Psoriatic arthritis is a chronic systemic inflammatory disease that presents with a variable clinical course and is typically associated with joint inflammation, together with cutaneous psoriasis. In recent decades, knowledge of the pathogenesis of psoriatic arthritis has advanced considerably and has allowed for development of new highly effective therapies, transforming the treatment landscape. Upadacitinib is a Janus kinase inhibitor (JAK) that is orally reversible with high selectivity for JAK1 and its signal transduction molecules. The results obtained in the phase III clinical trials (SELECT-PsA 1 and SELEC-PsA 2) demonstrated that upadacitinib was highly effective over placebo and non-inferior to adalimumab in several important domains of the disease. Improvements were observed in dactylitis, enthesitis and spondylitis as well as in physical function, pain, fatigue and overall quality of life. The safety profile of these results resembled that of adalimumab, apart from a slightly higher rate of herpes zoster infection, an increase of creatine kinase and an incidence of lymphopenia. However, none of these events was considered a serious adverse advent. Additionally, another analysis demonstrated that combining upadacitinib with methotrexate was associated with a similar efficacy to upadacitinib in monotherapy, both for patients that are naive to biologics treatment and for those previously treated with biologics. Therefore, upadacitinib is a new option for the treatment of psoriatic arthritis, presenting a series of beneficial characteristics. At this stage, it is important to collect long-term data to confirm the efficacy and safety profiles shown in clinical trials.
Background:Systemic Sclerosis (SSc) is a chronic disease with multi-organ manifestations that may contribute to disability and low quality of life.1 Therefore, anxiety and depression are more frequent in SSc patients than in general population.2Objectives:To assess the prevalence of anxiety and depression in a SSc cohort and to evaluate its correlation with function, quality of life and assessment of gastrointestinal (GI) involvement scores.Methods:A cross-sectional study was conducted evaluating a cohort of SSc patients. All patients answered to the Hospital Anxiety and Depression Scale (HADS) questionnaire. A cut-off score < 8 was considered normal. Health Assessment Questionnaire (HAQ), Scleroderma HAQ (SHAQ), 36-Item Short Form Health Survey (SF-36), EuroQol-5D (EQ-5D) and University Of California, Los Angeles, Scleroderma Clinical Trials Consortium Gastrointestinal Scale (UCLA SCTC GIT) 2.0 questionnaires were also obtained. Clinical data was obtained and analyzed.Results:We included 20 patients, 17 females [n = 17 (85%)], median (min, max) age was 52.5 (28, 75) years-old. Regarding disease classification, 13 (65%) had limited SSc, 4 (20%) had diffuse SSc and 3 (15%) had early SSc. A score ≥ 8 was found in 14 (70%) patients on HADS-A [median (min, max) = 9 (2, 19)] and in 12 (60%) patients on HADS-D [median (min, max) = 8 (1, 15)]. Depressive patients had significantly worst scores on the measures of function, such as HAQ and lung and gastrointestinal involvements and patient global assessment of SHAQ, of quality of life, such as EQ-5D and physical functioning, role physical, bodily pain, vitality, social functioning and mental health domains of SF-36, and on the UCLA SCTC GIT 2.0 scale. Anxious patients had significantly worst scores on social functioning and mental health domains of SF-36 and on the UCLA SCTC GIT 2.0 scale (Table 1).Conclusion:The prevalence of depression and anxiety on SSc patients is high and should not be neglected. Overall disability and multiorgan manifestations, particularly GI involvement, may contribute to a low quality of life and consequently to depression and anxiety.References:[1]Firestein & Kelley’s Textbook of Rheumatology 2-Volume Set, 11th Edition[2]Brett D. Thombs et al. Depression in Patients With Systemic Sclerosis: A Systematic Review of the Evidence. Arthritis & Rheumatism (Arthritis Care & Research) Vol. 57, 2007, pp 1089–1097Table 1.Function, quality of life and gastrointestinal (GI) involvement assessment according to HADS score.Results, median [min, max]HADS-D ≥ 8 (n = 12)HADS-D < 8 (n = 8)P-valueHADS-A ≥ 8 (n = 14)HADS-A < 8 (n = 6)P-valueSHAQ- GI involvement26.5 [0, 90]2 [0, 40]0.00918.5 [0, 90]2.5 [0, 40]0.091- Lung involvement48.5 [5, 90]2.5 [0, 30]0.00118 [0, 90]3 [0, 65]0.126- Patient global assessment67.5 [30, 100]4 [0, 85]0.01153.5 [2, 100]41.5 [0, 85]0.509HAQ1.375 [0.5, 2]0.1875 [0, 1]0.0011.25 [0, 2]0.875 [0, 1.125]0.147EQ5D0.3667 [-0.0573, 0.6937]0.6752 [0.2870, 1]0.0060.4640 [-0.0573, 0.7667]0.6752 [0.287, 1]0.075SF36- Physical functioning25 [15, 75]75 [50, 100]0.00140 [15, 100]72.5 [25, 85]0.106- Role physical31.25 [0, 75]72.875 [31.25, 100]0.02537.5 [0, 100]65.625 [31.25, 100]0.214- Bodily pain41 [0, 74]68 [20, 88]0.01141 [0, 88]61.5 [20, 74]0.428- Vitality25 [0, 43.75]65.625 [25, 75]0.00137.5 [0, 75]65.625 [12.5, 75]0.135- Social functioning37.5 [12.5, 87.5]87.5 [50, 100]0.00250 [12.5, 100]87.5 [87.5, 100]0.003- Mental health45 [25, 80]65.7 [51.4, 85]0.01245 [25, 75]77.5 [51.4, 85]0.005UCLA SCTC GIT 2.0- Reflux0.38 [0, 1.25]0 [0, 1.25]0.0240.25 [0, 1.25]0 [0, 1]0.139- Distension1 [0.5, 2]0.25 [0, 1.5]0.0171 [0.25, 2]0.125 [0, 1]0.024- Total0.44[0.1, 0.99]0.04 [0, 0.97]0.0100.34 [0.04, 0.99]0.02 [0, 0.44]0.018Disclosure of Interests:None declared
