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Rheumatoid arthritis (RA) patients might experience anxiety and depressive symptoms. Deficient vitamin D levels may be a trigger for these conditions. The aim of this study was to determine the frequency of depression, anxiety symptoms, and suicidal risk or ideation in patients with RA associated with vitamin D serum levels.In this cross-sectional study, we recruited RA patients older than 18 years, classified into 3 groups according to serum vitamin D levels: sufficient, ≥30 ng/mL; insufficient, 20-29 ng/mL; and deficient,20 ng/mL. Based on the self-reported Plutchik and the Hospital Anxiety and Depression Scale, we evaluated the association of suicidal risk, depression, and anxiety with the vitamin D levels in RA and the Rheumatoid Arthritis Quality-of-Life Questionnaire.We studied 72 patients with RA between January and October 2019. We found an inverse correlation between Plutchik score and suicidal risk with inadequate vitamin D levels, but not with the Hospital Anxiety and Depression Scale. Suicidal ideation was associated with a higher score on the Rheumatoid Arthritis Quality-of-Life Questionnaire.Despite the high prevalence of depressive and anxiety symptoms in RA patients, a Plutchik low correlation coefficient with inadequate serum levels of vitamin D was found. However, in the analysis of covariance, we were able to find that vitamin D levels remain associated with a reduction of suicide ideation. Further studies are needed to identify a risk profile for early psychological interventions to improve the quality of life in RA patients.

Autoimmune rheumatic diseases are a cluster of heterogeneous disorders that share some clinical symptoms such as pain, tissue damage, immune deregulation, and the presence of inflammatory mediators. Biologic disease-modifying antirheumatic drugs are some of the most effective treatments for rheumatic diseases. However, their molecular and pharmacological complexity makes them potentially immunogenic and capable of inducing the development of anti-drug antibodies. TNF inhibitors appear to be the main contributors to immunogenicity because they are widely used, especially in rheumatoid arthritis. Immunogenicity response on these treatments is crucial since the appearance of ADAs has consequences in terms of safety and efficacy. Therefore, this review proposes an overview of the immunogenicity of biological agents used in autoimmune rheumatic diseases highlighting the prevalence of anti-drug antibodies.

Introduction Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the production of autoantibodies such as anti-Sm. Studies in patients with SLE and murine models of lupus reveal that the most critical anti-Sm autoantibodies are predominantly direct against D1(83–119), D2, and B´/B epitopes. Objectives The present study aimed to analyze the induction of antigen-specific tolerance after prophylactic immunization with a DNA vaccine encoding the epitopes: D183-119, D2, B´/B, and B´/BCOOH in co-vaccination with IFN-γ or IL-10 in a murine model of lupus induced by pristane. Material and methods To obtain endotoxin-free DNA vaccines, direct cloning techniques using pcDNA were performed: D183-119, D2, B´/B, B´/BCOOH, IFN-γ, or IL-10. Lupus was induced by 0.5 mL of pristane via intraperitoneal in BALB/c female mice. Immunoprecipitation with K562 cells was metabolically labeled with 35S and ELISA to detect serum antibodies or mice IgG1, IgG2a isotypes. ELISA determined IL-10 and IFN-γ from splenocytes supernatants. Proteinuria was assessed monthly, and lupus nephritis was evaluated by immunofluorescence, and electron microscopy. Results The prophylactic co-vaccination with D2/IL-10 reduced the expression of kidney damage observed by electron microscopy, direct immunofluorescence, and H & E, along with reduced level of anti-nRNP/Sm antibodies (P = 0.048). Conclusion The prophylactic co-vaccination of IL-10 with D2 in pristane-induced lupus ameliorates the renal damage maybe by acting as prophylactic DNA tolerizing therapy.

