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The objective of this study was to assess the SARS‐CoV‐2–specific humoral and T cell response after a two‐dose regimen of SARS‐CoV‐2 vaccine in patients with rheumatoid arthritis (RA). In this observational study, patients with RA who are ≥18 years of age and vaccinated for SARS‐CoV‐2 according to the Argentine National Health Ministry's vaccination strategy were included. Anti–SARS‐CoV‐2 immunoglobulin G (IgG) antibodies (ELISA‐COVIDAR test), neutralizing activity (cytotoxicity in VERO cells), and specific T cell response (IFN‐γ ELISpot Assay) were assessed after the first and second dose. A total of 120 patients with RA were included. Mostly, homologous regimens were used, including Gam‐COVID‐Vac (27.5%), ChAdOx1 (24.2%), and BBIBP‐CorV (22.5%). The most frequent combination was Gam‐COVID‐Vac/mRNA‐1273 (21.7%). After the second dose, 81.7% presented with anti–SARS‐CoV‐2 antibodies, 70.0% presented with neutralizing activity, and 65.3% presented with specific T cell response. The use of BBIBP‐CorV and treatment with abatacept (ABA) and rituximab (RTX) were associated with undetectable antibodies and no neutralizing activity after two doses. BBIBP‐CorV was also associated with the absence of T cell response. The total incidence of adverse events was 357.1 events per 1,000 doses, significantly lower with BBIBP‐CorV (166.7 events per 1,000 doses, P< 0.02). In this RA cohort vaccinated with homologous and heterologous regimens against COVID‐19, 2 out of 10 patients did not develop anti‐SARS‐CoV‐2 IgG, 70% presented with neutralizing activity, and 65% presented with specific T cell response. The use of BBIBP‐CorV was associated with deficient humoral and cellular response, whereas treatment with ABA and RTX resulted in an impaired anti‐SARS‐CoV‐2 IgG formation and neutralizing activity.

ObjectivePsoriatic arthritis (PsA) is chronic disease that compromises multiple domains and might be associated with progressive joint damage, increased mortality, functional limitation, and considerably impaired quality of life. Our objective was to generate evidence-based recommendations on the management of PsA in Pan American League of Associations for Rheumatology (PANLAR) countries.MethodsWe used the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE)-ADOLOPMENT approach to adapt the 2019 recommendations of the European Alliance of Associations for Rheumatology. A working group consisting of rheumatologists from various countries in Latin America identified relevant topics for the treatment of PsA in the region. The methodology team updated the evidence and synthesized the information used to generate the final recommendations. These were then discussed and defined by a panel of 31 rheumatologists from 15 countries.ResultsTheses guidelines report 15 recommendations addressing therapeutic targets, use of antiinflammatory agents and corticosteroids, treatment with disease-modifying antirheumatic drugs (conventional synthetic, biologic, and targeted synthetic), therapeutic failure, optimization of biologic therapy, nonpharmacological interventions, assessment tools, and follow-up of patients with PsA.ConclusionHere we present a set of recommendations to guide decision making in the treatment of PsA in Latin America, based on the best evidence available, considering resources, medical expertise, and the patient’s values and preferences. The successful implementation of these recommendations should be based on clinical practice conditions, healthcare settings in each country, and a tailored evaluation of patients.

To study quality of sleep in patients with psoriatic arthritis (PsA) and to investigate the association of sleep disturbances with other variables.

ToPAS-2 is a questionnaire designed to detect cases of psoriatic arthritis (PsA) in patients with psoriasis (PsO).

To study quality of sleep in patients with psoriatic arthritis (PsA) and to investigate the association of sleep disturbances with other variables.

ToPAS-2 is a questionnaire designed to detect cases of psoriatic arthritis (PsA) in patients with psoriasis (PsO).

