BackgroundRheumatoid 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 ObjectivesTo evaluate serum levels of irisin and myostatin and body composition of RA patients and controls.Methods122 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.Table 1Irisin and myostatin serum levels of RA patients and controlsnIrisin (mean±SD)Myostatin (mean±SD) RA patients treated with biologics1331,71±7,69#2448,64±1114,90*#RA patients non-treated with biologics2725,93±6,893261,66±1156,28+Controls3030,36±10,954049,08±1610,01*p<0,05 RA patients treated with biologics vs controls; #p<0,05 RA patients treated with biologics vs RA patients non-treated with biologics;+p<0,05 RA patients non-treated with biologics vs controls.ResultsRA 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).ConclusionsRA 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 InterestNone declared
BackgroundRheumatoid arthritis (RA) patients suffer from joint pain and decreased physical capacity, like muscle wasting and fatigue. Fatigue is a clinical manifestation reported by 40-80% of patients with RA and is regarded as an important feature of the disease. Aerobic exercise may be beneficial for treating this feature in RA patients, however the mechanisms involved are still unclear.ObjectivesTo evaluate the effect of aerobic exercise training on the endurance exercise performance in collagen-induced arthritis (CIA) mice.MethodsMale DBA1/J mice with CIA [1] were randomly divided into 3 groups: wildtype with exercise (WT-EXE, n=4), CIA exercised (CIA-EXE, n=5) and CIA non-exercised (CIA, n=4). Endurance exercise performance test (fatigue) was analyzed in all groups prior to booster injection and each 15 days after protocol started. Eighteen days after the disease induction (booster), WT and CIA-EXE were submitted to training on an inclined treadmill (θ=5°), 45 minutes a day, 5 days per week for 6 weeks at 60% of their own endurance exercise performance. Variables analyzed were disease score, hindpaw nociception, body weight (g), fatigue (by endurance exercise performance in min) and relative muscle weight (muscle weight in mg divided by total animal weight in g). Data was analyzed with ANOVA Two-Way followed by Bonferroni and independent sample t-test and p<0.05 was considered significant. All data are represented as Mean ± SEM.ResultsBody weight was significantly higher in WT-EXE compared with CIA after 4 and 6 weeks of exercise. At week 6 of exercise, CIA-EXE had higher body weight than CIA. Fatigue test at 4 and 6 weeks of experiment was significantly different among all experimental groups; WT-EXE and CIA had, respectively, the highest and the lowest fatigue velocity. Gastrocnemius muscle weight was significantly heavier in control group than in CIA-EXE and CIA. Nociception and clinical score of arthritis did not differ between CIA-EXE and CIA.ConclusionsInclined aerobic exercise appears as an interesting intervention in RA to treat decreased physical capacity. Collagen-induced arthritis animals demonstrated decreased endurance, and consequently increased fatigue, characteristics of a good animal model to study fatigue. The exercise protocol used in this study was able to improve this feature, demonstrating that interventions used to treat physical disabilities in RA are also valid in this model. Further studies are necessary to clarify the mechanisms behind fatigue, especially when combining exercise training and common treatments of RA.ReferencesRosloniec EF, et al. Curr Protoc Immunol 2010; Chapter 15: Unit 15.5.1-25.AcknowledgementsFinancial support: CAPES, CNPq, FAPERGS, FIPE-HCPA.Disclosure of InterestNone declared
BackgroundRheumatoid arthritis is an autoimmune disease of unknown etiology associated with progressive disability, systemic complications like fatigue and muscle weakness, early death, and socioeconomic costs [1,2]. Nitric oxide (NO) have been related with inflammation and its regulation can lead to anti-inflammatory and anti-arthritic effects in CIA as well as induce muscle repair in muscle injury [3,4]. The role of NO in CIA muscle loss has not yet been studied.ObjectivesHow NO synthase inhibitor (NG-nitroL-arginie methy ester: L-NAME) and the NO donor (3-morpholinosydnonimine: SIN-1) affects CIA muscle loss?MethodsFemale Wistar rats with CIA [5] were separated in four groups: CIA (saline, n=10); L-NAME (30mg kg-1 n=10); and SIN-1 (0.3 mg kg-1, n=13), treated twice a day for 10 days after the onset of the disease, and a wildtype group (WT, n=8). Clinical score (arbitrary units – au), hind paw edema (mm), spontaneous locomotion (cm), and body weight (g) were analyzed. Ankle was collected and used for histological confirmation of the disease. Tibialis anterior (TA), gastrocnemious and soleus muscles were weighted (g). TA was used for histological analysis and immune stained for TNF-alfa, TGF-beta and IL-1beta. Serum was collected for albumin (g dL-1), total iron (μg dL-1) and ionized calcium (mg dL-1) analysis. Proper statistics were performed and p<.05 was set for critical limit. Data are in Mean ± SEM.ResultsAnkle histology confirmed that all CIA groups developed arthritis. In vivo analysis of hindpaw edema, clinical score, body and muscle weight, and spontaneous locomotion showed no difference among CIA groups. On the other hand, both L-NAME (48±6,5) and SIN-1 (48±6,5) groups have shown statistically decreased clinical score than saline (77±9,2) when analyzed by the area under curve. Muscle cross sectional area were higher in L-NAME (1074±315 μm) and SIN-1 (1115±303 μm) than saline (786±243 μm), however it did not reach WT diameter (1755±278 μm). Blood vessels diameter were smaller in L-NAME (287±121 μm) group compared to SIN-1 (524±169 μm) and saline (445±165 μm). Albumin was lower in all CIA groups (saline 3,8±0,2; L-NAME 3,9±0,1; SIN-1 3,7±0,1; WT 4,2±0,1), and ionized calcium had no difference among all groups. Iron was decreased in L-NAME (229±42) and SIN-1 (226±62) than WT (353±53). All CIA groups had shown increased immune cells infiltration shown by TNF-alfa, TGF-beta and IL-1beta immune staining.ConclusionsThe data above mentioned suggests that nitric oxide regulator drugs show good prospects as intervention for muscle loss. As was observed, even a simply drug that have main influence in vessel pressure shows preventive clinical score development and ameliorates muscle cross sectional area. The mechanism behind such findings will soon be depicted by molecular analysis.ReferencesMcInnes IB, Schett G. NEJM 2011;365(23):2205-19.Alver A, et al. Clinical Biochemistry 2011;44(17-18):1385-9.Gomaa A, et al. BJP 2009;158(7):1835-47.Filippin LI, et al. Nitric Oxide 2009;21(3-4):157-63.Rosloniec EF, et al. Curr ...
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