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| '''For patient information, click [[Amyloidosis (patient information)|here]]''' | | '''For patient information, click [[Amyloidosis (patient information)|here]]''' |
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| {{CMG}}; {{AE}} {{SHH}} | | {{CMG}}; {{AE}}{{Sab}}, {{HK}}, {{SHH}} |
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| ==Overview==
| | {{SK}} |
| In 1639, Nicolaus Fontanus [[Autopsy|autopsied]] a young man who had [[ascites|ascitis]], [[jaundice]], [[liver abscess]] and [[splenomegaly]] and his report has been the first description of amyloidosis. and in 1959, Cohen and Calkins assessed an ultra-thin sections of amyloidotic tissues by [[Electron microscope|electron microscopic]] examination. Amyloidosis may be classified based on [[precursor]] of amyloidogenic [[protein]] into different subtypes, include AL amyloidosis ([[Light chain|Light chains]] of [[Immunoglobulin|immunoglobulines]]), AA amyloidosis ([[Serum amyloid A|Serum amyloid A protein]]), AF amyloidosis (Mutant [[transthyretin]], [[Apolipoprotein A1|A1-apolipoprotein,]] [[gelsolin]], [[fibrinogen]], etc.), ATTRwt amyloidosis (Wild-type [[transthyretin]]), and AH amyloidosis (ß2-microglobulin). Amyloidosis also may classified by their extension of organ involvement as systemic amyloidosis ([[AL amyloidosis|primary amyloidosis]], [[AA amyloidosis|secondary amyloidosis]], hereditary amyloidosis) and Organ-specific amyloidosis ([[cardiac amyloidosis]], [[Hepatic amyloidosis with intrahepatic cholestasis|hepatic amyloidosis]], [[renal amyloidosis]], etc.). [[Amyloid]] is an abnormal insoluble [[extracellular]] [[protein]] that deposits in the different tissues and causes organic dysfunction. These abnormal [[Amyloid|amyloids]] derived from misfolding and aggregation of normally soluble [[Protein|proteins]]. In systemic amyloidosis, [[amyloid]] gradually accumulate and [[amyloid]] deposition is widespread in the viscera, [[blood vessel]] walls, and in the different [[Connective tissue|connective tissues]]. In organ-specific amyloidoses, [[amyloid]] deposition occurs only in the origin organ or tissue of [[precursor]] [[protein]]. In microscopy pathology of amyloidosis, [[amyloid]] is detectable as typical green [[birefringence]] under [[Polarization|polarized]] light after [[Congo red]] staining, linear non-branching [[Fibril|fibrils]], distinct [[X-rays|X-ray]] diffraction pattern consistent with Pauling's model of a cross-beta fibril.
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| == Historical Perspective == | | ==[[Amyloidosis overview|Overview]]== |
| *In 1639, Nicolaus Fontanus [[Autopsy|autopsied]] a young man who had [[ascites|ascitis]], [[jaundice]], [[liver abscess]] and [[splenomegaly]] and his report has been the first description of amyloidosis.<ref name="pmid218384133">{{cite journal |vauthors=Kyle RA |title=Amyloidosis: a brief history |journal=Amyloid |volume=18 Suppl 1 |issue= |pages=6–7 |date=June 2011 |pmid=21838413 |doi=10.3109/13506129.2011.574354001 |url=}}</ref>
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| *In 1854, Rudolph Virchow introduced the term of [[amyloid]] as an macroscopic abnormality in some tissues.<ref name="pmid10940217">{{cite journal |vauthors=Sipe JD, Cohen AS |title=Review: history of the amyloid fibril |journal=J. Struct. Biol. |volume=130 |issue=2-3 |pages=88–98 |date=June 2000 |pmid=10940217 |doi=10.1006/jsbi.2000.4221 |url=}}</ref>
