scholarly journals The Impact of Cigarette Smoking on Risk of Rheumatoid Arthritis: A Narrative Review

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 475 ◽  
Author(s):  
Yuki Ishikawa ◽  
Chikashi Terao
Keyword(s):  
Rheumatoid Arthritis ◽  
Environmental Factors ◽  
Cigarette Smoking ◽  
Cyclic Peptide ◽  
Bone Destruction ◽  
Narrative Review ◽  
Special Focus ◽  
Main Role ◽  
Genetic And Environmental Factors ◽  
The Impact

Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation and subsequent proliferation of synovial tissues, which eventually leads to cartilage and bone destruction without effective treatments. Anti-citrullinated cyclic peptide/protein antibody (ACPA) and rheumatoid factor (RF) are two main characteristic autoantibodies found in RA patients and are associated with unfavorable disease outcomes. Although etiologies and causes of the disease have not been fully clarified yet, it is likely that interactive contributions of genetic and environmental factors play a main role in RA pathology. Previous works have demonstrated several genetic and environmental factors as risks of RA development and/or autoantibody productions. Among these, cigarette smoking and HLA-DRB1 are the well-established environmental and genetic risks, respectively. In this narrative review, we provide a recent update on genetic contributions to RA and the environmental risks of RA with a special focus on cigarette smoking and its impacts on RA pathology. We also describe gene–environmental interaction in RA pathogenesis with an emphasis on cigarette smoking and HLA-DRB1.

Shared epitope defines distinct associations of cigarette smoking with levels of anticitrullinated protein antibody and rheumatoid factor

2019 ◽  
Vol 78 (11) ◽  
pp. 1480-1487 ◽  
Author(s):  
Yuki Ishikawa ◽  
Katsunori Ikari ◽  
Motomu Hashimoto ◽  
Koichiro Ohmura ◽  
Masao Tanaka ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Cigarette Smoking ◽  
Rheumatoid Factor ◽  
Cyclic Peptide ◽  
Shared Epitope ◽  
Asian Study ◽  
Allele Status ◽  
Acpa Level ◽  
The Impact ◽  
Production Mechanisms

ObjectsAlthough the association of cigarette smoking (CS) with susceptibility to rheumatoid arthritis (RA) has been established, the impact of CS on anticitrullinated cyclic peptide/protein antibody (ACPA) and rheumatoid factor (RF) levels in RA has yet been clear, especially in relation to shared epitope (SE) alleles.MethodsA total of 6239 subjects, the largest Asian study ever, from two independent Japanese cohorts were enrolled. Precise smoking histories, levels of ACPA and RF, and HLA-DRB1 allele status were withdrawn from databases. Associations between CS and high ACPA or RF levels, defined by the top quartiles, were evaluated. The effect of HLA-DRB1 alleles on the association was further investigated.ResultsCS at RA onset conferred the risks of high levels of both antibodies, especially RF (OR 2.06, p=7.4×10–14; ACPA, OR 1.29, p=0.012), suggesting that RF level is more sensitive to CS than ACPA level. The patients who had quitted CS before RA onset showed a trend of decreased risks of developing high levels of ACPA or RF, and the risks steadily decreased according to the cessation years. The association of CS with high ACPA level was observed only in subjects carrying SE alleles, while the association of high RF level was observed regardless of SE.ConclusionsCS confers the risks of high autoantibody levels in RA in different manners; CS interacts with SE alleles on ACPA level, while CS impacts on RF level despite SE allele. These data suggest novel distinct production mechanisms of RF and ACPA.

The Impact of Proinflammatory Cytokynes of Rheumatoid Polyarthritis on the Generalized Loss of Bone Mass

2018 ◽  
Vol 69 (9) ◽  
pp. 2541-2545
Author(s):  
Raluca Barzoi ◽  
Elena Rezus ◽  
Codruta Badescu ◽  
Razan Al Namat ◽  
Manuela Ciocoiu
Keyword(s):  
Rheumatoid Arthritis ◽  
Immune Cells ◽  
Osteoclast Differentiation ◽  
Bone Destruction ◽  
Nuclear Factor ◽  
Receptor Activator ◽  
Level Function ◽  
Rheumatoid Polyarthritis ◽  
The Impact ◽  
Nuclear Factor Kb

There is a bidirectional interaction between most immune cells and osteoblasts, osteoclasts and their precursor cells. The receptor activator of nuclear factor-kB ligand (RANKL)/RANK/osteoprotegerin (OPG) system plays an essential role in the formation of osteoblasts, but it also has implications in osteoclast biology and implicitly on the diseases characterized by bone loss. Proinflammatory cytokines existing at synovial level function as direct or indirect stimulators of osteoclast differentiation, but also of its survival or activity, although some cytokines may also play an antiosteocastogenic role. The fate of bone destruction is determined by the balance between osteoclastogenic and antiosteoclastogenic mediators. Our study has shown that the early initiation of the therapy with anti-TNF and anti-IL6 biological agents, in patients with rheumatoid arthritis, inhibits bone destruction, regardless of the anti-inflammatory activity in patients with rheumatoid arthritis.

