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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.
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 protein, being hardly detectable in normal situations and increasing quickly and dramatically during inflammation.5 In selected populations of patients with rheumatoid arthritis 5–20% of patients with longstanding disease will develop AA amyloidosis, depending upon the severity and duration of the arthritis in the population investigated.6 ,7
Although longstanding inflammation is necessary for the development of AA amyloidosis, it is not sufficient. Most people with a longstanding increase in SAA levels will never develop AA amyloidosis. In Europe AA amyloidosis is seen more often than in North America. Food, lifestyle, differences in drug treatment, other concurrent diseases, and genetic factors might be responsible for this difference. Genetic predisposition may be conditional for amyloid formation. One possible factor is homozygosity for SAA subtypes.8 ,9 Genetic research of diseases connected to the development of AA amyloidosis, such as familial …