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| *In 1867, Weber reported the first case of amyloidosis associated with [[multiple myeloma]].<ref name="pmid218384133">{{cite journal |vauthors=Kyle RA |title=Amyloidosis: a brief history |journal=Amyloid |volume=18 Suppl 1 |issue= |pages=6–7 |date=June 2011 |pmid=21838413 |doi=10.3109/13506129.2011.574354001 |url=}}</ref>
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| *In 1922, Bennhold introduced [[Congo red|Congo red staining]] of [[amyloid]] that remains the [[Gold standard (test)|gold standard]] for [[diagnosis]].<ref name="pmid11677276">{{cite journal |vauthors=Khan MF, Falk RH |title=Amyloidosis |journal=Postgrad Med J |volume=77 |issue=913 |pages=686–93 |date=November 2001 |pmid=11677276 |pmc=1742163 |doi= |url=}}</ref>
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| *In 1959, Cohen and Calkins used ultra-thin sections of amyloidotic tissues and assessed by [[Electron microscope|electron microscopic]] examination, explained the presence of non-branching [[Fibril|fibrils]] with indeterminate length and variable width.<ref name="pmid10940217">{{cite journal |vauthors=Sipe JD, Cohen AS |title=Review: history of the amyloid fibril |journal=J. Struct. Biol. |volume=130 |issue=2-3 |pages=88–98 |date=June 2000 |pmid=10940217 |doi=10.1006/jsbi.2000.4221 |url=}}</ref><ref name="pmid218384133">{{cite journal |vauthors=Kyle RA |title=Amyloidosis: a brief history |journal=Amyloid |volume=18 Suppl 1 |issue= |pages=6–7 |date=June 2011 |pmid=21838413 |doi=10.3109/13506129.2011.574354001 |url=}}</ref>
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| == Classification == | | ==[[Amyloidosis historical perspective|Historical Perspective]]== |
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| === Amyloidosis may be classified based on [[precursor]] of amyloidogenic [[protein]] into different subtypes, include:<ref name="pmid25378951">{{cite journal |vauthors=Real de Asúa D, Costa R, Galván JM, Filigheddu MT, Trujillo D, Cadiñanos J |title=Systemic AA amyloidosis: epidemiology, diagnosis, and management |journal=Clin Epidemiol |volume=6 |issue= |pages=369–77 |date=2014 |pmid=25378951 |pmc=4218891 |doi=10.2147/CLEP.S39981 |url=}}</ref><ref name="pmid24998818">{{cite journal |vauthors=Misumi Y, Ando Y |title=[Classification of amyloidosis] |language=Japanese |journal=Brain Nerve |volume=66 |issue=7 |pages=731–7 |date=July 2014 |pmid=24998818 |doi= |url=}}</ref> === | | ==[[Amyloidosis classification|Classification]]== |
| {| class="wikitable"
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| !Type
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| !Amyloidogenic protein/ fibril
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| !Clinical syndrome
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| |[[Primary amyloidosis|AL (primary amyloidosis)]]
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| |[[Light chain|Light chains]] of [[Immunoglobulin|immunoglobulines]] (most common type)
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| |[[Monoclonal gammopathy]]
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| |[[AA amyloidosis|AA (secondary amyloidosis)]]
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| |[[Serum amyloid A|Serum amyloid A protein]]
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| |[[Chronic inflammation|Chronic inflammatory diseases]]
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| |AF
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| |Mutant [[transthyretin]], [[Apolipoprotein A1|A1-apolipoprotein,]] [[gelsolin]], [[fibrinogen]], etc.
