ISSN 2398-2950      

Amyloidosis

ffelis

Introduction

  • Rare conditions with abnormal proteinaceous deposits within tissues.
  • Cause: familial disease in Abyssinians or Siamese or secondary to chronic inflammation.
  • Signs: related to organ affected. May be localized or systemic.
  • Diagnosis: histopathology, special staining and immunohistochemistry.
  • Treatment: few options.
  • Prognosis: guarded, usually progressive.

Pathogenesis

Etiology

  • Chronic inflammatory process.
  • Neoplasia.
  • Idiopathic.

Pathophysiology

  • Reactive systemic amyloidosis (Amyloid AA) in Abyssinians.
  • May be another form of AA amyloid in Oriental Shorthair Oriental shorthair and Siamese Siamese.
  • Amyloid protein deposited in a variety of tissues.
  • Most commonly liver and kidneys.
  • Chronic inflammation (infection, neoplasia)   →   persistently elevated serum amyloid A protein (SAA)   →   degraded to amyloid A (AA).
  • SAA is an acute phase protein produced by the liver in response to macrophage-derived cytokines (eg IL-1, IL-6, TNF) secreted during inflammation.
  • In normal animal AA is further degraded to soluble peptides.
  • Aberrant enzymic processing of protein   →   self-aggregation   →   fibrils deposited in beta-pleated sheet   →   abnormal protein deposits replace normal tissue   →   clinical signs related to site of deposition and organ dysfunction.
  • Genetic factors likely to have a role as amyloidosis is not always a sequel to inflammation.
  • Systemic amyloidosis: precursors distributed in vascular system; extensive amyloid deposition in renal glomerular mesangium and basement membranes (renal medullary deposition)   →   proteinuria and progressive renal disease   →   hypoalbuminemia and loss of antithrombin III in urine can   →   hypercoagulability   →   thrombosis (pulmonary, aortic).
  • Localized amyloidosis: protein precursors normally or abnormally concentrated in localized tissues.
  • Mechanism of hepatic hemorrhage development not clear but possibly due to increased tissue fragility and increased bleeding tendency.
  • Distinguish from AL (immunoglobulin light chain) and feline pancreatic islet amyloidosis (islet amyloid polypeptide).

Timecourse

  • Usually chronic, progressive over years.
  • Sometimes more acute.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Niewold T A, van der Linde-Sipman J S, Murphy C et al (1999) Familial amyloidosis in cats - Siamese and Abyssinian AA proteins differ in primary sequence and pattern of deposition. Amyloid (3), 205-209 PubMed.
  • Godfrey D R & Day M J (1998) Generalised amyloidosis in two Siamese cats - spontaneous liver haemorrhage and chronic renal failure. JSAP 39 (9), 442-7 PubMed.
  • Blunder A S & Smith K C (1992) Generalised amyloidosis and acute liver haemorrhage in four cats. JSAP 33 (12), 566-570 VetMedResource.

Other sources of information

  • Grauer G F & DiBartola S P (2000) Glomerular disease. In: Textbook of Veterinary Internal Medicine.5th edn. Ettinger S J & Feldman E C (eds). Philadelphia: W B Saunders Co. pp 1662-1678.
  • Van der Lindepimen JS et al (1997) Generalised AA-amyloidosis in Siamese and oriental cats. Vet Immunol immunopathol 56, 1-10.
  • Zuber R M (1997) Amyloidosis in Oriental Shorthair cats. In: Consultations in Feline Internal Medicine 3. August J R (ed). Philadelphia: W B Saunders Co. pp 337-340.
  • DiBartola S P (1992) Renal amyloidosis in dogs and cats. In: Current Veterinary Therapy XI. Kirk R W & Bonagura J D (eds). Philadelphia: W B Saunders Co. pp 823-826.
  • Johnson K H & O'Brien T D (1992) Amyloid and amyloidosis. In:Current Veterinary Therapy XI.Kirk R W & Bonagura J D (eds). Philadelphia: W B Saunders Co. pp 59-62.

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