Patients with rheumatoid arthritis (RA) experience inflamed and damaged joints. RA is an autoimmune disease in which proteins called autoantibodies, particularly anti-citrullinated protein autoantibodies, target the patient’s own joint tissue and organs by mistake, leading to symptomatic inflammation. Successful treatment can decrease the disease’s activity to a state known as remission. Patients in remission may experience little or no symptoms and it may be possible for some to then be able to decrease their treatment. Here, we report the results of a large, international study that looked at two treatments, abatacept and methotrexate, in patients with RA and anti-citrullinated protein autoantibodies. The study had two parts. Firstly, to see how many patients had success (remission) with weekly abatacept and/or methotrexate treatment, and secondly, to see if remission was maintained when treatment was either continued or decreased and stopped. The study showed that the number of patients in remission 6 months after treatment started was not greatly different between patients treated with both abatacept and methotrexate and those treated with just methotrexate. Those taking abatacept and methotrexate together had better remission rates 1 year later. More patients also stayed in remission when they continued to receive both abatacept and methotrexate compared with those who were just treated with abatacept or when their abatacept treatment was decreased and stopped. More patients stayed in remission when abatacept was decreased than when it was stopped. The results from this study may help determine possible future treatment reduction and/or withdrawal plans for some patients with RA.

Tofacitinib is a medicine used to treat rheumatoid arthritis (swollen and painful joints). A total of 4400 patients with moderate or severe rheumatoid arthritis who were taking part in tofacitinib clinical trials completed a survey about their general health and well-being at that time. We used their answers to determine whether they were likely to have depression or anxiety. We then looked at how common depression or anxiety was in patients with rheumatoid arthritis, and whether having depression or anxiety affected how patients responded to tofacitinib treatment. It is important to note that tofacitinib is not approved for the treatment of depression or anxiety, and these clinical trials were not designed to assess whether tofacitinib improved depression or anxiety symptoms. About 40% of patients likely had depression or anxiety when they started a clinical trial. This percentage decreased among patients who received tofacitinib treatment over a year. Patients treated with tofacitinib showed more improvement in their depression or anxiety than those treated with placebo. Over a year of treatment, tofacitinib improved signs and symptoms of rheumatoid arthritis, for example, the number of swollen or painful joints and fatigue. Having depression or anxiety did not change the way that patients responded to tofacitinib. This research shows how treating rheumatoid arthritis symptoms may also improve depression and anxiety symptoms. However, specially designed studies are needed to confirm this.

Rheumatoid arthritis (RA) is a disease that causes inflammation of the joints. Doctors have several ways of assessing how bad a patient’s disease is, and these often use a combination of signs and symptoms to develop a ‘score’. One method is called RAPID3, which is a score based on an overall assessment of the disease by the patient, the level of pain, and the amount of physical disability. An advantage of RAPID3 is that it is quick and easy to use, and since it uses only patient-reported symptoms, it can be measured easily via telemedicine, without the need for an in-person consultation. In this study, we decided to look into the effect of upadacitinib, a drug used for the treatment of RA, on RAPID3 score in patients with RA. We also investigated whether RAPID3 correlates with other ways of measuring RA severity, including scores that use physician-measured factors such as number of affected joints, as this can help show whether RAPID3 is a valid and useful tool. We found that upadacitinib led to long-term improvements in RAPID3 score, and that results were the same in different studies and patient groups, including patients who had not responded well to other treatments. We also found that RAPID3 correlated well with other measures, i.e., improvements in RAPID3 happened in parallel with improvements in other scores. Overall, these results suggest that RAPID3 can be a useful tool in patients with RA.

ObjectiveTo compare the Simplified Ankylosing Spondylitis Disease Activity Score (SASDAS) against the Ankylosing Spondylitis Disease Activity Score (ASDAS) for measuring and categorizing disease activity using data from the EMBARK trial (ClinicalTrials.gov: NCT01258738), a randomized controlled trial of etanercept (ETN) for axial spondyloarthritis (axSpA).MethodsPatients with early active axSpA received ETN 50 mg once weekly (n = 106) or placebo (PBO; n = 109) for 12 weeks in a double-blind manner; they then received open-label ETN for 92 weeks. For this analysis, ASDAS–C-reactive protein (CRP) and SASDAS-CRP were calculated at baseline, week 12, and week 24. The SASDAS was calculated by the linear addition of the ASDAS components without adjustment.ResultsA very strong correlation, as determined by the Spearman correlation coefficient, was observed between the ASDAS and SASDAS for continuous variables at baseline and during treatment. For pooled categorical data at baseline, the SASDAS placed 69.9% of patients in the same disease categories as the ASDAS but overestimated for 17.8% of patients and underestimated for 12.2% of patients. A similar pattern was seen postbaseline. Cohen weighted [Formula] statistics for all individual and pooled treatments and timepoints (0.54-0.73) reflected moderate to substantial agreement. The capacity to differentiate between treatments (ie, ETN and PBO/ETN) was higher with the ASDAS (effect size −0.74, 95% CI −1.03 to −0.46) compared with the SASDAS (effect size −0.51, 95% CI −0.79 to −0.23), but sensitivity to change was generally similar.ConclusionA very strong correlation between the SASDAS and ASDAS was observed when considering continuous variables; however, moderate to substantial agreement was observed for categorical data, and the SASDAS classified a lower proportion of patients as being in the inactive and low disease activity categories.

