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One of the consequences of pandemic is the increase in the prevalence of mental alterations such as anxiety, depression and stress. Since here, we aimed to determinate through a transversal and observational study prevalence of stress, anxiety and depression within hospitalized patients by COVID-19 as well as their likely association with the emotional impact received by relatives with hospitalized patients by COVID-19. Forty-five COVID-19 hospitalized patients with mean age of 54.4 ± 9.6 years and fifty-five relatives with mean age of 43.2 ± 11.8 years answered a questions battery and DASS-21 survey. Our results revealed high prevalence of depression, anxiety and stress assessed by DASS-21 subscales. We also identified risk factors associated with the emotional health such as age (< 50 years: depression OR = 2.99 [1.31, 6.80], p < .05 and anxiety OR = 2.83 [1.15, 6.93], p < .05), by gender (female: anxiety OR = 4.13 [1.57, 10.89], p < .05 and stress OR = 5.38 [2.27, 12.8], p < .05), by group of study (relatives: depression OR = 3.83 [1.63, 8.96]; p < .05, anxiety OR = 3.60 [1.46, 8.88]; p < .05 and stress OR = 3.30 [1.41, 7.70]; p < .05). Additionally, female gender and low socioeconomic status in patients (β = 3.23; 1.96) and relatives (β = 1.86; 2.31) were associated with higher scores in anxiety (p < .05) and stress (p < .05). We concluded that our sample of COVID-19 patients maintain a high prevalence of mental alterations and age, gender and socioeconomic status modify the magnitude of these disorders. Una de las consecuencias de la pandemia es el aumento de la prevalencia de alteraciones mentales como la ansiedad, la depresión y el estrés. En este estudio transversal y observacional se evaluó la prevalencia de estrés, ansiedad y depresión en pacientes hospitalizados por COVID-19 así como la probable asociación con el impacto emocional recibido por familiares de pacientes hospitalizados por COVID-19. Cuarenta y cinco pacientes hospitalizados por COVID-19 con una edad promedio de 54.4 ± 9.6 años y cincuenta y cinco familiares de pacientes hospitalizados con una edad promedio de 43.2 ± 11.8 años respondieron una batería de preguntas y la encuesta DASS-21. Nuestros resultados revelaron una alta prevalencia de depresión, ansiedad y estrés identificados por DASS-21. En este estudio identificamos factores de riesgo asociados a la salud emocional como la edad (< 50 años: depresión RM = 2.99 [1.31, 6.80] p < .05 y ansiedad RM = 2.83 [1.15, 6.93], p < .05), el género (mujeres: ansiedad RM = 4.13 [1.57, 10.89], p < .05 y estrés RM = 5.38 [2.27, 12.8], p < .05) y el grupo de estudio (familiares: depresión RM = 3.83 [1.63, 8.96]; p < .05 , ansiedad RM = 3.60 [1.46, 8.88]; p < .05 y estrés RM = 3.30 [1.41, 7.70]; p < .05). Además, el género femenino y el nivel socioeconómico bajo de los pacientes (β = 3.23; 1.96) y familiares (β = 1.86; 2.31) se asociaron con puntuaciones más altas en ansiedad (p < .05) y estrés (p < .05). Concluimos que la muestra de pacientes con COVID-19 mantiene una alta prevalencia de alteraciones mentales y que algunos factores sociodemográficos se asocian con la magnitud de estos trastornos.

Introduction: Idiopathic inflammatory myopathies (IIM) are a group of heterogeneous systemic autoimmune diseases characterized by muscle inflammation from unknown causes resulting in chronic weakness. Recent studies have shown the role of the cellular immune response affecting muscle fibers in polymyositis (PM), inclusion body myositis, and to a lesser extent, dermatomyositis (DM), wherein humoral immunity is more involved. The value of genetic factors of the class II major histocompatibility complex (MHC II) has also been highlighted. In studies of murine models, the presence of HLA-DR3 favors a higher risk of developing inflammatory muscle disease, including PM and juvenile DM. In recent years, few studies have provided timely information regarding this, thus the researchers initially proposed a review of existing literature to broaden the context regarding what was described and to visualize proposals that may enhance the understanding of this group of inflammatory pathologies. Methods: The design, implementation, analysis, and reporting of this study were followed according to the search with MeSH terms (Autoimmune myopathy, Inflammatory myopathies, Idiopathic inflammatory myopathies AND Major histocompatibility complex and genetics). We analyzed 12 articles for this review article. Conclusion: In the etiopathogenesis of IIM, both humoral and cellular immunity are observed, considering the presence of a trigger that causes the immune response. As for the immunogenetics, this review highlights what has been reported in Chinese and Mexican populations, where HLADRB1*09:01 is related to the presence of DM, and is observed as the first variant identified in various populations. This increases interest in this allele in the particular case to study DM and strengthens research that proposes the study of IIM independently for each nosological entity.

Toll-like receptor (TLR)-mediated signaling pathways induce a proinflammatory microenvironment to eradicate pathogens. However, in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), TLRs can promote chronic inflammation. It has been shown that some TLR4 and TLR9 single nucleotide polymorphisms (SNPs) are risk factors for RA and SLE, but these findings have not been replicated in all populations; thus, results are inconclusive. We evaluated the TLR4 Asp299Gly, Thr399Ile, - 1892G/A SNPs, and the TLR9 Pro545Pro SNP to assess potential associations with RA and SLE in Mexican patients. This study included 474 patients with RA, 283 patients with SLE, and 424 healthy controls. We used a 5' nuclease allelic discrimination assay to genotype individuals for the four TLR4 and TLR9 polymorphisms. We found that the genotype or allelic frequencies of the TLR4 Asp299Gly, Thr399Ile, - 1892G/A, and TLR9 Pro545Pro polymorphisms were similar between patients and controls. We found no association under different genetic models. A haplotype analysis of TLR4 showed no association with either RA or SLE. We found no significant differences in the allelic or genotypic frequencies of TLR4 Asp299Gly, Thr399IIe, - 1892G/A, or TLR9 Pro545Pro between patients and controls. These findings suggested that these variants are not risk factors for RA or SLE in Mexican patients.

