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ID PMID Title PublicationDate abstract
30024658 Anti-CCP antibodies and rheumatoid factor in systemic sclerosis: Prevalence and relationsh 2018 Sep BACKGROUND: It is known that anti-citrullinated protein (a-CCP) antibodies and rheumatoid factor (RF) can be present in systemic sclerosis (SSc) patients, particularly with joint involvement. OBJECTIVES: The aim of the study was to assess the prevalence of a-CCP antibodies and immunoglobulin M class (IgM) RF, and the relationships between their presence and joint manifestations in patients with SSc. MATERIAL AND METHODS: The study included 100 European Caucasian SSc patients hospitalized consecutively in the Department of Rheumatology and Connective Tissue Diseases (Lublin, Poland). Anti-citrullinated protein antibodies and IgM RF were determined using a commercial enzyme-linked immunosorbent assay (ELISA) test. RESULTS: Anti-citrullinated protein antibodies were found in 10 out of 100 (10%) SSc patients and IgM RF in 71 out of 100 (71%) SSc patients. In the study, 90/100 (90%) SSc patients had joint manifestations (arthralgia or arthritis), 34/100 (34%) had arthritis and 6/100 (6%) had a systemic sclerosis-rheumatoid arthritis (SSc-RA) overlap syndrome. Significantly higher a-CCP antibody levels (p = 0.012), erythrocyte sedimentation rate (ESR) (p = 0.029) and C-reactive protein (CRP) levels (p = 0.020) were observed in the SSc group with arthritis. A significant correlation was found between the group with arthritis and the presence of a-CCP antibodies, and between the arthralgia group and the presence of IgM RF. CONCLUSIONS: The prevalence of RF and a-CCP antibodies is relatively high in SSc, and joint involvement occurs frequently. There was a significantly higher prevalence of IgM RF in the group with joint manifestations. About 1/3 of SSc patients had symptoms of arthritis. Arthritis is connected with the presence of a-CCP antibodies, while arthralgia is connected with the presence of IgM RF.
30022480 Immune-bone interplay in the structural damage in rheumatoid arthritis. 2018 Oct The immune and bone systems maintain homeostasis by interacting closely with each other. Rheumatoid arthritis is a pathological consequence of their interplay, as activated T cell immune responses result in osteoclast-mediated bone erosion. An imbalance between forkhead box protein 3 (Foxp3)(+) regulatory T (T(reg) ) cells and T helper type 17 (Th17) cells is often linked with autoimmune diseases, including arthritis. Th17 cells contribute to the bone destruction in arthritis by up-regulating receptor activator of nuclear factor kappa-Î’ ligand (RANKL) on synovial fibroblasts as well as inducing local inflammation. Studies on the origin of Th17 cells in inflammation have shed light on the pathogenic conversion of Foxp3(+) T cells. Th17 cells converted from Foxp3(+) T cells (exFoxp3 Th17 cells) comprise the most potent osteoclastogenic T cell subset in inflammatory bone loss. It has been suggested that osteoclastogenic T cells may have developed originally to stop local infection in periodontitis by inducing tooth loss. In addition, Th17 cells also contribute to the pathogenesis of arthritis by modulating antibody function. Antibodies and immune complexes have attracted considerable attention for their direct role in osteoclastogenesis, and a specific T cell subset in joints was shown to be involved in B cell antibody production. Here we summarize the recent advances in our understanding of the immune-bone interplay in the context of the bone destruction in arthritis.
