Dyslipidaemia in Rheumatoid Arthritis: The Role of Inflammation, Drugs, Lifestyle and Genetic Factors

2010 ◽  
Vol 8 (3) ◽  
pp. 301-326 ◽  
Author(s):  
Tracey E. Toms ◽  
Deborah P. Symmons ◽  
George D. Kitas
Keyword(s):  
Rheumatoid Arthritis ◽  
Genetic Factors

scholarly journals Periodontitis and Rheumatoid Arthritis: The Same Inflammatory Mediators?

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Fulvia Ceccarelli ◽  
Matteo Saccucci ◽  
Gabriele Di Carlo ◽  
Ramona Lucchetti ◽  
Andrea Pilloni ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Proinflammatory Cytokines ◽  
Healthy Subjects ◽  
Structural Damage ◽  
Genetic Factors ◽  
The Many ◽  
Citrullinated Peptide ◽  
Anticyclic Citrullinated Peptide Antibodies ◽  
Peptide Antibodies

The strict link between periodontitis (PD) and rheumatoid arthritis (RA) has been widely demonstrated by several studies. PD is significantly more frequent in RA patients in comparison with healthy subjects: this prevalence is higher in individuals at the earliest stages of disease and in seropositive patients. This is probably related to the role of P. gingivalis in inducing citrullination and leading to the development of the new antigens. Despite the many studies conducted on this topic, there is very little data available concerning the possibility to use the same biomarkers to evaluate both RA and PD patients. The aim of the review is to summarize this issue. Starting from genetic factors, data from literature demonstrated the association between HLA-DRB1 alleles and PD susceptibility, similar to RA patients; moreover, SE-positive patients showed simultaneously structural damage to the wrist and periodontal sites. Contrasting results are available concerning other genetic polymorphisms. Moreover, the possible role of proinflammatory cytokines, such as TNF and IL6 and autoantibodies, specifically anticyclic citrullinated peptide antibodies, has been examined, suggesting the need to perform further studies to better define this issue.

Mutations of the cystic fibrosis gene in patients with bronchiectasis associated with rheumatoid arthritis

2010 ◽  
Vol 70 (4) ◽  
pp. 653-659 ◽  
Author(s):  
Xavier Puéchal ◽  
Thierry Bienvenu ◽  
Emmanuelle Génin ◽  
Jean-Marie Berthelot ◽  
Jean Sibilia ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Cystic Fibrosis ◽  
Genetic Factors ◽  
Genetic Defect ◽  
Family Members ◽  
Cystic Fibrosis Gene ◽  
Degree Relative ◽  
Family Based ◽  
Important Marker

ObjectivesIn cystic fibrosis, mutations of the CFTR gene lead to diffuse bronchiectasis (DB). DB is also associated with other diseases including rheumatoid arthritis (RA) in which the role of genetic factors in the predisposition to DB remains unclear.MethodsA family-based association study was carried out to determine whether the frequency of CFTR mutations was higher in patients with RA-associated DB and to determine whether a causal relationship could be established between the variant and the disease by evaluating its cosegregation with DB within families. Families of probands with RA-DB were included if one first-degree relative had RA and/or DB. The controls comprised healthy subjects requesting genetic counselling because their partner had cystic fibrosis.ResultsThe frequency of CFTR mutations was higher in family members with RA-DB or DB only than in unaffected relatives (p<0.005 for each comparison) and in unrelated healthy controls (p<0.001 for each comparison) but not in family members with RA only. CFTR mutations were more frequent in family members with RA-DB than in those with RA only (OR 5.30, 95% CI 2.48 to 11.33; p<5×10−5). They cosegregated with RA-DB in the families (sib-TDT=10.82, p=0.005).ConclusionsRA-DB should be added to the list of phenotypes in which CFTR mutations are pathogenic. CFTR mutation is the first genetic defect linked to an extra-articular feature of RA to be described. CFTR mutations in patients with RA appear to be an important marker of the risk of associated DB, which has been linked to a less favourable prognosis.

Genetics and epigenetics of rheumatoid arthritis

2020 ◽  
pp. 45-54
Author(s):  
Anne Barton
Keyword(s):  
Rheumatoid Arthritis ◽  
Treatment Response ◽  
Genetic Study ◽  
Genetic Factors ◽  
Family Studies ◽  
Genetic Component ◽  
Genetic Studies ◽  
Factors Associated ◽  
Increased Risk

Rheumatoid arthritis (RA) is known to have a genetic component: the evidence comes from twin and family studies as well as genetic studies themselves. Family studies consistently confirm that first degree relatives of patients with RA are at increased risk of developing the condition, supporting a genetic component. The most robust data comes from the Icelandic genealogical database. This chapter covers the basics of genetic studies in RA, designing the genetic study, RA-specific results and insights that can be gained from these. Detailed analyses of selected genetic regions are discussed, alongside genes that may indicate severity. Genetic factors associated with treatment response are also considered. Finally, the role of epigenetics is covered.

Role of Innate Immune Sensors, TLRs, and NALP3 in Rheumatoid Arthritis and Osteoarthritis

2014 ◽  
Vol 24 (4) ◽  
pp. 243-251 ◽  
Author(s):  
Yuya Takakubo ◽  
G. Barreto ◽  
Yrjo T. Konttinen ◽  
H. Oki ◽  
Michiaki Takagi
Keyword(s):  
Rheumatoid Arthritis ◽  
Innate Immune

Epigenetic factors and molecular markers of the risk of early pregnancy losses

GYNECOLOGY ◽  
2019 ◽  
Vol 21 (3) ◽  
pp. 9-16
Author(s):  
Nataly I Frolova ◽  
Tatiana E Belokrinitskaya
Keyword(s):  
Early Pregnancy ◽  
Genetic Factors ◽  
Molecular Genetic ◽  
Pregnancy Complication ◽  
Common Complication ◽  
Epigenetic Factors ◽  
Genetic Determination ◽  
Periconceptional Period ◽  
Combined Impact

Background. Miscarriage is a common complication in early pregnancy. Current studies have shown a higher prevalence of miscarriage, ranging from 10 to 20%. The review is devoted to modern concepts of etiology and pathogenesis of early pregnancy losses. Aim. Assess the role of epigenetic factors and molecular-genetic markers in the pathogenesis and prediction of early pregnancy losses Materials and methods. In order to write this review domestic and foreign publications were searched in Russian and international search systems (PubMed, eLibrary, etc.) for the last 10-15 years. Relevant articles from the peer-reviewed literature and clinical practice guidelines were included. Results. Many recent studies have proved the contribution of various epigenetic factors to the pathogenesis of spontaneous miscarriages, and the molecular-genetic determination such kinds of pregnancy complication has been confirmed. Conclusion. The miscarriage in early gestation is driven by combined impact of epigenetic and molecular-genetic factors, as well as the presence of intergenic interactions. It is may lead to deterioration of physiological functions, and maternal pathologenic pathways could be changed as during her periconceptional period as so during the pregnancy.

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