Bone impairment assessed by lumbar spine trabecular bone score (TBS) and HR-pQCT in male ankylosing spondylitis patients

Objectives. Low bone mineral density (BMD) and osteoporosis diagnosis in AS patients is based on data using dual-energy X-ray absorptiometry (DXA), which may be difficult to interpret due to the presence of syndesmophytes. The objective of this study is to evaluate bone mass and quality using areal (a) BMD, lumbar spine trabecular bone score (TBS) and HR-pQCT parameters in AS patients compared with healthy controls (HC). Methods. TBS and aBMD were evaluated using DXA. Volumetric bone mineral density (vBMD), bone microarchitecture and stiffness were analyzed at the distal tibia and radius using HR-pQCT. Seventy-three AS male patients and 52 agematched HC were evaluated. Results. Lower TBS values were observed in AS patients compared with HC (1.314 ± 0.121 vs. 1.396 ± 0.070, p<0.001); however, no difference was observed in lumbar spine aBMD between these two groups (1.080 ± 0.193 vs. 1.041 ± 0.118 g/cm2 , p=0.11). Lower trabecular vBMD (162.1 ± 39.6 vs. 186.8 ± 39.9 mg HA/cm3 , p<0.001), lower structural parameters Tb.Th (0.074 ± 0.012 vs. 0.080 ± 0.013 mm, p=0,044) and Tb.Sp (0.497 ± 0.110 vs. 0.448 ± 0.086 mm, p=0,039) and lower strength parameters stiffness (254250.8 ± 48477.7 vs. 291770.3 ± 52858.4 N/mm, p<0.001) and F.Load (12098.6 ± 2240. vs 13770.2 ± 2388.1 N, p=0,001) were observed in the trabecular compartment at the distal tibia in AS patients compared to HC. Conclusion. The lumbar spine TBS and HR-pQCT imaging measurements are superior technologies to detect impairment of bone mass and quality in AS patients compared to healthy subjects

Infliximab Induces Increase in Triglyceride Levels in Psoriatic Arthritis Patients

Objectives. To evaluate lipid profile changes after anti-TNF therapy in patients with psoriatic arthritis (PsA). Methods. Fifteen PsA patients (eight polyarticular, four oligoarticular, two axial, and one mutilating) under infliximab were included. None had dyslipoproteinemia or previous statin use. Total cholesterol (TC) and its fractions, inflammatory markers, and prednisone use were evaluated. Results. The comparisons of lipid levels between baseline and after three months (3M) of anti-TNF therapy showed that there was a significant increase in mean triglycerides (117.8 ± 49.7 versus 140.1 ± 64.1 mg/dL, P = 0.028) and VLDL-c (23.6 ± 10.5 versus 28.4 ± 13.7 mg/dL, P = 0.019) levels. In contrast, there were no differences in the mean TC (P = 0.28), LDL-c (P = 0.42), and HDL-c (P = 0.26) levels. Analysis of the frequencies of each lipid alteration at baseline and at 3M were alike (P > 0.05). Positive correlations were found between VLDL-c and CRP (r = 0.647, P = 0.009) and between triglycerides and CRP (r = 0.604, P = 0.017) levels at 3M. ESR reduction was observed after 3M (P = 0.04). Mean prednisone dose remained stable at beginning and at 3M (P = 0.37). Conclusion. This study demonstrated that anti-TNF may increase TG and VLDL-c levels in PsA patients after three months

PReS-FINAL-2177: Safety and lack of autoantibody production following influenza H1N1 vaccination in patients with juvenile idiopathic arthritis (JIA)