Rheumatoid arthritis (RA) and primary Sjögren's syndrome (pSS) are autoimmune diseases (ADs) characterized by joint damage and involvement of the salivary glands, respectively. ADs share some susceptibility loci, such as TNFSF4, which is a classical susceptibility gene associated with systemic lupus erythematosus, but its role in RA and pSS is not yet clear. Thus, the aim of this study was to determine whether three TNFSFS4 polymorphisms are associated with RA and pSS.Our case-control study included 500 controls, 459 patients with RA, and 210 patients with pSS from Mexico. TNFSF4 single nucleotide polymorphisms (SNPs) rs1234315C/T, rs2205960G/T, and rs704840T/G were genotyped using TaqMan probes and discrimination allelic assay.The three TNFSF4 SNPs were associated with susceptibility to RA (rs1234315C/T: odds ratio [OR] 1.4, p = 0.01; rs2205960G/T: OR 1.23, p = 0.03; rs704840T/G: OR 1.24, p = 0.02). An association between TNFSF4 rs1234315C/T and pSS was also observed (OR 1.28, p = 0.04), however, after Bonferroni correction, this association was lost.Our data suggest that TNFSF4 could be a risk factor in RA but not pSS in a Mexican population.

We conducted a case-control study in order to evaluate whether

Rheumatoid arthritis (RA) is a chronic inflammatory disease of autoimmune origin associated with many genetic traits, including genes related to the control of inflammation. The A20 protein, encoded by the TNFAIP3 gene, is a negative regulator of NF-kB-mediated inflammation. Several single nucleotide variants (SNVs) of TNFAIP3 are associated with susceptibility to RA in different ethnic groups, but not in Chileans, the only Latin Americans studied thus far. Objective. To examine the association of eight TNFAIP3 SNVs, four of them not previously studied, with RA in Mexican patients. Materials . We studied 471 RA patients (ACR-EULAR 2010) and eight TNFAIP3 SNVs: including, rs10499194C/T, rs6920220G/A and rs2230926T/G, which are associated with RA in European and Asian patients, in addition to rs373421182G/C, rs139054966T/G, rs5029924C/T, rs59693083A/G and rs61593413T/A, not previously examined in RA. All SNVs were evaluated by means of an allelic discrimination assay and TaqMan probes. Results. The allelic and genotypic frequencies of all SNVs examined were similar between cases and controls, and none of them was associated with RA under the allelic, codominant, dominant, and recessive models was observed. Conclusion. Our data indicate that the TNFAIP3 SNVs evaluated herein are not risk factors for RA in Mexican subjects.

Rheumatoid arthritis (RA) is a chronic inflammatory disease of autoimmune origin with many associated genetic traits, including genes related to the control of inflammation. The A20 protein, encoded by the TNFAIP3 gene, is a negative regulator of NF-kB mediated inflammation. Several single nucleotide variants (SNVs) of TNFAIP3 are associated with susceptibility to RA in different ethnic groups, none of which has been evaluated in Mexican patients.To examine the possible association of eight TNFAIP3 SNVs in Mexican patients with RA.We studied 471 patients with RA and 500 controls, as well as eight TNFAIP3 SNVs: including, rs10499194C/T, rs6920220G/A, and rs2230926T/G, which have been associated with RA in European or Asian patients, in addition to rs373421182G/C, rs139054966T/G, rs5029924C/T, rs59693083A/G and rs61593413T/A, not previously examined in RA. All SNVs were evaluated by means of an allelic discrimination assay using TaqMan probes.The allelic and genotypic frequencies of all SNVs examined were similar between cases and controls, and none of them was associated with RA under the allelic, codominant, dominant, and recessive models, as well as in haplotype combinations.Our data indicate that TNFAIP3 SNVs evaluated herein are not risk factors for RA in Mexican subjects.

Type I interferon (IFN-I) pathway plays a central role in the systemic lupus erythematosus (SLE) pathogenesis. Recent data suggest that SLE is associated with variants in IFN-I genes, such as tyrosine kinase 2 (TYK2), which is crucial in anti-viral immunity. Here, five TYK2 single nucleotide polymorphisms (SNPs) were genotyped in 368 childhood-onset SLE Mexican patients and 516 sex-matched healthy controls. Allele frequencies were also estimated in four indigenous groups. SLE protection was associated with TYK2 risk infection variants affecting residually its catalytic domain, rs12720356 (OR = 0.308; p = 0.041) and rs34536443 (OR = 0.370; p = 0.034), but not with rs2304256, rs12720270, and rs280500. This association was replicated in a 506 adult-onset SLE patients sample (OR = 0.250; p = 0.005, and OR = 0.277; p = 0.008, respectively). The minor alleles of both associated SNPs had a lower frequency in Mestizos than in Spaniards and were absent or rare in indigenous, suggesting that the presence of these alleles in the Mexican Mestizo population was derived from the Spaniards. For the first time, we report genetic variants with a protective effect in childhood- and adult-onset SLE Mexican population. Our results suggest that the frequency of IFN-I alleles associated with SLE, may have been shaped in populations exposed to infectious diseases for long periods, and this could be an explanation why Native American ancestry is associated with a higher SLE prevalence and an earlier onset.

Background Neutrophils play an important role in the pathogenesis of rheumatoid arthritis (RA). It has recently been reported that in addition to T helper (Th) 17 cells, other cells, including neutrophils, produce IL-17A, an important inflammatory cytokine involved in the pathogenesis of RA. The purpose of this study was to examine the presence of interleukin 17A-producing neutrophils in patients with RA. Methods We performed a cross-sectional study including 106 patients with RA and 56 healthy individuals. Whole peripheral blood cells were analyzed by flow cytometry to identify CD66b+ CD177+ IL-17A+ neutrophils and CD3+ CD4+ IL-17A+ T cells. Serum levels of IL-17A and IL-6 were measured by means of cytometry bead array (CBA). In purified neutrophils, mRNA levels of IL-17 and RORγ were measured by RT-PCR. In addition, purified neutrophils from patients and healthy controls were stimulated with the cytokines IL-6 and IL-23 to evaluate differences in their capacity to produce IL-17A. Results Neutrophils from RA patients expressed IL-17 and RORγ mRNA. Consequently, these cells also expressed IL-17A. Serum IL-17A levels but not Th17 cell numbers were increased in RA patients. Neutrophils positive for cytoplasmic IL-17A were more abundant in patients with RA (mean 1.2 ± 3.18%) than in healthy individuals (mean 0.07 ± 0.1%) (p

