scholarly journals Rheumatoid Arthritis Associated Episcleritis and Scleritis: An Update on Treatment Perspectives

2021 ◽  
Vol 10 (10) ◽  
pp. 2118
Author(s):  
Veronique Promelle ◽  
Vincent Goeb ◽  
Julie Gueudry
Keyword(s):  
Rheumatoid Arthritis ◽  
Potential Role ◽  
Topical Steroids ◽  
Rheumatoid Vasculitis ◽  
Ocular Complications ◽  
Increased Risk ◽  
Effective Option ◽  
Close Cooperation ◽  
Inflammatory Drugs

Episcleritis and scleritis are the most common ocular inflammatory manifestation of rheumatoid arthritis. Rheumatoid arthritis (RA) accounts for 8% to 15% of the cases of scleritis, and 2% of patients with RA will develop scleritis. These patients are more likely to present with diffuse or necrotizing forms of scleritis and have an increased risk of ocular complications and refractory scleral inflammation. In this review we provide an overview of diagnosis and management of rheumatoid arthritis-associated episcleritis and scleritis with a focus on recent treatment perspectives. Episcleritis is usually benign and treated with oral non-steroidal anti- inflammatory drugs (NSAIDs) and/or topical steroids. Treatment of scleritis will classically include oral NSAIDs and steroids but may require disease-modifying anti-rheumatic drugs (DMARDs). In refractory cases, treatment with anti TNF biologic agents (infliximab, and adalimumab) is now recommended. Evidence suggests that rituximab may be an effective option, and further studies are needed to investigate the potential role of gevokizumab, tocilizumab, abatacept, tofacitinib, or ACTH gel. A close cooperation is needed between the rheumatology or internal medicine specialist and the ophthalmologist, especially when scleritis may be the first indicator of an underlying rheumatoid vasculitis.

scholarly journals SAT0014 ENDOTHELIAL PROGENITOR CELLS: ROLE IN ENDOTHELIAL DAMAGE OF INTERSTITIAL LUNG DISEASE ASSOCIATED TO RHEUMATOID ARTHRITIS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 937.1-937
Author(s):  
V. Pulito-Cueto ◽  
S. Remuzgo-Martínez ◽  
F. Genre ◽  
V. M. Mora-Cuesta ◽  
D. Iturbe Fernández ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Potential Role ◽  
Endothelial Damage ◽  
Research Support ◽  
Endothelial Progenitor