30173153 Clinical Responses and Synovial Vascularity in Obese Rheumatoid Arthritis Patients Treated 2018 Dec OBJECTIVE: Obese patients with rheumatoid arthritis (RA) report more joint swelling and tenderness and often have poorer responses to therapy than nonobese patients. The aim of this posthoc analysis of the MUSICA trial was to compare imaging and clinical disease activity measures in obese and nonobese patients with RA. METHODS: MUSICA evaluated methotrexate (MTX) 20 mg/week versus 7.5 mg/week in combination with adalimumab (ADA) in RA patients with an inadequate response to MTX. Patients were categorized by baseline body mass index as normal (< 25), overweight (≥ 25 to < 30), or obese (≥ 30). Synovial vascularity and hypertrophy, swollen and tender joint counts (SJC and TJC), American College of Rheumatology (ACR) responses, and low disease activity (LDA), defined as Clinical Disease Activity Index < 10 and 28-joint count Disease Activity Score using C-reactive protein (DAS28-CRP) < 3.2, were assessed at weeks 12 and 24. RESULTS: Patient characteristics were similar among groups at baseline. Obese patients had numerically smaller changes from baseline to weeks 12/24 in SJC, TJC, DAS28-CRP, and synovial hypertrophy and vascularity versus nonobese patients. Significantly fewer obese patients reached ACR20/50 at weeks 12 and 24, and LDA at Week 12; this difference was especially apparent in patients receiving 7.5 mg/week MTX but was no longer significant at Week 24. CONCLUSION: Obese patients with RA had worse clinical and ultrasonographic responses than nonobese patients, which were partly overcome with time. Obese patients may experience better and faster clinical improvements if ADA is initiated with high-dose (20 mg/week) rather than low-dose MTX. [ClinicalTrials.gov: NCT01185288].
29694580 [Profile of spending on the treatment of rheumatoid arthritis for patients of the Unified 2018 Apr Rheumatoid arthritis (RA) is a chronic condition that affects about 1% of the adult population. In a historical cohort of Minas Gerais State, 11,573 RA patients registered in the Outpatient Information System (SIA) between 2008 and 2013 were identified. For this study we adopted the public funding body's perspective and the values were adjusted by the national inflation index (IPCA) of December 2015. Etanercept was the most expensive treatment. The mean cohort age was 52 years old and most of the patients were women. Multiple regression analysis indicated a negative association between higher expenditure and age, female sex, and diagnosis at entry in the cohort and positive association between high expenditure and the Human Development Index (HDI) of the municipality and use of tumor necrosis factor agents. This study identified the factors that have an impact on RA drug treatment expenditure. Also, we showed that methods that enable extracting demographic and expenditure data of administrative information systems may represent important tools in the construction of economic studies to subsidize economic health evaluations, especially from the standpoint of the managers.
29452286 Risk factor analysis of adjacent segment disease requiring surgery after short lumbar fusi 2018 Sep BACKGROUND CONTEXT: The influence of rheumatoid arthritis (RA) on the lumbar spine has received relatively little attention compared with cervical spine, and few studies have been conducted for adjacent segment disease (ASD) after lumbar fusion in patients with RA. PURPOSE: The present study aims to determine the incidence of ASD requiring surgery (ASDrS) after short lumbar fusion and to evaluate risk factors for ASDrS, including RA. STUDY DESIGN: This is a retrospective cohort study. PATIENT SAMPLE: The present study included 479 patients who underwent lumbar spinal fusion of three or fewer levels, with the mean follow-up period of 51.2 (12-132) months. OUTCOME MEASURES: The development of ASD and consequent revision surgery were reviewed using follow-up data. METHODS: The ASDrS-free survival rate of adjacent segments was calculated through Kaplan-Meier method. The log-rank test and Cox regression analysis were used to evaluate risk factors comprising RA, age, gender, obesity, osteoporosis, diabetes, smoking, surgical method, and the number of fusion segments. RESULTS: After short lumbar fusion, revision surgery for ASD was performed in 37 patients (7.7%). Kaplan-Meier analysis predicted that the ASDrS-free survival rate of adjacent segments was 97.8% at 3 years, 92.7% at 5 years, and 86.8% at 7 years. In risk factor analysis, patients with RA showed a 4.5 times higher risk of ASDrS than patients without RA (p<.001), and patients with three-segment fusion showed a 2.7 times higher risk than patients with one- or two-segment fusion (p=.005). CONCLUSIONS: Adjacent segment disease requiring surgery was predicted in 13.2% of patients at 7 years after short lumbar fusion. Rheumatoid arthritis and the number of fusion segments were confirmed as risk factors.
