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HAEM5:Immunoglobulin-related (AL) amyloidosis (view source)

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<blockquote class='blockedit'>{{Box-round|title=HAEM5 Conversion Notes|This page was converted to the new template on 2023-11-30. The original page can be found at [[HAEM4:Primary Amyloidosis]].

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<blockquote class='blockedit'>{{Box-round|title=HAEM5 Conversion Notes|This page was converted to the new template on 2023-12-04. The original page can be found at [[HAEM4:Primary Amyloidosis]].

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==Primary Author(s)*==

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*A member of the group of “monoclonal immunoglobulin deposition diseases” that are characterized by visceral and soft tissue deposition of aberrant immunoglobulin (Ig), which subsequently results in organ dysfunction<ref>{{Cite journal|last=Aucouturier|first=Pierre|last2=Khamlichi|first2=Ahmed A.|last3=Touchard|first3=Guy|last4=Justrabo|first4=Eve|last5=Cogne|first5=Michel|last6=Chauffert|first6=Bruno|last7=Martin|first7=Francois|last8=Preud'homme|first8=Jean-Louis|date=1993|title=Heavy-Chain Deposition Disease|url=http://www.nejm.org/doi/abs/10.1056/NEJM199311043291905|journal=New England Journal of Medicine|language=en|volume=329|issue=19|pages=1389–1393|doi=10.1056/NEJM199311043291905|issn=0028-4793}}</ref><ref>{{Cite journal|last=J|first=Buxbaum|date=1992|title=Mechanisms of disease: monoclonal immunoglobulin deposition. Amyloidosis, light chain deposition disease, and light and heavy chain deposition disease|url=https://pubmed.ncbi.nlm.nih.gov/1582976/|language=en|pmid=1582976}}</ref><ref>{{Cite journal|last=Herzenberg|first=Andrew M.|last2=Lien|first2=John|last3=Magil|first3=Alex B.|date=1996|title=Monoclonal heavy chain (immunoglobulin G3) deposition disease: report of a case|url=https://linkinghub.elsevier.com/retrieve/pii/S0272638696901419|journal=American Journal of Kidney Diseases|language=en|volume=28|issue=1|pages=128–131|doi=10.1016/S0272-6386(96)90141-9}}</ref><ref>{{Cite journal|last=Kambham|first=Neeraja|last2=Markowitz|first2=Glen S.|last3=Appel|first3=Gerald B.|last4=Kleiner|first4=Morton J.|last5=Aucouturier|first5=Pierre|last6=D'Agati|first6=Vivette D.|date=1999|title=Heavy chain deposition disease: The disease spectrum|url=https://linkinghub.elsevier.com/retrieve/pii/S0272638699704324|journal=American Journal of Kidney Diseases|language=en|volume=33|issue=5|pages=954–962|doi=10.1016/S0272-6386(99)70432-4}}</ref><ref name=":3">{{Cite journal|last=Ra|first=Kyle|last2=Ma|first2=Gertz|date=1995|title=Primary systemic amyloidosis: clinical and laboratory features in 474 cases|url=https://pubmed.ncbi.nlm.nih.gov/7878478/|language=en|pmid=7878478}}</ref><ref>{{Cite journal|last=Preud'homme|first=Jean-Louis|last2=Aucouturier|first2=Pierre|last3=Touchard|first3=Guy|last4=Striker|first4=Liliane|last5=Khamlichi|first5=Ahmed Amine|last6=Rocca|first6=Anna|last7=Denoroy|first7=Luc|last8=Cogné|first8=Michel|date=1994|title=Monoclonal immunoglobulin deposition disease (Randall type). Relationship with structural abnormalities of immunoglobulin chains|url=https://linkinghub.elsevier.com/retrieve/pii/S0085253815586365|journal=Kidney International|language=en|volume=46|issue=4|pages=965–972|doi=10.1038/ki.1994.355}}</ref><ref>{{Cite journal|last=Preud'Homme|first=Jean-Louis|last2=Aucouturier|first2=Pierre|last3=Touchard|first3=Guy|last4=Khamlichi|first4=Amhed Amine|last5=Rocca|first5=Anna|last6=Denoroy|first6=Luc|last7=Cogne|first7=Michel|date=1994|title=Monoclonal immunoglobulin deposition disease: A review of immunoglobulin chain alterations|url=https://linkinghub.elsevier.com/retrieve/pii/0192056194900329|journal=International Journal of Immunopharmacology|language=en|volume=16|issue=5-6|pages=425–431|doi=10.1016/0192-0561(94)90032-9}}</ref><ref>{{Cite journal|last=Serpell|first=L. C.|last2=Sunde|first2=M.|last3=Blake|first3=C. C. F.|date=1997|title=The molecular basis of amyloidosis|url=http://link.springer.com/10.1007/s000180050107|journal=Cellular and Molecular Life Sciences|volume=53|issue=12|pages=871|doi=10.1007/s000180050107}}</ref><ref name=":0">McKenna RW, et al., (2017). Plasma cell neoplasms: Monoclonal immunoglobulin deposition diseases, in World Health Organization Classification of Tumours of Haematopoietic and Lymphoid Tissues, Revised 4th edition. Swerdlow, SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J, Arber DA, Hasserjian RP, Le Beau MM, Orazi A, and Siebert R, Editors. IARC Press: Lyon, France, p254-255. </ref>

