Treatment aims in rheumatoid arthritis

ESC CardioMed ◽  
2018 ◽  
pp. 1120-1121
Author(s):  
Oliver Distler ◽  
Adrian Ciurea
Keyword(s):  
Rheumatoid Arthritis ◽  
Cardiovascular Disease ◽  
Risk Factor ◽  
Systemic Inflammation ◽  
Independent Risk Factor ◽  
Joint Destruction ◽  
Joint Inflammation ◽  
High Grade

Treatment of rheumatoid arthritis aims at targeting joint inflammation, inhibiting joint destruction, limiting extra-articular involvement, and preventing systemic co-morbidities, the most important being cardiovascular disease. Rheumatoid arthritis has been shown to be an independent risk factor for cardiovascular disease, mostly through high-grade systemic inflammation.

scholarly journals Does rheumatoid arthritis equal diabetes mellitus as an independent risk factor for cardiovascular disease? A prospective study

2009 ◽  
Vol 61 (11) ◽  
pp. 1571-1579 ◽  
Author(s):  
Mike J. L. Peters ◽  
Vokko P. van Halm ◽  
Alexandre E. Voskuyl ◽  
Yvo M. Smulders ◽  
Maarten Boers ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Diabetes Mellitus ◽  
Cardiovascular Disease ◽  
Risk Factor ◽  
Prospective Study ◽  
Independent Risk Factor ◽  
A Prospective Study

scholarly journals Serum uric acid is an independent risk factor for cardiovascular disease and mortality in hypertensive patients

2012 ◽  
Vol 35 (11) ◽  
pp. 1087-1092 ◽  
Author(s):  
Tatsuo Kawai ◽  
Mitsuru Ohishi ◽  
Yasushi Takeya ◽  
Miyuki Onishi ◽  
Norihisa Ito ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Uric Acid ◽  
Risk Factor ◽  
Serum Uric Acid ◽  
Independent Risk Factor ◽  
Hypertensive Patients

scholarly journals Fibroblast Like Synovial Cell Subsets in Rheumatoid Arthritis

2021 ◽  
Author(s):  
Søren Lomholt ◽  
Morten A. Nielsen ◽  
Maithri P. Aspari ◽  
Peter B. Jørgensen ◽  
Adam P. Croft ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Cartilage Damage ◽  
Joint Destruction ◽  
Human Leukocyte ◽  
Synovial Cell ◽  
Joint Inflammation ◽  
Nuclear Factor Κb ◽  
Sequencing Studies ◽  
Sublining Layer ◽  
Lymphoid Structures

Fibroblasts like synoviocytes (FLS) play several significant roles in rheumatoid arthritis (RA) pathophysiology. This chapter will describe known roles of FLS in disease initiation, joint inflammation, disease persistence and joint destruction. It will describe the newly characterized subsets of FLS based on single cell RNA sequencing studies, and their association to specific aspects of the disease. Finally, we will discuss the future of targeting FLS in the treatment of RA. The FLS in the synovial lining layer are identified by surface complement decay-accelerating factor (CD55) along with lubricin and metallopeptidase expression. Pathological activation of this lining layer subset result in bone and cartilage damage in mice. FLS of the sublining layer are often characterized by THY1 expression, but recent studies have highlighted a heterogeneity where several distinct subsets are identified by additional markers. Sublining FLS expressing human leukocyte antigen-DRA (HLA-DRA) produce C-X-C motif chemokine 12 (CXCL12) and receptor activator of nuclear factor-κB ligand (RANKL) and seems to constitute a pro-inflammatory subset that is associated with inflammation and tertiary lymphoid structures. Another subset of FLS characterized by CD34 expression may discriminate a common progenitor fibroblast subset. Taken together, studies isolating and characterizing gene expression in synovial FLS report both associations of unknown importance and markers that may impose protective or destructive features. This supports evidence of FLS as active players in RA pathology capable of cellular recruitment, local cellular crosstalk and promotion of joint destruction. These discoveries may serve as an atlas for synovial activation in RA and have identified several potential fibroblast markers for the development of targeted treatment.

