Breast cancer survivors in this study encountered some problems in returning to work, mainly linked to the sequelae of their disease and its treatment rather than to discrimination by employers or colleagues.
Background The spondyloarthritis (SpA) patients treated under TNF inhibitors (TNFi) with detectable antidrug antibodies (ADA) often develop loss of efficacy. Concomitant therapy with methotrexate (MTX) appears to reduce the the immunogenicity of biological drugs. Objectives To analyze if the use of combined therapy with MTX and TNFi can reduce the incidence of ADA and whether its effect is MTX dose dependent in SpA patients. Methods In this retrospective observational study, 162 SpA patients (including ankylosing spondylitis, Psoriatic SpA, SpA associated with inflammatory bowel disease and undifferentiated SpA) were included. The patients are treated with infliximab (Ifx) or adalimumab (Ada). The presence of ADA were measured at baseline and before each administration by ELISA to complete a follow up of 3 years. The patients were divided in two groups [MTX-15 (dose <15 mg/week) and MTX+15 (≥15 mg/week)] to study the influence of baseline MTX dose on immunogenicity. The statistical analysis was performed using SPSS 11.0. Results Eighty nine out of 162 (54,9%) patients were male. Eighty five out of 162 (52,5%) patients received Ifx and 77 out of 162 (47,5%) Ada. The mean duration of treatment was 13.38±9.19 years to Ifx and 12.71±10.46 years for Ada. Forty five patients received MTX weekly at baseline [25/85 (29.4%)in Ifx and 20/77 (26%)in Ada]. The mean dose of MTX was 15,9±4.76 mg/week. Twenty nine out of 162 (17,9%) patients developed ADA, and ADA presence was significantly higher in SpA patients on Ifx therapy [21/85 (24.7%) in Ifx vs 8/77 (10.4%) in Ada, p=0.018)]. The presence of ADA was less frequent in SpA patients taking MTX [3/162 (1.8%) with MTX vs 26/162 (16%) without MTX, p=0.021]. No statistically differences were observed in the influence of baseline MTX dose on the ADA appearance (in Ifx: 2/18 (11,1%) in MTX+15 vs 1/9 (11,1%)in MTX-15, p=1,0; in Ada: 1/17 (5,9%) in MTX+15 vs 0/4 (0,0%)in MTX-15, p=1,0). Conclusions In this cohort of SpA patients treated with Ifx and Ada, the use of MTX has a preventive effect on the ADA development. However, the baseline MTX dose is not a determinant factor to get this effect. Further prospective studies are needed to confirm these data. Disclosure of Interest A. Villalba Yllan: None declared, C. Plasencia Grant/research support: Pfizer, D. Pascual-Salcedo Grant/research support: Pfizer, Speakers bureau: Pfizer, D. Peiteado: None declared, L. Nuño: None declared, G. Bonilla: None declared, R. del Moral: None declared, A. Balsa Grant/research support: Pfizer, Speakers bureau: Pfizer, Roche, Abbvie, E. Martin Mola Speakers bureau: Pfizer, Roche, Abbvie, Amgen DOI 10.1136/annrheumdis-2014-eular.5819
BackgroundTocilizumab (TCZ), a humanized anti-IL-6 receptor antibody, represents a new treatment strategy for RA patients.Several studies have demonstrated the association between high serum levels of TNF-inhibitors and a good clinical response in patients with RA. Little evidence exists on this relationship for other biological therapies.ObjectivesTo evaluate the association between TCZ serum through levels and disease activity in a cohort of RA patients after one year of treatment with TCZ.Methods34 RA patients treated with Tocilizumab were included. Clinical activity was assessed using the Disease Activity Score 28 (DAS28-ESR) and the Clinical and Simplified Activity Index (CDAI and SDAI), serological improvement by C-Reactive Protein- CRP- and Erythrocyte Sedimentation Rate-ESR, clinical improvement by the delta-DAS 28 and response to treatment using EULAR criteria at baseline and after one year of treatment. We stratified all patients into quartiles according to the tocilizumab levels (μg/ml) as follows: IQR1: <3,4, IQR2: 3,4–11,2, IQR3: 