Background: Patients with immune-mediated rheumatic diseases (IMRD) undergoing immunosuppressive treatment are at greater risk of infection. Infectious are one of the main causes of death in this group of patients. Although vaccination impacts in reducing the incidence of infections, the vaccine coverage of the general population in Brazil has been falling over the years. Objectives: To present the preliminary results on influenza and pneumococcal (PCV10/13 and PPV23) vaccination coverage in patients with juvenile IMRD in Brazil. Methods: This is a cross-sectional multicenter study designed to evaluate the vaccination coverage of patients under 18 years, from 2019 to 2022. Investigators from Pediatric Rheumatology outpatient clinics representing the five regions of Brazil were invited to participate. The clinical data were collected in medical records and in vaccination cards using a standardized protocol. Vaccination was evaluated considering the immunization schedule for the current year of inclusion based on the National Immunization Program and Reference Centers for special groups. Clinical and demographic data were sex, age, education level, diagnosis, time since diagnosis, current and previous treatments, disease activity and analysis of the vaccination card. Results were expressed using frequencies and percentages for qualitative variables, and measures of central tendency (mean or median) and measures of dispersion (standard deviation - SD) for quantitative ones. Comparisons of variables were performed using Student's t-test or Mann-Whitney test. A significance level of 5% was considered. Results: Two-hundred twenty-nine patients were included, 48% were diagnosed with juvenile idiopathic arthritis and 23% with systemic lupus erythematosus; 70.8% were female with mean age of 12 years (SD 4.17) and average time of diagnosis of 3.77 years (SD 3.17). Regarding treatment, 22.68% were using biological agents, 8.24% were in corticosteroids (>20mg/day or >2mg/kg/day or pulse therapy with methylprednisolone), and 2.4% in cyclophosphamide. According to specific disease activity criteria, 51.89% of patients were in remission. Of total, 178 (61.16%) patients were not vaccinated against influenza in last campaign; 130 of 188 (69.14%) patients had complete schedule for PCV10/13 but only 12.4% (31/250) received PPV23. Conclusion: These results show the low vaccination coverage against influenza and pneumococcal vaccines among patients with juvenile IMRD. Additional studies are necessary to identify the reasons to the decline the vaccination among immunosuppressed children. REFERENCES: [1] MAKAROVA E et al. Vaccination coverage in children with juvenile idiopathic arthritis, inflammatory bowel diseases, and healthy peers: Cross-sectional electronic survey data. World J Clin Pediatr 2023 March 9; 12(2): 45-56. [2] Chevallard M et. al. Active vaccination campaign to increase seasonal influenza vaccination coverage: a monocenter experience in a cohort of Italian patients with systemic autoimmune diseases. Clinical Rheumatology 2023 42:923–928. https://doi.org/10.1007/s10067-022-06380-z. [3] Balažiová B, Kuková Z, Mišíková D, Novosedlíková K, Dallos T. Real-life vaccination coverage in Slovak children with rheumatic diseases. Front. Pediatr. 10:956136. doi: 10.3389/fped.2022.956136. [4] Furer V, Rondaan C, Heijstek MW, et al. 2019 update of EULAR recommendations for vaccination in adult patients with autoimmune inflammatory rheumatic diseasesAnn Rheum Dis 2020;79:39–52 Acknowledgements: NIL. Disclosure of Interests: None declared.