The presence of myositis-specific antibodies (MSA), was recently reported in healthy individuals, cancer patients without myopathy and paraneoplastic rheumatic syndromes. We sought to analyze the frequency of MSA, myositis-associated antibodies (MAA) and autoantibodies related to systemic autoimmune rheumatic diseases (SARD) in breast cancer patients. One hundred fifty-two breast cancer patients were enrolled in a cross-sectional study. Clinical information was collected, and autoantibodies tested by immunoprecipitation of an 35S-methionine-labeled K562 cell extract, enzyme-linked immunosorbent assay (ELISA) and Western blot when indicated. All statistical tests were performed using the software statistical package for the social science (SPSS) ver. 19.0 (IBM Inc., NYSE, USA). Autoantibodies associated with SARD: anti-52 kD ribonucleoprotein/tripartite motif-containing 21 (anti-Ro52/TRIM21) was found in 5.9% (9/152), anti-Sjögren syndrome-related antigen A/60 kD ribonucleoprotein antibody (anti-SSA/Ro60) in 3.9% (6/152) and anti-Su antigen/Argonaute 2 antibody (anti-Su/Ago2) in 2.6% (4/152). Meanwhile, anti-transcription intermediary factor-1γ (anti-TIF-1γ, p155/140) antibody was positive in 2 cases and anti-polymyositis/scleroderma antibody was detected in one case. As a whole, 14.47% (22/152) of breast cancer patients showed autoantibodies associated with SARD. These specific autoantibodies were not associated with the presence of rheumatic diseases except one rheumatoid arthritis patient positive for anti-Ro52/TRIM21. Autoantibodies to TIF-1γ were found in two patients with breast cancer without dermatomyositis (DM). More common specificities were autoantibodies anti-SSA/Ro60, anti-Ro52/TRIM21 and anti-Su/Ago2. More studies are needed in order to establish the biological meaning of the presence of SARD-associated autoantibodies in breast cancer.

Background: type-2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by hyperglycemia, insulin resistance (IR), and abnormal fatty acid metabolism in which the CD36 receptor has been implicated in glucose and lipid dysregulation. Objective: to evaluate the contribution of polymorphism CD36 rs3211938 to metabolic profile in T2DM Mexican mestizos from western Mexico. Methods: we included 115 individuals classified as non-T2DM (NT2DM) adults and T2DM patients. Polymorphism CD36 rs3211938 was assessed by PCR-RFLP. Anthropometric and metabolic markers were measured by routine methods, and insulin and oxidized LDL (ox-LDL) were measured by ELISA. Results: the distribution of genotypes between NT2DM and T2DM patients was different (p0.001), as was the allele frequency (p = 0.002). NT2DM TG carriers showed the lowest levels of basal insulin and HOMA-IR index in comparison with TT carriers (p0.05 and p0.05, respectively). In the T2DM group TG carriers showed high BMI, WHR, and weight values (p = 0.001; p ≤ 0.05 and p0.05, respectively), and the highest levels of basal glucose, HDL-cholesterol, ox-LDL, and HOMA-IR (p0.001; p0.001; p0.001, and p = 0.001, respectively) in comparison with diabetic TT carriers. Conclusion: the CD36 rs3211938 TG genotype is associated with high levels of glucose, ox-LDL, HDL-cholesterol, and IR, and with increased BMI in Mexican mestizo T2DM patients from western Mexico.Antecedentes: la diabetes mellitus de tipo 2 (DMT2) es un trastorno metabólico crónico caracterizado por hiperglucemia, resistencia a la insulina (RI) y metabolismo anormal de ácidos grasos en el que se ha implicado el receptor CD36 en la disregulación de la glucosa y los lípidos. Objetivo: evaluar la contribución del polimorfismo CD36 rs3211938 al perfil metabólico en individuos mestizos mexicanos con DMT2 del occidente de México. Métodos: se incluyeron 115 individuos clasificados en adultos sin DMT2 (NDMT2) y pacientes con DMT2. El polimorfismo CD36 rs3211938 se identificó mediante PCR-RFLP. Las mediciones antropométricas y metabólicas se realizaron mediante métodos de rutina y la insulina y las LDL-oxidadas (LDL-ox) se midieron por ELISA. Resultados: las distribuciones de los genotipos entre los pacientes NDMT2 y DMT2 fueron diferentes (p0,001), así como la frecuencia alélica (p = 0,002). Los individuos NDMT2 portadores del genotipo TG mostraron niveles más bajos de insulina basal e índice HOMA-IR en comparación con los portadores del genotipo TT (p0,05 y p0,05, respectivamente). En el grupo DMT2, los portadores del genotipo TG presentaron valores elevados de índice de masa corporal (IMC), índice cintura-cadera (ICC) y peso (p = 0,001; p0,05 y p0,05, respectivamente) y niveles más altos de glucosa basal, HDL-colesterol, LDL-ox y HOMA-IR (p0,001; p0,001; p0,001 y p = 0,001, respectivamente) en comparación con los portadores del genotipo TT. Conclusión: el genotipo TG del polimorfismo CD36 rs3211938 se asocia a altos niveles de glucosa, ox-LDL, HDL-colesterol y RI, y a aumentos del IMC en los pacientes mestizos mexicanos con DMT2 del occidente de México.