Solitary fibrous tumor (SFT) is a rare mesenchymal ubiquitous tumor reported in the pleura and a wide variety of extrapleural locations, most frequently in the orbits and extremities. Approximately 78-88% of SFTs are benign and 12-22% are malignant. Although tumor characteristics are highly dependent on the location there are unifying features in MR imaging suggesting SFT: well-circumscribed, often lobulated nodular lesion, delayed contrast enhancement and the presence of fibrous contents which are hypointense on T1 and T2-weighted MRI imaging. There are many SFT differential diagnosis, highly dependent to the tumor location. Due to its rarity the diagnosis of extrapleural SFTs may be challenging. Histopathologic analysis is always required to confirm the diagnosis and to allow the distinction between the benign and malignant forms. We review pleural and extrapleural SFTs, presenting diagnostic clues, differential diagnosis and prognostic factors.
Background:Anti-tumour necrosis factor alpha (anti-TNF-α) therapy is commonly used to treat inflammatory conditions such as rheumatoid arthritis (RA). Autoantibodies namely antinuclear antibodies (ANA) induced by these treatments are well established. However, anti-TNF-α-induced systemic lupus erythematosus (SLE) is rarely described and its incidence is yet unknown.Objectives:This study aimed to determine the prevalence of ANA seroconversion and to characterize the development of SLE induced by anti-TNF-α therapy in patients with RA over time.Methods:An observational retrospective cohort study was conducted with at least one year of follow-up. Patients with diagnosis of RA, according to American College of Rheumatology criteria (ACR), and registered on Rheumatic Diseases Portuguese Register (Reuma.pt) who started their first anti-TNFα between 2003 and 2019 were included. Patients with positive ANA (titer ≥100) and/or positive double-strand DNA (dsDNA) antibodies and/or with a diagnosis of SLE at their first visit were excluded. Demographic, clinical and laboratory data were obtained by consulting Reuma.pt. As there are no recognized criteria for drug-induced SLE, the diagnosis of SLE induced by anti-TNF-α was considered if there is a temporal relationship between clinical manifestations and anti-TNF-α-therapy, the presence of at least 1 serologic ACR criteria (ANA or anti-dsDNA) and at least 1 nonserologic ACR criteria (arthritis, serositis, hematologic disorder or malar rash) [1]. Continuous variables are presented with mean, standard deviation, median, quartile 1 and quartile 3. Categorical variables are presented with absolute and relative frequencies.Results:A total of 211 patients (mean age of 49.9±10.9 years old; 84.4% female) were included with a median follow-up time of 6 [3-14] years. We found a seroconversion rate for ANA of 75.4% (n=159) with median treatment duration of 31 [8.5-70.5] months. The most common titre was 1/100 with diffuse and speckled patterns. ANA seroconversion was higher for etanercept (47.8%, n=76) than with adalimumab (23.9%, n=38), infliximab (13.8%, n=22), golimumab (12.6%, n=20) or certolizumab (1.9%, n=3). SLE induced by anti-TNF-α occurred in two patients (0.9%) with erosive and seropositive (rheumatoid factor and anti-citrullinated protein antibodies) RA previously treated with two conventional synthetic disease-modifying antirheumatic drugs, including methotrexate. The first patient, a female with 66 years old and 17 years of disease duration, developed SLE after 16 months of infliximab, with constitutional symptoms, abrupt worsening of polyarthritis, ANA titer of 1/320 diffuse pattern and positive dsDNA (248 UI/mL) antibodies. The second patient, a woman with 43 years old and 11 years of disease duration, developed SLE after 41 months of adalimumab with malar rash and ANA titer of 1/320 diffuse pattern, positive dsDNA (285 UI/mL), positive anti-histone antibodies and hypocomplementemia. In these two cases, anti-TNF-α therapy was stopped and recovery was spontaneous without treatment. The first patient switched to adalimumab and the second switched to golimumab without recurrence of SLE for more than ten years.Conclusion:We found a high rate of ANA