Immunoglobulin levels in systemic lupus erythematosus: A narrative review

Lupus ◽  
2021 ◽  
pp. 096120332110047
Author(s):  
Ibrahim Almaghlouth ◽  
Sindhu R Johnson ◽  
Eleanor Pullenayegum ◽  
Dafna Gladman ◽  
Murray Urowitz
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Narrative Review ◽  
Special Focus ◽  
Immunoglobulin Level ◽  
Systemic Lupus ◽  
External Threats ◽  
Self Tolerance ◽  
Low Levels ◽  
The Impact

Immunoglobulins play a fundamental role in the protection of the human body against internal and external threats. They also contribute to the immune system homeostasis and maintenance of self-tolerance. Hypogammaglobulinemia is occasionally encountered in routine clinical practice by rheumatologists. Low levels of immunoglobulins can occur as primary or secondary issues and may predispose patients to various forms of infection. However, the impact of the low immunoglobulin level abnormality varies with the underlying condition. In this narrative review, we shed light on the overall types and functions of immunoglobulins for clinicians. We discuss important principles of immunoglobulin measurements. We then consider the primary and secondary causes of low immunoglobulins with a special focus on hypogammaglobulinemia in patients with systemic lupus erythematosus (SLE).

scholarly journals Impact of Genetic and Environmental Factors on hsCRP Concentrations and Response to Therapeutic Agents

2009 ◽  
Vol 55 (2) ◽  
pp. 256-264 ◽  
Author(s):  
Jian Shen ◽  
Jose M Ordovas
Keyword(s):  
Environmental Factors ◽  
Genetic Polymorphisms ◽  
Genetic Variants ◽  
Inflammatory Marker ◽  
Lipid Lowering ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Fenofibrate Treatment ◽  
Genetic And Environmental Factors ◽  
The Impact

Abstract Background: Inflammation plays an instrumental role in all stages of atherosclerosis. High-sensitivity C-reactive protein (hsCRP), a systemic inflammatory marker, has been gaining recognition as an independent risk factor for cardiovascular disease (CVD). Both baseline hsCRP concentrations and drug-induced hsCRP changes are highly variable and potentially subject to genetic regulation. Content: This review summarizes the current studies examining the effect of genetic and environmental factors on baseline plasma hsCRP concentrations, with a main focus on C-reactive protein, pentraxin-related (CRP) genetic polymorphisms and various dietary components that affect hsCRP concentrations. We also address the association of CRP genetic variations with CVD risk, a relationship that may support or refute the causality of CRP in the atherosclerotic process. Moreover, we discuss the impact of CRP genetic polymorphisms on hsCRP changes in response to 3-week fenofibrate treatment in the genetic intervention of the Genetics of Lipid Lowering Drugs and Diet Network study. Summary: Genetic variants on the CRP locus and other loci and dietary and lifestyle factors are responsible for the interindividual variability of plasma hsCRP concentrations. CRP genetic variants further influence differing plasma hsCRP response after 3-week fenofibrate treatment in patients with metabolic syndrome. Future studies focusing on the influence and interaction of genetic variation on the hsCRP response to dietary and other behavior modification as well as drug treatment could have important implications for the development of more personalized preventive and therapeutic approaches to reduce CVD.

scholarly journals Nutrition in the Intensive Care Unit—A Narrative Review

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2851
Author(s):  
Aileen Hill ◽  
Gunnar Elke ◽  
Arved Weimann
Keyword(s):  
Critically Ill ◽  
Feeding Strategy ◽  
Interdisciplinary Approach ◽  
Nutrition Therapy ◽  
Narrative Review ◽  
Optimal Timing ◽  
Special Focus ◽  
Prognostic Impact ◽  
Specific Patient ◽  
The Impact