Osteoporosis (OP) is highly prevalent in rheumatoid arthritis (RA) and is influenced by genetic factors. Single-nucleotide polymorphism (SNP) rs2073618 in the TNFRSF11B osteoprotegerin (OPG) gene has been related to postmenopausal OP although, to date, no information has been described concerning whether this polymorphism is implied in abnormalities of bone mineral density (BMD) in RA. We evaluated, in a case-control study performed in Mexican-Mestizo women with RA, whether SNP rs2073618 in the TNFRSF11B gene is associated with a decrease in BMD. RA patients were classified as follows: (1) low BMD and (2) normal BMD. All patients were genotyped for the rs2073618 polymorphism by PCR-RFLP. The frequency of low BMD was 74.4%. Higher age was observed in RA with low BMD versus normal BMD (62 and 54 years, resp.; p<0.001). Worse functioning and lower BMI were observed in RA with low BMD (p=0.003 and p=0.002, resp.). We found similar genotype frequencies in RA with low BMD versus RA with normal BMD (GG genotype 71% versus 64.4%, GC 26% versus 33%, and CC 3% versus 2.2%, resp.; p=0.6). We concluded that in Mexican-Mestizo female patients with RA, the rs2073618 polymorphism of the TNRFS11B gene is not associated with low BMD.

To compare bone turnover marker (BTM) levels and bone mineral density (BMD) between patients with ankylosing spondylitis (AS) and healthy controls (HC) and to evaluate, in AS, the association between BTM levels and clinical variables, spinal syndesmophytes, and BMD using multivariate analysis.Seventy-eight AS patients were compared with 58 HC matched by gender. Spinal syndesmophytes in AS and other characteristics were assessed. C-terminal telopeptide fragments of type I collagen (CTX), bone-specific alkaline phosphatase (BAP), osteocalcin (OC) serum levels, and BMD of the lumbar spine, femoral neck, and forearm were evaluated.AS males and females had lower BAP levels than their respective HC (p 0.001 and p = 0.001). AS patients with bridging syndesmophytes had higher OC levels than AS patients either with non-bridging syndesmophytes (p = 0.001) or without spinal syndesmophytes (p 0.001). OC and CTX levels correlated significantly with the modified Stoke Ankylosing Spondylitis Spinal Score (mSASSS). In the multivariate linear regression adjusted by age, gender, the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), BMD in the lumbar spine, and C-reactive protein (CRP), we observed an association between BAP levels and anti-tumour necrosis factor (anti-TNF) use (p = 0.05) whereas OC levels were associated with mSASSS (p 0.001) and anti-TNF use (p = 0.05), and CTX levels were exclusively associated with mSASSS (p = 0.03). In the logistic regression analysis, only OC levels were associated with the presence of syndesmophytes in AS [odds ratio (OR) 2.42, 95% confidence interval (CI) 1.19-5.75].We observed an increase in OC levels in AS patients with syndesmophytes. BTM levels were associated with the severity of spinal damage. Future longitudinal studies should evaluate whether these BTMs should be included as tools to determine the prognosis and progression of spinal damage.