Background: Telomeres are protein complexes located at the top of each arm of chromosomes, essential for maintaining the stability of the genome. Telomere shortening is found in physiological aging and senescence-related to systemic lupus erythematosus (SLE). Objectives: To compare the relative telomere length (TL) in patients with SLE and controls and to correlate the TL with clinical characteristics, treatments, disease activity, and damage. Methods: A cross-sectional study comparing SLE patients and controls, from 18 to 60 years old, matched by sex and age. Clinical and demographic data from all participants were collected, and relative TL by qPCR. For cases, previous and current history, disease activity, damage, cognitive assessment, fatigue, presence of depression, anxiety, stress symptoms, and physical activity were analyzed. Results were obtained using frequencies and percentages for qualitative characteristics and measures of central tendency and standard deviation for quantitative ones. Comparisons of relative TL and other variables were performed using the t-Student test when assumptions of normality and homoscedasticity were satisfied and the Mann-Whitney test otherwise. A significance level of 5% was considered. Results: Sixty SLE patients and 55 controls were included. Among patients, 75% were diagnosed in adulthood; 86.7% were female (mean age 37 years); 15% had antiphospholipid syndrome (APS), 51.7% had a previous history of nephritis, and 23.3% had neuropsychiatric involvement. Among controls, 87.3% were female (mean age 38 years). There was no difference between groups regarding sex and age (p=0.924 and p=0.737, respectively). SLE patients had a median relative TL of 0.80 versus 1.07 in the control group (p=0.005). In the multiple regression model (R2=18.4%), patients with anxiety symptoms in a moderate grade had lower TL (p=0.015) when compared to patients without or with low-grade anxiety symptoms. In contrast, patients with APS had longer telomere when compared to patients without APS (p=0.007). There was no association with disease activity or damage. Conclusion: Brazilian SLE patients have shorter telomeres than controls. Telomere length in SLE patients was associated with anxiety symptoms. Longitudinal studies are essential to evaluate clinical implications related to TL. REFERENCES: [1] LEE, Y. H. et al. Association between shortened telomere length and systemic lupus erythematosus: a meta-analysis. Lupus, v. 26, n. 3, p. 282-288, Mar 2017.[2] BRIDGES, J. et al. Leukocyte Telomere Length and Childhood Onset of Systemic Lupus Erythematosus in the Black Women’s Experiences Living with Lupus Study. ACR Open Rheumatol, v. 4, n. 5, p. 426-431, May 2022.[3] HAQUE, S. et al. Shortened telomere length in patients with systemic lupus erythematosus. Arthritis Rheum, v. 65, n. 5, p. 1319-23, May 2013.[4] UGARTE-GIL, M. F. et al. Circulating CD4+CD28null and extra-thymic CD4+CD8+ double positive T cells are independently associated with disease damage in systemic lupus erythematosus patients. Lupus, v. 25, n. 3, p. 233-40, Mar 2016. Acknowledgements: Brazilian Society of Rheumatology for funding this study. Disclosure of Interests: None declared.Table 1Comparisons of relative telomere length between patients and controlsCharacteristicsCases (n = 60)Controls (n = 55)p-valueTL, mean (SD), median0.91 (0.51)/ 0.80 (0.29-2.94)1.10 (0.45)/ 1.07 (0.38-2.32)0.005*Cases comparisonChildhood-onset SLE0.83 (0.45)/ 0.70 (0.33-1.95)-0.591*Adulthood-onset SLE0.93 (0.54)/ 0.82 (0.29-2.94)-Table data are presented as mean (SD), and median (minimum and maximum values). SD: standard deviation; SLE: systemic lupus erythematosus; TL: telomere length. *U of Mann-Whitney

Axial Spondyloarthritis (axSpA) is a chronic inflammatory rheumatic disease whose pathophysiology is also associated with intestinal dysbiosis and leaky gut (increased permeability of the intestinal barrier to bacteria and their products).Gliadin, a type of gluten that can induce the release of zonulin (a modulator of intercellular tight junctions), may be related to the higher permeability in bowel mucosal epithelium.This pilot study aimed to evaluate if a 12-week gluten-free diet may improve systemic and intestinal inflammation, intestinal permeability, and clinical outcomes in patients with active axSpA.

the Brazilian Universal Health System (BUHS) enact several policies to reduce access barriers to biological medicines, favoring biosimilars. After seven years since the authorization of the first biosimilars, we investigated the major gaps that hinders a greater participation of these products in the market.

