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Letters to the Editor |
1 Department of Clinical Pathology, Juntendo University, School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan, Fax 81-03-3813-0293, E-mail toshiyam{at}med.juntendo.ac.jp
To the Editor:
MacGregor et al. (1) reported a twin-study of the genetic contribution to baseline serum concentrations of two acute-phase proteins, C-reactive protein and serum amyloid A protein (SAA). In their discussion, they stated that no studies had been reported of associations between particular isoforms and different baseline values of SAA. Although twins were not used as subjects, we earlier reported genetic effects on SAA serum concentrations.
Acute-phase SAA is divided into two major isotypes, SAA1 and SAA2, which are coded at different loci. The dominant isotype, SAA1, consists of six allelic variants (SAA1.1 to SAA1.6) (2). In the Japanese population, three major alleles, SAA1.1 (52Val, 57Ala), SAA1.3 (52Ala, 57Ala), and SAA1.5 (52Ala, 57Val), which differ from each other in SAA1 exon 3 structure, appear with approximately equal frequencies (0.30–0.35). Among 280 healthy Japanese (3), the mean serum SAA concentrations in SAA1.5 homozygotes, SAA1.5 heterozygotes, and non-SAA1.5 carriers were 5.7, 4.1, and 2.2 mg/L, respectively (analyzed after logarithmic conversion of the raw data). The mean SAA concentration (SD range) was 4.5 (2.6–7.8) mg/L in SAA1.5 carriers, whereas that in noncarriers was 2.2 (1.4–3.6) mg/L (P <0.001). The SAA/C-reactive protein ratio was significantly higher in SAA1.5 carriers than in noncarriers in Japanese patients with rheumatoid arthritis (4). More recently we reported that human recombinant SAA1.5 protein is cleared from the circulation more slowly than other isoforms in mice (5). Differences in plasma clearance may therefore be one of the possible factors responsible for such genetic effects.
The differences in SAA isoforms are not likely to be attributable to a method effect of the analytical method because we used an assay (6) that has been confirmed by polyacrylamide gel electrophoresis analysis (7).
SAA1 allele frequencies in the United Kingdom have been reported to be 0.76, 0.19, and 0.05 for SAA1.1, SAA1.5 (originally considered as SAA1.2), and SAA1.3, respectively (8). It is predicted that 
35% of the English population (individuals homozygous and heterozygous for SAA1.5) have a tendency to have higher SAA serum concentrations.
As MacGregor et al. (1) noted, SAA may have some role in atherogenesis. We are also interested to learn whether the genetic effects causing the differences in serum SAA concentrations have any associations with atherogenic diseases.
References
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