Rheumatoid Arthritis in the Aged

Nesher, Gideon; Moore, Terry L.

doi:10.2165/00002512-199303060-00003

Cited by 20 publications

(2 citation statements)

References 121 publications

(87 reference statements)

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“…Importantly, young DBA/1 mice (8–14 weeks old) did not respond to oral LPS administration, as serum IL-6 levels were not raised in these animals, indicating that aged mice are more susceptible to bacterial toxins present in the GI tract. This observation supports a possible link between immunosenescence and an age-related proinflammatory state [ 48 ], as well as the increased incidence of RA in the elderly [ 37 ].…”

Section: Introductionsupporting

confidence: 80%

“…Indeed, RA mainly develops in women older than 40 and men older than 60 years old as reviewed elsewhere [ 37 ] and develops long after the emergence of preclinical symptoms such as fatigue, malaise, and diffuse musculoskeletal pain [ 38 ]. In fact, we have observed that the majority of RA patients (14/18: 78%) suffer from GI disorders such as constipation (66%) or diarrhea (11%) [ 32 ].…”

Section: Introductionmentioning

confidence: 99%

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Slipping through the Cracks: Linking Low Immune Function and Intestinal Bacterial Imbalance to the Etiology of Rheumatoid Arthritis

Terato¹,

Christopher²,

Shionoya³

2015

Autoimmune Diseases

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Autoimmune diseases (ADs) are considered to be caused by the host immune system which attacks and destroys its own tissue by mistake. A widely accepted hypothesis to explain the pathogenic mechanism of ADs is “molecular mimicry,” which states that antibodies against an infectious agent cross-react with a self-antigen sharing an identical or similar antigenic epitope. However, this hypothesis was most likely established based on misleading antibody assay data largely influenced by intense false positive reactions involved in immunoassay systems. Thus reinvestigation of this hypothesis using an appropriate blocking agent capable of eliminating all types of nonspecific reactions and proper assay design is strongly encouraged. In this review, we discuss the possibility that low immune function may be the fundamental, common defect in ADs, which increases the susceptibility to potential disease causative pathogens located in the gastrointestinal tract (GI), such as bacteria and their components or dietary components. In addition to these exogenous agents, aberrations in the host's physical condition may disrupt the host defense system, which is tightly orchestrated by “immune function,” “mucosal barrier function,” and “intestinal bacterial balance.” These disturbances may initiate a downward spiral, which can lead to chronic health problems that will evolve to an autoimmune disorder.

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Section: Introductionsupporting

confidence: 80%

Section: Introductionmentioning

confidence: 99%

Slipping through the Cracks: Linking Low Immune Function and Intestinal Bacterial Imbalance to the Etiology of Rheumatoid Arthritis

Terato¹,

Christopher²,

Shionoya³

2015

Autoimmune Diseases

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Tolerance and effectiveness of anti–tumor necrosis factor α therapies in elderly patients with rheumatoid arthritis: A population‐based cohort study

Genevay

Finckh

Ciurea

et al. 2007

Arthritis & Rheumatism

113

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Objective. Limited data have been published on tolerance to and efficacy of classic or biologic disease-modifying antirheumatic drugs in elderly patients with rheumatoid arthritis (RA). The goal of the present study was to evaluate the tolerance to and effectiveness of anti-tumor necrosis factor (anti-TNF) agents in elderly patients (>65 years old) with RA (ERA) in comparison with younger patients (YRA). Methods. The Swiss Clinical Quality Management program for RA is a longitudinal population-based cohort. All patients who had received at least 1 dose of anti-TNF agents between January 1997 and November 2005 were included and categorized according to their age. Tolerance was assessed by analyzing discontinuation rates of anti-TNF agents. Effectiveness of these agents was assessed by analyzing RA disease activity (Disease Activity Score in 28 joints [DAS28]) and functional disability (Health Assessment Questionnaire [HAQ]) after anti-TNF initiation.Results. Among 1,571 patients with RA treated with anti-TNF agents, 344 were >65 years of age at treatment initiation. Drug discontinuation rates (median time 3 years) and mean change in DAS28 scores at 2 years (-0.65 versus -0.58) were identical in ERA and YRA. However, HAQ score improved significantly less in ERA (-0.02) than in YRA (-0.1) and a subsequent analysis revealed that this finding was essentially due to patients >75 years of age. Conclusion. Age in itself should not interfere with the decision to treat elderly patients with RA with anti-TNF agents. In a subset of patients ages >75 years, no functional improvement according to HAQ should be expected despite improvements in disease activity.

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Arthritic disease is more severe in older rats in a kaolin/carrageenan-induced arthritis model

Kim

Yeom

et al. 2011

Rheumatol Int

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This study examined in an arthritis animal model whether elderly onset rheumatoid arthritis (EORA) is a more severe disease than younger onset rheumatoid arthritis. Arthritis was induced by injecting 5% kaolin/carrageenan into the left tibiotarsal ankles of 18-month-old and 4-week-old rats. Various parameters were measured to evaluate the arthritic progression of kaolin/carrageenan-induced arthritis in the rats. Immunohistochemical staining of arthritic joints was performed to determine the degree of inflammation in old and young rats. Measurements of ankle volume and thickness, arthritic index, number of squeaks, and the paw pressure test showed the 18-month-old rats had more severe disease than the young rats in a kaolin/carrageenan-induced arthritis model. The degree of inflammation and MMP-1 expression of arthritic joints in old rats was significantly higher than that of young rats based on histological evaluation with hematoxylin and eosin (H&E) staining and immunochemistry. More severe disease symptoms were found in old rats with EORA, but the molecular mechanisms still remain to be elucidated. Understanding the molecular mechanisms will be helpful to develop clinical protocols to efficiently treat patients with EORA, which is difficult to control with current protocols.

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Rheumatoid Arthritis in the Aged

Cited by 20 publications

References 121 publications

Slipping through the Cracks: Linking Low Immune Function and Intestinal Bacterial Imbalance to the Etiology of Rheumatoid Arthritis

Slipping through the Cracks: Linking Low Immune Function and Intestinal Bacterial Imbalance to the Etiology of Rheumatoid Arthritis

Tolerance and effectiveness of anti–tumor necrosis factor α therapies in elderly patients with rheumatoid arthritis: A population‐based cohort study

Arthritic disease is more severe in older rats in a kaolin/carrageenan-induced arthritis model

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