Introduction Vaccination is an effective tool against several infectious agents including influenza. In 2010, the Advisory Committee on Immunization Practices (ACIP) recommended influenza A H1N1/2009 immunization for high risk groups, including juvenile idiopathic arthritis (JIA) patients and more recently the EULAR task force reinforced the importance of vaccination in immunosuppressed pediatric rheumatologic patients. We have recently shown that Influenza A H1N1/2009 vaccination generated protective antibody production with short-term safety profile among 93 JIA patients, but the possible impact of the vaccine in autoimmune response in JIA have not been studied. Therefore, we aimed to assess the production of some autoantibodies generated following influenza H1N1 vaccination in JIA patients. Objectives To assess the autoimmune response and H1N1 serology following influenza H1N1 vaccination in patients with JIA. Methods Cepa A/California/7/2009 (NYMC X-179A) anti-H1N1 was used to vaccinate JIA patients: 1 dose of immunization was given to all participants and those <9yrs of age received a second booster 3 weeks apart. Sera were analyzed before and 3 weeks following complete vaccination. Serology against H1N1 virus was performed by hemagglutination inhibition antibody assay, rheumatoid factor (RF) by latex fixation test, antinuclear antibodies (ANA) by IIF, IgM and IgG anticardiolipin (aCL) by ELISA.Results Among 98 JIA patients that were vaccinated, 58 sera were available for this study. Mean age of 58 JIA patients was 23.9 ± 9.5 yrs, 38 were females and 20 males with mean disease duration of 14.7 ± 10.1 yrs. JIA subtypes were: 33 (57%) poliarticular, 10 (17%) oligoarticular, 6 (10%) systemic and 9 (16%) other. Sixteen patients were off drugs while 42 (72%) were under different pharmacotherapy: 32 (55%) were on 1 DMARD/IS, 10 (17%) on 2 DMARDs/IS, 19 (33%) antimalarials, 29 (50%) MTX, 8(14%) sulfasalazine, 6 (10%) anti-TNFs, 4 (7%) abatacept; no patient was using prednisone >0.5 mg/kg/d. Seroprotection rates against H1N1 influenza increased from 23 to 83% and seroconversion rates were achieved in 78% JIA. Prior to vaccination, 31(53.4%) JIA patients were ANA+, 6(10.3%) RF+, and 4 (7%) IgM + IgG aCL+. After complete H1N1 vaccination, positivity for ANA remained the same whereas 1 patient became negative for IgG aCL, and another for RF, IgM and IgG aCL. One (1.7%) patient turned low titer IgG aCL+. Conclusion Vaccination of JIA patients against pandemic influenza A (H1N1) generated successful protective antibody production without the induction of autoantibody production, except for 1 patient that became positive for low titer IgG aCL, supporting its safety

Low sclerostin levels: a predictive marker of persistent inflammation in ankylosing spondylitis during anti-tumor necrosis factor therapy?

Abstract\ud \ud \ud \ud Introduction\ud \ud Sclerostin levels have been reported to be low in ankylosing spondylitis (AS), but there is no data regarding the possible role of this Wnt inhibitor during anti-tumor necrosis factor (TNF) therapy. The present study longitudinally evaluated sclerostin levels, inflammatory markers and bone mineral density (BMD) in AS patients under anti-TNF therapy.\ud \ud \ud \ud Methods\ud \ud Thirty active AS patients were assessed at baseline, 6 and 12 months after anti-TNF therapy regarding clinical parameters, inflammatory markers, BMD and baseline radiographic damage (mSASSS). Thirty age- and sex-matched healthy individuals comprised the control group. Patients' sclerostin levels, sclerostin binding low-density lipoprotein receptor-related protein 6 (LRP6) and BMD were evaluated at the same time points and compared to controls.\ud \ud \ud \ud Results\ud \ud At baseline, AS patients had lower sclerostin levels (60.5 ± 32.7 vs. 96.7 ± 52.9 pmol/L, P = 0.002) and comparable sclerostin binding to LRP6 (P = 0.387) than controls. Improvement of Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Bath Ankylosing Spondylitis Functional Index (BASFI), Bath Ankylosing Spondylitis Metrology Index (BASMI), Ankylosing Spondylitis quality of life (ASQoL) was observed at baseline vs. 6 vs. 12 months (P < 0.01). Concomitantly, a gradual increase in spine BMD (P < 0.001) and a positive correlation between baseline mSASSS and spine BMD was found (r = 0.468, P < 0.01). Inflammatory parameters reduction was observed comparing baseline vs. 6 vs. 12 months (P <0.01). Sclerostin levels progressively increased [baseline (60.5 ± 32.7) vs. 6 months (67.1 ± 31.9) vs. 12 months (72.7 ± 32.3) pmol/L, P <0.001]. At 12 months, the sclerostin levels remained significantly lower in patients compared to controls (72.7 ± 32.3 vs. 96.70 ± 52.85 pmol/L, P = 0.038). Moreover, sclerostin serum levels at 12 months were lower in the 10 patients with high C reactive protein (CRP) (≥ 5 mg/l) compared to the other 20 patients with normal CRP (P = 0.004). Of note, these 10 patients with persistent inflammation also had lower sclerostin serum levels at baseline compared to the other patients (P = 0.023). Univariate logistic regression analysis demonstrated that AS patients with lower sclerostin serum levels had an increased risk to have high CRP at 12 months (odds ratio = 7.43, 95% CI 1.23 to 45.01, P = 0.020) than those with higher sclerostin values.\ud \ud \ud \ud Conclusions\ud \ud Persistent low sclerostin levels may underlie continuous inflammation in AS patients under anti-TNF therapy.This study was supported by grants from Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP #2009/51897-5 to EB), Conselho Nacional de Desenvolvimento Científico e Tecnológico (#300248/2008-3 to CAS, #301411/2009-3 to EB and #300559/2009-7 to RMRP) Federico Foundation (to CGSS, CAS, EB and RMRP)

