Aim of the study is to search for correlations between the MEFV genotype and the SAA polymorphisms with the clinical manifestations of FMF and the occurrence of amyloidosis in a large cohort of Armenian patients.
Treatment with weekly rilonacept provided marked and lasting improvement in the clinical signs and symptoms of CAPS, and normalized the levels of SAA from those associated with risk of developing amyloidosis.
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.
Influence of Serum Amyloid A (SAA1) and SAA2 gene polymorphisms on renal amyloidosis, and on SAA/C-reactive protein values in patients with familial mediterranean fever in the Turkish population.
Apart from the apparent inherent amyloidogenicity of SAA, it can not be excluded that certain amino acid substitutions could enhance its amyloidogenicity but also could contribute to tissue predilection in amyloidosis.
In Caucasian patients with JCA, the presence of the homozygous SAA1 alpha genotype indicates high risk of amyloidosis and should encourage early and aggressive anti-inflammatory therapy to keep circulating SAA levels as low as possible.
Because only SAA2-derived products deposit in mouse amyloid tissues, the resistance of SJL mice to amyloidosis seems to be due to defective SAA2 gene expression.