Rationale: There is neither a gold standard definition nor a universal consensus to diagnose sarcopenia in patients with chronic hepatitis C (CHC). Thus, we aimed to compare the prevalence of sarcopenia and the agreement and discrepancies between the European Working Group on Sarcopenia in Older People (EWGSOP1), the EWGSOP2 and The Foundation for the National Institutes of Health Biomarkers Consortium Sarcopenia Project (FNIH) consensuses in CHC. Methods: Dual-energy X-ray absorptiometry was used to assess muscle mass by quantifying appendicular lean mass (ALM) adjusted for squared height (ALM/ht2) or for body mass index (ALMBMI). Muscle function was evaluated by handgrip strength. The Controlling Nutritional Status score was used to assess the nutritional status. Results: This cross-sectional study included 103 CHC outpatients followed at the tertiary care ambulatory (mean age, 50.6 ± 11.3 years; 74.8% males; 67.0% non-cirrhotic; 33.0% with compensated cirrhosis). Sarcopenia prevalence was 8.7%, 9.7% and 9.7%, according to EWGSOP1, EWGSOP2 and FNIH consensuses, respectively. There is neither sex- nor liver disease severity-specific differences in the prevalence of sarcopenia between the criteria applied. Sixteen (15.5%) patients fulfilled at least one of these criteria, and 3/16 (18.8%) were diagnosed as sarcopenic by the three consensuses simultaneously. Sarcopenic obesity was identified in 9/16 (56.3%) patients, and 6/9 (66.7%) of these met only FNIH consensus. Conclusion: This is the first study to demonstrate that the revised EWGSOP2 did not affect sarcopenia diagnosis in CHC patients. In overweight patients, the ALM adjusted by BMI appears to be more feasible to detect sarcopenia in CHC. Disclosure of Interest: None declared

IntroductionLa douleur résiduelle reste un obstacle à l’amélioration de la qualité de vie chez les patients atteints de PR. L’association d’upadacitinib à un traitement de fond par MTX a permis des améliorations plus importantes de la douleur qu’avec l’adalimumab (ADA)+MTX et le placebo (PBO)+MTX dans l’étude SELECT-COMPARE [1]. L’objectif de cette analyse post hoc était de décrire les niveaux de réduction de la douleur et de douleur résiduelle après un traitement par UPA+MTX vs ADA+MTX et PBO+MTX chez des patients atteints de PR ayant ou non présenté une atténuation de l’inflammation aux semaines 12 et 26 (S12 et S26).Patients et méthodesUne évaluation en sous-groupes a été effectuée selon qu’une atténuation de l’inflammation (définie par l’absence de synovite et une CRP<6 mg/L) ait été atteinte aux S12 et 26. La douleur était mesurée à l’aide d’une échelle EVA. La variation moyenne par rapport à l’inclusion de la douleur aux S12 et 26 ainsi que les réductions ≥ 30 %, ≥ 50 % ou ≥ 70 % de la douleur entre l’inclusion et les S12 et 26 ont été évaluées. Pour les analyses de variation par rapport à l’inclusion, la moyenne des moindres carrés entre les groupes, l’IC à 95 % et la valeur de p nominale sont basés sur l’analyse du modèle de covariance.RésultatsUne atténuation de l’inflammation à la S26 a été obtenue chez respectivement 41 (6,3 %), 60 (18,3 %) et 187 (28,7 %) des patients recevant le PBO, l’ADA et l’UPA ; une inflammation était toujours présente chez respectivement 610 (93,7 %), 267 (81,7 %) et 464 (71,3 %) des patients. Des différences ont été observées entre les caractéristiques à l’inclusion. Parmi les patients avec atténuation de l’inflammation, l’amélioration de la douleur a été plus importante avec UPA (moyenne [IC à 95 %] : −42,9 [−46,6, −39,1]) qu’avec ADA (−34,7 [−41,1, −28,0] ; p nominale=0,038) ou PBO (−33,1 [−41,0, −25,2] ; p nominale=0,029) à S12 ; les résultats de variation par rapport à l’inclusion étaient numériquement similaires à la semaine 26. Les valeurs moyennes absolues pour la douleur ont montré une tendance similaire. Parmi les patients avec inflammation résiduelle, une tendance similaire a été observée, qui était significative pour UPA versus PBO aux S12 et 26 et pour UPA versus ADA à la semaine 12. Pour la réduction ≥ 30 %, ≥ 50 % ou ≥ 70 % de la douleur par rapport à l’inclusion, le taux de réponse avec UPA était numériquement plus élevé qu’avec ADA ou PBO aux S12 et 26 (significatif pour l’UPA vs PBO à la semaine 12 pour la réduction ≥ 50 %) chez les patients présentant une atténuation de l’inflammation. Parmi les patients avec inflammation résiduelle, des taux de réponse significativement plus importants ont été observés avec UPA vs PBO aux S12 et 26 et vs ADA à S12 pour les réductions ≥ 30 %, ≥ 50 % et ≥ 70 % de la douleur par rapport à l’inclusion.ConclusionChez les patients avec atténuation de l’inflammation ainsi que chez ceux avec inflammation résiduelle après 1re et 26 semaines de traitement, l’amélioration de la douleur était plus importante avec UPA qu’avec l’ADA ou PBO aux semaines 12 et 26. Ces résultats suggèrent que UPA est efficace pour réduire la douleur chez les patients atteints de PR active avec atténuation de l’inflammation à 3 ou 6 mois.