Background: While consent exists, that nutritional status has prognostic impact in the critically ill, the optimal feeding strategy has been a matter of debate. Methods: Narrative review of the recent evidence and international guideline recommendations focusing on basic principles of nutrition in the ICU and the treatment of specific patient groups. Covered topics are: the importance and diagnosis of malnutrition in the ICU, the optimal timing and route of nutrition, energy and protein requirements, the supplementation of specific nutrients, as well as monitoring and complications of a Medical Nutrition Therapy (MNT). Furthermore, this review summarizes the available evidence to optimize the MNT of patients grouped by primarily affected organ system. Results: Due to the considerable heterogeneity of the critically ill, MNT should be carefully adapted to the individual patient with special focus on phase of critical illness, metabolic tolerance, leading symptoms, and comorbidities. Conclusion: MNT in the ICU is complex and requiring an interdisciplinary approach and frequent reevaluation. The impact of personalized and disease-specific MNT on patient-centered clinical outcomes remains to be elucidated.

scholarly journals The role of microbiome in rheumatoid arthritis treatment

2019 ◽  
Vol 11 ◽  
pp. 1759720X1984463 ◽  
Author(s):  
Rahul Bodkhe ◽  
Baskar Balakrishnan ◽  
Veena Taneja
Keyword(s):  
Rheumatoid Arthritis ◽  
Immune System ◽  
Gut Microbiota ◽  
Autoimmune Disorder ◽  
Host Immune System ◽  
Microbial Composition ◽  
Drug Induced ◽  
Partial Restoration ◽  
Genetic And Environmental Factors ◽  
The Impact

Rheumatoid arthritis (RA) is an autoimmune disorder with multifactorial etiology; both genetic and environmental factors are known to be involved in pathogenesis. Treatment with disease-modifying antirheumatic drugs (DMARDs) plays an essential role in controlling disease progression and symptoms. DMARDs have immunomodulatory properties and suppress immune response by interfering in various pro-inflammatory pathways. Recent evidence has shown that the gut microbiota directly and indirectly modulates the host immune system. RA has been associated with dysbiosis of the gut microbiota. Patients with RA treated with DMARDs show partial restoration of eubiotic gut microbiome. Hence, it is essential to understand the impact of DMARDs on the microbial composition and its consequent influences on the host immune system to identify novel therapies for RA. In this review, we discuss the importance of antirheumatic-drug-induced host microbiota modulations and possible probiotics that can generate eubiosis.

Combined influence of genetic and environmental factors in age of rheumatoid arthritis onset

2011 ◽  
Vol 32 (10) ◽  
pp. 3097-3102 ◽  
Author(s):  
Luis Rodríguez-Rodríguez ◽  
José Ramón Lamas ◽  
Jezabel Varadé ◽  
Pilar Tornero-Esteban ◽  
Lydia Abasolo ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Environmental Factors ◽  
Genetic And Environmental Factors

scholarly journals Combat exposure severity as a moderator of genetic and environmental liability to post-traumatic stress disorder

2013 ◽  
Vol 44 (7) ◽  
pp. 1499-1509 ◽  
Author(s):  
E. J. Wolf ◽  
K. S. Mitchell ◽  
K. C. Koenen ◽  
M. W. Miller
Keyword(s):  
Environmental Factors ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Combat Exposure ◽  
Shared Environment ◽  
Post Traumatic Stress ◽  
Post Traumatic ◽  
Genetic And Environmental Factors ◽  
The Impact

BackgroundTwin studies of veterans and adults suggest that approximately 30–46% of the variance in post-traumatic stress disorder (PTSD) is attributable to genetic factors. The remaining variance is attributable to the non-shared environment, which, by definition, includes combat exposure. This study used a gene by measured environment twin design to determine whether the effects of genetic and environmental factors that contribute to the etiology of PTSD are dependent on the level of combat exposure.MethodThe sample was drawn from the Vietnam Era Twin Registry (VETR) and included 620 male–male twin pairs who served in the US Military in South East Asia during the Vietnam War era. Analyses were based on data from a clinical diagnostic interview of lifetime PTSD symptoms and a self-report measure of combat exposure.ResultsBiometric modeling revealed that the effects of genetic and non-shared environment factors on PTSD varied as a function of level of combat exposure such that the association between these factors and PTSD was stronger at higher levels of combat exposure.ConclusionsCombat exposure may act as a catalyst that augments the impact of hereditary and environmental contributions to PTSD. Individuals with the greatest exposure to combat trauma were at increased risk for PTSD as a function of both genetic and environmental factors. Additional work is needed to determine the biological and environmental mechanisms driving these associations.

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