The BLK and BANK1 genes have been consistently associated with systemic lupus erythematosus (SLE), primarily in European or Asian-derived populations. However, this finding has not been replicated in Latin-American patients. Our study included 881 women from Mexico: 487 healthy controls and 394 SLE patients. The BLK rs13277113A/G-rs2736340T/C as well as BANK1 rs10516487G/A (R61H)-rs3733197G/A (A383T) single nucleotide polymorphisms (SNPs) were evaluated using a TaqMan® SNP genotyping assay. Our data showed that the BLK rs2736340T/C and rs13277113A/G polymorphisms are associated with susceptibility to SLE (C vs T, OR 1.60, p = 2×10−5; G vs A, OR 1.53, p = 9 × 10−5, respectively). We also identified an association between the functional BANK1 R61H polymorphism and SLE (A vs G, OR 1.56, p = 0.002). In addition, we observed a genetic interaction between BLK (rs2736340T/C, rs13277113A/G) and BANK1 (R61H and A383T) associated with susceptibility to SLE. This is the first study documenting an association between BLK and BANK1 and SLE in a Latin-American population. Our data confirm previous reports: BLK and BANK1 are factors associated with SLE. Thus, both genes are universal loci for this autoimmune disease.

La granulomatosis con poliangeitis es una vasculitis de pequenos vasos asociada a la presencia de anticuerpos anticitoplasma de neutrofilos, con manifestaciones cardiacas que son poco frecuentes, como pericarditis, miocarditis, arteritis coronaria y enfermedad valvular. Reportamos el caso de un paciente de 49 anos con reciente diagnostico de granulomatosis con poliangeitis, quien presento infarto agudo del miocardio. Se considero la actividad de la enfermedad como causa del infarto. Las manifestaciones clinicas cardiovasculares en la granulomatosis con poliangeitis son relevantes por ser marcadores de mal pronostico. Granulomatosis with polyangiitis is a small vessel vasculitis associated to anti-neutrophil cytoplasmic antibodies, in which the cardiac manifestations are not common, as pericarditis, cardiomyopathy, coronary artery disease and vascular disease. We report a clinical case of a 49-year-old man with a recent diagnosis of granulomatosis with polyangiitis, he presented myocardial infarction. Disease activity was considered the cause of myocardial infarction. Cardiovascular clinical manifestations in granulomatosis with polyangiitis are relevant because are markers of poor prognosis.

BLK and BANK1 in primary Sjögren's syndrome (pSS) have scarcely been evaluated and the results are inconclusive. The aim of our study was to determine whether single nucleotide variants (SNVs) located within BLK or BANK1 are associated with susceptibility, clinical and serological features, and smoking in pSS. BLK rs13277113A/G, BANK1 rs10516487G/A and rs3733197G/A were genotyped in 203 cases and 424 controls using a TaqMan® SNP genotyping assay. The BLK rs13277113A allele showed association with pSS under the allelic (OR 1.35, p = 0.02), and recessive (OR 1.83, p = 0.003) model, while, BANK1 rs3733197G/A showed association under the dominant model (OR 2.90, p = 0.043). Interactions between BANK1 and BLK genotypes also showed association (OR 2.36, p 0.0001). In addition, BLK rs13277113A/G was associated with protection against arthritis and BANK1 rs10516487G/A with both arthritis and keratoconjunctivitis sicca, meanwhile, BANK1 rs3733197G/A was associated with smoking in patients with pSS. This is the first study to describe an association between BLK and susceptibility to pSS in a Latin-American population. Our data also shows a first evidence of association between interactions of BLK and BANK1 in pSS, and association of BLK and BANK1with arthritis, keratoconjunctivitis sicca and smoking in patients with pSS.

The aim of this study was to examine the association of three TNFSF4 single nucleotide variants (SNVs) with systemic lupus erythematosus (SLE) susceptibility in Mexican patients.Genotypes of the TNFSF4 rs1234315T/C, rs2205960G/T, and rs704840T/G SNVs were determined using a TaqMan assay. In our study, we included 395 patients with SLE and 500 controls.Our information shows a significant difference in the allelic and genotypic frequency of the three TNFSF4 SNVs between cases and controls. Thus, our data showed an association between TNFSF4 rs1234315T/C (T vs. C, OR 1.40, p = 0.00087), rs2205960G/T (G vs. T, OR 1.32, p = 0.0037), and rs704840T/G (T vs. G, OR 1.41, p = 0.0003) and SLE susceptibility in Mexican subjects. Besides, we conducted a meta-analysis to determine the role of TNFSF4 rs2205960G/T and SLE susceptibility; our results showed that this variant is a risk factor for SLE in Latin Americans and Asians.Our results show that TNFSF4 rs1234315T/C, rs2205960G/T, and rs704840T/G are risk factors to SLE in Mexicans. This is the first study to document an association between TNFSF4 rs704840T/G and SLE in a Latin American population. In addition, our meta-analysis showed that TNFSF4 rs2205960G/T is a risk factor for Asians and Latin Americans. Key Point • The TNFSF4 rs1234315T/C, rs2205960G/T, and rs704849T/G SNVs are risk factors to SLE in patients from Mexico.

Introducción: la esclerosis sistémica presenta complicaciones esofágicas hasta en el 96 % de los casos. El diagnóstico de los trastornos motores se basa en la manometría. Objetivo: describir los síntomas del tracto gastrointestinal superior y evaluar la motilidad esofágica en pacientes con esclerosis sistémica. Materiales y métodos: se realizó una serie de casos que incluyó a 24 pacientes con esclerosis sistémica. Las manifestaciones clínicas se obtuvieron de los expedientes clínicos y se realizó manometría esofágica. Resultados: los 24 pacientes fueron de sexo femenino (100 %), con edad promedio 53.5 años y evolución de la enfermedad de 5.8 años. También los 24 pacientes (100 %) presentaron síntomas gastrointestinales superiores. En la manometría el promedio de la presión basal del esfínter esofágico superior fue de 32.59 mmHg. (DS ±6.78) con presión residual de 0.95 mmHg. (DS ±16.29) y amplitud de ondas del cuerpo esofágico de 14.01 mmHg. (DS ±7.06). La presión basal del esfínter esofágico inferior fue de 8.85 mmHg. (DS ±10.71) con presión residual del de 1.28 mmHg. (DS ±16.06), con porcentaje del índice de relajación del 15.79% y con ondas no transmitidas del 91.2 %. Discusión: los síntomas descritos del tracto gastrointestinal superior y los trastornos motores esofágicos son similares a los reportados en la literatura; en el presente estudio fue común la hipotensión del esfínter esofágico inferior y la aperistalsis esofágica, favoreciendo el desarrollo de complicaciones. La manometría es esencial para el diagnóstico temprano de la dismotilidad esofágica en la esclerosis sistémica así como para la prevención de sus complicaciones. Actualmente no hay estándares de guías clínicas que recomienden la vigilancia especializada por manometría.

