Secondary, AA, Amyloidosis

Papa, Riccardo; Lachmann, HJ

doi:10.1016/j.rdc.2018.06.004

Cited by 155 publications

(125 citation statements)

References 115 publications

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“…In AA amyloidosis, amyloid fibrils are derived from serum amyloid A protein, which is an acute phase reactant produced by the liver [15,16]. AA is typically associated with an underlying chronic inflammatory process and remains the leading cause of systemic amyloidosis in developing countries, due to the high prevalence of associated, underlying, infectious diseases [15,[17][18][19]. AA can develop in association with hereditary auto-inflammatory diseases, both monogenic (familial Mediterranean fever) as well as polygenic, including inflammatory bowel disease [15].…”

Section: Aamentioning

confidence: 99%

The Pathology of Amyloidosis in Classification: A Review

2020

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Background: The amyloidoses are a rare and heterogeneous group of disorders that are characterized by the deposition of abnormally folded proteins in tissues ultimately leading to organ damage. The deposits are mainly extracellular and are recognizable by their affinity for Congo red and their yellow-green birefringence under polarized light. Current classification of amyloid in medical practice is based on the amyloid protein type. To date, 36 proteins have been identified as being amyloidogenic in humans. Summary: in clinical practice, it is critical to distinguish between treatable versus non-treatable amyloidoses. Moreover, amyloidoses with a genetic component must be distinguished from the sporadic types and systemic amyloidoses must be distinguished from the localized forms. Among the systemic amyloidoses, AL continues to be the most common amyloid diagnosis in the developed world; other clinically significant types include AA, ALECT2, and ATTR. The latter is emerging as an underdiagnosed type in both the hereditary and wild-type setting. Other hereditary amyloidoses include AFib, several amyloidoses derived from apolipoproteins, AGel, ALys, etc. In a dialysis setting, systemic amyloid derived from β 2 microglobulin (Aβ2M) should be considered, although a very rare hereditary variant has also been reported; several amyloido-ses may be typically associated with aging and several iatrogenic types have also emerged. Determination of the amyloid protein type is imperative before specific therapy can be implemented and the current methods are briefly summarized. A brief overview of the target organ involvement by amyloid type is also included. Key Messages: (1) Early diagnosis of amyloidosis continues to pose a significant challenge and requires the participation of many clinical and laboratory specialties. (2) Determination of the protein type is imperative before specific therapy can be implemented. (3) While mass spectrometry has emerged as the preferred method of amyloid typing, careful application of immune methods is still clinically useful but caution and experience, as well as awareness of the limitations of each method, are necessary in their interpretation. (4) While the spectrum of amyloidoses continues to expand, it is critical to distinguish between those that are currently treatable versus those that are untreatable and avoid causing harm by inappropriate treatment.

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Section: Aamentioning

confidence: 99%

The Pathology of Amyloidosis in Classification: A Review

2020

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“…Most (43 out of 49 [1], 35 out of 41 [28] and 44 out of 58 [29]) of the associated diseases listed earlier in the literature appear to be strongly or weakly associated (Tables 1 and 2). Fifteen diseases have now been assessed differently.…”

Section: Assessment Of Associations Compared To Previous Listsmentioning

confidence: 90%

“…Lists of diseases causing AA amyloidosis have been published [1,[27][28][29]. From a clinical perspective, there is a need for an updated, reliable and comprehensive list.…”

Section: Introductionmentioning

confidence: 99%

Causes of AA amyloidosis: a systematic review

Brunger

Nienhuis

Bijzet

et al. 2019

Amyloid

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From a clinical perspective, there is a need for a reliable and comprehensive list of diseases causing AA amyloidosis. This list could guide clinicians in the evaluation of patients with AA amyloidosis in whom an obvious cause is lacking. In this systematic review, a PubMed, Embase and Web of Science literature search were performed on causes of AA amyloidosis published in the last four decades. Initially, 4066 unique titles were identified, but only 795 full-text articles and letters were finally selected for analysis. Titles were excluded because of non-AA type of amyloidosis, language, no fulltext publication or irrelevance. Hundred and fifty diseases were initially reported to be associated with the development of AA amyloidosis. The presence of AA amyloid was proven in 208 articles (26% of all) of which 140 (67%) showed a strong association with an underlying disease process. Disease associations were categorized and 48 were listed as strong, 19 as weak, 23 as unclear, and 60 as unlikely. Most newly described diseases are not really unexpected because they often cause longstanding inflammation. Based on the spectrum of identified causes, a pragmatic diagnostic approach is proposed for the AA amyloidosis patient in whom an obvious underlying disease is lacking.

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“…Secondary amyloidosis, the predominant type of amyloidosis in patients with IBD, is characterised by extracellular deposition of serum amyloid A, an acute phase reactant protein in different parts of the kidneys, leading to proteinuria or renal insufficiency [38]. Deposition of amyloid in the glomeruli will usually lead to proteinuria and/or nephrotic syndrome, while interstitial amyloid accumulation will result in renal insufficiency [39].…”

Section: Amyloidosismentioning

confidence: 99%

Renal involvement in paediatric inflammatory bowel disease

Mutalib

2019

Pediatr Nephrol

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Inflammatory bowel disease (IBD), which includes Crohn's disease, ulcerative colitis and inflammatory bowel disease unclassified, is a chronic inflammatory disorder that predominantly affects the gastrointestinal (GI) tract and has a rising incidence in both children and adults. Symptoms are caused by inappropriate inflammatory response triggered by interaction between the environment, gut microbiome and host immune system in a genetically susceptible individual. Extranintestinal manifestations of IBD are common and can affect any body system outside the gut; they can precede or run parallel to GI inflammation. Renal involvement in IBD is uncommon and can be part of extraintestinal manifestation or metabolic complications of IBD. Many medications used to treat IBD can cause renal damage. Renal manifestation in children with IBD can range from asymptomatic biochemical abnormalities to variable stages of renal impairment with significant morbidity and even mortality burden.

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Secondary, AA, Amyloidosis

Cited by 155 publications

References 115 publications

The Pathology of Amyloidosis in Classification: A Review

The Pathology of Amyloidosis in Classification: A Review

Causes of AA amyloidosis: a systematic review

Renal involvement in paediatric inflammatory bowel disease

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