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Ann Rheum Dis 2000;59:577-579 ( August )

Leader

Where has secondary amyloid gone?

The first 150 words of the full text of this article appear below.

	Introduction

There is a growing clinical impression that the incidence of amyloid secondary to rheumatoid disease is declining. Recent studies from Finland strongly support this impression.^1-3 The prevalence of amyloidosis in patients with rheumatoid arthritis who died in 1989 (about 6%)¹ was lower than in earlier studies.⁴ In a recent cohort of patients with early rheumatoid arthritis followed up for 8-14 years no one died from amyloidosis.² In a hospital for rheumatic diseases the annual number of biopsies positive for amyloid decreased from more than 60 in 1987 to fewer than 10 recently.³ The question arises whether this is a true decline of the incidence or a more concealed clinical presentation of this type of amyloidosis.

	Development of AA amyloidosis

Secondary amyloidosis is nowadays called systemic AA amyloidosis. It is associated with chronic inflammation and results from systemic deposition of the acute phase reactant serum amyloid A protein (SAA) in a fibrillar structure. SAA behaves similarly to C reactive . . . [Full text of this article]

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