espanolIntroduccion: Los pacientes con artritis reumatoide pueden desarrollar enfermedad tiroidea autoinmune (ETA), cuyo diagnostico clinico puede ser dificil debido a que ambas comparten sintomas como artralgias, mialgias, rigidez matutina o fatiga. Objetivo: Determinar la prevalencia de ETA en pacientes con artritis reumatoide. Metodo: Estudio transversal que incluyo 78 pacientes con artritis reumatoide y 81 controles clinicamente sanos pareados por edad y sexo. A ambos grupos se realizo cuantificacion de anticuerpos antitiroideos, pruebas de funcion tiroidea, ultrasonido y biopsia de glandula tiroides cuando la puntuacion de Thyroid Imaging Reporting and Data System (TIRADS) fue ≥ 4. Resultados: 24.4 % de los pacientes con artritis reumatoide presento hipotiroidismo (p = 0.003) y altos titulos de anticuerpos antitiroideos versus controles clinicamente sanos; 53 % de los ultrasonidos tiroideos resulto normal en pacientes hipotiroideos; en pacientes con artritis reumatoide positivos para anticuerpos antitiroideos se encontro perfusion incrementada en 40 %. Los casos clasificados como TIRADS 4 fueron enviados a aspiracion, con resultado histopatologico benigno. Conclusiones: Se demostro el valor clinico agregado de la evaluacion tiroidea en pacientes con artritis reumatoide, conforme a la prevalencia de hipotiroidismo subclinico, positividad de anticuerpos antitiroideos y anomalias en el ultrasonido independientes de la funcion tiroidea normal o alterada. EnglishIntroduction: Patients with rheumatoid arthritis can develop autoimmune thyroid disease (ATD), the clinical diagnosis of which can be difficult because both entities share symptoms such as arthralgia, myalgia, morning stiffness or fatigue. Objective: To determine the prevalence of ATD in patients with rheumatoid arthritis. Method: Cross-sectional study that included 78 patients with rheumatoid arthritis and 81 clinically healthy controls matched by age and gender. Both groups underwent anti-thyroid antibodies quantification, thyroid function tests, thyroid ultrasound and thyroid gland biopsy when the Thyroid Imaging Reporting and Data System (TIRADS) score was ≥ 4. Results: Hypothyroidism was found in 24.4% of patients with rheumatoid arthritis (p = 0.003), as well as high titers of anti-thyroid antibodies versus clinically healthy controls; 53% of thyroid ultrasounds were normal in hypothyroid patients, and increased perfusion was found in 40% of rheumatoid arthritis patients who tested positive for anti-thyroid antibodies. Cases classified as TIRADS 4 underwent aspiration with benign histopathological results. Conclusions: Thyroid assessment added clinical value was demonstrated in patients with rheumatoid arthritis, according to the prevalence of subclinical hypothyroidism, anti-thyroid antibodies positivity and ultrasound abnormalities, regardless of normal or altered thyroid function.

The main cause of death in rheumatoid arthritis (RA) is cardiovascular events. We evaluated the relationship of anticyclic citrullinated peptide (anti-CCP) antibody levels with increased carotid intima-media thickness (cIMT) in RA patients.Methods. Forty-five anti-CCP positive and 37 anti-CCP negative RA patients, and 62 healthy controls (HC) were studied. All groups were assessed for atherogenic index of plasma (AIP) and cIMT. Anti-CCP, C-reactive protein (CRP), and levels of tumor necrosis factor alpha (TNFα) and interleukin-6 (IL-6) were measured by enzyme-linked immunosorbent assay (ELISA).Results. The anti-CCP positive RA patients showed increased cIMT compared to HC and anti-CCP negative (P<0.001). Anti-CCP positive versus anti-CCP negative RA patients, had increased AIP, TNFαand IL-6 (P<0.01), and lower levels of high density lipoprotein cholesterol (HDL-c) (P=0.02). The cIMT correlated with levels of anti-CCP (r=0.513,P=0.001), CRP (r=0.799,P<0.001), TNFα(r=0.642,P=0.001), and IL-6 (r=0.751,P<0.001). In multiple regression analysis, cIMT was associated with CRP (P<0.001) and anti-CCP levels (P=0.03).Conclusions. Levels of anti-CCP and CRP are associated with increased cIMT and cardiovascular risk supporting a clinical role of the measurement of cIMT in RA in predicting and preventing cardiovascular events.

Posttranslational modifications (PTMs) are defined as covalent modifications occurring in a specific protein amino acid in a time- and signal-dependent manner. Under physiological conditions, proteins are posttranslationally modified to carry out a large number of cellular events from cell signaling to DNA replication. However, an absence, deficiency, or excess in PTMs of a given protein can evolve into a target to trigger autoimmunity, since PTMs arise in the periphery and may not occur in the thymus; hence, proteins with PTMs never tolerize developing thymocytes. Consequently, when PTMs arise during cellular responses, such as inflammation, these modified self-antigens can be taken up and processed by the antigen-presenting cells (APCs). Autoreactive T cells, which recognize peptides presented by APCs, can then infiltrate into host tissue where the modified antigen serves to amplify the autoimmune response, eventually leading to autoimmune pathology. Furthermore, a PTM occurring in an amino acid residue can induce changes in the net charge of the protein, leading to conformational modifications in the tertiary and quaternary structure of the protein, especially interaction with human leukocyte antigen (HLA) molecules. Molecular mimicry (MM) was until now the prevailing hypothesis explaining generation of autoimmunity; nevertheless, experimental animal models need inflammation via infection or other immunogens to ensure autoimmunity; MM alone is not sufficient to develop autoimmunity. PTMs could arise as an additive factor to MM, which is required to start an autoimmune response. PTMs have been found to be present in different pathologic conditions such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), antiphospholipid syndrome, and primary biliary cirrhosis. The aim of the present review is to expose protein posttranslational modifications and the evidence suggesting their role in the generation of autoimmunity.

