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Where has secondary amyloid gone?
| The first 150 words of the full text of this article appear below. |
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Introduction |
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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.
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Development of AA amyloidosis |
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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
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