Tumor necrosis factor (TNF) plays an important role in the pathogenesis of rheumatoid arthritis (RA). Different genetic variants including the TNF -308G/A polymorphism are associated with RA susceptibility. However, these findings have not been replicated in all populations. The aim of this study was to determine whether the TNF -1031T/C (rs1799964), -376G/A (rs1800750), -308G/A (rs1800629) -238G/A (rs361525), and TNFR1 -609G/T polymorphisms are associated with RA susceptibility in a sample of Mexican patients. Our study included 499 patients with RA and 492 healthy controls. The genotypes of the TNF polymorphisms were obtained using TaqMan assay. The genotype and allele frequencies of the TNF -1031T/C, -376G/A, -308G/A, -238G/A, and TNFR1 -609G/T polymorphisms were similar among RA cases versus healthy controls, and no association with RA susceptibility was identified. Our results suggest that the TNF -1031T/C, -376G/A, -308G/A, -238G/A, and TNFR1 -609G/T polymorphisms are not associated with RA susceptibility in a sample of Mexican patients.

Systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) are treated with immunosuppressive purine analogs, 6-mercaptopurine/6-thioguanine/azathiopurine, which are inactivated by thiopurine S-methyltransferase (TPMT). Non-synonymous polymorphisms in TPMT are associated with increased risk of adverse effects in patients treated with thiopurines. This study aimed to determine the frequency of the most common mutant TPMT alleles in Mexican patients with SLE (a prototype autoimmune disease) and RA (one of the most common autoimmune diseases in Mexico). Five hundred fifty-three consecutive patients from Central Mexico with SLE (178) and RA (375) were included. Subjects were genotyped to identify TPMT*2 (rs1800462), TPMT*3A (rs1800460 and rs1142345), TPMT*3B (rs1800460), and TPMT*3C (rs1142345) mutant alleles. DNA samples were assayed with the 5' exonuclease technique and TaqMan probes. Mutant alleles were detected in 6.2 and 5.2% of SLE and RA cases, respectively. Of note, 12.4% of SLE cases and 10.1% of RA cases carried mutant genotypes. Among those, the null genotype (TPMT*2/*3A, 0.3%) and the TPMT*3B (0.5%) and TPMT*3C (1.0%) alleles were found in RA, but not SLE cases. Mexican SLE cases displayed the highest frequency of mutant TPMT genotypes worldwide. TPMT genotyping should be performed for Mexican patients with SLE and RA before prescribing purine analogs.

// Isidro Aleman-Avila 1, 2 , Mayra Jimenez-Morales 1 , Olga Beltran-Ramirez 1 , Rosa Elda Barbosa-Cobos 3 , Silvia Jimenez-Morales 4 , Fausto Sanchez-Munoz 5 , Guillermo Valencia-Pacheco 6 , Luis M. Amezcua-Guerra 5 , Yaneli Juarez-Vicuna 5 , Dulce Milagro Razo-Blanco Hernandez 7 , Maria Concepcion Aguilera-Cartas 8 , Ricardo F. Lopez-Villanueva 9 , Oscar Peralta-Zaragoza 10 , Carlos Tovilla-Zarate 11 and Julian Ramirez-Bello 1 1 Endocrine and Metabolic Disease Unit Research, Hospital Juarez of Mexico, Mexico City, Mexico 2 Superior School of Medicine Postgraduate Program, National Polytechnic Institute, Mexico City, Mexico 3 Rheumatology Department, Hospital Juarez of Mexico, Mexico City, Mexico 4 Laboratory of Cancer Genomics, National Institute of Genomic Medicine, Mexico City, Mexico 5 Immunology Department, National Institute of Cardiology, Mexico City, Mexico 6 Hematology Laboratory, Regional Research Center, Autonomous University of Yucatan, Yucatan, Mexico 7 Research Direction, Hospital Juarez of Mexico, Mexico City, Mexico 8 Endocrinology Department, Hospital Juarez of Mexico, Mexico City, Mexico 9 Rheumatology Department, Regional Hospital General (ISSSTE), Health Service Yucatan, Yucatan, Mexico 10 Direction of Chronic Infections and Cancer, Research Center in Infection Diseases, National Institute of Public Health, Cuernavaca, Mexico 11 Multidisciplinary Academic Division of Comalcalco, Juarez Autonomous University of Tabasco, Comalcalco, Mexico Correspondence to: Julian Ramirez-Bello, email: dr.julian.ramirez.hjm@gmail.com Keywords: systemic lupus erythematosus, rheumatoid arthritis, Graves’ disease, microRNA gene, susceptibility Received: December 21, 2016 Accepted: June 30, 2017 Published: July 27, 2017 ABSTRACT Recently, different microRNA (miRNA) gene polymorphisms have been evaluated in patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and Graves’ disease (GD). In the present study, we examined three single-nucleotide polymorphisms (SNPs) located in the pre-miR-146a (rs2910164G/C), pre-miR-196a-2 (rs11614913C/T), and pre-miR-499 (rs3746444A/G) genes. Our study population included 900 Mexican patients with RA, SLE, or GD, as well as 486 healthy control individuals with no family history of inflammatory or autoimmune diseases. Genotyping was performed using TaqMan probes and a 5′ exonuclease assay. None of the investigated SNPs were associated with RA or GD susceptibility under any genetic model (co-dominant, recessive, or dominant). Genotype and allele frequencies of the miR-196a-2 rs11614913C/T polymorphism were similar between SLE cases and controls. In contrast, the miR-146a rs2910164G/C and miR-499 rs3746444A/G polymorphisms were associated with SLE susceptibility. These SNPs were not associated with lupus nephritis (LN). Our results suggest that polymorphisms in miR-146a, miR-196a-2 , and miR-499 are not associated with RA or GD susceptibility. This is the first report documenting that the miR-146a rs2910164G/C and miR-499 rs3746444 polymorphisms are associated with SLE susceptibility but not with LN.