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| |Familial [[polyneuropathy]]/[[cardiomyopathy]]/[[nephropathy]]
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| |ATTRwt
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| |Wild-type [[transthyretin]]
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| |[[Senile]] [[restrictive cardiomyopathy]] _ [[Transthyretin]]-related amyloidosis wild-type
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| |-
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| |AH
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| |ß2-microglobulin
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| |Long-term [[hemodialysis]]
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| |}
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| === Amyloidosis also may classified by their extension of organ involvement as below:<ref name="pmid21360109">{{cite journal |vauthors=Bilginer Y, Akpolat T, Ozen S |title=Renal amyloidosis in children |journal=Pediatr. Nephrol. |volume=26 |issue=8 |pages=1215–27 |date=August 2011 |pmid=21360109 |pmc=3119800 |doi=10.1007/s00467-011-1797-x |url=}}</ref><ref name="pmid28134587">{{cite journal |vauthors=Khoor A, Colby TV |title=Amyloidosis of the Lung |journal=Arch. Pathol. Lab. Med. |volume=141 |issue=2 |pages=247–254 |date=February 2017 |pmid=28134587 |doi=10.5858/arpa.2016-0102-RA |url=}}</ref> === | | ==[[Amyloidosis pathophysiology|Pathophysiology]]== |
| {| class="wikitable"
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| !Classification
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| !subtypes
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| !Causes
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| !Important clinical findings
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| | rowspan="3" |Systemic amyloidosis
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| |[[AL amyloidosis|Primary amyloidosis (AL)]]
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| * Aggregation and deposition of [[immunoglobulin]] [[Light chain|light chains]] that usually produced by [[plasma cell]] clones
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| * [[Nephrotic syndrome]]
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| * [[Restrictive cardiomyopathy]]
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| * [[Peripheral neuropathy]]
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| * [[Hepatomegaly]] with elevated [[liver enzymes]]
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| * [[Macroglossia]]
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| * [[Purpura]] and an unexplained [[Hemorrhagic diathesis|bleeding diathesis]]
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| |[[AA amyloidosis|Secondary amyloidosis (AA)]]
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| * Chronic [[inflammation]] ([[Tuberculosis|TB]], [[familial mediterranean fever]], [[rheumatoid arthritis]] and [[multiple myeloma]])
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| * [[Nephrotic syndrome]]
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| * [[Congestive heart failure|Heart failure]]
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| |[[Heredity|Hereditary]] amyloidosis
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| * Amyloidogenic [[Mutation|mutations]] and subsequently deposition of [[Amyloid|amyloids]]
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| * [[Congestive heart failure|Heart failure]]
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| * [[Cardiac arrhythmia|Arrhythmia]]
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| | rowspan="5" |Organ-specific amyloidosis
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| |[[Renal amyloidosis]]
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| | rowspan="5" |
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| * [[AL amyloidosis|Immunoglobulin light-chain amyloidosis (AL amyloidosis)]]
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| * [[Transthyretin-related hereditary amyloidosis|Transthyretin-related amyloidosis]] (associated with familial/mutant or senile/wild-type [[Transthyretin|TTR]])
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| * [[Proteinuria]]
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| * [[Nephrotic syndrome]]
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| * [[Chronic renal failure]]
| | ==[[Amyloidosis causes|Causes]]== |
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| |[[Cardiac amyloidosis]]
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| * [[Systolic dysfunction]]
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| * [[Diastolic dysfunction]]
| | ==[[Amyloidosis differential diagnosis|Differentiating Amyloidosis from other Diseases]]== |
| * [[Cardiac arrhythmia|Arrhythmia]]
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| |[[Hepatic amyloidosis with intrahepatic cholestasis|Hepatic amyloidosis]]
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| * [[Hepatomegaly]]
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| * Elevated [[liver enzymes]]
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| |Amyloid neuropathy
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| * [[Peripheral neuropathy]] and [[autonomic neuropathy]]
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| * [[Neurodegenerative disease|Neurodegenerative disorders]]
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| ** [[Parkinson's disease|Parkinson]], [[Alzheimer's disease|Alzheimer]], and [[Huntington's disease]]
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| |Gastrointestinal amyloidosis