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*These monoclonal Ig deposition diseases overlap as clinically similar conditions—but likely represent chemically distinctive manifestations of similar pathological processes, which can be placed into two major categories: 1) primary amyloidosis (detailed herein); 2) [[~~Light Chain and Heavy Chain Deposition Disease~~|light chain and heavy chain deposition diseases]]<ref name=":0" /><ref name=":1">{{Cite journal|last=Ra|first=Kyle|last2=A|first2=Linos|last3=Cm|first3=Beard|last4=Rp|first4=Linke|last5=Ma|first5=Gertz|last6=Wm|first6=O'Fallon|last7=Lt|first7=Kurland|date=1992|title=Incidence and natural history of primary systemic amyloidosis in Olmsted County, Minnesota, 1950 through 1989|url=https://pubmed.ncbi.nlm.nih.gov/1558973/|language=en|pmid=1558973}}</ref>

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*These monoclonal Ig deposition diseases overlap as clinically similar conditions—but likely represent chemically distinctive manifestations of similar pathological processes, which can be placed into two major categories: 1) primary amyloidosis (detailed herein); 2) [[HAEM5:Monoclonal immunoglobulin deposition disease|light chain and heavy chain deposition diseases]]<ref name=":0" /><ref name=":1">{{Cite journal|last=Ra|first=Kyle|last2=A|first2=Linos|last3=Cm|first3=Beard|last4=Rp|first4=Linke|last5=Ma|first5=Gertz|last6=Wm|first6=O'Fallon|last7=Lt|first7=Kurland|date=1992|title=Incidence and natural history of primary systemic amyloidosis in Olmsted County, Minnesota, 1950 through 1989|url=https://pubmed.ncbi.nlm.nih.gov/1558973/|language=en|pmid=1558973}}</ref>

*An acquired systemic amyloidosis, primary amyloidosis or the preferred term “AL amyloidosis,” results from a plasma cell (pc) or in rare instances, a lymphoplasmacytic neoplasm

*AL amyloidosis is a rare clonal plasma cell dyscrasia, with a particularly devastating clinical phenotype that results from the extracellular amyloid fibril deposition in vital organs<ref name=":14">{{Cite journal|last=Ah|first=Bryce|last2=Rp|first2=Ketterling|last3=Ma|first3=Gertz|last4=M|first4=Lacy|last5=Ra|first5=Knudson|last6=S|first6=Zeldenrust|last7=S|first7=Kumar|last8=S|first8=Hayman|last9=F|first9=Buadi|date=2009|title=Translocation t(11;14) and survival of patients with light chain (AL) amyloidosis|url=https://pubmed.ncbi.nlm.nih.gov/19211640/|language=en|doi=10.3324/haematol.13369|pmc=PMC2649355|pmid=19211640}}</ref><ref name=":4">{{Cite journal|last=G|first=Merlini|date=2017|title=AL amyloidosis: from molecular mechanisms to targeted therapies|url=https://pubmed.ncbi.nlm.nih.gov/29222231/|language=en|doi=10.1182/asheducation-2017.1.1|pmc=PMC6142527|pmid=29222231}}</ref><ref>{{Cite journal|last=Ryšavá|first=Romana|date=2019|title=AL amyloidosis: advances in diagnostics and treatment|url=https://academic.oup.com/ndt/article/34/9/1460/5123556|journal=Nephrology Dialysis Transplantation|language=en|volume=34|issue=9|pages=1460–1466|doi=10.1093/ndt/gfy291|issn=0931-0509}}</ref>

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==Links==

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[[Monoclonal Immunoglobulin Deposition Diseases]]

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[[HAEM4:Monoclonal Immunoglobulin Deposition Diseases]]

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