Les patients atteints de rhumatismes inflammatoires chroniques ont un risque accru d’événements cardiovasculaires majeurs (MACE), et de maladie thromboembolique veineuse profonde (MTEV) par rapport à la population générale. L’objectif de cette analyse était de décrire les événements et les facteurs de risque de MACE et de MTEV dans les programmes d’essais cliniques de l’upadacitinib (UPA), dans la polyarthrite rhumatoïde (PR), le rhumatisme psoriasique (RP) et la spondylarthrite ankylosante (SA). Une synthèse des événements indésirables apparus sous traitement (EIAT) de MACE et de MTEV dans 9 essais pivots randomisés et contrôlés (6 dans la PR ; 2 dans le RP ; 1 dans la SA) a été effectuée pour UPA 15 mg UPA 30 mg, adalimumab (ADA) 40 mg et MTX. Les EIAT étaient définis comme survenant pendant ou après la première administration du médicament et jusqu’à 30 jours après la dernière administration pour UPA et MTX ou 70 jours pour ADA. Les EIAT de MACE (décès d’origine cardiovasculaire, infarctus du myocarde non fatals et accidents vasculaires cérébraux non fatals) et de MTEV (embolies pulmonaires et thromboses veineuses profondes) étaient confirmés par un comité indépendant d’adjudication des événements cardiovasculaires, en aveugle. Les patients n’étaient pas censurés au moment de l’événement ; les données sont présentées sous forme de taux d’événements ajustés en fonction de l’exposition (TEAE) en nombre d’événements pour 100 patients-années (date de cut-off au 30 juin 2021). Le délai de survenue d’un événement était analysé en utilisant la méthode de Kaplan–Meier et les TEAE étaient évalués selon des intervalles de 6 mois. Compte tenu du nombre limité d’événements, les régressions de Cox étaient limitées à des analyses univariées et évaluaient la relation entre les facteurs de risque potentiels et la survenue de MACE et MTEV chez les patients sous UPA. Au total, 4298 patients ont reçu ≥ 1 dose d’UPA 15 mg et 2125 ont reçu de l’UPA 30 mg, 1008 patients ont reçu de l’ADA 40 mg et 314 patients ont reçu du MTX. À l’inclusion, 40–50 % des patients présentaient au moins 2 facteurs de risque CV et la proportion de patients âgés de ≥ 65 ans allait de 6 % à 23 %. Sur les 41 MACE rapportés dans le groupe UPA 15 mg dans la PR et le RP, seuls 2 patients atteints de RP n’avaient pas au moins 1 facteur de risque CV à l’inclusion. Deux MTEV fatales ont été rapportées dans l’ensemble des essais, toutes deux dans le groupe PR sous UPA 15 mg. Un chevauchement des intervalles de confiance a été observé avec les différentes doses d’UPA et les comparateurs pour les taux de MACE ainsi que pour les taux de MTEV à la fois dans la PR et le RP. Aucune tendance de délai de survenue des événements pour les TEAE à 6 mois d’intervalle sur 42 mois n’a été observée chez les patients recevant de l’UPA (données non présentées). Dans les analyses univariées, les facteurs potentiellement associés à la survenue de MACE ou de MTEV chez les patients atteints de PR recevant de l’UPA 15 mg incluaient un âge d’au moins 65 ans, la présence d’une hypertension à l’inclusion, le diabète, un tabagisme actif, un antécédent d’événement CV ou de MTEV, ainsi que l’utilisation d’aspirine, de statines ou d’antithrombotiques. Dans le RP, l’utilisation d’aspirine était associée à un risque accru de MACE. Les MACE et MTEV confirmés par le comité d’adjudication avec l’UPA étaient peu fréquents et les taux étaient cohérents avec ceux rapportés dans les populations atteintes de PR, RP et SA. Les caractéristiques des patients associées à la survenue de MACE et de MTEV épousaient les facteurs de risque connus de ces événements.

