Development of amyloidosis in patients with rheumatoid arthritis under TNF-blocking agents

Roque, Rafael; Ramiro, Sofía; Cordeiro, Ana; Gonçalves, Pedro de Araújo; Canas, Silva Da; Santos, María José

doi:10.1007/s10067-011-1732-3

Cited by 4 publications

(2 citation statements)

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“…Etanercept (ETN) and infliximab (IFX), both tumor necrosis factor α (TNFα) antagonists, can lower SAA levels in RA patients with AA amyloidosis [55,56]. This effect ameliorates both RA inflammation and AA amyloidosis, reduces the number of swollen and tender joints, lowers or normalizes proteinuria, and improves renal function [57,58]. Although a small number of patients with AA amyloidosis secondary to RA received ETN, this drug had benefits for both RA inflammation and AA amyloidosis, even in SAA1.3/1.3 allele-carrying RA patients ( Table 2) [59][60][61][62].…”

Section: Treatment With Biological Dmards For Aa Amyloidosis Secondarmentioning

confidence: 99%

Developments in the Treatment of Amyloid A Amyloidosis Secondary to Rheumatoid Arthritis

Nakamura¹

2016

Exploring New Findings on Amyloidosis

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Amyloidosis refers to a heterogeneous group of diseases in which a soluble precursor, misfolded protein, and subsequently aggregates into highly structured protein fibrils with a cross--pleated structure. Of these diseases, amyloid A AA amyloidosis is a complication of long-standing inflammatory diseases such as rheumatoid arthritis RA . Treatment of this amyloidosis with RA aims to stop serum AA protein production. Immunosuppressants have reportedly been useful for both RA inflammation and AA amyloidosis. Also, biologics are effective for these specific pathological processes by targeting key players in each inflammation. In addition to the above-mentioned medications, agents both inhibiting AA fibrillogenesis and destabilizing AA fibrils have recently been employed. Phagocytes play important roles in the regression of AA fibrils. Renal involvement is the most common complication in AA amyloidosis. Peritoneal dialysis, hemodialysis, and even renal transplantation are available for patients with end-stage renal disease and AA amyloidosis. This chapter thus discusses current developments in the treatment of AA amyloidosis secondary to RA.

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Section: Treatment With Biological Dmards For Aa Amyloidosis Secondarmentioning

confidence: 99%

Developments in the Treatment of Amyloid A Amyloidosis Secondary to Rheumatoid Arthritis

Nakamura¹

2016

Exploring New Findings on Amyloidosis

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“…This result suggests that the earlier the intervention with biologics, the better the outcome for patients. ETN alone may therefore be efficacious, without MTX [49][50][51][52][53]. Table 3 shows that the change in serum creatinine value was not statistically significant, when using a cutoff value as less than 2.0 mg/dl at the initial-visit, it was demonstrated that the creatinine value improved significantly at the lastvisit.…”

Section: Biologicsmentioning

confidence: 99%

Therapeutic Strategies in Amyloid A Amyloidosis Secondary to Rheumatoid Arthritis

Nakamura¹

2013

Amyloidosis

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Amyloidosis is a disorder of protein conformation and metabolism that results in the deposition of insoluble amyloid fibrils in tissues, which causes organ dysfunction; systemic amyloidosis is characterized by failure of multiple organs and the presence of amyloid precursor protein in the serum [1-3]. Reactive amyloid A (AA) amyloidosis is one of the most severe complications of several chronic disorders, particularly rheumatoid arthritis (RA) [4], and indeed, most patients with reactive AA amyloidosis have an underlying rheumatic disease. An extra-articular complication of RA, AA amyloidosis is a serious, potentially life-threatening disorder caused by deposition in organs of AA amyloid fibrils, which derive from the circulatory acute-phase reactant, serum amyloid A protein (SAA) [5]. AA amyloidosis secondary to RA is thus one of the intractable conditions found in patients with collagen vascular diseases and is an uncommon yet important complication of RA [6]. However, the actual pathological mechanisms that are responsible for the relationship between SAA and AA amyloidosis have not been fully elucidated. With new biological therapies, both treatment and understanding of the roles of cytokines and inflammatory cellular events in RA have seen considerable progress. Biologics are recommended for patients with RA who have a suboptimal response or an intolerance to traditional disease-modifying anti-rheumatic drugs (DMARDs), such as methotrexate (MTX). Early diagnosis and rapidly subsequent treatment are essential because patients with advanced disease can't usually undergo intensive therapy. Specific treatment of AA amyloidosis caused by RA aims to stop SAA production. Cytotoxics such as chlorambucil and cyclophosphamide (CYC) and biologics such as anti-tumor necrosis factor (TNF)α inhibitors and anti-interleukin (IL)-6 receptor antibody are reportedly useful for both RA and AA amyloidosis [7, 8]. By the way, the genetic predisposition allele SAA1.3, one of SAA1 gene

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Case of Secondary Amyloidosis in a Patient with Ankylosing Spondylitis Refractory to TNF-α Inhibitors

Lee

Park

et al. 2014

Korean J Med

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Development of amyloidosis in patients with rheumatoid arthritis under TNF-blocking agents

Cited by 4 publications

References 5 publications

Developments in the Treatment of Amyloid A Amyloidosis Secondary to Rheumatoid Arthritis

Developments in the Treatment of Amyloid A Amyloidosis Secondary to Rheumatoid Arthritis

Therapeutic Strategies in Amyloid A Amyloidosis Secondary to Rheumatoid Arthritis

Case of Secondary Amyloidosis in a Patient with Ankylosing Spondylitis Refractory to TNF-α Inhibitors

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