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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
AYSIN BAKKALOGLU, ALI DUZOVA, SEZA OZEN, BANU BALCI, NESRIN BESBAS, REZAN TOPALOGLU, FATIH OZALTIN, and ENGIN YILMAZ
ABSTRACT.
Methods. SAA1 and SAA2 gene polymorphisms and SAA levels were determined in 74 patients with FMF (39 female, 35 male; median age 11.5 yrs, range 1.0–23.0). All patients were on colchicine therapy. SAA1 and SAA2 gene polymorphisms were analyzed using polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). SAA and C-reactive protein (CRP) values were measured and SAA/CRP values were calculated. Results. The median SAA level was 75 ng/ml (range 10.2–1500). SAA1 gene polymorphisms were: a/a genotype in 23 patients (31.1%), a/ß genotype in 30 patients (40.5%), a/g genotype in one patient (1.4 %), ß/ß genotype in 14 patients (18.9%), ß/g genotype in 5 patients (6.8 %), and g/g genotype in one patient (1.4%). Of the 23 patients who had a/a genotype for the SAA1 polymorphism, 7 patients had developed renal amyloidosis (30.4%) compared to only one patient without this genotype (1/51; 2.0%); p < 0.001. SAA2 had no effect on renal amyloidosis. SAA1 and SAA2 genotypes had no significant effect on SAA levels. SAA/CRP values were significantly lower in patients with the SAA1a/a genotype, compared to other SAA1 genotypes: 0.16 (0.025–1.96) versus 0.23 (0.012–28.20), p < 0.05. Conclusion. SAA1a/a genotype is one genetic factor that confers a significant risk for amyloidosis in the Turkish FMF population. Neither the SAA1 nor SAA2 genotypes had a significant effect on SAA level. (J Rheumatol 2004;31:1139-42) Key Indexing Terms:
FAMILIAL MEDITERRANEAN FEVER
From the Departments of Pediatrics, Pediatric Nephrology, and Medical Biology, and the Rheumatology Unit, Hacettepe University Faculty of Medicine, Ankara, Turkey. A. Bakkaloglu, MD, Professor of Pediatrics; A. Duzova, MD, Assistant Professor of Pediatrics; S. Ozen, MD, Professor of Pediatrics; N. Besbas, MD, Professor of Pediatrics; R. Topaloglu, MD, Professor of Pediatrics; F. Ozaltin, MD, Fellow in Pediatric Nephrology, Department of Pediatrics, Pediatric Nephrology and the Rheumatology Unit; B. Balci, PhD; E. Yilmaz, PhD, Associate Professor of Medical Biology, Department of Medical Biology. Address reprint requests to Dr. A. Bakkaloglu, Department of Pediatrics, Hacettepe University Faculty of Medicine, 06100, Ankara, Turkey. E-mail: aysin@hacettepe.edu.tr Submitted August 26, 2002; revision accepted January 6, 2004.
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