ObjectiveThe aim of this study was to assess the immune response after a third dose of SARS-CoV-2 vaccine in patients with rheumatoid arthritis (RA) with undetectable antibody titers after the primary regimen of 2 doses.MethodsPatients with RA with no seroconversion after 2 doses of SARS-CoV-2 vaccine and who received a third dose of either an mRNA or vector-based vaccine were included. Anti-SARS-CoV-2 IgG antibodies, neutralizing activity, and T cell responses were assessed after the third dose.ResultsA total of 21 nonresponder patients were included. At the time of vaccination, 29% were receiving glucocorticoids and 85% biologic disease-modifying antirheumatic drugs (including 6 taking abatacept [ABA] and 4 taking rituximab [RTX]). The majority (95%) received the BNT162b2 vaccine and only one of them received the ChAdOx1 nCoV-19 vaccine. After the third dose, 91% of the patients presented detectable anti-SARS-CoV-2 IgG and 76% showed neutralizing activity. Compared to other treatments, ABA and RTX were associated with the absence of neutralizing activity in 4 out of 5 (80%) patients and lower titers of neutralizing antibodies (median 3, IQR 0-20 vs 8, IQR 4-128; P= 0.20). Specific T cell response was detected in 41% of all patients after the second dose, increasing to 71% after the third dose. The use of ABA was associated with a lower frequency of T cell response (33% vs 87%, P= 0.03).ConclusionIn this RA cohort, 91% of patients who failed to seroconvert after 2 doses of SARS-CoV-2 vaccine presented detectable anti-SARS-CoV-2 IgG after a third dose. The use of ABA was associated with a lower frequency of specific T cell response.

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Background: In patients with rheumatoid arthritis (RA), qualitative alterations of low and high-density lipoproteins (LDL and HDL, respectively) might partially explain their increased cardiovascular risk. Tocilizumab has been associated with an increase in lipids, including triglyceride (TG) and cholesterol levels. The aim of this study is to evaluate the effect of tocilizumab on certain LDL and HDL characteristics (oxidized LDL levels, HDL-associated enzymes, chemical composition of both total HDL and HDL3c subpopulation, and their capacity to promote cellular cholesterol efflux) at baseline and 3 months after the start of treatment in patients with RA. Methods: Twenty-eight RA patients (ACR/EULAR 2010 criteria) with indication of treatment with tocilizumab were included in the present study. Clinical assessment [Health assessment questionnaire (HAQ)], disease activity score 28 (DAS28), high-sensitivity C reactive protein (hsCRP) concentration, lipid profile, and lipoprotein (a) [Lp(a)] levels were evaluated in all patients at baseline and after 3 months of treatment with tocilizumab. Lipoprotein characteristics were evaluated through the levels of oxidized LDL (OxLDL), the activity of paraoxonase (PON) 1, the composition of total HDL and small, dense HDL3c subpopulation, and their ability to promote cellular cholesterol efflux. Results: After 3 months of treatment with tocilizumab, HAQ (− 23%, p&lt; 0.05), DAS28 (− 49%, p&lt; 0.001), and hsCRP (− 94%, p&lt; 0.01) levels decreased significantly. Total cholesterol (TC), LDL-C, non-HDL-C, and apo B levels showed a significant increase after treatment (TC: + 7.0%, p&lt; 0.01; LDL-C: + 10%, p&lt; 0.01; non-HDL-C: + 9.9%, p&lt; 0.01; and apo B: + 9.6%, p&lt; 0.05). Decreases in Lp(a) and OxLDL levels were also observed after treatment [Lp(a): − 50%, p&lt; 0.01; and oxLDL: − 5.4%, p&lt; 0.05]. The latter was in accordance with the increment detected in PON activity. No changes were observed in HDL capacity to promote cholesterol efflux (p> 0.05) in the whole group. Conclusions: Treatment with tocilizumab reduced hsCRP levels and displayed positive effects on certain lipoprotein-related parameters, such as a potent decrease inLp(a) and a reduction in OxLDL levels. Moreover, HDL capacity to promote cellular cholesterol efflux was maintained after 3 months of treatment.