28880689 Prodromal signs and symptoms of serious infections with tocilizumab treatment for rheumato 2018 May OBJECTIVE: To search for signs and symptoms before serious infection (SI) occurs in tocilizumab (TCZ)-treated rheumatoid arthritis (RA) patients. METHODS: Individual case safety reports, including structured (age, sex, adverse event [AE]) and unstructured (clinical narratives) data, were analyzed by automated text mining from a Japanese post-marketing AE-reporting database (16 April 2008-10 April 2015) assuming the following: treated in Japan; TCZ RA treatment; ≥1 SI; unable to exclude causality between TCZ and SIs. RESULTS: The database included 7653 RA patients; 1221 reports met four criteria, encompassing 1591 SIs. Frequent SIs were pneumonia (15.9%), cellulitis (9.9%), and sepsis (5.0%). Reports for 782 patients included SI onset date; 60.7% of patients had signs/symptoms ≤28 days before SI diagnosis, 32.7% had signs/symptoms with date unidentified, 1.7% were asymptomatic, and 4.9% had unknown signs/symptoms. The most frequent signs/symptoms were for skin (swelling and pain) and respiratory (cough and pyrexia) infections. Among 68 patients who had normal laboratory results for C-reactive protein, body temperature, and white blood cell count, 94.1% had signs or symptoms of infection. CONCLUSION: This study identified prodromal signs and symptoms of SIs in RA patients receiving TCZ. Data mining clinical narratives from post-marketing AE databases may be beneficial in characterizing SIs.
30013029 Multi-omics monitoring of drug response in rheumatoid arthritis in pursuit of molecular re 2018 Jul 16 Sustained clinical remission (CR) without drug treatment has not been achieved in patients with rheumatoid arthritis (RA). This implies a substantial difference between CR and the healthy state, but it has yet to be quantified. We report a longitudinal monitoring of the drug response at multi-omics levels in the peripheral blood of patients with RA. Our data reveal that drug treatments alter the molecular profile closer to that of HCs at the transcriptome, serum proteome, and immunophenotype level. Patient follow-up suggests that the molecular profile after drug treatments is associated with long-term stable CR. In addition, we identify molecular signatures that are resistant to drug treatments. These signatures are associated with RA independently of known disease severity indexes and are largely explained by the imbalance of neutrophils, monocytes, and lymphocytes. This high-dimensional phenotyping provides a quantitative measure of molecular remission and illustrates a multi-omics approach to understanding drug response.
29611761 Safety and effectiveness of iguratimod in patients with rheumatoid arthritis: Final report 2019 Mar OBJECTIVES: We evaluated the long-term (52 weeks) safety and effectiveness of iguratimod (IGU) in patients with rheumatoid arthritis (RA). METHODS: This multicenter, prospective, observational study included all evaluable RA patients who received IGU since its market launch in 2012. We evaluated adverse events (AEs); adverse drug reactions (ADRs); ADRs of special interest, including liver and renal dysfunctions, interstitial lung disease, gastrointestinal and blood disorders, and infection; and change in Disease Activity Score 28-C-reactive protein (DAS28-CRP) at week 52. RESULTS: Safety and effectiveness were analyzed in 2666 and 1614 patients, respectively. The incidences of AEs, serious AEs, ADRs, and serious ADRs were 46.92, 7.35, 38.26, and 4.58%, respectively. The incidence of ADRs peaked at approximately 4 weeks of treatment. Subsequently, the ADR incidence did not increase over time. Improvement of RA activity was shown up to week 52. CONCLUSION: Long-term treatment with IGU in patients with RA resulted in a tolerable safety profile and an improvement in RA activity. IGU could be considered a useful treatment option for patients with RA.
29302905 The efficacy of probiotic supplementation in rheumatoid arthritis: a meta-analysis of rand 2018 Feb Probiotics are considered as -immunomodulatory agents; their efficacy as an adjunct therapy option for rheumatoid arthritis (RA), however, remains controversial. The main aim of the present meta-analysis, therefore, was to compare available data from the published randomized, controlled trials (RCTs) recruiting adults with RA which compared probiotics with placebo. The English literature search was performed using Ovid version of Medline, EmBase, Web of Science, and the Central Cochrane library through October 2016 and supplemented by hand searching reference lists. Among 240 citations identified, 4 RCTs (153 participants; 89% female) were included. All data were pooled using a standardized mean difference (SMD) with a 95% CI. Compared to the placebo, probiotics did not change the inflammatory parameters (erythrocyte sedimentation rate, tumor necrosis factor [TNF]-α, interleukin [IL]-1β, IL-6, IL-10, and IL-12) and oxidative stress indices (total antioxidant capacity and malondialdehyde) significantly. The borderline significant reduction as a result of probiotic administration was only determined in C-reactive protein [SDM - 0.32 (95% CI - 0.65 to 0.00)]. Among disease activity indices (disease activity score [DAS], tender joint count, and swollen joint count), DAS showed a significant improvement following probiotic treatment with a SMD (95% CI) of - 0.58 (- 0.97 to - 0.19). The number of trials was too small to determine if a strain-, dose-, or duration-response effect was present. Probiotics seem to be less effective in RA; however, to reach a firm conclusion, we need further evidence.