Background:Interstitial lung disease (ILD) is one of the most significant comorbidities of rheumatoid arthritis (RA), increasing the mortality in these patients [1,2]. Although the pathogenesis of ILD associated to RA (RA-ILD+) remains poorly defined [1], it is known that vascular tissue plays a crucial role in lung physiology [3]. In this context, a population of cells termed endothelial progenitor cells (EPC) are involved in vasculogenesis and endothelial tissue repair [4]. Previous reports suggest the implication of EPC in different conditions such as RA and idiopathic pulmonary fibrosis (IPF), the most common and destructive ILD [5,6]. Nevertheless, little is known about their specific role in RA-ILD+.Objectives:The purpose of this study was to shed light on the potential role of EPC in endothelial damage in RA-ILD+.Methods:Peripheral venous blood was collected from a total of 68 individuals (18 with RA-ILD+, 17 with RA-ILD-, 19 with IPF and 14 healthy controls). All subjects were recruited from the Rheumatology and Pneumology departments of Hospital Universitario Marqués de Valdecilla, Santander, Spain. Quantification of EPC was analyzed by the expression of surface antigens by flow cytometry. The combination of antibodies against the stem cell marker CD34, the immature progenitor marker CD133, the endothelial marker VEGF receptor 2 (CD309) and the common leukocyte antigen CD45 was used. EPC were considered as CD34+, CD45Low, CD309+and CD133+. All statistical analyses were performed using Prism software 5 (GraphPad).Results:EPC frequency was significantly increased in patients with RA-ILD+, RA-ILD-and IPF compared to controls (p=0.001, p=0.002, p< 0.0001, respectively). Nevertheless, patients with RA, both RA-ILD+and RA-ILD-, showed a lower frequency of EPC than those with IPF (p= 0.048, p= 0.006, respectively).Conclusion:Our results provide evidence for a potential role of EPC as a reparative compensatory mechanism related to endothelial damage in RA-ILD+, RA-ILD-and IPF patients. Interestingly, EPC frequency may help to establish a differential diagnostic between patients with IPF and those who have an underlying autoimmune disease (RA-ILD+).References:[1] J Clin Med 2019; 8: 2038;[2] Arthritis Rheumatol 2015; 67: 28-38;[3] Nat Protoc 2015; 10: 1697-1708;[4] Science 1997; 275: 964-966;[5] Rheumatology (Oxford) 2012; 51: 1775-1784;[6] Angiogenesis 2013; 16: 147-157.Acknowledgments:Personal funds, VP-C: PREVAL18/01 (IDIVAL); SR-M: RD16/0012/0009 (ISCIII-ERDF); LL-G: PI18/00042 (ISCIII-ERDF); RL-M: Miguel Servet type I CP16/00033 (ISCIII-ESF).Disclosure of Interests:Verónica Pulito-Cueto: None declared, Sara Remuzgo-Martínez: None declared, Fernanda Genre: None declared, Victor Manuel Mora-Cuesta: None declared, David Iturbe Fernández: None declared, Sonia Fernández-Rozas: None declared, Leticia Lera-Gómez: None declared, Pilar Alonso Lecue: None declared, Javier Rodriguez Carrio: None declared, Belén Atienza-Mateo: None declared, Virginia Portilla: None declared, David Merino: None declared, Ricardo Blanco Grant/research support from: AbbVie, MSD, Roche, Consultant of: Abbvie, Eli Lilly, Pfizer, Roche, Bristol-Myers, Janssen, UCB Pharma and MSD, Speakers bureau: Abbvie, Eli Lilly, Pfizer, Roche, Bristol-Myers, Janssen, UCB Pharma. MSD, Alfonso Corrales Speakers bureau: Abbvie, Jose Manuel Cifrián-Martínez: None declared, Raquel López-Mejías: None declared, Miguel A González-Gay Grant/research support from: Pfizer, Abbvie, MSD, Speakers bureau: Pfizer, Abbvie, MSD

scholarly journals Potential role of acetylsalicilic acid and other non-steroidal anti-inflammatory drugs in cancer risk reduction (literature review)

2021 ◽  
Vol 23 (3) ◽  
Author(s):  
V. V. Buheruk ◽  
O. B. Voloshyna ◽  
L. I. Kovalchuk ◽  
I. V. Balashova ◽  
O. V. Naidionova
Keyword(s):  
Cancer Risk ◽  
Acetylsalicylic Acid ◽  
Potential Role ◽  
Task Force ◽  
Current Systematic Review ◽  
Anti Cancer ◽  
Cancer Types ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

The aim of this review is to analyze and summarize the existing evidence regarding the possibilities of using acetylsalicylic acid (ASA) and other non-steroidal anti-inflammatory drugs (NSAIDs) to reduce cancer risk. Conclusions. Chronic inflammation facilitates the onset and progress of tumour growth. Anti-cancer properties of acetylsalicylic acid and other non-steroidal anti-inflammatory drugs are mediated via cyclooxygenase COX-dependent mechanisms, as well as other tumorigenic pathways. Current systematic review addresses potential role of ASA and other NSAIDs in reduction of cancer risk for the following localizations: head and neck, lungs, gastrointestinal tract, breast, ovaries, prostate, and skin. The role of ASA in primary prevention of colorectal cancer in specific populations is presented in 2016 U. S. Preventive Services Task Force guidelines. Studies indicate heterogeneous protective potential of ASA against different cancer types, depending on studied population, duration of intake and dose. Influence of non-aspirin NSAIDs on cancer morbidity and mortality is more controversial.

scholarly journals Rheumatoid arthritis: influence of inflammation and anti-inflammatory therapy on cardiovascular risk factors

2020 ◽  
pp. 32-44
Author(s):  
D. I. Trukhan ◽  
D. S. Ivanova ◽  
K. D. Belus
Keyword(s):  
Rheumatoid Arthritis ◽  
Risk Factors ◽  
Cardiovascular Risk ◽  
Cardiovascular Diseases ◽  
Cardiovascular Risk Factors ◽  
Chronic Inflammation ◽  
Pharmacological Intervention ◽  
Increased Risk ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