11,2–18,5 and IQR4 >18.5. A last observation carried forward analysis (LOCF) was performed at the first year of treatment, so patients that dropped out of the therapy before this period were included. Blood samples were collected just before intravenous (i.v) infusion. Serum drug levels were determined by a capture enzymelinked immunosorbent assay (ELISA).ResultsThe baseline demographic and clinical characteristics are shown in Table 1. When patients were categorised into quartiles, IQR1 comprised 8 (24,2%) patients; IQR2, 7 (21,2%); IQR3, 8 (24,2%) and IQR4, 10 (30,3%). Clinical activity (DAS28, CDAI and SDAI) was statistically significant higher in patients with lower serum through levels at the first year [DAS28 (IQR1: 4,46 ±1,5, IQR2: 2,58 ± 0,87, IQR 3: 3,6± 0,79; IQR4: 2,17 ± 0,74; p=0,001), CDAI (IQR1: 23±13,9, IQR2: 7,72 ± 4,44, QIR 3: 13,38± 4,35, IQR4: 6,33 ± 4,62; p=0,003) and SDAI (IQR1: 19,46 ±15,5, IQR2: 9,51± 7,4, IQR3: 12,59 ± 6,31, IQR4: 4,55 ± 3,73; p=0,005)] and also was the number of swollen joints (IQR1: 7,5 ± 6,6, IQR2: 2,29 ±2,06, IQR3: 5,63 ± 4,3, IQR4: 1,1 ± 1,6, p=0,013) and tender joints (IQR1: 5,5 ± 5,7, IQR2: 1,71 ± 2,06, IQR3: 3,13 ± 2,8, IQR4: 0,8 ± 0,9, p=0,014). In addition, the EULAR reponse was worse in those patients with lower serum drug levels [non-responders: 4 (66,7%) in IQR1 vs 1 (16,7%) in IQR2 vs 1 (16,7%) in IQ3 vs 0 (0%) in IQR4, moderate responders: 3 (37,5%) in IQR1 vs 0 (0%) in IQR2 vs 4 (50%) in IQR3 vs 1 (12,5%) in IQR4 and good responders: 1 (5,3%) in IQR1 vs 6 (31,6%) in IQR2 vs 3 (37,5%) in IQR3 vs 9 (47,4%) in IQR4, p=0,006]. In terms of acute-phase reactants, the mean ESR tended to be higher in patients with lower TCZ levels (IQR1: 22,6±14,8 vs IQR2: 5,6±1,6 vs IQR 3: 9,4 ±3,5 vs IQR4: 6,4 ± 3,5, p=0,005), and also CRP levels (RIQ1: 10,2±17,4 vs RIQ2: 2,3 ± 3,4 vs RIQ3 0,56 ± 0,4 vs RIQ 4: 0,42 ± 0,66, p=NS)].ConclusionsThe presence of low serum Tocilizumab levels correlates with a worse clinical disease activity. Consequ...
BackgroundDespite the fact that genetic and serological risk factors have been studied in rheumatoid arthritis (RA), the symptoms phase of preclinical RA is poorly characterised. Taking into account the importance of early diagnosis and effective treatment for the prevention of structural damage and long-term disability in RA, it is important to find clinical or image variables that identify patients with clinically suspected arthralgias at risk of developing a chronic arthritis (CSA).ObjectivesTo identify baseline clinical, immunological and ultrasound variables in patients with arthralgias clinically suspected of progression to chronic arthritis.MethodsLongitudinal prospective study of patients with CSA and follow-up from November 2015 in pre-arthritis clinics. Patients were assessed at baseline and every 6 months until 2 years, with clinical, laboratory and ultrasound data using standardised protocols. The criteria for eligible patients for inclusion in the study were:≤12 months of symptoms onset, inflammatory arthralgias (predominance in nights or mornings, improvement during the day or with movement, and morning stiffness of ≥30 min), and the involvement of small joints of hands or feet. Patients with clinical synovitis at baseline visit, patients with fibromyalgia or osteoarthritis were excluded.ResultsTwenty-six patients were recruited in 26 months of the study (1 male, 25 female), with an average baseline age of 44.7±12.6 years, an average delay time of symptoms to first visit of 8.7±3.3 months, a mean follow-up time of 7.7±8.1 months an average body mass index (BMI) of 27.7±7.2. Five patients had familial background of autoimmune diseases in first degree relatives (RA, psoriasis, inflammatory bowel disease), 6 (23.1%) were seropositive (RF and/or ACPA), 7 (26.9%) had increased baseline acute-phase reactants (PAR), and 11 (47.8%) were smokers or former smokers. Most of the patients reported