Misdiagnosis of hereditary amyloidosis as AL (primary) amyloidosis

N Engl J Med. 2002 Jun 6;346(23):1786-91. doi: 10.1056/NEJMoa013354.

Abstract

Background: Hereditary, autosomal dominant amyloidosis, caused by mutations in the genes encoding transthyretin, fibrinogen A alpha-chain, lysozyme, or apolipoprotein A-I, is thought to be extremely rare and is not routinely included in the differential diagnosis of systemic amyloidosis unless there is a family history.

Methods: We studied 350 patients with systemic amyloidosis, in whom a diagnosis of the light-chain (AL) type of the disorder had been suggested by clinical and laboratory findings and by the absence of a family history, to assess whether they had amyloidogenic mutations.

Results: Amyloidogenic mutations were present in 34 of the 350 patients (9.7 percent), most often in the genes encoding fibrinogen A alpha-chain (18 patients) and transthyretin (13 patients). In all 34 of these patients, the diagnosis of hereditary amyloidosis was confirmed by additional investigations. A low-grade monoclonal gammopathy was detected in 8 of the 34 patients (24 percent).

Conclusions: A genetic cause should be sought in all patients with amyloidosis that is not the reactive systemic amyloid A type and in whom confirmation of the AL type cannot be obtained.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Amyloidosis / diagnosis*
  • Amyloidosis / genetics
  • Amyloidosis, Familial / complications
  • Amyloidosis, Familial / diagnosis*
  • Apolipoprotein A-I / genetics
  • DNA Mutational Analysis
  • Diagnostic Errors*
  • Female
  • Fibrinogen / genetics
  • Genotype
  • Heterozygote
  • Humans
  • Kidney / diagnostic imaging
  • Kidney / pathology
  • Middle Aged
  • Muramidase / genetics
  • Paraproteinemias / complications
  • Point Mutation*
  • Prealbumin / genetics
  • Radionuclide Imaging

Substances

  • Apolipoprotein A-I
  • Prealbumin
  • Fibrinogen
  • Muramidase