Objective.To evaluate longterm drug survival (proportion of patients still receiving treatment) and discontinuation of etanercept (ETN), infliximab (IFX), adalimumab (ADA), certolizumab pegol (CZP), and golimumab (GOL) using observational data from patients with rheumatoid arthritis (RA).Methods.Following a systematic literature review, drug survival at 12 and 12–24 months of followup was estimated by summing proportions of patients continuing treatment and dividing by number of studies. Drug survival at ≥ 36 months of followup was estimated through Metaprop.Results.There were 170 publications included. In the first-line setting, drug survival at 12 months with ETN, IFX, or ADA was 71%, 69%, and 70%, respectively, while at 12–24 months the corresponding rates were 63%, 57%, and 59%. In the second-line setting, drug survival at 12 months with ETN, IFX, or ADA was 61%, 69%, and 55%, respectively, while at 12–24 months the corresponding rates were 53%, 39%, and 43%. Drug survival at ≥ 36 months with ETN, IFX, or ADA in the first-line setting was 59% (95% CI 46–72%), 49% (95% CI 43–54%), and 51% (95% CI 41–60%), respectively, while in the second-line setting the corresponding rates were 56% (95% CI 52–61%), 48% (95% CI 40–55%), and 41% (95% CI 36–47%). Discontinuation of ETN, IFX, and ADA at 36 months of followup was 38–48%, 42–62%, and 38–59%, respectively. Data on CZP and GOL were scarce.Conclusion.After > 12 months of followup, more patients with RA receiving ETN remain on treatment compared with other tumor necrosis factor inhibitors.

Psoriatic arthritis (PsA) is a chronic, systemic inflammatory disease. This study assessed the cost-effectiveness of secukinumab, an interleukin-17A inhibitor, versus other biologics in PsA from the Argentinean social security perspective.

Background: AVERT-2 (a phase IIIb, two-stage study) evaluated abatacept + methotrexate versus methotrexate alone, in methotrexate-naive, anti-citrullinated protein antibody-positive patients with early (≤ 6 months), active RA. This subanalysis investigated whether individual patients who achieved the week 24 Simplified Disease Activity Index (SDAI) remission primary endpoint could sustain remission to 1 year and then maintain it following changes in therapy. Methods: During the 56-week induction period (IP), patients were randomized to weekly subcutaneous abatacept 125 mg + methotrexate or abatacept placebo + methotrexate. Patients completing the IP who achieved SDAI remission (≤ 3.3) at weeks 40 and 52 entered a 48-week de-escalation (DE) period. Patients treated with abatacept + methotrexate were re-randomized to continue weekly abatacept + methotrexate, or de-escalate and then withdraw abatacept (after 24 weeks), or receive abatacept monotherapy. Proportions of patients achieving sustained SDAI and Boolean remission, and Disease Activity Score in 28 joints using C-reactive protein (DAS28 [CRP]) &lt; 2.6, were assessed. For patients achieving early sustained SDAI remission at weeks 24/40/52, flow between disease activity categories and individual trajectories was evaluated; flow was also evaluated for later remitters (weeks 40/52 but not week 24). Results: Among patients treated with abatacept + methotrexate (n/N= 451/752) at IP week 24, 22% achieved SDAI remission, 17% achieved Boolean remission, and 42% achieved DAS28 (CRP) &lt; 2.6; of these, 56%, 58%, and 74%, respectively, sustained a response throughout IP weeks 40/52. Among patients with a sustained response at IP weeks 24/40/52, 82% (14/17) on weekly abatacept + methotrexate, 81% (13/16) on abatacept monotherapy, 63% (12/19) who de-escalated/withdrew abatacept, and 65% (11/17) on abatacept placebo + methotrexate were in SDAI remission at end of the DE period; rates were higher than for later remitters in all arms except abatacept placebo + methotrexate. Conclusions: A high proportion of individual patients achieving clinical endpoints at IP week 24 with abatacept + methotrexate sustained their responses through week 52. Of patients achieving early and sustained SDAI remission through 52 weeks, numerically more maintained remission during the DE period if weekly abatacept treatment continued. Trial registration: NCT02504268 (ClinicalTrials.gov), registered July 21, 2015.

