Alan S Cohen, Amyloid Program, Boston University School of Medicine, Boston, USA

Copyright © 1998 Elsevier Ltd. All Rights Reserved.

Although a waxy tissue deposit was observed in pathologic laboratories in the early eighteenth century, it was Rudolph Virchow in 1854 who called these 'lardaceous deposits' of the liver and spleen amyloid, when he found them to stain with iodine and sulfuric acid. This belief that the material was made up of carbohydrates (i.e. cellulose) was challenged, and the proteinaceous nature of the substance was generally accepted by the turn of the century. Most amyloid was thought to be related to chronic infections (tuberculosis, osteomyelitis) and subsequently to chronic inflammation (rheumatoid arthritis) and the term secondary or reactive amyloid has persisted in the clinical literature. In 1886, it was noted that amyloid could appear de novo and the then unusual clinical form named primary or idiopathic amyloid was discovered. The association of amyloid with aging, especially in the brain and heart, was long known, but regarded as incidental epiphen-omena until recent years. Finally in 1952, in Portugal, a hereditary amyloid polyneuropathy was described, and has led to a growing literature of multiple kinships of hereditary amyloid.

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