Objective. There is a lack of information about the genotype frequencies of IL-6 −174G/C and −572G/C polymorphisms in Mexicans with rheumatoid arthritis (RA). Therefore, the aim of this study was to evaluate the association of the IL-6 −174G/C and −572G/C polymorphisms in Mexican mestizo with RA.Methods. We included 137 patients with RA and 102 healthy controls. Patients were assessed for clinical characteristics. IL-6 −174G/C and −572G/C polymorphisms were genotyped using PCR-RFLP analysis. Allele and genotype frequencies and the Hardy-Weinberg equilibrium were computed. Odds ratios (ORs) were computed to identify the risk for RA associated with the presence of GG genotype in comparison with the GC or CC genotypes.Results. The genotype −174GG occurred at a higher frequency in cases and controls (77.4% versus 78.4%,P=0.845). We found similar results for the genotype −572GG (54% in patients versus 60.8% in controls,P=0.295).Conclusions. This is the first study to evaluate the association of −174G/C and −572G/C polymorphisms of the IL-6 gene with RA in Mexican mestizo patients. These two polymorphisms were not associated with RA in the studied sample. Additional studies are required to evaluate if these IL-6 polymorphisms have relevance to the development of more severe disease.

Citation Martinez-Garcia EA, Chavez-Robles B, Sanchez-Hernandez PE, Nunez-Atahualpa L, Martin-Maquez BT, Munoz-Gomez A, Gonzalez-Lopez L, Gamez-Nava JI, Salazar-Paramo M, Davalos-Rodriguez I, Petri MH, Zuniga-Tamayo D, Vargas-Ramirez R, Vazquez-Del Mercado M. IL-17 Increased in the third trimester in healthy women with term labor. Am J Reprod Immunol 2011; 65: 99–103 Introduction The function, peripheral blood expression, and physiologic importance of IL-17 is not well established. Detection of IL-17 in sera and plasma samples from patients with pre-eclampsia has been reported with inconsistent results. To establish the l levels of the IL-17 at peripheral level, we studied prospectively a cohort of 13 healthy pregnant women. Objective To evaluate the changes in serum levels of IL-17 in healthy pregnant women in a prospective cohort. Material and Methods Thirteen healthy pregnant women were prospectively followed to evaluate serum levels of IL-17. Each patient was evaluated at each trimester. IL-17 levels were measured by ELISA. The statistical analysis was done using repeated measures anova and Bonferroni′s multiple comparison test. Results IL-17 levels were significantly increased from first trimester with a mean of 14.61 up to 31.78 pg/mL at third trimester (P

Phosphorylation is the most important post-translational event at a cellular level that is regulated by protein kinases. MAPK is a key player in the important cellular signaling pathway. It has been hypothesized that phosphorylation might have a role in the induction of break tolerance against some autoantigens such as SRP72. The aim of this study was to explore the pathways of phosphorylation and overexpression of the SRP72 polypeptide, using an in vitro model of Jurkat cells stimulated by recombinant human (rh)IL-1β in the presence of MAPK inhibitors. We used Jurkat cells as a substrate stimulated with rhIL-1β in the presence of MAPK inhibitors at different concentrations in a time course in vitro experiment by immunoprecipitation, immunoprecipitation-Western blotting, and real time PCR. Our results showed that rhIL-1β causes up-regulation of protein expression and phosphorylation of SRP72 in Jurkat cells. Inhibitors of the MAPK pathway ERK1/2 or p38α/β down-regulate the expression of SRP72 autoantigen in Jurkat cells stimulated by rhIL-1β. Our results highlight the importance of studying the pathways of activation and overexpression of autoantigens. It will be necessary to perform careful research on various kinases pathways, including MAPK in dermatomyositis and other rheumatic diseases, to help to explain the routes of activation and inhibition of autoantigens. The understanding of this process may help to develop new therapies to prevent and control the loss of tolerance toward own normal proteins.