28388293 Long-term safety and effectiveness of adalimumab for the treatment of Japanese patients wi 2018 Jan OBJECTIVES: To determine the safety and effectiveness of and identify associated factors in long-term adalimumab (ADA) treatment of Japanese patients with rheumatoid arthritis (RA). METHODS: Of 7740 patients participating in the all-case postmarketing surveillance study, 552 were enrolled in the present study and observed for 3 years. The safety and effectiveness of ADA were analyzed in 509 and 430 patients, respectively. RESULTS: Adverse drug reactions (ADRs) were reported in 34.2% of patients (23.3/100 person-years [PYs]); serious ADRs (SADRs) were reported in 10.6% (5.9/100 PYs). The most common ADRs and SADRs were infection (16.5%) and serious infection (6.1%), respectively. Seven patients (1.4%) developed malignancies. Multivariate analysis revealed that the risk factors for SADRs were age ≥65 years and respiratory disorder at baseline. The proportion of patients who achieved remission (28-joint count Disease Activity Score based on four erythrocyte sedimentation rates <2.6) increased from 3.3% at baseline to 49.2% at 36 months. Significant predictors of failure to achieve remission were female sex, age ≥65 years, blood disorders and advanced structural change at baseline. CONCLUSIONS: Overall, no unknown safety issues were noted during the 3-year treatment with ADA in Japanese patients with RA.
30297333 Rheumatoid arthritis-associated DNA methylation sites in peripheral blood mononuclear cell 2019 Jan OBJECTIVES: To identify novel DNA methylation sites significant for rheumatoid arthritis (RA) and comprehensively understand their underlying pathological mechanism. METHODS: We performed (1) genome-wide DNA methylation and mRNA expression profiling in peripheral blood mononuclear cells from RA patients and health controls; (2) correlation analysis and causal inference tests for DNA methylation and mRNA expression data; (3) differential methylation genes regulatory network construction; (4) validation tests of 10 differential methylation positions (DMPs) of interest and corresponding gene expressions; (5) correlation between PARP9 methylation and its mRNA expression level in Jurkat cells and T cells from patients with RA; (6) testing the pathological functions of PARP9 in Jurkat cells. RESULTS: A total of 1046 DNA methylation positions were associated with RA. The identified DMPs have regulatory effects on mRNA expressions. Causal inference tests identified six DNA methylation-mRNA-RA regulatory chains (eg, cg00959259-PARP9-RA). The identified DMPs and genes formed an interferon-inducible gene interaction network (eg, MX1, IFI44L, DTX3L and PARP9). Key DMPs and corresponding genes were validated their differences in additional samples. Methylation of PARP9 was correlated with mRNA level in Jurkat cells and T lymphocytes isolated from patients with RA. The PARP9 gene exerted significant effects on Jurkat cells (eg, cell cycle, cell proliferation, cell activation and expression of inflammatory factor IL-2). CONCLUSIONS: This multistage study identified an interferon-inducible gene interaction network associated with RA and highlighted the importance of PARP9 gene in RA pathogenesis. The results enhanced our understanding of the important role of DNA methylation in pathology of RA.
29404828 Tumor necrosis factor (TNF) and TNFR1 polymorphisms are not risk factors for rheumatoid ar 2018 Jun Tumor necrosis factor (TNF) plays an important role in the pathogenesis of rheumatoid arthritis (RA). Different genetic variants including the TNF -308G/A polymorphism are associated with RA susceptibility. However, these findings have not been replicated in all populations. The aim of this study was to determine whether the TNF -1031T/C (rs1799964), -376G/A (rs1800750), -308G/A (rs1800629) -238G/A (rs361525), and TNFR1 -609G/T polymorphisms are associated with RA susceptibility in a sample of Mexican patients. Our study included 499 patients with RA and 492 healthy controls. The genotypes of the TNF polymorphisms were obtained using TaqMan assay. The genotype and allele frequencies of the TNF -1031T/C, -376G/A, -308G/A, -238G/A, and TNFR1 -609G/T polymorphisms were similar among RA cases versus healthy controls, and no association with RA susceptibility was identified. Our results suggest that the TNF -1031T/C, -376G/A, -308G/A, -238G/A, and TNFR1 -609G/T polymorphisms are not associated with RA susceptibility in a sample of Mexican patients.