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| * Nonspecific findings
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| ** [[Dyspepsia]], [[abdominal pain]], [[diarrhea]], [[malabsorption]]
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| |}
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| == Pathophysiology == | | ==[[Amyloidosis epidemiology and demographics|Epidemiology and Demographics]]== |
| *[[Amyloid]] is an abnormal insoluble [[extracellular]] [[protein]] that deposits in the different tissues and causes organic dysfunction and a wide variety of clinical syndromes.<ref name="pmid23979488">{{cite journal |vauthors=Gillmore JD, Hawkins PN |title=Pathophysiology and treatment of systemic amyloidosis |journal=Nat Rev Nephrol |volume=9 |issue=10 |pages=574–86 |date=October 2013 |pmid=23979488 |doi=10.1038/nrneph.2013.171 |url=}}</ref><ref name="pmid23227278">{{cite journal |vauthors=Baker KR, Rice L |title=The amyloidoses: clinical features, diagnosis and treatment |journal=Methodist Debakey Cardiovasc J |volume=8 |issue=3 |pages=3–7 |date=2012 |pmid=23227278 |pmc=3487569 |doi= |url=}}</ref>
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| *These abnormal [[Amyloid|amyloids]] derived from misfolding and aggregation of normally soluble [[Protein|proteins]].<ref name="pmid16409147">{{cite journal |vauthors=Pepys MB |title=Amyloidosis |journal=Annu. Rev. Med. |volume=57 |issue= |pages=223–41 |date=2006 |pmid=16409147 |doi=10.1146/annurev.med.57.121304.131243 |url=}}</ref>
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| *[[Amyloid]] deposition can disrupt tissue structure of involved organ and consequently leads to organ failure.<ref name="pmid26155101">{{cite journal |vauthors=Jerzykowska S, Cymerys M, Gil LA, Balcerzak A, Pupek-Musialik D, Komarnicki MA |title=Primary systemic amyloidosis as a real diagnostic challenge - case study |journal=Cent Eur J Immunol |volume=39 |issue=1 |pages=61–6 |date=2014 |pmid=26155101 |pmc=4439975 |doi=10.5114/ceji.2014.42126 |url=}}</ref>
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| ===Systemic Amyloidosis===
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| *In systemic amyloidosis, [[amyloid]] gradually accumulate and [[amyloid]] deposition is widespread in the viscera, [[blood vessel]] walls, and in the different [[Connective tissue|connective tissues]].<ref name="pmid23227278">{{cite journal |vauthors=Baker KR, Rice L |title=The amyloidoses: clinical features, diagnosis and treatment |journal=Methodist Debakey Cardiovasc J |volume=8 |issue=3 |pages=3–7 |date=2012 |pmid=23227278 |pmc=3487569 |doi= |url=}}</ref><ref name="pmid16409147">{{cite journal |vauthors=Pepys MB |title=Amyloidosis |journal=Annu. Rev. Med. |volume=57 |issue= |pages=223–41 |date=2006 |pmid=16409147 |doi=10.1146/annurev.med.57.121304.131243 |url=}}</ref>
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| ====Primary Amyloidosis (AL)====
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| *[[AL amyloidosis|Primary (AL) amyloidosis)]] is the most common type of amyloidosis. It results from aggregation and deposition of monoclonal [[Immunoglobulin|immunoglobulin (Ig)]] [[Light chain|light chains]] that usually produced by [[plasma cell]] clones.
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| *Change in the [[secondary structure]] or [[tertiary structure]] of a monoclonal [[light chain]] results in abnormal folding of the [[light chain]] that abnormally form [[amyloid]] [[Fibril|fibrils]].<ref name="pmid22909024">{{cite journal |vauthors=Desport E, Bridoux F, Sirac C, Delbes S, Bender S, Fernandez B, Quellard N, Lacombe C, Goujon JM, Lavergne D, Abraham J, Touchard G, Fermand JP, Jaccard A |title=Al amyloidosis |journal=Orphanet J Rare Dis |volume=7 |issue= |pages=54 |date=August 2012 |pmid=22909024 |pmc=3495844 |doi=10.1186/1750-1172-7-54 |url=}}</ref>
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| *This type of amyloidosis most frequently involve the [[kidney]] (usually [[proteinuria]] with the [[nephrotic syndrome]]) and the [[heart]].<ref name="pmid116772762">{{cite journal |vauthors=Khan MF, Falk RH |title=Amyloidosis |journal=Postgrad Med J |volume=77 |issue=913 |pages=686–93 |date=November 2001 |pmid=11677276 |pmc=1742163 |doi= |url=}}</ref>
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| *In [[AL amyloidosis|primary (AL) amyloidosis]] survival rate depends on:<ref name="pmid229090242">{{cite journal |vauthors=Desport E, Bridoux F, Sirac C, Delbes S, Bender S, Fernandez B, Quellard N, Lacombe C, Goujon JM, Lavergne D, Abraham J, Touchard G, Fermand JP, Jaccard A |title=Al amyloidosis |journal=Orphanet J Rare Dis |volume=7 |issue= |pages=54 |date=August 2012 |pmid=22909024 |pmc=3495844 |doi=10.1186/1750-1172-7-54 |url=}}</ref>
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| **Type of organ involvement ([[amyloid]] heart disease is the main prognostic factor)
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| **The severity of different organs involvement
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| **[[Hematology|Haematological]] response to treatment
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| *The median [[Survival analysis|survival]] of patients with [[AL amyloidosis]] is aproximately 3.8 years.<ref name="pmid21483018">{{cite journal |vauthors=Merlini G, Seldin DC, Gertz MA |title=Amyloidosis: pathogenesis and new therapeutic options |journal=J. Clin. Oncol. |volume=29 |issue=14 |pages=1924–33 |date=May 2011 |pmid=21483018 |pmc=3138545 |doi=10.1200/JCO.2010.32.2271 |url=}}</ref>
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| For more information about primary amyloidosis click [[AL amyloidosis|'''here''']].