Immunogenicity and Reactogenicity of 2009 Influenza A (H1N1) Inactivated Monovalent Non-Adjuvanted Vaccine in Elderly and Immunocompromised Patients

Background\ud \ud Immunosuppressed individuals present serious morbidity and mortality from influenza, therefore it is important to understand the safety and immunogenicity of influenza vaccination among them.\ud Methods\ud \ud This multicenter cohort study evaluated the immunogenicity and reactogenicity of an inactivated, monovalent, non-adjuvanted pandemic (H1N1) 2009 vaccine among the elderly, HIV-infected, rheumatoid arthritis (RA), cancer, kidney transplant, and juvenile idiopathic arthritis (JIA) patients. Participants were included during routine clinical visits, and vaccinated according to conventional influenza vaccination schedules. Antibody response was measured by the hemagglutination-inhibition assay, before and 21 days after vaccination.\ud Results\ud \ud 319 patients with cancer, 260 with RA, 256 HIV-infected, 149 elderly individuals, 85 kidney transplant recipients, and 83 with JIA were included.\ud \ud The proportions of seroprotection, seroconversion, and the geometric mean titer ratios postvaccination were, respectively: 37.6%, 31.8%, and 3.2 among kidney transplant recipients, 61.5%, 53.1%, and 7.5 among RA patients, 63.1%, 55.7%, and 5.7 among the elderly, 59.0%, 54.7%, and 5.9 among HIV-infected patients, 52.4%, 49.2%, and 5.3 among cancer patients, 85.5%, 78.3%, and 16.5 among JIA patients. The vaccine was well tolerated, with no reported severe adverse events.\ud Conclusions\ud \ud The vaccine was safe among all groups, with an acceptable immunogenicity among the elderly and JIA patients, however new vaccination strategies should be explored to improve the immune response of immunocompromised adult patients. (ClinicalTrials.gov, NCT01218685)Fundação Butantan funded the study, and employed several of the authors. The funder had a role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

Mortality from gastrointestinal congenital anomalies at 264 hospitals in 74 low-income, middle-income, and high-income countries: a multicentre, international, prospective cohort study