29471588 Brief Report: Attenuated Effectiveness of Tumor Necrosis Factor Inhibitors for Anti-Human 2018 Jul OBJECTIVE: To evaluate the effectiveness of tumor necrosis factor (TNF) inhibitors for the treatment of human T lymphotropic virus type I (HTLV-I)-positive patients with rheumatoid arthritis (RA) in an area endemic for HTLV-I infection. METHODS: We conducted an observational study of 585 RA patients in whom TNF inhibitors were newly introduced as a first biologic disease-modifying antirheumatic drug in an area in southwestern Japan that is endemic for HTLV-I infection. RESULTS: Fifty patients (8.5%) were anti-HTLV-I antibody-positive. The ages of the patients in this group were significantly higher at entry compared with the ages of patients who were anti-HTLV-I antibody-negative (n = 535). The median Disease Activity Score in 28 joints using the erythrocyte sedimentation rate (DAS28-ESR) was 5.21. Among the total group of patients, 82% were anti-citrullinated protein antibody (ACPA)-positive. The persistence rate of TNF inhibitors at 24 weeks was 89%. The median DAS28-ESR was significantly decreased at 24 weeks in each group. The European League Against Rheumatism (EULAR) response rate was significantly better in the anti-HTLV-I antibody-negative patients (P = 0.0277). Multiple regression analysis demonstrated that anti-HTLV-I antibody status was significantly associated with the EULAR response rate and change in the DAS28-ESR and was prominent especially in the ACPA-negative subjects. No patients developed adult T cell leukemia/lymphoma (ATL) or HTLV-I-associated myelopathy (HAM) during the 24-week treatment period. CONCLUSION: The efficacy of TNF inhibitors may be attenuated in anti-HTLV-I antibody-positive patients with RA. ATL and HAM did not develop when TNF inhibitors were used for 24 weeks, but the long-term risk is not known.
30413926 Risk of hospitalization for heart failure in rheumatoid arthritis patients treated with et 2019 Feb To estimate biologic influence on heart failure (HF) risk in rheumatoid arthritis. Retrospective cohort (RECORD Study of Italian Society for Rheumatology) study on administrative healthcare databases. We identified 2527 patients treated with either etanercept (n = 1690) or abatacept (n = 837). HF incidence rate was higher in the abatacept cohort than in the etanercept cohort with a 2.38 (95% CI 1.08-5.27) crude competing risk HR (SHR) for abatacept of developing HF, not confirmed after adjustment for prespecified confounders (SHR 1.43; 95% CI 0.51-3.98). Abatacept, compared to etanercept, is prescribed to patients with a worse cardiovascular profile but does not increase the risk of developing HF, when confounding factors are accounted for.