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| ====Secondary Amyloidosis (AA)==== | | ==[[Amyloidosis risk factors|Risk Factors]]== |
| *[[AA amyloidosis|Secondary amyloidosis]] is associated with chronic [[inflammation]] (such as [[tuberculosis]] or [[rheumatoid arthritis]]).<ref name="pmid116772762">{{cite journal |vauthors=Khan MF, Falk RH |title=Amyloidosis |journal=Postgrad Med J |volume=77 |issue=913 |pages=686–93 |date=November 2001 |pmid=11677276 |pmc=1742163 |doi= |url=}}</ref>
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| *[[AA amyloidosis|Secondary or reactive amyloidosis (AA)]] is approximately 45% of all systemic amyloidosis.<ref name="pmid119640392">{{cite journal |vauthors=Röcken C, Shakespeare A |title=Pathology, diagnosis and pathogenesis of AA amyloidosis |journal=Virchows Arch. |volume=440 |issue=2 |pages=111–122 |date=February 2002 |pmid=11964039 |doi=10.1007/s00428-001-0582-9 |url=}}</ref>
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| *[[Pathogenesis]] of [[AA amyloidosis|secondary amyloidosis]] is multifactorial that include:
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| **[[Primary structure]] of the [[precursor]] protein
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| **Acute phase response
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| **Nonfibril [[Protein|proteins]] ([[amyloid]] P component, [[Apolipoprotein E|apo E]], [[Glycosaminoglycan|GAGs]], [[Proteoglycan|proteoglycans]] and [[basement membrane]] [[Protein|proteins]])
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| **[[Receptor (biochemistry)|Receptors]]
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| **[[Lipid metabolism]]
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| **[[Protease|Proteases]]
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| For more information about secondary amyloidosis click '''[[AA amyloidosis|here]]'''.
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| ====Hereditary Amyloidosis==== | | ==[[Amyloidosis screening|Screening]]== |
| *Hereditary (or familial) amyloidosis are [[Autosome|autosomal]] [[Dominance relationship|dominant]] diseases that [[inherited]] variant [[Protein|proteins]] cause the production and deposition of [[amyloid]] fibrils.<ref name="pmid116772762">{{cite journal |vauthors=Khan MF, Falk RH |title=Amyloidosis |journal=Postgrad Med J |volume=77 |issue=913 |pages=686–93 |date=November 2001 |pmid=11677276 |pmc=1742163 |doi= |url=}}</ref>
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| *Hereditary amyloidosis are due to amyloidogenic [[Mutation|mutations]] and subsequently deposition of [[Amyloid|amyloids]], include:<ref name="pmid24497558">{{cite journal |vauthors=Mahmood S, Palladini G, Sanchorawala V, Wechalekar A |title=Update on treatment of light chain amyloidosis |journal=Haematologica |volume=99 |issue=2 |pages=209–21 |date=February 2014 |pmid=24497558 |pmc=3912950 |doi=10.3324/haematol.2013.087619 |url=}}</ref>
| | ==[[Amyloidosis natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
| **[[Transthyretin|Transthyretin (TTR)]] (most common [[inherited]] [[mutation]])
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| **[[Fibrinogen]]
| | ==Diagnosis== |
| **[[Apolipoprotein A1]]
| | [[Amyloidosis diagnostic study of choice|Diagnostic study of choice]] | [[Amyloidosis history and symptoms|History and Symptoms]] | [[Amyloidosis physical examination|Physical Examination]] | [[Amyloidosis laboratory findings|Laboratory Findings]] | [[Amyloidosis electrocardiogram|Electrocardiogram]] | [[Amyloidosis x ray|X-ray]] | [[Amyloidosis echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[Amyloidosis CT scan|CT scan]] | [[Amyloidosis MRI|MRI]] | [[Amyloidosis other imaging findings|Other Imaging Findings]] | [[Amyloidosis other diagnostic studies|Other Diagnostic Studies]] |