Rheumatoid arthritis is a frequent and one of the most severe immuno-inflammatory diseases in humans, which determines the great medical and socio-economic importance of this pathology. One of the priority problems of modern cardiac rheumatology is an increased risk of cardiovascular complications in rheumatoid arthritis. In patients with rheumatoid arthritis, traditional cardiovascular risk factors for cardiovascular diseases (metabolic syndrome, obesity, dyslipidemia, arterial hypertension, insulin resistance, diabetes mellitus, smoking and hypodynamia) and a genetic predisposition are expressed. Their specific features also have a certain effect: the “lipid paradox” and the “obesity paradox”. However, chronic inflammation as a key factor in the development of progression of atherosclerosis and endothelial dysfunction plays a leading role in morbidity and mortality from cardiovascular diseases in rheumatoid arthritis. This review discusses the effect of chronic inflammation and its mediators on traditional cardiovascular risk factors and its independent significance in the development of CVD. Drug therapy (non-steroidal anti-inflammatory drugs, glucocorticosteroids, basic anti-inflammatory drugs, genetically engineered biological drugs) of the underlying disease also has a definite effect on cardiovascular risk factors in patients with rheumatoid arthritis. A review of studies on this problem suggests a positive effect of pharmacological intervention in rheumatoid arthritis on cardiovascular risk factors, their reduction to a level comparable to the populations of patients not suffering from rheumatoid arthritis. The interaction of rheumatologists, cardiologists and first-contact doctors (therapist and general practitioner) in studying the mechanisms of the development of atherosclerosis in patients with rheumatoid arthritis will allow in real clinical practice to develop adequate methods for the timely diagnosis and prevention of cardiovascular diseases in patients with rheumatoid arthritis.

scholarly journals Decreased MiR-128-3p alleviates the progression of rheumatoid arthritis by up-regulating the expression of TNFAIP3

2018 ◽  
Vol 38 (4) ◽  
Author(s):  
Zhongbin Xia ◽  
Fanru Meng ◽  
Ying Liu ◽  
Yuxuan Fang ◽  
Xia Wu ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
T Cells ◽  
Peripheral Blood ◽  
Potential Role ◽  
Enzyme Linked Immunosorbent Assay ◽  
Normal Person ◽  
Synovial Joint ◽  
Peripheral Blood Mononuclear

Background: Rheumatoid arthritis (RA) is a inflammatory disease that characterized with the destruction of synovial joint, which could induce disability. Inflammatory response mediated the RA. It has been reported that MiR-128-3p is significantly increased in RA, while the potential role was still unclear. Methods: T cells in peripheral blood mononuclear cell (PBMC) were isolated from the peripheral blood from people of RA and normal person were used. Real-time PCR was performed to detect the expression of MiR-128-3p, while the protein expression of tumor necrosis factor-α-induced protein 3 (TNFAIP3) was determined using Western blot. The levels of IL-6 and IL-17 were measured using enzyme-linked immunosorbent assay (ELISA). The expression of CD69 and CD25 was detected using flow cytometry. The RA mouse model was constructed for verification of the role of MiR-128-3p. Results: The expression of MiR-128-3p was significantly increased, while TNFAIP3 was decreased, the levels of IL-6 and IL-17 were also increased in the T cells of RA patients. Down-regulated MiR-128-3p significantly suppressed the expression of p-IkBα and CD69, and CD25in T cells. MiR-128-3p targets TNFAIP3 to regulate its expression. MiR-128-3p knockdown significantly suppressed the activity of nuclear factor κB (NF-κB) and T cells by up-regulating TNFAIP3, while cells co-transfected with si-TNFAIP3 abolished the effects of MiR-128-3p knockdown. The in vivo experiments verified the potential role of MiR-128-3p on RA. Conclusion: Down-regulated MiR-128-3p significantly suppressed the inflammation response of RA through suppressing the activity of NF-κB pathway, which was mediated by TNFAIP3.

scholarly journals Prior Routine Use of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) and Important Outcomes in Hospitalised Patients with COVID-19