seroconversion induced by anti-TNFα therapy in patients with RA. However, similar to previous literature, only 0.9% of patients developed SLE with mild manifestations without major organ involvement. Although the drug with the highest ANA seroconversion rate was etanercept, those responsible for induced SLE were infliximab and adalimumab. Patients improved after discontinuation of therapy and tolerated an alternative anti-TNF-α drug without recurrence of induced SLE over time. Therefore, ANA and SLE induced by anti-TNF-α should be considered and reported in the follow-up of RA patients. Further research is needed to explore the impact of this adverse event on the outcomes of treatment over time.References:[1]Hochberg MC. Arthritis Rheum. 1997;40(9):1725.Disclosure of Interests:None declared
Background:Vitamin D, a fat soluble vitamin that is mainly involved in the regulation of calcium/phosphate metabolism, has a increasingly understood role in immunomodulatory activity, both in innate and adaptive immune system. In rheumatoid arthritis (RA), vitamin D showed to suppress the proliferation of synoviocytes and to reduce the production of proinfammatory cytokines, in vitro. (1) Recently the hypothesis has been raised that vitamin D has a negative association with RA activity. (2)Objectives:This study aimed to evaluate the relationship between the 25-hydroxyvitamin D (25(OH) vitD) level, RA activity and response to a first biologic disease-modifying drug (bDMARD).Methods:This is a longitudinal, retrospective study including consecutive patients with the diagnosis of RA followed at our rheumatology department. Demographic, clinical, and laboratorial data were collected from our national database at baseline, 6 and 12 months after initiation of a first bDMARD. Statistical analysis was performed using SPSS 23.0. Correlations between variables were studied using Spearman correlation analysis and comparison between groups was performed using Wilcoxon and Kruskal-Wallis tests; p<0.05 was considered statistically significant.Results:Mean age of patients (n=236) was 51.5 ± 11.2 years old, 192 (81.4%) were females with a median disease duration of 10.1 [4.7, 16.7] years. Seropositivity for anti-citrullinated protein antibodies was present in 192 (81.4%) patients and for rheumatoid factor in 175 (74.2%). The majority exhibited a very high or high disease activity at baseline (median DAS28 5.75 [4.99 – 6.63]) and 90% (n=212) of them were concomitantly using corticosteroids and/or other disease-modifying anti-rheumatic drugs (117 with methotrexate (MTX), 62 with leflunomide and 32 with sulfasalazine). Regarding bDMARD, 56.8% (n=134) initiated an TNF alpha inhibitor.After 6 and 12 months from a bDMARD initiation there was a significant reduction of ESR, CRP levels, TJCs, SJCs and DAS28 (all p-values < 0.001), as expected. Median baseline serum 25(OH) vitD concentrations was 25.5 [16.5, 30.0] ng/ml; notably, 34.2% of our sample was affected by hypovitaminosis D at baseline (25(OH) vitD< 20 ng/mL).Among our study population 42.5% patients were responders to first bDMARD (23.8% good and 18.7% moderate responders) according to the EULAR response criteria. Disease remission (DAS28 < 2.6) was achieved by 17.6% of patients.The percentage of good responders was significantly lower in the subgroup of patients with hypovitaminosis D compared to subjects with normal 25(OH) vitamin D levels at baseline (p=0.002), as it was for the percentage of disease remission (p=0.015).The bivariate correlation analyses showed that 25(OH) vit D levels at baseline correlated with CRP levels and good response to RA treatment after 12 months (Spearman’s coefficient -0.201, p = 0.028; Spearman’s coefficient 0.255, p < 0.019, respectively). 25(OH) vit D levels at baseline, 6 and 12 months after bDMARD initiation did not correlate with age, BMI, ESV, number of tender or swollen joints, DAS28, HAQ or with SDAI or CDAI at 6 or 12 months of treatment.Conclusion:In patients with RA, basal 25(OH) vit D levels correlated with response to a bDMARD. These results suggest a role of basal vitamin D status in the prediction of disease evolution and support the hypothesis that vitamin D has an immunomodulatory potential.References:[1]Huhtakangas JA, Veijola J, Turunen S et al. 1,25(OH)2D3 and calcipotriol, its hypocalcemic analog, exert a long-lasting anti-infammatory and anti-proliferative effect in synoviocytes cultured from patients with rheumatoid arthritis and osteoarthritis. J Steroid Biochem Mol Biol 2017; 173: 13- 22.[2]Lee YH, Bae SC. Vitamin D level in rheumatoid arthritis and its correlation with the disease activity: a meta-analysis. Clin Exp Rheumatol. 2016 Sep-Oct;34(5):827-833. Epub 2016 Apr 6. PMID: 27049238.Disclosure of Interests:None declared
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