Summary Background Congenital anomalies are the fifth leading cause of mortality in children younger than 5 years globally. Many gastrointestinal congenital anomalies are fatal without timely access to neonatal surgical care, but few studies have been done on these conditions in low-income and middle-income countries (LMICs). We compared outcomes of the seven most common gastrointestinal congenital anomalies in low-income, middle-income, and high-income countries globally, and identified factors associated with mortality. Methods We did a multicentre, international prospective cohort study of patients younger than 16 years, presenting to hospital for the first time with oesophageal atresia, congenital diaphragmatic hernia, intestinal atresia, gastroschisis, exomphalos, anorectal malformation, and Hirschsprung’s disease. Recruitment was of consecutive patients for a minimum of 1 month between October, 2018, and April, 2019. We collected data on patient demographics, clinical status, interventions, and outcomes using the REDCap platform. Patients were followed up for 30 days after primary intervention, or 30 days after admission if they did not receive an intervention. The primary outcome was all-cause, in-hospital mortality for all conditions combined and each condition individually, stratified by country income status. We did a complete case analysis. Findings We included 3849 patients with 3975 study conditions (560 with oesophageal atresia, 448 with congenital diaphragmatic hernia, 681 with intestinal atresia, 453 with gastroschisis, 325 with exomphalos, 991 with anorectal malformation, and 517 with Hirschsprung’s disease) from 264 hospitals (89 in high-income countries, 166 in middleincome countries, and nine in low-income countries) in 74 countries. Of the 3849 patients, 2231 (58·0%) were male. Median gestational age at birth was 38 weeks (IQR 36–39) and median bodyweight at presentation was 2·8 kg (2·3–3·3). Mortality among all patients was 37 (39·8%) of 93 in low-income countries, 583 (20·4%) of 2860 in middle-income countries, and 50 (5·6%) of 896 in high-income countries (p<0·0001 between all country income groups). Gastroschisis had the greatest difference in mortality between country income strata (nine [90·0%] of ten in lowincome countries, 97 [31·9%] of 304 in middle-income countries, and two [1·4%] of 139 in high-income countries; p≤0·0001 between all country income groups). Factors significantly associated with higher mortality for all patients combined included country income status (low-income vs high-income countries, risk ratio 2·78 [95% CI 1·88–4·11], p<0·0001; middle-income vs high-income countries, 2·11 [1·59–2·79], p<0·0001), sepsis at presentation (1·20 [1·04–1·40], p=0·016), higher American Society of Anesthesiologists (ASA) score at primary intervention (ASA 4–5 vs ASA 1–2, 1·82 [1·40–2·35], p<0·0001; ASA 3 vs ASA 1–2, 1·58, [1·30–1·92], p<0·0001]), surgical safety checklist not used (1·39 [1·02–1·90], p=0·035), and ventilation or parenteral nutrition unavailable when needed (ventilation 1·96, [1·41–2·71], p=0·0001; parenteral nutrition 1·35, [1·05–1·74], p=0·018). Administration of parenteral nutrition (0·61, [0·47–0·79], p=0·0002) and use of a peripherally inserted central catheter (0·65 [0·50–0·86], p=0·0024) or percutaneous central line (0·69 [0·48–1·00], p=0·049) were associated with lower mortality. Interpretation Unacceptable differences in mortality exist for gastrointestinal congenital anomalies between lowincome, middle-income, and high-income countries. Improving access to quality neonatal surgical care in LMICs will be vital to achieve Sustainable Development Goal 3.2 of ending preventable deaths in neonates and children younger than 5 years by 2030

Low sclerostin levels: a predictive marker of persistent inflammation in ankylosing spondylitis during anti-TNF therapy

