ISSN 2398-2969      

Amyloidosis

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Introduction

  • Pathogenesis: abnormal proteinaceous deposits accumulate within tissues.
  • Signs: depend on which tissues are disrupted by amyloid accumulation.
  • May be systemic or localized: kidneys often affected , also liver and spleen.
  • Treatment: few options: colchicine and dimethyl sulfoxide (DMSO) have been tried.
  • Prognosis: usually progressive until death.
  • Familial and sporadic forms also occur.

Pathogenesis

Etiology

  • Abnormal protein deposits disrupt and replace functioning tissue.
  • Classified by chemical identity of precursor protein.
  • Abnormal protein not processed normally and peptide units with beta-pleated sheet structure assembled into fibrils. Amyloid fibrils derive from 15 precursor proteins (human): only 3 found in animals to date.
  • Different etiopathogenesis for different precursor proteins.
  • Amyloid fibrils comprise a polymer of repeated peptide units; different repeats for different forms of amyloid.
  • AA amyloidosis ('reactive' amyloidosis) by far the most common kind in both sporadic and familial cases.
  • Clinical signs relate to specific site of amyloid deposition.

Predisposing factors

General
  • Infection, inflammation, neoplasia → acute phase reactant protein production (serum amyloid A, SAA).
  • Truncation and polymerization of SAA → beta-pleated sheet → AA amyloidosis.
  • Not all dogs with inflammatory disease develop amyloidosis, so may be genetic component.

Pathophysiology

  • Secondary 'reactive' (AA) amyloidosis: persistent stimulus (infection, inflammation or neoplasia) → release of macrophage-derived cytokines → liver produces acute phase protein serum amyloid A → modified → deposited in tissues → aggregation into fibrils; sporadic or familial.Most common type of amyloid.
  • Primary (AL) amyloidosis: immunoglobulin light chain derived.(Rare).
  • Localized amyloidosis: protein precursors normally or abnormally concentrated in localized tissues. Apoprotein in A1 amyloidosis deposits in pulmonary arterial wall. Amyloid plaques in cerebral cortex of aged dogs.

Timecourse

  • Chronic, progressive.

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.
  • Jull B (1999) Pulmonary thrombosis and glomerular amyloidosis in a dog. Vet Med 94 (8), 686-689 VetMedResource.
  • Faunt K K et al (1998) Isolated right ventricular hypertrophy with severe pulmonary vascular apolipoprotein A1-derived amyloidosis in a dog. JAAHA 34 (1), 35-37 PubMed.
  • Venco L et al (1998) Pulmonary thromboembolism in a dog with renal amyloidosis. Vet Radiol Ultrasound 39 (6), 564-565 PubMed.

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). W B Saunders, Philadelphia. pp 1662-1678.
  • Mason N J & Day M J (1996)Renal amyloidosis in related English Foxhounds.JSAP37, 255-260.
  • Johnson K H & O'Brien T D (1992)Amyloid and amyloidosis.In: Kirk R W & Bonagura J D (eds)Current Veterinary Therapy XI.W B Saunders, Philadelphia. pp 59-62.
  • DiBartola S P, Tarr M J, Parker A T, Powers J D, Pultz J A (1989)Clinicopathological findings in dogs with renal amyloidosis - 59 cases (1976-1986).JAVMA195, 358-364.

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