To evaluate the long‐term clinical and imaging efficacy of etanercept in patients with early, active nonradiographic axial spondyloarthritis (SpA). Adult patients who satisfied the Assessment of SpondyloArthritis international Society (ASAS) classification criteria for axial SpA (but not the modified New York radiographic criteria), with symptom duration >3 months to <5 years, and who were unresponsive to ≥2 nonsteroidal antirheumatic drugs (NSAIDs) received double‐blind etanercept 50 mg/week or placebo for 12 weeks, followed by open‐label etanercept 50 mg/week to week 104. Clinical, magnetic resonance imaging (MRI; Spondyloarthritis Research Consortium of Canada [SPARCC] scores), and safety outcomes at 104 weeks were analyzed. Of 215 randomized patients (etanercept: n = 106; placebo: n = 109), 205 entered the study (etanercept/etanercept: n = 100; placebo/etanercept: n = 105) and 169 completed the open‐label period (etanercept/etanercept: n = 83; placebo/etanercept: n = 86). At week 104, 61 of 81 (75%), 49 of 81 (61%), 48 of 80 (60%), and 57 of 81 (70%) patients who received etanercept throughout the trial achieved ASAS20, ASAS40, Ankylosing Spondylitis Disease Activity Score (ASDAS) inactive disease, and Bath Ankylosing Spondylitis Disease Activity Index criteria for 50% improvement (BASDAI 50) scores, respectively (observed). From baseline to week 104, continued improvements in clinical outcomes (ASDAS–C‐reactive protein: −1.5 and −1.7; BASDAI: −3.3 and −3.8 [last observation carried forward]), and SPARCC MRI scores (sacroiliac joint: −6.0 and −3.4; spinal: −2.1 and −0.8 [observed]) were seen in patients receiving etanercept/etanercept and placebo/etanercept. During the study, 8% in the etanercept/etanercept group and 7% in the placebo/etanercept group had serious adverse events; no new safety signals were seen. Patients with early, active nonradiographic axial SpA and an inadequate response to at least 2 NSAIDs demonstrated improvement in clinical and imaging outcomes that were sustained through 104 weeks of etanercept treatment.

Objective.To define whether Amerindian genetic ancestry correlates with clinical and therapeutic variables in admixed individuals with rheumatoid arthritis (RA) from Latin America.Methods.Patients with RA (n = 1347) and healthy controls (n = 1012) from Argentina, Mexico, Chile, and Peru were included. Samples were genotyped for the Immunochip v1 using the Illumina platform. Clinical data were obtained through interviews or the clinical history.Results.Percentage of Amerindian ancestry was comparable between cases and controls. Morning stiffness (p < 0.0001, OR 0.05), rheumatoid factor (RF; p < 0.0001, OR 0.22), radiographic changes (p < 0.0001, OR 0.05), and higher number of criteria were associated with lower Amerindian ancestry after Bonferroni correction. Higher Amerindian ancestry correlated only with weight loss (pBonferroni< 0.0001, OR 2.85). Increased Amerindian ancestry correlated with higher doses of azathioprine (p < 0.0001, OR 163.6) and sulfasalazine (p < 0.0001, OR 48.6), and inversely with methotrexate (p = 0.001, OR 0.35), leflunomide (p = 0.001, OR 0.16), and nonsteroidal antiinflammatory drugs (pBonferroni= 0.001, OR 0.37). Only the presence of RF and weight loss were modified after confounders adjustment.Conclusion.Amerindian ancestry protects against most major clinical criteria of RA, but regarding the association of RF with increased European ancestry, age, sex, and smoking are modifiers. Ancestry also correlates with the therapeutic profiles.