Introdução: Baixas concentrações séricas de esclerostina foram descritas em pacientes com Espondilite Anquilosante (EA). No entanto, não existem dados sobre a importância deste inibidor da via de sinalização Wnt em pacientes com EA durante o tratamento com anti fator de necrose tumoral alfa (TNFa). Objetivos: Avaliar longitudinalmente os níveis séricos de esclerostina e sua associação com inflamação e densidade mineral óssea (DMO) em pacientes com EA em tratamento com anti-TNFa. Métodos: Trinta pacientes com EA em atividade foram avaliados no início, 6 e 12 meses, após terapia anti-TNFa em relação aos parâmetros clínicos (BASDAI, BASFI, BASMI e ASQoL), marcadores inflamatórios e dano radiológico basal (mSASSS). Trinta indivíduos saudáveis pareados por idade e sexo constituíram o grupo controle. As análises laboratoriais de esclerostina e da ligação de esclerostina ao receptor LRP6 e a DMO foram realizadas nos pacientes nos mesmos períodos de avaliação e comparadas aos controles. Resultados: Na avaliação inicial, pacientes com EA apresentavam menores concentrações séricas de esclerostina [60,5 (32,7) vs. 96,7 (52,9) pmol/l,P=0,002] e níveis similares de ligação de esclerostina ao receptor LRP6 (P=0,387) em relação aos controles. Foi observado melhora do BASDAI, BASFI, BASMI, ASQoL comparando tempo basal vs. 6 vs. 12 meses (P<0,01). Concomitantemente, observou-se um aumento gradual da DMO da coluna lombar (P<0,001) e no início do estudo os pacientes apresentavam uma correlação positiva entre avaliação radiológica basal (mSASSS) e a DMO da coluna lombar (r=0,468, P<0,01). Foi observada também uma redução dos marcadores inflamatórios comparando tempo basal vs. 6 vs. 12 meses (P<0,01). Os níveis de esclerostina aumentaram progressivamente após o tratamento com anti-TNFa [60,5 (32,7) vs. 67,1 (31,9) vs. 72,7 (32,3) pmol/l, P<0,001]. Entretanto, após 12 meses de terapia anti-TNFa as concentrações séricas de esclerostina permaneceram significativamente mais baixos em relação os controles [72,7 (32,3) vs. 96,7 (52,9) pmol/l, P=0,038]. Além disso, aos 12 meses, os níveis séricos de esclerostina ficaram mais baixos nos 10 pacientes que ainda apresentavam proteína C reativa elevada (PCR=5mg/l), comparados aos pacientes que apresentaram normalização dos níveis de PCR (P=0,004). Interessantemente, estes 10 pacientes com inflamação persistente já apresentavam concentrações séricas mais baixas de esclerostina quando comparados aos demais pacientes (P=0,023) antes do tratamento com anti- TNFa. A análise de regressão logística demonstrou que os pacientes com EA com níveis baixos de esclerostina apresentam um risco aumentado de apresentar PCR alta após 12 meses de tratamento (odds ratio = 7,43, 95% IC 1,23-45,01, P=0,020) quando comparados aos pacientes com níveis altos de esclerostina no tempo basal. Conclusão: Concentrações persistentemente baixas de esclerostina estão associados a inflamação contínua em pacientes com EA tratados com terapia anti-TNFa.Introduction: Sclerostin levels have been reported to be low in ankylosing spondylitis (AS), but there is no data regarding the possible role of this Wnt inhibitor during anti tumor necrosis factor alpha (TNFa) therapy. Objectives: The present study longitudinally evaluated sclerostin levels, inflammatory markers and bone mineral density (BMD) in AS patients under anti-TNFa therapy. Methods: Thirty active AS patients were assessed at baseline, 6 and 12 months after anti-TNFa therapy regarding clinical parameters (BASDAI, BASFI, BASMI and ASQoL), inflammatory markers, BMD and baseline radiographic damage (mSASSS). Thirty age- and sex-matched healthy individuals comprised the control group. Patients\' sclerostin levels, sclerostin binding LRP6 and BMD were evaluated at the same time points and compared to controls. Results: At baseline, AS patients had lower sclerostin levels [60.5 (32.7) vs. 96.7 (52.9) pmol/l, P=0.002] and comparable sclerostin binding to LRP6 (P=0.387) than controls. Improvement of BASDAI, BASFI, BASMI, ASQoL was observed at baseline vs. 6 vs. 12 months (P<0.01). Concomitantly, a gradual increase in spine BMD (P<0.001) and a positive correlation between baseline mSASSS and spine BMD was found (r=0.468, P<0.01). Inflammatory parameters reduction was observed comparing baseline vs. 6 vs. 12 months (P<0.01). Sclerostin levels progressively increased [60.5 (32.7) vs. 67.1 (31.9) vs. 72.7 (32.3) pmol/l, P<0.001] after anti-TNFa treatment. At 12 months, the sclerostin levels remained significantly lower in patients compared to controls [72.7 (32.3) vs. 96.70 (52.85) pmol/l, P=0.038]. Moreover, sclerostin serum levels at 12 months were lower in the 10 patients with high CRP (=5mg/l) compared to the other 20 patients with normal CRP (P=0.004). Of note, these 10 patients with persistent inflammation also had lower sclerostin serum levels at baseline compared to the other patients (P=0.023). Univariate logistic regression analysis demonstrated that AS patients with lower sclerostin serum levels had an increased risk to have high CRP at 12 months (odds ratio=7.43, 95% CI 1.23-45.01, P=0.020) than those with higher sclerostin values. Conclusion: Persistent low sclerostin levels may underlie continuous inflammation in AS patients under anti-TNFa therapy

Pesquisa de autoanticorpos em pacientes com artrite psoriásica sob terapia anti-TNF&#945; Autoantibodies in patients with psoriatic arthritis on anti-TNF&#945; therapy