Thyrotropin stimulating hormone (TSH) suppression in patients with differentiated thyroid cancer (DTC) aims to decrease the growth and proliferation of thyroid cancer cells. However, the effect of TSH-suppressive therapy on bone microarchitecture remains undefined. Cross-sectional study including 43 women with DTC undergoing TSH-suppressive therapy (sTSH) compared to 20 women also on levothyroxine (LT4) therapy but with TSH in the low-normal range (nTSH) since the thyroid surgery. Bone mineral density (BMD) was measured by dual-energy X-ray absorptiometry (DXA), and trabecular bone score (TBS) was evaluated using the TBS iNsigth software. Fracture risk assessed by FRAX, with and without TBS, was calculated. The relationship between suppressive therapy-related parameters and bone parameters was investigated. The TBS mean values were not significantly different in the sTSH and nTSH groups (1.273 ± 0.12 vs 1.307 ± 0.14, p = 0.7197). In both groups, postmenopausal women had degraded microarchitecture (TBS 1.216 ± 0.11 vs 1.213 ± 0.09, p = 0.9333), while premenopausal women had normal microarchitecture (1.328 ± 0.11 vs 1.401 ± 0.12, p = 0.195). The percentage of all postmenopausal women with degraded TBS was 54.7%, while the percentage of osteoporosis diagnoses was 16.1%. The TBS-adjusted FRAX-probability of fracture was similar in sTSH and nTSH groups. Body mass index (BMI) and menopausal status were the only variables associated with TBS and BMD. Trabecular microarchitecture assessed by TBS was similar between women on long-term suppressive therapy in DTC and those on LT4 replacement therapy aiming at a TSH level within the low-normal reference range. Low TBS values were observed in postmenopausal women of both groups, suggesting that not only suppressed TSH levels but also a low-normal TSH is associated with deteriorated bone microarchitecture in postmenopausal women following total thyroidectomy.

Rationale: Sarcopenia is a remarkable finding in patients with chronic hepatitis C (CHC). However, the potential factors behind the skeletal muscle loss have not been completely clarified. We evaluate independent associations between host-, disease-, nutritional- and virus-related factors with sarcopenia and its components [appendicular muscle mass index (ASMI) and handgrip strength (HGS)]. Additionally, we appraised the association between sarcopenia and Bioelectrical Impedance Analysis (BIA)-derived phase angle (PhA).

