Successful treatment of renal AA amyloidosis in familial Mediterranean fever with pegylated alpha-2a interferon

Yoshida, Hiroaki; Yokoyama, Keitaro; Yaginuma, Tatsuhiro; Ohkido, Ichiro; Yamamoto, Hayato; Utsunomiya, Yasushi; Kawakami, Masanobu; Hosoya, Takuma

doi:10.5414/cn106447

Cited by 10 publications

(2 citation statements)

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“…Anti-IL-1 Case series [111,112,149,150] Anti-IL-6 Case series [120,122,[151][152][153][154] Interferon-α2a Case [155] Anti-TNF Case series [156,157] PFM in amyloid deposits and improved survival [84]. If SAA is not available, CRP values 5 mg/L in FMF children or 8.75 mg/L in FMF adults during attack-free periods can be a convenient substitute to guide therapeutic decisions [124].…”

Section: Treatment Of Complicationsmentioning

confidence: 99%

Familial Mediterranean fever, from pathogenesis to treatment: a contemporary review

Tufan¹,

Lachmann²

2020

Turk J Med Sci

111

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Familial Mediterranean fever (FMF) (OMIM #249100) is the most common hereditary autoinflammatory disease in the world. FMF is caused by gain of function mutations of MEFV gene which encodes an immune regulatory protein, pyrin. Over the last few years, we have witnessed several new developments in the pathogenesis, genetic testing, diagnosis, comorbidities, disease related damage and treatment approaches to FMF. Elucidation of some of the pathogenic mechanisms has led to the discovery of pathways involved in inflammatory, metabolic, cardiovascular and degenerative diseases. The use of next generation sequencing in FMF has revealed many new gene variants whose clinical significance may be clarified by developing functional assays and biomarkers. Clinically, although FMF is considered an episodic disease characterized by brief attacks, recent systematic studies have defined several associated chronic inflammatory conditions. Colchicine is the mainstay of FMF treatment, and interleukin (IL)-1 antagonists are the treatment of choice in refractory or intolerant cases. Experience of IL-1 antagonists, anakinra and canakinumab, is now available in thousands of colchicine resistant or intolerant FMF patients. In this contemporary review, we surveyed current FMF knowledge in the light of these recent advances.

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Section: Treatment Of Complicationsmentioning

confidence: 99%

Familial Mediterranean fever, from pathogenesis to treatment: a contemporary review

Tufan¹,

Lachmann²

2020

Turk J Med Sci

111

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“…[ 8 ] However, its beneficial effect in the other causes of AA amyloidosis is not clear. [ 9 ] In addition, case reports and small case series involving patients with FMF and other rheumatic diseases have reported some success with various immunosuppressives and immunomodulators such as azathioprine, [ 10 ] chlorambucil, [ 11 ] methotrexate, [ 12 ] interferon-alpha, [ 13 ] and cyclophosphamide. [ 14 ] In the last decade, biologic agents targeting proinflammatory cytokines such as tumor necrosis factor alpha (TNF-α), interleukin (IL)-1, and IL-6 have been tried in patients with AA amyloidosis.…”

Section: Introductionmentioning

confidence: 99%

Long-term follow-up of secondary amyloidosis patients treated with tumor necrosis factor inhibitor therapy

Esatoğlu

Hatemi²,

Uğurlu³

et al. 2017

Medicine

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There are no treatment modalities, which were proven to prevent the deposition of amyloid, proteinuria, and loss of renal function due to amyloidosis. Anti-tumor necrosis factor agents (anti-TNFs) were shown to decrease the production of serum amyloid A protein.We aimed to evaluate the long-term efficacy and safety of anti-TNFs in secondary (AA) amyloidosis patients treated in a single center.Thirty-seven patients with AA amyloidosis were started an anti-TNF for AA amyloidosis between March 2001 and June 2008 and followed until May 2016 unless deceased. They were surveyed for the endpoints of death, development of end-stage renal disease (ESRD), switch to another agent due to worsening of amyloidosis and adverse events.Among the 37 patients, 12 (32%) had died, 9 (24%) had ESRD, and 8 (22%) had started another group of biologic due to worsening of amyloidosis indicated by an increase in proteinuria, 5 (14%) patients are still doing well with anti-TNFs, and 3 (8%) are off treatment at the end of a median follow-up of 10 (interquartile range [IQR]: 5.5–10.5) years since the start of anti-TNFs and 10 (IQR: 8–13) years since the diagnosis of AA amyloidosis. Most common serious adverse events were sepsis and thrombotic events observed in 8 and 4 patients, respectively.Treatment with anti-TNFs may be associated with a higher survival rate compared with historic cohorts of AA amyloidosis, especially when started early with a lower serum creatinine level at baseline. Caution is needed regarding serious adverse events, especially infections.

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Mechanisms of cardiovascular complications in chronic kidney disease: research focus of the Transregional Research Consortium SFB TRR219 of the University Hospital Aachen (RWTH) and the Saarland University

et al. 2018

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Patients with chronic kidney disease (CKD) exhibit a massively increased risk for cardiovascular (CV) events, and traditional strategies to improve CV outcome have largely failed in the context of CKD. This review article summarizes the current understanding of the pathophysiology of CVD in patients with CKD, defines the gaps in knowledge and describes the structure of the German Transregional Research Consortium SFB TRR219 which addresses "Mechanisms of Cardiovascular Complications in Chronic Kidney Disease".

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Successful treatment of renal AA amyloidosis in familial Mediterranean fever with pegylated alpha-2a interferon

Cited by 10 publications

References 0 publications

Familial Mediterranean fever, from pathogenesis to treatment: a contemporary review

Familial Mediterranean fever, from pathogenesis to treatment: a contemporary review

Long-term follow-up of secondary amyloidosis patients treated with tumor necrosis factor inhibitor therapy

Mechanisms of cardiovascular complications in chronic kidney disease: research focus of the Transregional Research Consortium SFB TRR219 of the University Hospital Aachen (RWTH) and the Saarland University

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