INTRODUÇÃO: A terapia imunobiológica anti-TNF&#945; tem-se mostrado efetiva no tratamento de pacientes com artrite psoriásica (APs) refratária. No entanto, não está bem definido o risco de desenvolvimento de autoanticorpos comumente encontrados nas doenças reumatológicas em pacientes com APs na vigência desse tratamento. OBJETIVO: avaliar a indução de autoanticorpos específicos durante a terapia anti-TNF&#945; em pacientes com APs. PACIENTES E MÉTODOS: Foram analisadas amostras de soro de 23 pacientes com APs (mulheres: 61%, idade: 45,04 ± 12,68 anos, quadro poliarticular: 69,6%, duração da doença: 13,3 ± 7,7 anos, infliximabe: 82,60%) obtidas imediatamente antes (basal) e cerca de um ano após a introdução da terapia anti-TNF (última amostra) (385 ± 131,45 dias). A pesquisa incluiu a detecção de anticorpos antinucleares (ANA) e anticorpos para dsDNA (imunofluorescência indireta em células Hep-2 e em Crithidia luciliae, respectivamente); RNP e Sm (hemaglutinação passiva); Ro/SS-A e/ou La/SS-B, cromatina, histona, peptídeo citrulinado (CCP) e cardiolipina (ELISA). RESULTADOS: A pesquisa basal de ANA revelou positividade em 47,8% dos pacientes, com predomínio do padrão nuclear homogêneo (81,8%). Todas as amostras de soro testadas foram negativas para fator reumatoide e anticorpos anticardiolipina, RNP, Sm, Ro/SS-A, La/SS-B, histona e dsDNA, enquanto dois pacientes apresentaram positividade para anticromatina e um para anti-CCP. Todas as amostras de ANA positivas no tempo basal, exceto uma, mantiveram essa reatividade após a introdução da terapia anti-TNF. Reatividade "de novo" ANA foi observada em quatro dos pacientes originalmente negativos (33,3%). Anticorpos anti-Ro/SS-A, La/SS-B, cardiolipina, histona, dsDNA e fator reumatoide foram sistematicamente negativos em todas as amostras finais de soro testadas e positividade anticromatina foi detectada em outros três pacientes. CONCLUSÃO: Nossos achados mostram que a terapia anti-TNF induziu positividade ANA em um terço dos pacientes com APs e o uso concomitante de metotrexato não alterou esse achado. Além disso, todos os soros foram sistematicamente negativos para a maioria dos autoanticorpos específicos de doenças reumatológicas testados após a introdução da terapia biológica.INTRODUCTION: Anti-TNF&#945; therapy has been effective in the treatment of patients with refractory psoriatic arthritis (PSA). However, the risk of developing autoantibodies commonly found in rheumatic diseases in PSA patients undergoing this therapy is not clear. OBJECTIVE: To evaluate the induction of specific autoantibodies after anti-TNF&#945; therapy in PSA patients. PATIENTS AND METHODS: Serum samples from 23 PSA patients (women: 61%, age: 45.04 ± 12.68 years, polyarticular: 69.6%, disease duration: 13.3 ± 7.7 years, infliximab: 82.60%) obtained immediately before (baseline) and approximately one year after the introduction of anti-TNF therapy (last sample) (385 ± 131.45 days), were analyzed. The analysis included detection of antinuclear antibodies (ANA) and anti-dsDNA antibodies (indirect immunofluorescence on Hep-2 cells and Crithidia luciliae, respectively); anti-RNP and anti-Sm (passive hemagglutination); and anti-Ro/ SS-A and/or anti-La/SS-B, anti-chromatin, anti-histones, anti-citrullinated peptide (CCP), and anti-cardiolipin (ELISA) antibodies. RESULTS: At baseline, ANA was positive in 47.8% of patients, with predominance of homogeneous nuclear pattern (81.8%). All baseline serum samples were negative for rheumatoid factor and antibodies to cardiolipin, RNP, Sm, Ro/SS-A, anti-La/SS-B, anti-histone, and anti-dsDNA antibodies, while two patients were positive for anti-chromatin and one for anti-CCP. All ANA-positive samples at baseline, except for one, remained positive after the introduction of anti-TNF therapy; however, de novo ANA reactivity was observed in four originally negative patients (33.3%). Anti-Ro/SS-A, La/SS-B, cardiolipin, histones, dsDNA, and rheumatoid factor antibodies remained negative in all final serum samples tested, and anti-chromatin positivity was detected in three other patients. CONCLUSION: Our findings have shown that anti-TNF therapy induced ANA positivity in one third of PSA patients. The concomitant use of methotrexate did not interfere with this finding. In addition, all serum samples were systematically negative for specific rheumatic autoantibodies tested after the introduction of the biological treatment