Serum amyloid A1 -13 T/C alleles in Turkish familial Mediterranean fever patients with and without amyloidosis

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Abstract

Previously reported studies concerning the effect of homozygosity of the1.1allele of theSAAgene found a correlation between this haplotype and susceptibility to amyloidosis in FMF patients. Another report revealed a strong association betweenSAA1-13T/C and secondary amyloidosis in the rheumatoid arthritis patient group. In this study, we aimed to determine the effect ofSAA1-13T/C in FMF patients with and without amyloidosis. The study cohort, consisting of 166 patients with FMF was divided into two groups, according to the presence (n=66) or absence (n=100) of renal amyloidosis at study entry.MEFV genemutation analysis and allelic variant ofSAA1gene -13 T/C was analyzed according to the previously described techniques.SAA1-13 T allele frequencies were 0.5816, 0.23 and 0.4242 in controls, FMF patients and FMF-amyloidosis patients respectively. The difference between controls vs. FMF patients and FMF-amyloidosis patients were 0.0002 and 0.1673 respectively. It was 0.0071 for FMF-patients vs. FMF-amyloidosis. When 694 M/V homozygous nonamyloid-FMF group was compared with 694 M/V carriers of the FMF-amyloidosis group, the difference was 0.049. When carrying ‘TT allele was considered, the difference between controls vs. FMF patients and FMF-amyloidosis patients were 0.0001 and 0.58. It was 0.0003 for FMF patients vs. FMF-amyloidosis. When 694 M/V homozygous nonamyloid-FMF group was compared with 694 M/V carriers of the FMF-amyloidosis group, the difference was 0.03. Carrying SAA-13T in homozygote state revealed a 7.9 (95% CI 3.6 17.5) fold risk for the occurrence of amyloidosis when compared with FMF patients without amyloidosis. This was 8.75 (95% CI 3.0 - 25.1) when 694 M/V homozygotes were taken into consideration. Our data revealed that the genotypeSAA1-13T has at least an effect on the development of amyloidosis. As more data on this polymorphism accumulate, we will understand its effect on the pathogenesis of amyloidosis in FMF.

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