29693122 TNF‑α increases inflammatory factor expression in synovial fibroblasts through the toll 2018 Jun Osteoarthritis is a type of joint disease that may lead to other joint diseases. Previous research has demonstrated that tumor necrosis factor (TNF)‑α is associated with osteoarthritis activity and pathology. The possible mechanisms of the TNF‑α‑mediated signaling pathway have not been clearly elaborated in synovial fibroblasts. The present study aimed to investigate the potential mechanisms of TNF‑α in a mouse model of iodoacetate‑induced osteoarthritis. Reverse transcription‑quantitative polymerase chain reaction, ELISA, western blotting and immunohistochemistry were performed to evaluate the role of TNF‑α in the progression of osteoarthritis. The results revealed that the serum levels of TNF‑α, interleukin (IL)‑1β, IL‑4 and IL‑6 were significantly upregulated in a mouse model of iodoacetate‑induced osteoarthritis compared with healthy mice (P<0.01). TNF‑α, IL‑1β, IL‑4 and IL‑6 mRNA and protein levels were also significantly upregulated in synovial fibroblasts in the experimental mice (P<0.01). It was demonstrated that TNF‑α increased pro‑inflammation factors matrix metalloproteinase (MMP)‑3, MMP‑9, nuclear factor (NF)‑κB and receptor activator of NF‑κB ligand (RANKL) in synovial fibroblasts. It was also observed that the toll‑like receptor (TLR)‑3 was significantly upregulated and extracellular signal‑regulated kinase (ERK) and protein kinase B (AKT) were significantly downregulated in synovial fibroblasts in osteoarthritis mice (P<0.01). An in vitro assay demonstrated that TNF‑α inhibitor decreased mRNA and protein levels of IL‑1β, IL‑4 and IL‑6 in synovial fibroblasts. The knockdown of TLR‑3 abolished the TNF‑α upregulated mRNA and protein levels of IL‑1β, IL‑4 and IL‑6 in synovial fibroblasts. In addition, the knockdown of TLR‑3 also reversed TNF‑α‑upregulated ERK and AKT expression in synovial fibroblasts. In vivo assays demonstrated that TNF‑α inhibitor significantly decreased the deposition of IL‑1β, IL‑4 and IL‑6 as well as bone destruction and significantly increased the body weight and osteoarthritis score for osteoarthritic mice (P<0.01). TNF‑α inhibitor decreased TLR‑3 and significantly increased the expression and phosphorylation of ERK and AKT in articular cartilage (P<0.01). In conclusion the results of the present study indicate that TNF‑α serves an essential role in synovial fibroblasts in osteoarthritis, suggesting that inhibition of TNF‑α may decrease inflammation via the TLR‑3‑mediated ERK/AKT signaling pathway in a mouse model of monosodium iodoacetate‑induced osteoarthritis.
29859232 Lipid nanoparticles with minimum burst release of TNF-α siRNA show strong activity agains 2018 Aug 10 TNF-α siRNA has shown promising therapeutic benefits in animal models of rheumatoid arthritis. However, there continues to be a need for siRNA delivery systems that have high siRNA encapsulation efficiency and minimum burst release of TNF-α siRNA, and can target inflamed tissues after intravenous administration. Herein we report a novel acid-sensitive sheddable PEGylated solid-lipid nanoparticle formulation of TNF-α-siRNA, AS-TNF-α-siRNA-SLNs, prepared by incorporating lipophilized TNF-α-siRNA into solid-lipid nanoparticles composed of biocompatible lipids such as lecithin and cholesterol. The nanoparticles are approximately 120 nm in diameter, have a high siRNA encapsulation efficiency (>90%) and a minimum burst release of siRNA (<5%), and increase the deilvery of the siRNA in chronic inflammation sites in mouse models, including in a mouse model with collagen-induced arthritis. Importantly, in a mouse model of collagen antibody-induced arthritis that does not respond to methotrexate therapy, intravenous injection of the AS-TNF-α-siRNA-SLNs significantly reduced paw thickness, bone loss, and histopathological scores. These findings highlight the potential of using this novel siRNA nanoparticle formulation to effectively treat arthritis, potentially in patients who do not respond adequately to methotrexate.
30583799 [Pharmaceutical interviews for rheumatoid arthritis patients: Perceptions and expectations 2019 Mar INTRODUCTION: Rheumatoid arthritis has a low level of medication adherence. Abroad, the community pharmacist has a positive impact on the patients' adherence in several chronic diseases. In France, community pharmacists' missions are developing with the implementation of pharmaceutical interviews. OBJECTIVE: To evaluate community pharmacists' perceptions on the interest and feasibility of pharmaceutical interviews targeting patients with rheumatoid arthritis. METHOD: Semi-structured interviews were conducted between August and October 2017, with pharmacists in the Auvergne-Rhône-Alpes region. The inductive analysis of the interview verbatim was realized by two independent persons. RESULTS: Fifteen community pharmacists highlighted barriers in recruiting patients for the interviews currently possible at the pharmacy, the complexity of the organization and the financing, a weakness of the hospital-to-community liaison. Nevertheless pharmacists were motivated to expand the service to other pathologies. Regarding rheumatoid arthritis, pharmacists would see them in the form of structured interviews preferentially at the pharmacy, in connection or even "prescribed" by physicians for optimal and multi-professional information sharing. Prior training and funding for these interviews should be considered to motivate pharmacists to this activity. CONCLUSION: This study allowed to discuss with community pharmacists their expectations and needs to widen the service of pharmaceutical interviews in the rheumatoid arthritis. These results will have to be taken into account to build a support interviews model for rheumatoid arthritis patients who can be integrated in their daily pharmaceutical activity.