Background Comorbidities are an important issue to consider in patients with rheumatic diseases (RD), as well as the clinical assessment of the autoimmune disease. Looking for concomitant diseases is a necessary step for a global approach of the rheumatic patient, knowingly that some diseases are more frequent in patients with RD than in the general population and could influence the course of RD and achievement of treatment goals1. Despite this, there is a need of new evidence about primary Sjogren’s Syndrome (pSS) comorbidities and their association with clinical outcomes. Objectives To determine the prevalence of comorbidities in patients with pSS in mexican population. Methods This was a national, multicenter, cross-sectional, and observational study. We included 393 patients with pSS, diagnosed according to the American-European Consensus Group (AECG) criteria 2002 or ACR/EULAR 2012 criteria. Comorbidities, serological profile of autoantibodies, Schirmer’s test, sialometry and histopathological assessment from minor salivary gland biopsies reported in the medical records were evaluated by a rheumatologist. The comparisons between the study groups were carried out using the two-tailed Student’s t test, χ2 test, and unidirectional. A value of p Results At least one comorbidity were reported in 310 (78.9%) patients, 2 to 4 comorbidities were reported in 183 (46.6%), and only 18 (4.6%) had a least 5 comorbidities. Thyroid disease was the most frequent comorbidity, observed in 91 (23.2%) subjects, being hypothyroidism the main cause. Smoking (21.9%) and hypertension (19.6%) were in second and third place. Psychiatric disease was present in 62 (15.8%) patients being depression and anxiety disorders the most frequent, appearing in 49 (79%) and 12 (19.35%) patients respectively. Regarding malignancy, we documented 10 (2.5%) patients with lymphoma, and 4 (1%) patients with breast cancer. The rest of comorbidities are shown at Figure 1 and Table 1. There was no significant difference for each variable measured between the groups except for the mean age (p= 0.001). Conclusion The systematic evaluation of comorbidities in patients with pSS is essential for an integral management. Physicians should be aware that these conditions might directly impact quality of life, prognosis, treatment response and healthcare costs. We encourage further research for the identification of new approaches in benefit of the patients. References [1] Yurkovich, et al. (2014). Overall and Cause-Specific Mortality in Patients With Systemic Lupus Erythematosus: A Meta-Analysis of Observational Studies. Arthritis Care & Research, 66(4), 608–616. https://doi.org/10.1002/acr.22173. Disclosure of Interests None declared

Background: Golimumab is a human anti-TNF monoclonal antibody that has shown efficacy in RA. In the RA pathophysiology, the elevation of TNF modulates the cellular immune response, which leads to a sustained activation of T-cell response; however, it is unknown whether anti-TNF interferes with the immunophenotype of T-cell. Objectives: To evaluate activation (CD25, CD69) and exhausted (PD-1, TIM-3, LAG-3, CTLA-4) markers of T-cells in RA patients treated with Golimumab. Methods: We included 14 patients with RA diagnosis (Criteria ACR/EULAR 2010), with moderate to severe activity; 11 non-responders to synthetic DMARDs (NR-DMARDs) and 3 responders to synthetic DMARDs with pharmacological toxicity (R-DMARDs). All patients were treated with Golimumab during 24 weeks. The questionnaire SF-36, DAS28-CRP, power Doppler signal and expression of CD25, CD69, PD-1, TIM-3, LAG-3 and CTLA-4, in T-cell were evaluated at 0 and 24 weeks. Results: Clinical variables evaluated in patients with Rheumatoid Arthritis are shown in tables 1 and 2. The frequency of LAG-3+ on CD4+ T-cells increased after 24 weeks of treatment with Golimumab (p = 0.013) (figure 1). The expression of LAG-3 in CD4+ T-cells (r = -0.586, p = 0.028) (Figure 2) and CD8+ T-cells (r = -0.617, p = 0.019) (Figure 3) inversely correlated with DAS28-CRP after treatment. At the beginning of treatment NR-DMARDs patients showed higher expression of CD25 in CD8+ T-cells and lower expression of TIM-3 in CD4+ and CD8+ T-cells with respect to R-DMARDs. After 24 weeks of treatment, a lower frequency of CD69+ and LAG-3+ T-cells was found and increased of CD25+ T-cells compared to R-DMARDs. Conclusion: Golimumab treatment increased the expression of LAG-3 in T-cells, suggesting a negative regulator of antigen presentation of T-cells. References [1] Tahir Z, Kavanaugh A. The role of golimumab in inflammatory arthritis. A review of the evidence. Ther Adv Musculoskel Dis2018;9:181–194. [2] Cuda C, Pope R, Perlman H. The inflammatory role of phagocyte apoptotic pathways in rheumatic diseases. Nat rev Rheumatol2016;12: 543-555. [3] Wherry E, Kurachi M. Molecular and celular insights into T cell exhaustion. Nat rev Inmunol 2015;15: 486-496. [4] Burmester G, Feist E, Dorner T. Emerging cell and cytokine targets in rheumatoid arthritis. Nat rev Inmunol2013;15:1-10. [5] McKinney E, Lee J, Jayne D, Lyons P. T-cell exhaustion, co-stimulation and clinical outcome in autoimmunity and infection. Nat rev Inmunol2015;523: 612-616. Disclosure of Interests: None declared

Introduction BLK has been identified as a risk factor to rheumatoid arthritis (RA) primarily in Asian or European-derived populations. However, this finding has not been evaluated in other populations such as Latin-Americans, except for Colombians. On the other hand, BANK1 single nucleotide variants (SNVs) have been scarcely studied in RA patients. Objective The aim of this study was to determine whether the BLK rs2736340T/C, rs13277113A/G, and BANK1 rs10516487G/A (R61H) and rs3733197G/A (A383T) polymorphisms are risk factors to RA in a sample of patients from Central Mexico. Materials and Methods We studied 957 women; 487 controls and 470 patients with RA by means of a TaqMan® SNP genotyping assay with fluorescent probes for the BLK rs13277113A/G, rs2736340T/C and BANK1 10516487G/A (R61H) and rs3733197G/A (A383T) variants. Result The BLK rs2736340T/C and rs13277113A/G variants were associated with risk for RA: C vs T; OR 1.39, p = 0.001, and G vs A; OR 1.37, p = 0.004, respectively. In addition, there was also an association between BANK1 R61H and RA: A vs G; OR 1.49, p = 0.003, but no with BANK1 A383T. We also identified an interaction significant between genotypes of BLK rs2736340T/C-BANK1 rs10516487G/A and RA: OR 1.65, p = 0.0001. Conclusions Our data suggest that both BLK and BANK1 confer susceptibility to RA in Mexican patients. The individual association of BANK1 rs1054857G/A with RA had not been previously reported in a particular population (except for pooled patients from several countries), therefore, our study presents the first evidence of association between this BANK1 variant and RA.