OBJECTIVE: To describe differential characteristics of axial involvement in ankylosing spondylitis (AS) as compared with that seen in psoriatic arthritis (PsA) and inflammatory bowel disease (IBD) in a cohort of Ibero-American patients. METHODS: This study included 2044 consecutive patients with spondyloarthritis (SpA; ESSG criteria). Demographic, clinical, disease activity, functional ability, quality of life, work status, radiologic, and therapeutic data were evaluated and collected by RESPONDIA members from different Ibero-American countries between June and December 2006. Patients selected for analysis met modified New York criteria (mNY) for AS. RESULTS: A total of 1264 patients met the New York criteria for AS: 1072 had primary AS, 147 had psoriatic, and 45 had IBD-associated spondylitis. Median disease duration was comparable among the 3 patient groups. Patients with primary AS were significantly younger (p = 0.01) and presented a higher frequency of males (p = 0.01) than the other 2 groups. Axial manifestations such as inflammatory back pain and sacroiliac pain were significantly more frequent in patients with primary AS (p = 0.05) versus other groups, whereas frequency of dactylitis, enthesitis, and peripheral arthritis was more common in patients with psoriatic spondylitis (p = 0.05). Spinal mobility was significantly more limited in patients with primary AS versus the other 2 groups (p = 0.0001). Radiologic changes according to BASRI total score were equally significant in primary AS. Disease activity (BASDAI), functional ability (BASFI), and quality of life (ASQoL) scores were comparable in the 3 groups. CONCLUSION: Patients with primary AS had more severe axial involvement than those with spondylitis associated with psoriasis or IBD. Functional capacity, disease activity, and quality of life were comparable among the groups studied.

The objective of this study was to assess the prevalence of rheumatoid arthritis (RA) in the population of a city of 70,000 inhabitants located in Buenos Aires, Argentina.

Analyze disability determinants in a cohort of Argentine patients with rheumatoid arthritis (RA).

To evaluate work status and its determinants among ankylosing spondylitis (AS) patients in our country.

Audiovestibular disorders have been described in several autoimmune diseases but have not been studied in patients with ankylosing spondylitis (AS). The aim of this study was to evaluate the audiovestibular function in patients with AS.

Osteoarthritis (OA) of the knee is a common cause of chronic disability in patients with quadriceps muscle weakness. Beneficial effects have been proposed for functional electrostimulation (FES) and exercise at the muscle level.

The Health Assessment Questionnaire (HAQ) is one of the most frequently used instruments to assess functional capacity in activities of daily living.

The presence of eosinophilia in peripheral blood has been considered by some authors as an indicator of bad prognosis in patients with rheumatoid arthritis (RA); however, the methodology and the number of patients included in those studies were not appropriate.

OBJECTIVE :Proteasomes are targets of humoral autoimmune response in patients with connective tissue diseases and other organ-specific autoimmune diseases. The finding of circulating proteasomes in psoriasis, the multiplicity of mechanisms regulated by proteasomes that are also implicated in the pathogenesis of psoriatic arthritis (PsA), and the increasing evidence linking PsA and autoimmunity led us to evaluate whether the 20S proteasome represents an antibody target in PsA. METHODS: Serum samples from 36 patients with PsA and 30 age- and sex-matched healthy subjects were tested for the presence of anti-20S proteasome antibodies (anti-20S antibody). Additional controls included 24 patients with systemic lupus erythematosus (SLE) and 20 with rheumatoid arthritis (RA). The associations of anti-20S antibodies with clinical, laboratory, and therapeutic measures were evaluated. RESULTS: 27.8% of the PsA patients were positive for anti-20S antibody compared to 41.6% of the SLE group and 5% of the RA group. None of the healthy subjects were seropositive for anti-20S antibody. In PsA, anti-20S seropositivity was not associated with the presence of other autoantibodies or with a particular subgroup of articular involvement. CONCLUSION: Immunoreactivity against proteasomes occurs frequently in patients with PsA. This finding supports the concept of PsA as an autoimmune disease and opens new avenues for investigating its pathogenesis.