Citation Martinez-Garcia EA, Sanchez-Hernandez PE, Chavez-Robles B, Nunez-Atahualpa L, Martin-Marquez BT, Arana-Argaez VE, Garcia-Iglesias T, Gonzalez-Lopez L, Gamez-Nava JI, Petri MH, Velazquez-Rodriguez J, Salazar-Paramo M, Davalos-Rodriguez IP, Daneri-Navarro A, Vazquez-Del Mercado M. The distribution of CD56dimCD16+ and CD56brightCD16− Cells are associated with prolactin levels during pregnancy and menstrual cycle in healthy women. Am J Reprod Immunol 2011; 65: 433–437 Problem The pregnancy and menstrual cycle (MC) are the main physiologic events linked to the human reproduction. An adequate neuroendocrine axis is mandatory for the homeostasis in both events. To analyze the distribution of NK, T, Treg cells, expression of their receptors and to associate with hormone levels in pregnant and MC in healthy women. Method of Study We studied two groups of healthy women: 13 pregnant women followed up at 1st, 2nd and 3rd trimesters and 11 women in the 5th and 21st day of the MC. The distribution of NK, T, Treg cells population, expression of their receptors and hormone levels were quantified. Results In pregnant women, we found an association of NK cells CD56dimCD16+ with prolactin levels. This finding was also was observed for CD56brigthCD16− being statistical significant during 1st trimester for both subpopulations. During MC, correlation of CD56dimCD16+, CD56brightCD16− cells with prolactin in follicular and luteal phase was found. Conclusion This is the first report where these cell subpopulations have been analyzed prospectively. Even we can argue the random effect for the small number of women is interesting that prolactin showed the more consistent correlation with CD56dimCD16+, CD56brigthCD16− cells during both events studied.

Objective. To evaluate whether serum titers of second-generation anticyclic citrullinated peptide antibodies (anti-CCP2) are associated with the severity and extent of interstitial lung disease in rheumatoid arthritis (RA-ILD).Methods. In across-sectional study, 39 RA-ILD patients confirmed by high-resolution computed tomography (HRCT) were compared with 42 RA without lung involvement (RA only). Characteristics related to RA-ILD were assessed in all of the patients and serum anti-CCP2 titers quantified.Results. Higher anti-CCP2 titers were found in RA-ILD compared with RA only (medians 77.9 versus 30.2 U/mL,P<0.001). In the logistic regression analysis after adjustment for age, disease duration (DD), smoke exposure, disease activity, functioning, erythrocyte sedimentation rate, and methotrexate (MTX) treatment duration, the characteristics associated with RA-ILD were higher anti-CCP2 titers (P=0.003) and + RF (P=0.002). In multivariate linear regression, the variables associated with severity of ground-glass score were anti-CCP2 titers (P=0.02) and with fibrosis score DD (P=0.01), anti-CCP2 titers (P<0.001), and MTX treatment duration (P<0.001).Conclusions. Anti-CCP2 antibodies are markers of severity and extent of RA-ILD in HRCT. Further longitudinal studies are required to identify if higher anti-CCP2 titers are associated with worst prognosis in RA-ILD.

Patients with rheumatoid arthritis (RA) have a higher risk for atherosclerosis. There is no clinical information about scavenger receptor CD36 and the development of subclinical atherosclerosis in patients with RA. The aim of this study was to evaluate the association between membrane expression of CD36 in peripheral blood mononuclear cells (PBMC) and carotid intima-media thickness (cIMT) in patients with RA.Methods. We included 67 patients with RA from the Rheumatology Department of Hospital Civil “Dr. Juan I. Menchaca,” Guadalajara, Jalisco, Mexico. We evaluated the cIMT, considering subclinical atherosclerosis when >0.6 mm. Since our main objective was to associate the membrane expression of CD36 with subclinical atherosclerosis, other molecules related with cardiovascular risk such as ox-LDL, IL-6, and TNFαwere tested.Results. We found low CD36 membrane expression in PBMC from RA patients with subclinical atherosclerosis (P<0.001). CD36 mean fluorescence intensity had negative correlations with cIMT (r= −0.578,P<0.001), ox-LDL (r= −0.427,P= 0.05), TNFα(r= −0.729,P<0.001), and IL-6 (r= −0.822,P<0.001).Conclusion. RA patients with subclinical atherosclerosis showed low membrane expression of CD36 in PBMC and increased serum proinflammatory cytokines. Further studies are needed to clarify the regulation of CD36 in RA.