MH: none. individuals with early RA, and to investigate their associations with disease activity, treatment response, ultrasound findings and radiographic damage. Methods Disease-modifying antirheumatic drug (DMARD)-na?ve individuals with early Methylproamine RA, classified according to the 2010 American College of Rheumatology (ACR)/Western Little league Against Rheumatism (EULAR) criteria, were included in the ARCTIC trial and assessed in the present analysis. During follow up, individuals were monitored regularly and treatment was modified relating to a predetermined protocol, starting with methotrexate monotherapy with prednisolone bridging. Analysis of 16 different ACPA reactivities focusing on citrullinated peptides from fibrinogen, alpha-1 enolase, vimentin, filaggrin and histone was performed using a multiplex chip-based assay. Samples from 0, 3, 12 and 24?weeks were analysed. Settings were blood donors with related characteristics to the individuals (age, gender, smoking status). Results A total of 217 individuals and 94 settings were included. Median [25, 75 percentile] quantity of ACPA reactivities in all individuals was 9 [4, 12], and were most common in anti-cyclic citrullinated peptide /rheumatoid factor-positive individuals 10 [7, 12]. Methylproamine Disease activity actions and ultrasound scores at baseline were reduced ACPA reactivity-positive compared to ACPA reactivity-negative individuals. ACPA reactivity levels decreased after 3?weeks of DMARD treatment, most pronounced for fibrinogen 60C74 to 62% of baseline antibody level, with least switch in filaggrin 307C324 to 81% of baseline antibody level, both test and Mann-Whitney U test, as appropriate. Correlation between anti-CCP/ACPA reactivity levels and quantity of ACPA reactivities and disease activity actions, ultrasound and radiography scores were assessed using Spearmans rank correlation coefficient. Spearmans correlation was classified as very fragile, weak, moderate, strong or very strong [41]. Association between quantity of ACPA reactivities and treatment response was evaluated using the Mann-Whitney U test. Association between anti-CCP/ACPA reactivity status and continuous variables was evaluated from the Mann-Whitney U test, and association with categorical variables was assessed from the chi-square test. ACPA reactivity median levels at baseline and follow-up appointments were compared by paired samples using the Wilcox test, comparing each time point with the baseline level. A value <0.05 was considered statistically significant. Statistical analyses were performed using Stata Statistical Software, version 14 (StataCorp LLC, TX, USA) and R Statistical Software, version 3.4.0 (copyright 2017, The R Foundation for Statistical Computing). Results Patient characteristics A total of 217 individuals and 94 healthy settings were included in the study. Baseline characteristics relating to autoantibody subgroups are provided in Table?1. Presence of ACPA reactivities was seen mainly in individuals positive for anti-CCP and RF (Table?1), but ACPA reactivities also occurred more frequently Methylproamine in anti-CCP/RF negative individuals than in settings (0 (0, 1) vs. 0 (0, 0), (%)?Fib 60-74cit162 (75)160 (90)2 (5)136 (88)26 (41)134 (91)0 (0)0 (0)?Vim 60-75cit159 (73)152 (85)7 (18)130 (84)29 (46)128 Rabbit Polyclonal to LRP11 (87)5 (16)5 (5)?H4 31-50cit145 (67)142 (80)3 (8)119 (77)26 (41)118 (80)2 (6)1 (1)?CEP-1140 (65)137 (77)3 (8)117 (76)23 (37)115 (78)1 (3)1 (1)?Fil 307-324cit136 (63)134 (75)2 (5)113 (73)23 (37)112 (76)1 (3)0 (0)?Fib 573cit123 (57)121 (68)2 (5)99 (64)24 (38)99 (67)2 (6)0 (0)?Fib 36-52cit117 (54)116 (65)1 (3)96 (62)21 (33)96 (65)1 (3)2 (2)?H3 1-30cit107 (49)106 (60)1 (3)93 (60)14 (22)92 (63)0 (0)0 (0)?H4 14-34cit105 (48)103 (58)2 (5)90 (58)15 (24)88 (60)0 (0)3 (3)?H3 21-44cit96 (44)94 (53)2 (5)80 (52)16 (25)79 (54)1 (3)1 (1)?Fib 621-635cit93 (43)92 (52)1 (3)78 (51)15 (24)77 (52)0 (0)1 (1)?Vim 2-17cit88 (41)87 (49)1 (3)80 (52)8 (13)79 (54)0 (0)0 (0)?Fib 36-50cit79 (36)79 (44)0 (0)67 (44)12 (19)67 (46)0 (0)0 (0)?Fib 591cit69 (32)66 (37)3 (8)56 (36)13 (21)55 (37)2 (6)1 (1)?Fib 74cit66 (30)60 (34)6 (15)54 (35)12 (19)51 (35)3 (9)3 (3)?Fib 72cit27 (12)24 (13)3 (8)21 (14)6 (1)20 (14)2 (6)2 (2) Open in a separate window rheumatoid arthritis; anti-cyclic citrullinated peptide, rheumatoid element, Disease Activity Score, vehicle der Heijde revised Sharp score, joint space narrowing, anti-citrullinated protein antibody, fibrinogen, citrullinated, vimentin, histone, citrullinated enolase peptide-1, filaggrin; figures referring to amino acid sequence, not relevant aMean (SD) bNumber (percentage) cMedian [25, 75 percentile] Open in a separate windowpane Fig. 1 Quantity of anti-citrullinated protein antibody (ACPA) reactivities relating to autoantibody status. a All individuals with rheumatoid arthritis.