Literature DB >> 10571824

A case of hereditary amyloidosis transthyretin variant Met 30 with amyloid cardiomyopathy, less polyneuropathy, and the presence of giant cells.

Y Nakamura1, C Yutani, M Nakazato, Y Date, T Baba, Y Goto.   

Abstract

Transthyretin-Met 30 (TTR-Met 30) is a variant of transthyretin and is usually associated with familial amyloid polyneuropathy. It is rare that patients with TTR-Met 30 will primarily develop amyloid cardiomyopathy. This report presents a patient with late-onset TTR-Met 30 who primarily developed amyloid cardiomyopathy, with less amyloid polyneuropathy in the peripheral nervous system than is usually seen. An autopsy was performed, and histological examination revealed many foreign-body giant cells and macrophages in the area of amyloid deposition that was found in nearly all of the organs.

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Year:  1999        PMID: 10571824     DOI: 10.1046/j.1440-1827.1999.00962.x

Source DB:  PubMed          Journal:  Pathol Int        ISSN: 1320-5463            Impact factor:   2.534


  1 in total

1.  Antibodies to human serum amyloid P component eliminate visceral amyloid deposits.

Authors:  Karl Bodin; Stephan Ellmerich; Melvyn C Kahan; Glenys A Tennent; Andrzej Loesch; Janet A Gilbertson; Winston L Hutchinson; Palma P Mangione; J Ruth Gallimore; David J Millar; Shane Minogue; Amar P Dhillon; Graham W Taylor; Arthur R Bradwell; Aviva Petrie; Julian D Gillmore; Vittorio Bellotti; Marina Botto; Philip N Hawkins; Mark B Pepys
Journal:  Nature       Date:  2010-10-20       Impact factor: 49.962

  1 in total

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