OBJECTIVES To evaluate the incidence of COVID-19 and its main outcomes in rheumatic disease (RD) patients on hydroxychloroquine (HCQ) compared to household cohabitants (HC). METHODS This is a 24-week nationwide prospective multi-centre cohort with a control group without RD and not using HCQ. All participants were monitored through scheduled phone interviews performed by health professionals. Details regarding COVID-19 symptoms, and epidemiological, clinical, and demographic data were recorded on a specific web-based platform. COVID-19 was defined according to the Brazilian Ministry of Health criteria and classified as mild, moderate or severe. RESULTS A total of 9,585 participants, 5,164 (53.9%) RD patients on HCQ and 4,421 (46.1%) HC were enrolled from March 29th, 2020 to September 30th, 2020, according to the eligibility criteria. COVID-19 confirmed cases were higher in RD patients than in cohabitants [728 (14.1%) vs. 427 (9.7%), p<0.001] in a 24-week follow-up. However, there was no significant difference regarding outcomes related to moderate/ severe COVID-19 (7.1% and 7.3%, respectively, p=0.896). After multiple adjustments, risk factors associated with hospitalisation were age over 65 (HR=4.5; 95%CI 1.35-15.04, p=0.014) and cardiopathy (HR=2.57; 95%CI 1.12-5.91, p=0.026). The final survival analysis demonstrated the probability of dying in 180 days after a COVID-19 diagnosis was significantly higher in patients over 65 years (HR=20.8; 95%CI 4.5-96.1) and with 2 or more comorbidities (HR=10.8; 95%CI 1.1-107.9 and HR=24.8; 95%CI 2.5-249.3, p=0.006, respectively). CONCLUSIONS Although RD patients have had a higher COVID-19 incidence than individuals from the same epidemiological background, the COVID-19 severity was related to traditional risk factors, particularly multiple comorbidities and age, and not to underlying RD and HCQ.

Rheumatoid arthritis (RA), psoriatic arthritis (PsA), and ankylosing spondylitis (AS) are inflammatory diseases with different bone remodeling patterns. Fibroblast-like synoviocytes (FLS) are cells involved in the transition from an acute and reparable phase to a chronic and persistent stage in these diseases. The distinction of joint phenotypes involves inflammatory cytokines such as tumor necrosis factor alpha (TNF-α), interleukin (IL)-17, and IL-22 directly or through key signaling pathways such as Wnt. To evaluate the role of FLS as the source of Wnt antagonists (sFRP3/FRZB and Dkk1) in the synovia, levels of TNF- α, IL-17, IL-22, Dkk1, and sFRP3 were measured by ELISA directly in the synovial fluid of patients with RA, PsA, or AS. Dkk1 and sFRP3 were also measured in the FLS culture supernatants after different inflammatory stimulus. sFRP3 and Dkk1 are constitutively expressed by FLS. IL-22 and sFRP3 were positively correlated (r=0.76; P<0.01) in synovial fluid. The stimulation of FLS with IL-22, but not TNF-alpha and IL-17, increased the production of sFRP3. No stimulus altered the basal expression of Dkk1. These results showed, for the first time, the ability of IL-22 to increase the expression of sFRP3/FRZB by human FLS in both in vitro and ex vivo models. This finding linked IL-22 to local inhibition of Wnt signaling and possibly to blockade of osteogenesis. Furthermore, FLS presented as a source of this inhibitor in synovial fluid, assigning to this cell a bone injury mechanism.

Objectives: This study aimed to determine whether estrogen deficiency is a sole risk factor for osteoporosis or is also associated with age, through indicators such as gender, age, and time since menopause. Methods: A cross-sectional study was conducted evaluating 938 postmenopausal women who underwent bone mineral densitometry. We collected the following data: age, ethnic group, body mass index, smoking, and time since menopause. These data were correlated to the presence of osteoporosis, according to the T-score of the femur and lumbar spine. Results: The prevalence of osteoporosis was 37.8%. Ethnic group (p = 0.47) and smoking habits (p = 0.19) were not associated with osteoporosis. In the group of women with osteoporosis, mean age was significantly higher (p < 0.001), mean body mass index was significantly lower (p < 0.001), and time since menopause was significantly higher (p < 0.001) than in the group of women with no osteoporosis. After multivariate analysis was performed, the only variables that remained independently associated with osteoporosis were body mass index and time since menopause. Higher body mass index was a protective factor (odds ratio = 0.80 [95% confidence interval 0.76; 0.84], p < 0.001). Time since menopause represented a risk factor for osteoporosis (odds ratio = 1.04 [1.02; 1.06], p < 0.001). When divided into categories, the risk increased after 20 years of menopause and gradually every 5 years. Conclusion: Time since menopause and body mass index were the most important factors associated with osteoporosis, confirming that estrogen deficiency, and not age, is the major cause of the disease.

