Arthritis (RA). Material and methods: A descriptive cross-sectional study with 71 patients with established RA. The instruments used were: DAS-28, HAQ and SF-36, and the following parameters were determined: the erythrocyte sedimentation rate, capillary blood glucose; total cholesterol (TC) and its fractions, thyroid hormones, antinuclear antibodies (ANA), rheumatoid factor (RF) and antibodies against citrullinated proteins (ACPAs). Patients were classified into groups HAQ ≤ 1 (mild dysfunction) and HAQ > 1 (moderate and severe dysfunction) and, according to the HAQ scores, in groups treated with corticosteroids (CS) and without CS. Results: 9 patients were male and 62 female with mean age and duration of disease of 53.45 (±10.7) and 9.9 (±8.6), respectively. RF was positive in 52 (76%), ACPAs in 54 (76.1%) and ANA in 12 (16.9%). Thirty-six patients (50.7%) had systemic hypertension, 9 (12.68%) diabetes mellitus, 16 (22.5%) hypothyroidism, 33 (46.5%) dyslipidemia and 8 (11.27%) were smokers. The results of TC > 240 were found in 53.8% for group HAQ > 1 (26) and in 24.4% for group HAQ ≤ 1 (45) (p = 0.020). These groups did not differ as to presence of comorbidities or drug treatment. Triglyceride levels >200 for the group with CS (42.4%) versus without CS (18.42%) were significant (p = 0.025). Conclusion: An association of increased TC and triglycerides with results of HAQ ≤ 1 and with CS use was noted, reinforcing the importance of screening risk factors associated with cardiovascular disease in RA.

http://www.scielo.br/pdf/rbr/v55n6/en_0482-5004-rbr-55-06-0493.pdf

Risk factors for cardiovascular disease in rheumatoid arthritis patients from Mato Grosso do Sul

Objective. Dyslipidemia, a risk factor for cardiovascular diseases, is more prevalent in patients with rheumatoid arthritis (RA) than in the general population. We investigated whether single-nucleotide polymorphisms (SNP) modulating low-density lipoprotein (LDL) cholesterol affect susceptibility, severity, and progression of RA. Methods. We enrolled 302 patients with RA and 1636 healthy controls, and investigated the SNP modulating LDL cholesterol. Clinical characteristics of RA, serum adipocytokine concentrations, and radiographic severity were analyzed according to genotype score based on the number of unfavorable alleles. The influence of genotype score on radiographic progression was also investigated using multivariable logistic models. Results. We identified 3 SNP (rs688, rs693, and rs4420638) modulating LDL cholesterol in Koreans, which correlated well with LDL cholesterol levels in both patients with RA and controls. Among them, 2 SNP, rs688 and rs4420638, were more prevalent in patients with RA than in controls. In patients with RA carrying more unfavorable alleles (genotype score ≥ 3), disease activity measures, serum adipocytokine levels, and radiographic severity were all increased. The genotype score was an independent risk factor for radiographic progression of RA over 2 years, and its effect was greater than the influence of conventional risk factors. Conclusion. SNP modulating LDL cholesterol influence the risk, activity, and severity of RA. These results provide the first evidence that genetic mechanisms linked to dyslipidemia may directly contribute to the susceptibility and prognosis of RA, a representative of chronic inflammatory diseases, explaining the high incidence of dyslipidemia in RA.

https://www.jrheum.org/content/jrheum/40/6/798.full.pdf

Association of polymorphisms modulating low-density lipoprotein cholesterol with susceptibility, severity, and progression of rheumatoid arthritis.

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Association of polymorphisms modulating low-density lipoprotein cholesterol with susceptibility, severity, and progression of rheumatoid arthritis.