scholarly journals THE RISK OF FALLS IN PATIENTS WITH RHEUMATOID ARTHRITIS

2017 ◽  
Vol 54 (6) ◽  
pp. 705-711 ◽  
Author(s):  
N. V. Toroptsova ◽  
A. Yu. Feklistov
Keyword(s):  
Rheumatoid Arthritis ◽  
Risk Factors ◽  
Risk Factor ◽  
Independent Risk Factor ◽  
Risk Of Falls ◽  
Relationship Of ◽  
The Relationship

The paper discusses the materials of investigations dealing with falls as an independent risk factor for fractures in patients with rheumatoid arthritis (RA). It gives data on the incidence and possible risk factors of falls in this category of patients. According to the data obtained, the prevalence of falls in different countries varies from 10 to 50%, which may be related to differences in the methods of collecting information, and the relationship of the investigated factors with the risk of falls in patients with RA is uniquely unproven and calls for further investigations.

IgG Glycosylation Changes and MBL2 Polymorphisms: Associations with Markers of Systemic Inflammation and Joint Destruction in Rheumatoid Arthritis

2012 ◽  
Vol 39 (3) ◽  
pp. 463-469 ◽  
Author(s):  
LONE N. TROELSEN ◽  
SØREN JACOBSEN ◽  
JODIE L. ABRAHAMS ◽  
LOUISE ROYLE ◽  
PAULINE M. RUDD ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Systemic Inflammation ◽  
Joint Destruction ◽  
Serum Levels ◽  
High Expression ◽  
Markers Of Inflammation ◽  
Spearman's Rho ◽  
Spearman’S Rho ◽  
Factor Α ◽  
Igg Glycosylation

Objective.To examine whether IgG glycosylation changes and MBL2 genotypes are associated with systemic inflammation and joint destruction in rheumatoid arthritis (RA).Methods.IgG N-glycan content was determined from serum in 118 patients with RA by high-throughput glycan analysis using normal-phase high-pressure liquid chromatography. MBL2 extended genotypes (YA/YA, YA/XA, XA/XA, YA/YO, XA/YO, YO/YO) were determined. Systemic inflammation was assessed by serum levels of C-reactive protein (CRP), interleukin 6 (IL-6), and tumor necrosis factor-α (TNF-α). Joint destruction was assessed by total Sharp score (TSS) and alloplastic surgery records.Results.IgG hypogalactosylation was significantly correlated to IL-6 (Spearman’s rho = 0.32, p < 0.001), CRP (Spearman’s rho = 0.31, p < 0.001), TSS (Spearman’s rho = 0.25, p = 0.01), and alloplastic replacement of joints (Spearman’s rho = 0.18, p = 0.05). In multivariate analysis including age, CRP, anticitrullinated protein antibodies (ACPA), and other confounders, IgG hypogalactosylation was significantly associated with TSS (p = 0.014) and alloplastic joint replacement (OR 76.5, p = 0.041) in patients homozygous for the high expression MBL2 genotype YA/YA, but not in carriers of lower expression genotypes.Conclusion.Decreased galactosylation of IgG correlated to markers of inflammation, i.e., IL-6 and CRP. Only in patients homozygous for high expression of the MBL2 genotype YA/YA was IgG hypogalactosylation associated with markers of joint destruction. Our results suggest that inflammation-associated decreased galactosylation of IgG combined with high expression MBL2 genotypes are involved in the pathophysiology of RA.

Specific diseases: renal disease

ESC CardioMed ◽  
2018 ◽  
pp. 2670-2673
Author(s):  
Susanna Price
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Risk Factor ◽  
Kidney Disease ◽  
Renal Disease ◽  
Independent Risk Factor ◽  
Hospital Admissions ◽  
Kidney Injury ◽  
Potential Methods

Chronic kidney disease is a global health burden, with an estimated prevalence of 11–13%, with the majority of patients diagnosed as stage 3, and is an independent risk factor for cardiovascular disease. The incidence of acute kidney injury is increasing, and estimated to be present in one in five acute hospital admissions, and there is a bidirectional relationship between acute and chronic kidney disease. The relevance to the patient with cardiovascular disease relates to increased perioperative risk, as reduced kidney function is an independent risk factor for adverse postoperative cardiovascular outcomes including myocardial infarction, stroke, and progression of heart failure. Furthermore, patients undergoing cardiovascular investigations are at risk of developing acute kidney injury, in particular where iodinated contrast is administered. This chapter reviews the classification of renal disease and its impact on cardiovascular disease, as well as potential methods for reducing the development of contrast-induced acute kidney injury.

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