Introducao: O uso da dinâmica de captacao do gadolinio (Gd) a ressonância magnetica (DCRM) tem evoluido recentemente como um metodo importante para avaliar varias doencas do sistema osteomuscular, principalmente em tumores e artropatias. O metodo ainda foi pouco explorado na avaliacao das tendinopatias e no pos operatorio de rupturas tendineas. Materiais e metodos: Foram 12 coelhos brancos, machos, raca Nova Zelândia adultos, dois grupos foram designados sendo os operados (n = 8), com resseccao da porcao tendinea central de Aquiles e o grupo controle ( n=4) , em quatro semana, e apos a realizacao da ressonância magnetica com uso de tecnica de avaliacao dinâmica do meio de contraste, os animais foram sacrificados, para analise histologica dos tendoes. Resultados: O principal achado deste estudo foi a diferenca ( p <0,001) do pico maximo de realce de contraste, na DCRM dinâmica na RM de Aquiles entre o grupo operado e controle, sendo o grupo operado oque apresenta maior captacao de contraste. Os tendoes operados apresentavam a histologia desorganizacao de sua arquitetura, fibras tendineas de aspecto desordenado, com neoformacao vascular e proliferacao de fibroblastos. Conclusao: DCRM e uma tecnica com potencial de demonstrar as alteracoes do padrao de vascularizacao do tendao de Aquiles no pre e pos operatorio. A DCRM apresenta potencial para ser usada em estudos para controle de tratamento e diagnostico da tendinose a cirurgia.

Objective. The objective of the study was to compare the production of metalloproteinases (MMP)-1, -3 and interleukin (IL)-6 by fibroblast-like synoviocytes (FLS) derived from synovial fluid (FD-FLS), and FLS derived from synovial tissue (TD-FLS) of patients with primary osteoarthritis (OA). The more accessible FD-FLS could facilitate the study of the role of these cells in OA pathophysiology. Methods. MMP-1, MMP-3, and IL-6 levels were measured in the supernatant culture at baseline and 22 hours after stimulation with TNF-alpha and IL-1 beta. Results. There was no difference at baseline between MMP-1, MMP-3 and IL-6 production by FD-FLS and TD-FLS. Analogous to baseline, stimulation of FD-FLS and TD-FLS with IL-1 beta and TNF-alpha did not result in difference on MMP-3 and IL-6 production. However, TD-FLS produced more MMP-1 than FD-FLS after stimulation with IL-1 beta (p=0.01). Additionally, there was a positive correlation for production of MMP-1, MMP-3 and IL-6 between FD-FLS and TD-FLS (r=0.40 and p<0.0008; r=0.66 and p<0.0001; r=0.76 and p<0.0001, respectively). Supporting this statistical significant positive correlation, the Bland-Altman plotting, showed a homogeneous distribution of the values and low mean disagreement rates between all results of FD-FLS and TD-FLS (23.1%, 56.8% and 48.1%, respectively). Conclusion. Our data demonstrated functional similarity between FD-FLS and TD-FLS and support the use of a more accessible source of FLS for the study of the pathogenesis of joint destruction and therapeutic targets in primary OA.