Objetive: To identify the patients with RA at highest risk of TB, prior to the use of biological therapy antiTNF. Method: We carried out a study of two phases considered three groups, in the first we performed a case and control study in the Hospital Juarez de Mexico, in the second phase, the results of phase one were analyzed with those obtained in the group of patients identified with Poncet´s disease. We compared the classes I and II of the HLA of patients naive to biologic treatment with healthy controls. Result: We have identified several candidate alleles that will help to advance the personalized treatment of RA that takes into account the genetic risk to develop TB, particularly the alleles B27 and DQB1*0301. Conclusion: Patients with RA have an increased risk to develop TB and severe complications derived from it. This infectious process is related to the use of biologic.

ResumenAntecedentesLas muertes por tuberculosis a nivel mundial han superado los 2,5 millones de casos por año. La enfermedad de Poncet es una forma poco frecuente de tuberculosis, caracterizada por un cuadro de poliartritis.Caso clínicoVarón de 24 años de edad, quien presentó rigidez matinal, artralgias, artritis bilateral simétrica de interfalángicas proximales, carpos, rodillas, tobillos, hombros y adenomegalias a nivel cervical, submandibular, supraclavicular izquierda, axilar e inguinal, sin fiebre. Resultados de laboratorio: velocidad de sedimentación globular 44mm/hora, proteína C reactiva 4.35, niveles de complemento C3 y C4 normales, factor reumatoide y anticuerpos anti-péptido C citrulinado negativos, anticuerpos antinucleares positivos con patrón moteado fino 1:320 y citoplásmico 1:160; anticuerpos anti-Smith, anti-ADN de doble cadena, antígeno A de síndrome de Sjogren's y antígeno B de síndrome de Sjogren's negativos. Reporte histológico del tejido ganglionar cervical con lesiones granulomatosas compatibles con tuberculosis. Se descartaron artritis reumatoide y lupus eritematoso sistémico. Se inició tratamiento antifímico remitiendo el cuadro clínico. Se concluyó el diagnóstico de enfermedad de Poncet.ConclusiónEl diagnóstico diferencial entre tuberculosis y enfermedades articulares inflamatorias de etiología autoimune es un reto clínico.AbstractBackgroundDeaths due to tuberculosis have reached 2.5 million cases per year worldwide. Poncet's disease is an infrequent form of tuberculosis characterised by a clinical picture of polyarthritis.Clinical caseA 24-year-old male presented with morning stiffness, arthralgias, bilateral symmetric arthritis of the proximal interphalangeal joints, wrists, knees, ankles, and shoulders, and adenomegalies at the cervical, submandibular, left supraclavicular, axillary and inguinal levels, without fever. Laboratory results were as follows: ESR 44mm/h, C-reactive protein 4.35, normal levels of complement C3 and C4, negative rheumatoid factor and anticyclic citrullinated peptide antibodies, positive antinuclear antibodies with fine speckled pattern (1:320) and cytoplasm (1:160) pattern and negative anti-Smith, -double-stranded DNA, Sjogren's syndrome-antigen A and Sjogren's syndrome-antigen B. Histological report of cervical node tissue revealed granulomatous lesions compatible with tuberculosis. Rheumatoid arthritis and systemic lupus erythematosus were ruled out. Anti-tuberculosis agents were initiated that resolved the clinical picture. Diagnosis of Poncet's disease was confirmed.ConclusionThe differential diagnosis between tuberculosis and autoimmune inflammatory joint diseases is a clinical challenge.

Following publication, it was brought to the authors' attention by Dr. Julia Toscano-Garibay that she did not participate as a reviewer of the final version of this manuscript prior to its submission and publication in Clinical Rheumatology.

The AIRE gene influences the expression of a wide array of self-antigens in the thymus, and is essential to the negative selection of self-reactive T cells and establishment of central tolerance. Single nucleotide variants (SNVs) such as rs878081C/T (Ser196Ser) and rs2075876G/T at this locus have been associated with susceptibility to rheumatoid arthritis, mainly in Asian populations, but its role in systemic lupus erythematosus (SLE) has not been documented. We performed a case-control association study with 379 SLE patients and 460 controls from central Mexico. In addition, we replicated our finding in another group of 179 SLE patients and 97 controls from the same region of Mexico. In the first group, we identified that the AIRE Ser196Ser synonymous variant was associated with SLE (OR 1.4, p = 0.009), meanwhile, in the second group we observed the following: OR 1.7, p = 0.024. No association was found between these AIRE SNVs and lupus nephritis. Our results suggest that AIRE is a risk factor for SLE in our population. This study is the first to document an association between AIRE and SLE susceptibility.