2020 ◽  
Vol 9 (8) ◽  
pp. 2586 ◽  
Author(s):  
Eilidh Bruce ◽  
Fenella Barlow-Pay ◽  
Roxanna Short ◽  
Arturo Vilches-Moraga ◽  
Angeline Price ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Severe Acute Respiratory Syndrome ◽  
Observational Study ◽  
Potential Role ◽  
Multivariable Analysis ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Hospitalised Patients ◽  
Inflammatory Drugs

Coronavirus disease 2019 (COVID-19) infection causes acute lung injury, resulting from aggressive inflammation initiated by viral replication. There has been much speculation about the potential role of non-steroidal inflammatory drugs (NSAIDs), which increase the expression of angiotensin-converting enzyme 2 (ACE2), a binding target for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to enter the host cell, which could lead to poorer outcomes in COVID-19 disease. The aim of this study was to examine the association between routine use of NSAIDs and outcomes in hospitalised patients with COVID-19. This was a multicentre, observational study, with data collected from adult patients with COVID-19 admitted to eight UK hospitals. Of 1222 patients eligible to be included, 54 (4.4%) were routinely prescribed NSAIDs prior to admission. Univariate results suggested a modest protective effect from the use of NSAIDs, but in the multivariable analysis, there was no association between prior NSAID use and time to mortality (adjusted HR (aHR) = 0.89, 95% CI 0.52–1.53, p = 0.67) or length of stay (aHR 0.89, 95% CI 0.59–1.35, p = 0.58). This study found no evidence that routine NSAID use was associated with higher COVID-19 mortality in hospitalised patients; therefore, patients should be advised to continue taking these medications until further evidence emerges. Our findings suggest that NSAID use might confer a modest benefit with regard to survival. However, as this finding was underpowered, further research is required.

Differential diagnosis between rheumatoid arthritis and psoriatic arthritis: the value of ultrasound findings at metacarpophalangeal joints level

2011 ◽  
Vol 70 (6) ◽  
pp. 1111-1114 ◽  
Author(s):  
Marwin Gutierrez ◽  
Emilio Filippucci ◽  
Fausto Salaffi ◽  
Luca Di Geso ◽  
Walter Grassi
Keyword(s):  
Rheumatoid Arthritis ◽  
Differential Diagnosis ◽  
Psoriatic Arthritis ◽  
Synovial Fluid ◽  
Potential Role ◽  
Power Doppler ◽  
Extensor Tendon ◽  
Synovial Hypertrophy ◽  
Ultrasound Findings

ObjectiveTo investigate the potential of ultrasound (US) in the differential diagnosis between rheumatoid arthritis (RA) and psoriatic arthritis (PsA) at metacarpophalangeal (MCP) joints level.Methods18 RA patients and 20 PsA patients with clinical involvement of MCP joints were included. All US examinations were performed by two rheumatologists investigating: presence of joint cavity widening (JCW), synovial fluid and/or synovial hypertrophy, peritenon extensor tendon inflammation (PTI) and intra-articular or peri-tendinous power Doppler (PD) signal.ResultsA total of 83 MCP joints in 18 RA patients were assessed. In all of these the authors found different degrees of JCW. 15 of 83 (18%) MCP joints showed synovial fluid, whereas 68 of 83 (82%) MCP joints showed synovial hypertrophy. In 72 of 83 (86.7%) MCP joints intra-articular PD was detected. No PTI pattern was found in these patients.In PsA patients, a total of 82 MCP joints in 20 patients were assessed. 54 of 82 (65.8%) MCP joints showed PTI pattern (p = 0.001). In 50 of these 54 (92.5%) MCP joints extra-articular PD signal was detected (p = 0.001). 28 of 82 (34.1%) MCP joints showed different degrees of JCW. 6 of 28 (21.4%) MCP joints presented synovial fluid, whereas 22 of 28 (78.5%) MCP joints showed synovial hypertrophy. In 8 of 82 (9.7%) MCP joints the JCW and PTI patterns were found contemporaneously.ConclusionsPreliminary results demonstrate that PTI pattern is a higher characteristic of PsA, which suggests a potential role of US in the differential diagnosis between RA and PsA at MCP joints level.

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