29434155 Hyperplasia of Lymphoid Follicles and Lymphangiectasia in the Parietal Pleura in Bucillami 2018 Jul 1 Yellow nail syndrome (YNS) pleurisy is often difficult to control, and pathological examinations have rarely been reported. We herein report a case of bucillamine-induced YNS in which histopathology of the parietal pleura revealed hyperplasia of the lymphoid follicles and lymphangiectasia. Even after the discontinuation of bucillamine, the pleurisy and lymphedema showed no change. Based on the histopathological findings showing similarity to rheumatoid pleurisy, we administered corticosteroid treatments, and both the pleurisy and lymphedema improved. The findings in the present case suggest that, in bucillamine-induced YNS, pleurisy may be related to inflammation caused by rheumatoid arthritis in addition to abnormalities in lymphatic vessels.
30383451 Fas receptor induces apoptosis of synovial bone and cartilage progenitor populations and p 2019 Mar Rheumatoid arthritis (RA) is an inflammatory joint disease that eventually leads to permanent bone and cartilage destruction. Fas has already been established as the regulator of inflammation in RA, but its role in bone formation under arthritic conditions is not completely defined. The aim of this study was to assess the effect of Fas inactivation on the bone damage during murine antigen-induced arthritis. Subchondral bone of wild-type (WT) and Fas-knockout (Fas(-/-)) mice was evaluated by histomorphometry and microcomputerized tomography. Proportions of synovial bone and cartilage progenitors were assessed by flow cytometry. Synovial bone and cartilage progenitors were purified by fluorescence-activated cell sorting and expression of Fas and Fas-induced apoptosis were analyzed in vitro. Results showed that Fas(-/-) mice developed attenuated arthritis characterized by preserved epiphyseal bone and cartilage. A proportion of the earliest CD200(+) bone and cartilage progenitors was reduced in WT mice with arthritis and was unaltered in Fas(-/-) mice. During osteoblastic differentiation in vitro, CD200(+) cells express the highest levels of Fas and are removed by Fas ligation. These results suggest that Fas-induced apoptosis of early CD200(+) osteoprogenitor population represents potential mechanism underlying the impaired bone formation in arthritis, so their preservation may represent the bone-protective mechanism during arthritis.-Lazić Mosler, E., Lukač, N., Flegar, D., Fadljević, M., Radanović, I., Cvija, H., Kelava, T., Ivčević, S., Šućur, A., Markotić, A., Katavić, V., Marušić, A., Grčević, D., Kovačić, N. Fas receptor induces apoptosis of synovial bone and cartilage progenitor populations and promotes bone loss in antigen-induced arthritis.
29313071 Glucocorticoids, Inflammation and Bone. 2018 May The current review on glucocorticoids (GCs), inflammation and bone is focused on three aspects: (1) the mutual effects between GCs, inflammation and bone in inflammatory rheumatic diseases, (2) current views on fracture risk assessment in patients using GCs and (3) non-pharmacological and pharmacological treatment to prevent fractures in GC-using patients with inflammatory rheumatic diseases. The use of GCs results in increased risk for fractures due to both direct and indirect negative effects of GCs on bone mass, and on bone and muscle strength. However, also the underlying inflammatory rheumatic disease is associated with the increased bone loss and fracture risk due to the chronic inflammation itself, and due to disability/immobility caused by active disease or joint destruction. The rapid and strong anti-inflammatory effect of GCs in patients with rheumatoid arthritis seems to balance the negative effects of GCs on bone in the early, active phase of the disease. Recently, an update of the American College of Rheumatology guidelines for prevention and treatment of GC-induced osteoporosis was published with renewed recommendations. To prevent fractures, general measures, including treatment of the underlying inflammatory disease adequately (even with GCs when indicated), a healthy lifestyle, including adequate calcium and vitamin D supplementation, and regular weight bearing exercises are important. In rheumatic patients with high fracture risk using GCs, especially when the cumulative dose is high and/or the underlying inflammatory disease is active, treatment with anti-osteoporotic drugs, usually an oral bisphosphonate, is indicated.