a progression of the arthralgias (55%) and a subjective joint swelling at some point (70%). Of 24 patients, 8 (33.3%) developed clinical arthritis (7 RA, 1 undifferentiated arthritis), with a longer follow-up (15.7±7.4 vs. 7.5±7.2 months, p=0.016), greater baseline HAQ (11.8±8.3 vs. 3.9±4.8, p=0.033) and higher percentage of moderate inflammatory activity in the baseline ultrasound (83.3% vs. 8.3%, p=0.004), compared to patients that didn’t develop arthritis. There was a trend towards a higher seropositivity, (37.7% vs. 18.8%), a higher patient global disease assessment (45±29 vs. 30±27 on a 100 mm scale), higher patient pain scores (using a visual analogue pain 100 mm scale) (58±41 vs. 34±23) among patients who eventually developed arthritis, although not statistically significant. No differences were found with PAR, BMI, age, smoking habit or painful joint count at baseline visit.ConclusionsIn our pre-arthritis clinics of patients with clinically suspicious arthralgias, 33% progressed to arthritis, underlying the importance of these clinics. Functional disability and ultrasound at baseline visit are especially useful ...
Background There is wide scientific evidence about the involvement of smoking in the susceptibility to rheumatoid arthritis. However, the effect of smoking on the activity of the disease and its clinical course is controversial. Objectives To analyze the impact of smoking on disease activity in a cohort of patients with recent onset rheumatoid arthritis. Methods We included a cohort of patients from an Early Arthritis Clinic (EAC), followed up between January 1993 and December 2012. All patients gave informed consent to the study. Patients were included with early arthritis (less than one year of disease duration to the onset), who met the criteria of the American College of Rheumatology (ACR) 1987 for RA at some time during the disease course, and were followed up for two years. Microcrystalline and infectious arthritis were excluded, as well as patients who previously had been treated with disease modifying antirheumatic drugs. Patients were monitored for clinical and analytical data using standardized protocols every six months. The influence of active smoking in disease activity, functional disability and serological variables were studied. Every six months we assessed: number of tender (out of 68) joints (NTJ), number of swollen (out of 68) joints (NSJ), DAS, change in DAS (ΔDAS), HAQ, erythrocyte sedimentation rate (ESR), rheumatoid factor (RF) and anti-citrullinated protein antibodies (ACPA). Results 398 patients were included in the study, with a mean age at onset of 51.8 years (± 16.1 SD) and a predominance of women (77.6%). Patients were referred to the EAC with a mean of 17.7 weeks (± 13.1 SD) from the onset of symptoms. Active smokers were 27.6% of the patients. At baseline most patients had a subacute (88.7%), symmetrical (88.9%), RF-positive (81.3%), ACCP-positive (67, 5%) polyarthritis (83.1%). Smokers were younger at disease onset (49 ± 13.4 years smokers vs. 52.9 ± 13.4 in nonsmokers, p = 0.022), with a predominance of males (43% males vs. 23% women, p <0.001), positive RF (30.5% vs. RF positive. 13.4% RF negative, P = 0.005) and positive ACPA (35.2% ACPA-positive vs. 16.2% ACPA-negative; p <0.001). No significant differences in relation to smoking were found in terms of extension, course, symmetry, NTJ, NSJ, DAS, HAQ and ESR at months 0, 6, 12, 18 or 24. However, improvement in disease activity in active smokers was lower at 12 months (ΔDAS 1.29 ± 0.99 in smokers vs. 1.66 ± 1.30 in nonsmokers, p = 0.032) and at 24 months (ΔDAS 1.28 ± 1.20 in smokers vs. 1.9 ± 1.22 in non-smokers, p = 0.004). Conclusions Active smoking has a negative impact on the activity of patients with recent onset rheumatoid arthritis, with less improvement as compared to non-smokers. Disclosure of Interest None Declared
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