Background Rheumatoid arthritis (RA) is an independent risk factor for cardiovascular disease (CVD). The renin-angiotensin system (RAS) is a hormonal cascade with important role in hydroelectrolytic homeostasis, blood pressure and regulation of cardiovascular remodeling. Angiotensin II (Ang II) acts as a proinflammatory mediator (1). Objectives To investigate the association of serum levels of RAS components with the presence of subclinical atherosclerosis using carotid ultrasonography in women with RA. Methods Women with RA according to ACR/EULAR 2010 or ACR 1987 criteria and without clinical ischemic CVD were included. Disease activity was assessed using the DAS28. The presence of atherosclerotic plaques and the thickness of the medium-intimal complex (EMI) of the arterial wall in the common carotid artery were evaluated by ultrasonography, Serum levels of angiotensin (Ang) II, Ang-(1-7), angiotensin converting enzyme (ECA) and ECA II were determined by enzyme immunoassay. Results 50 women with RA, mean age 48.2 years (±7.32), mean duration of disease of 15.35 years (±8.56), DAS28 of 4.02 (±1.41) and CDAI of 14.23 (±11.53) were included. Seven patients presented altered EMI, eight had atherosclerotic plaque. The prevalence of risk factors for CVD was: 12% of smoking, 12% of family history of premature CVD, 46% of arterial hypertension, 10% of diabetes, 62% of dyslipidemia, 94% of abdominal obesity and 46% of metabolic syndrome. The control group consisted of 30 healthy women, mean age of 46.3 years (±7.72). RA patients had a higher serum concentration of Ang II (p<0.01), Ang-(1-7) (p<0.01), and ACE (p<0.01) than the control group (table 1). There was a negative correlation between ECA II and EMI (p=0.041, rho -0.290). EMI correlated positively with age (p=0.022, rho 0.324), disease duration (p=0.012, rho 0.315) and overall Framingham risk (p=0.008, rho 0.368) and Ang II correlated positively with DAS28 (p=0.034, rho 0.301) and CDAI (p=0.040, rho 0.291). Conclusions Imbalance of RAS components, especially Ang II and ECA II, may be associated to CVD in RA patients. Ultrasonography of the carotid arteries can identify patients that could benefit from ECA blockade. Reference: [1] Chang Y, Wei W. Angiotensin II in inflammation, immunity and rheumatoid arthritis. Clin Exp Immunol 2015;179:137-145. doi: 10.1111/cei.12467 Acknowledgements: National Council for Scientific and Technological Development (CNPq), Foundation for Research Support of Minas Gerais (FAPEMIG) Disclosure of Interest: None declared

Background Rheumatoid arthritis (RA) patients have loss of muscle mass. The balance between muscle protein synthesis and degradation is regulated by cytokines and growth factors, named myokines, such as irisin and myostatin. Myokines are mainly expressed by skeletal muscle and exert systemic effects promoting crosstalk among different tissues. Irisin increases cortical bone mass and its low levels are related to muscle atrophy and obesity[,1, 2 while myostatin is a negative regulator of muscle growth and regeneration and has a direct role in osteoclastogenesis of inflammatory bone destruction[.3, 4 Objectives To evaluate serum levels of irisin and myostatin and body composition of RA patients and controls. Methods 122 female patients with RA, mean age 53 years, mean disease activity score (DAS28) 4.09, mean disease duration 11.2 years and mean body mass index 27.33 kg/m2 were included. 69 age and sex-matched healthy subjects were enrolled as control group. Irisin (Phoenix Pharmaceuticals) and myostatin (R and D Systems) serum levels were evaluated by ELISA. Fat mass index (FMI;Kg/m2) and appendicular lean mass index (ALMI;Kg/m2) were assessed by total body dual-energy x-ray absorptiometry. Student’s t test and Spearman correlation were performed. Significance was set at p<0.05. Results RA patients had decreased serum levels of irisin (25,61±8,25 vs 30,36±10,95 ng/ml; p<0.05) and myostatin (3011,28±1271,11 vs 4049,08±1610,01 pg/ml; p<0.05), decreased ALMI (6,09±0,88 vs 6,50±1,10; p<0.05) and increased FMI (11,26±3,30 vs 9,44±2,65; p<0.05), compared to controls. No correlations were observed among irisin and myostatin levels and ALMI and FMI. Of the 122 RA patients, 40 were analysed for the use of biologic medication. Serum levels of irisin and myostatin were different between RA patients treated and non-treated with biologics (table 1). Conclusions RA patients presented loss of lean mass and gain of fat mass, as well as lower irisin and myostatin serum levels, in comparison with controls. Additionally, the use of biologic medication by patients impacted on myokines serum levels. Further analyses are needed for a better comprehension of irisin and myostatin roles in RA, and to verify their correlation to other RA features. References [1] Colaianni G, et al. Proc Natl Acad Sci2015;112(39):12157–62. [2] Chang J, et al. Geriatr Gerontol Int. 2017;17(11):2266–2273. [3] Huang Z, et al. Cell Signal2011;23(9):1441–6. [4] Dankbar B, et al. Nat Med2015;21(9):1085–90. Disclosure of Interest None declared