Background A rheumatic disease may be a casual factor in the pathogenesis of a neoplastic disease, as in other cases, cancer may lead to the development of paraneoplastic rheumatic manifestations that may be the only initial symptoms1. Lazarus et al. demonstrated in its cohort study with 112 patients that of the 22% of patients who developed some neoplasm during the study, the most prevalent was lymphoma with 44%. according to the same study, patients with pss present a risk 37.5 times more than that of the general population. of generating lymphoma, with another risk 2.6 times of developing another type of cancer2.it was also shown that in patients with pss there is an incidence of 320 cases per 100 000 a year of presenting non-hodgkin’s lymphoma3. In our country there are no epidemiological studies to know the prevalence of cancer in patients with pss, so these numbers are difficult to estimate Objectives Determine the prevalence of cancer in patients with ss in the mexican population. Methods Cross-sectional, observational study was conducted in which 393 patients were included, of which 221 (52%) came from the national institute of medical sciences and nutrition ”salvador zubiran”, 92 (23.4%) from the university hospital ”Jose E Gonzalez” and 80 (20.6%) of the juarez mexico hospital/ABC medical centre whom fulfilled the diagnosis of ssp according to the 2002/2012 criteria of the american college of rheumatology/european league against rheumatism. Bivariate anailsis was performed, normality was demonstrated using the K.S test, the student’s T test was used for the numerical variables and the chi2 test for the categorical ones, and no difference was found between the characteristics of patients with or without cancer. Results We include 393 patients, the majority were women (n=377, 95.9%) with an average age of 56.4 (±13.60), of these 23 (5.85%) had some type of neoplasm regardless of their malignancy. the most prevalent was lymphoma with 9 cases (34.6%), followed by breast cancer with 5 (19.2%), 3 (11.5%) of basal cell cancer and 2 (7.7%) cases of cervical uterine cancer Conclusions We confirmed lymphoma as the most prevalent neoplasia in a cohort of non-Caucasian pSS patients. We observed the presence of non-hematologicalmalignancy 60.86% of our patients, whether it risk is increased in pSS population still needs to be addressed. References [1] Bellan M, Boggio E, Sola D, Gibbin A, Gualerzi A, Favretto S, … Sainaghi PP. Association between rheumatic diseases and cancer: results from a clinical practice cohort study. Internal and Emergency Medicine2017;12(5):621–627. [2] Lazarus MN. Incidence of cancer in a cohort of patients with primary Sjogren’s syndrome. Rheumatology2006;45(8):1012–1015. [3] Nishishinya MB, Pereda CA, Munoz-Fernandez S, Pego-Reigosa JM, Rua-Figueroa I, Andreu JL, … Santamaria EL. Identification of lymphoma predictors in patients with primary Sjogren’s syndrome: A systematic literature review and meta-analysis. Rheumatology International2015;35(1):17–26. Disclosure of Interest None declared

AIM Recent studies highlight the importance of the interleukin (IL)-17A cytokine in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). There are also reports of associations between some single nucleotide polymorphisms (SNPs) in IL-17A and RA but not SLE. Notably, these findings have not been replicated in all studied populations. The aim of this study was to investigate whether the IL-17A -737 T/C (rs8193036), -444A/G (rs3819024), -197G/A (rs2275913), and -121G/A (rs8193037) SNPs conferred susceptibility to SLE (or lupus nephritis) or to RA in a Mexican population. METHODS The study included 1367 Mexican subjects, 501 with RA, 367 with SLE, and 499 healthy controls. IL-17A was genotyped using a TaqMan 5' allelic discrimination assay. RESULTS Our results showed that the IL-17A -737 T/C, -444A/G, -197G/A, and -121G/A SNPs had similar genotype and allele frequencies in patients with SLE (or lupus nephritis) or RA and in controls. However, an IL-17A haplotype (TAGA) showed an association with SLE susceptibility (odds ratio 2.43, P = 0.004) but not with RA susceptibility. CONCLUSIONS These results confirm that the IL-17A -737T/C, -444A/G, -197G/A, and -121G/A SNPs are not risk factors for RA, but the IL-17A TAGA haplotype is a risk factor for SLE. This is the first report to document an association between IL-17A and SLE susceptibility in adults.

The TNF -238G/A (rs361525) and -308G/A (rs1800629) polymorphisms have consistently been associated with systemic lupus erythematosus (SLE) in several populations; however, these findings have not been verified in all populations. Here, we aimed to examine whether the TNF -238G/A, -308G/A, -376G/A (rs1800750), and -1031T/C (rs1799964) polymorphisms confer SLE or lupus nephritis (LN) susceptibility in a Mexican population. Our study included 442 patients with SLE and 495 controls. For genotyping, we used the TaqMan 5′ allele discrimination assay. The TNF -238G/A and -1031T/C polymorphisms were associated with SLE susceptibility (odds ratio (OR) 2.1, p = 0.0005 and OR 1.4, p = 0.003, respectively). Gender stratification showed a strong association between TNF -238G/A and SLE in women (OR 2.2, p = 0.00006), while TNF -1031T/C had an OR of 1.5 (p = 0.007). With regard to the TNF -376G/A polymorphism, this also showed association with SLE susceptibility (OR 1.95, p = 0.036) and LN (OR 3.5, p = 0.01). In conclusion, our study provides the first demonstration of association between the TNF -376G/A polymorphism and SLE and LN susceptibility. In addition, our study is the second documenting an association of TNF -1031T/C with SLE susceptibility. We also observed a strong association between TNF -238G/A and SLE susceptibility. The TNF 308G/A polymorphism was not associated with SLE or LN.

Background Levels of circulating vascular endothelial growth factor (VEGF) (a potent endothelial-cell-specific angiogenic factor) have been correlated with disease activity in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). In addition, several single nucleotide polymorphisms (SNPs), including the VEGFA -2578C/A, have been associated with RA in some populations. By contrast, the role of different VEGFA SNPs in the susceptibility to SLE has received little attention. Thus, the present study aimed to determine whether the VEGFA -2578C/A, -1154G/A and -634G/C polymorphisms confer risk or were associated with reduced risk of RA or SLE in a Mexican population. Methods The present study included 903 women from Mexico: 405 were patients with RA, 282 had SLE and 216 were healthy individuals. The genotypes were obtained with TaqMan probes. Results The data obtained in the present study suggest that the VEGFA -2578C/A and -634G/C polymorphisms are not risk factors for RA or SLE; however, VEGFA -1154G/A was associated with reduced risk in women with RA (odds ratio = 0.6, pc = 0.0051) but not with SLE (odds ratio = 0.7, pc = 0.13). Conclusions The present study is the first to document an association between VEGFA -1154G/A and reduced risk in women with RA but not with SLE.