| **[[Apolipoprotein A2]]
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| **[[Lysozyme]]
| | ==Treatment== |
| **[[Gelsolin]] [[Gene|genes]]
| | [[Amyloidosis medical therapy|Medical Therapy]] | [[Amyloidosis surgery|Surgery]] | [[Amyloidosis primary prevention|Primary Prevention]] | [[Amyloidosis secondary prevention|Secondary Prevention]] | [[Amyloidosis cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Amyloidosis future or investigational therapies|Future or Investigational Therapies]] |
| ===Organ-specific Amyloidosis=== | |
| *In this type of amyloidoses, [[amyloid]] deposition occurs only in the origin organ or tissue of [[precursor]] [[protein]].<ref name="pmid23451869">{{cite journal |vauthors=Blancas-Mejía LM, Ramirez-Alvarado M |title=Systemic amyloidoses |journal=Annu. Rev. Biochem. |volume=82 |issue= |pages=745–74 |date=2013 |pmid=23451869 |pmc=4044913 |doi=10.1146/annurev-biochem-072611-130030 |url=}}</ref>
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| *Some [[Neurodegenerative disease|neurodegenerative disorders]] such as [[Parkinson's disease]], [[Alzheimer's disease|Alzheimer]], and [[Huntington's disease]] may occur in localised amyloidosis.
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| *Localised amyloidoses can accure due to deposition of [[intracellular]] and/or [[extracellular]] [[amyloid]].
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| **[[Huntington's disease]]: [[intracellular]] [[protein]] deposition
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| **[[Parkinson's disease]]: [[intracellular]] [[protein]] deposition
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| **[[Alzheimer's disease]]: [[intracellular]] ([[Tau protein]] [[Fibril|fibrils]]) and [[extracellular]] ([[amyloid]] β fibrils) deposition
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| ===Microscopic Pathology===
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| In microscopy pathology of amyloidosis, [[amyloid]] is detectable as:<ref name="pmid119640392">{{cite journal |vauthors=Röcken C, Shakespeare A |title=Pathology, diagnosis and pathogenesis of AA amyloidosis |journal=Virchows Arch. |volume=440 |issue=2 |pages=111–122 |date=February 2002 |pmid=11964039 |doi=10.1007/s00428-001-0582-9 |url=}}</ref><ref name="pmid116772762">{{cite journal |vauthors=Khan MF, Falk RH |title=Amyloidosis |journal=Postgrad Med J |volume=77 |issue=913 |pages=686–93 |date=November 2001 |pmid=11677276 |pmc=1742163 |doi= |url=}}</ref>
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| *Typical green [[birefringence]] under [[Polarization|polarized]] light after [[Congo red]] staining (appears in red under normal light)
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| *Linear non-branching [[Fibril|fibrils]] (indefinite length with an approximately same diameter)
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| *Distinct [[X-rays|X-ray]] diffraction pattern consistent with Pauling's model of a cross-beta fibril
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| ==Case Studies== | | ==Case Studies== |
| [[Amyloidosis case study one|Case #1]] | | [[Amyloidosis case study one|Case #1]] |
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| {{Metabolic pathology}}
| | [[Category:Disease]] |
| | | [[Category:Cardiology]] |
| [[Category:Medicine]] | | [[Category:Pulmonology]] |
| <references />
| | [[Category:Immunology]] |