Objective: To investigate the possible association between HLA and Dermatomyositis (DM) in the Mexican mestizo population. Methods: HLA class I (A and B) and class II (DRB1* and DQB1*) were determined in 36 Mexican mestizo patients with DM and 72 healthy controls. Results: A positive association was identified among alleles HLA A*01:01 (OR 3.5 (1.30-9.54), p

The aim of the is study is to examine the role of serum substance P (SP) levels as a simple biomarker for rheumatoid arthritis (RA) disease activity, its correlation with other markers of disease activity, and with selected clinical parameters. The study comprised 90 RA patients and 24 healthy controls. RA activity was assessed by means of the disease activity 28-C-reactive protein (DAS28-CRP) index and ultrasound power Doppler (USPD) by the German ultrasound score based on seven joints. SP serum values were obtained by means of an ELISA commercial kit. Statistics were achieved by the Student's t test and Spearman correlation analysis with Bonferroni correction. As a group, RA patients had significantly increased levels of SP compared with healthy controls (p

The functional PTPN22 R620W polymorphism (rs2476601) is clearly associated with susceptibility to several autoimmune diseases (ADs). However, the PTPN22 R263Q polymorphism (rs33996649) has been scarcely explored in different ADs. Here we aimed to examine the associations of the PTPN22 R620W and R263Q polymorphisms with susceptibility to or protection against rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and Graves' disease (GD) among Mexican patients.We conducted a case-control study including 876 patients (405 with SLE, 388 with RA, and 83 with GD) and 336 healthy control individuals. PTPN22 genotypes were determined using the TaqMan 5' allele discrimination assay.PTPN22 R620W was associated with GD susceptibility (OR 4.3, p = 0.004), but was not associated with SLE (OR 1.8, p = 0.19). We previously demonstrated that this polymorphism is associated with RA susceptibility (OR 4.17, p = 0.00036). Moreover, PTPN22 R263Q was associated with protection against SLE (OR 0.09, p = 004) and RA (OR 0.28, p = 0.045), but was not associated with GD.Our data provide the first demonstration that PTPN22 R620W confers GD susceptibility among Latin-American patients. Moreover, this is the second report documenting the association of PTPN22 R263Q with protection against SLE and RA.

A variety of ophthalmic manifestations can occur in patients who have systemic vasculitides and may be the presenting feature. Ocular involvement is frequently found and can result in significant morbidity, even in blindness. Early diagnosis and treatment may improve visual outcome. The management is challenging and requires a multidisciplinary approach. Treatment of ocular manifestations and systemic disease usually follows the same path. The mainstay of treatment is the use of systemic corticosteroids, usually combined with steroid-sparing immunosuppressive drugs. New, promising, emerging therapies rely on the development of biologic agents, which seem useful in the ocular manifestations of systemic vasculitides.

Introduction Rheumatoid Arthritis (RA) is a systemic and chronic inflammatory disease, which affects 1–1.5% of population worldwide. Synovial membrane, cartilage and bone are the main sites affected by inflammation. The inflammatory process in RA leads to increased production of inflammatory cytokines IL-8, TNF-a, IL-6, IL-1b, IL-15, IL-18 e IL-17A in synovial fluid and serum. In addition to Th17, others cells such as gd T cells, iNKTs, mast cells and neutrophils also produce IL-17A. In mouse model of RA, IL-17A producing neutrophils seems to be important for the onset of the disease. Thus, we hypothesize that the population of IL-17A producing neutrophils is increased in patients with RA. Objective To analyze the frequency of IL-17A producing neutrophils in peripheral blood of patients with RA. Methods Peripheral blood from 68 patients with rheumatoid arthritis and 15 healthy donors has been collected, erythrocytes were lysed and peripheral blood leukocytes were stained for surface marker CD177 and for intracellular detection of IL-17A. Cells were analyzed by flow cytometry. It was also evaluated the frequency TH17 cells by flow cytometry using standard protocol. Results IL-17A producing neutrophils are increased in peripheral blood of patients with RA (0–19.5% Mean 1.66%) compared with healthy donors where no neutrophils IL-17A+ were observed (0–0.1% mean 0.05%). Surprisingly, Th17 cells were not detected in peripheral blood of patients with RA. Conclusion Neutrophils might be the most important source of IL-17A during the inflammatory response observed in patients with RA since we do not detect TH17 cells in these patients.

La coexistencia entre la enfermedad de Castleman y polimiopatia inflamatoria idiopática es poco conocida por cuanto existe pocos casos referentes a estas dos patologías juntas. Las características histopatológicas de los nódulos linfáticos asociados en estas dos entidades son similares, haciendo su diferenciación más difícil. La resolución quirúrgica del tumor conlleva, en la mayoría de casos a la mejoría de las manifestaciones autoinmunes, aunque en ciertos casos, el uso de glucocorticoides, radioterapia, quimioterapia y tratamiento biológicos pueden ser usados cuando la opción quirúrgica no es suficiente. Se propone como parte de la fisiopatología de la enfermedad de Castleman, compartida en ciertas enfermedades autoinmunes, la inmunoactivación celular asociada con niveles altos de interleukina 6 y otros reactantes de fase aguda, así como ciertos procesos infecciosos como el virus de inmunodeficiencia adquirida y el virus del Epstein-Barr. Se presenta el caso de una mujer de 17 años con diagnóstico de enfermedad de Castleman variante hialino vascular y polimiositis.

A variety of ophthalmic manifestations can occur in patients who have systemic vasculitides and may be the presenting feature. Ocular involvement is frequently found and can result in significant morbidity, even in blindness. Early diagnosis and treatment may improve visual outcome. The management is challenging and requires a multidisciplinary approach. Treatment of ocular manifestations and systemic disease usually follows the same path. The mainstay of treatment is the use of systemic corticosteroids, usually combined with steroid-sparing immunosuppressive drugs. New, promising, emerging therapies rely on the development of biologic agents, which seem useful in the ocular manifestations of systemic vasculitides.

Background Deaths due to tuberculosis have reached 2.5 million cases per year worldwide. Poncet's disease is an infrequent form of tuberculosis characterised by a clinical picture of polyarthritis. Clinical case A 24-year-old male presented with morning stiffness, arthralgias, bilateral symmetric arthritis of the proximal interphalangeal joints, wrists, knees, ankles, and shoulders, and adenomegalies at the cervical, submandibular, left supraclavicular, axillary and inguinal levels, without fever. Laboratory results were as follows: ESR 44 mm/h, C-reactive protein 4.35, normal levels of complement C3 and C4, negative rheumatoid factor and anticyclic citrullinated peptide antibodies, positive antinuclear antibodies with fine speckled pattern (1:320) and cytoplasm (1:160) pattern and negative anti-Smith, -double-stranded DNA, Sjogren's syndrome-antigen A and Sjogren's syndrome-antigen B. Histological report of cervical node tissue revealed granulomatous lesions compatible with tuberculosis. Rheumatoid arthritis and systemic lupus erythematosus were ruled out. Anti-tuberculosis agents were initiated that resolved the clinical picture. Diagnosis of Poncet's disease was confirmed. Conclusion The differential diagnosis between tuberculosis and autoimmune inflammatory joint diseases is a clinical challenge.