Prevalence of HLA-B27 in the New Zealand population: effect of age and ethnicity
1 Department of Surgical Sciences, Dunedin School of Medicine, University of Otago, PO Box 913, Dunedin 9054, New Zealand
2 Department of Biochemistry, University of Otago, PO Box 56, Dunedin 9056, New Zealand
3 Department of Medicine, University of Otago, PO Box 7343, Wellington 6242, New Zealand
4 Wellington Regional Rheumatology Unit, Hutt Hospital, Private Bag 31907, Lower Hutt 5040, New Zealand
5 Department of Rheumatology Waikato Hospital, Private Bag 3200, Hamilton 3240, New Zealand
6 Department of Rheumatology and Immunology Christchurch Hospital, PO Box 4710, Christchurch 8140, New Zealand
7 Department of Medicine, Christchurch School of Medicine, PO Box 4345, Christchurch 8140, New Zealand
8 Department of Rheumatology Timaru Hospital, Private Bag 911, Timaru, Dunedin, New Zealand
9 Department of Rheumatology, Dunedin Hospital, Private Bag 1921, Dunedin 9054, New Zealand
10 Department of Medicine, Dunedin School of Medicine, PO Box 56, Dunedin 9054, New Zealand
Arthritis Research & Therapy 2013, 15:R158 doi:10.1186/ar4341Published: 22 October 2013
HLA-B27 genotyping is commonly used to support a diagnosis of ankylosing spondylitis (AS). A recent study has suggested that HLA-B27 may adversely affect longevity. The objectives of this study were to determine, for the first time, the prevalence of HLA-B27 in the New Zealand population, and to test whether HLA-B27 prevalence declines with age.
117 Caucasian controls, 111 New Zealand Māori controls, and 176 AS patients were directly genotyped for HLA-B27 using PCR-SSP. These participants and a further 1103 Caucasian controls were genotyped for the HLA-B27 tagging single nucleotide polymorphisms (SNPs) rs4349859 and rs116488202. All AS patients testing positive for HLA-B27 of New Zealand Māori ancestry underwent high resolution typing to determine sub-allele status.
HLA-B27 prevalence was 9.2% in New Zealand Caucasian controls and 6.5% in Māori controls. No decline in HLA-B27 prevalence with age was detected in Caucasian controls (p = 0.92). Concordance between HLA-B27 and SNP genotypes was 98.7-99.3% in Caucasians and 76.9-86% in Māori. Of the 14 AS patients of Māori ancestry, 1 was negative for HLA-B27, 10 were positive for HLAB*2705, and 3 positive for HLAB*2704. All cases of genotype discordance were explained by the presence of HLAB*2704.
HLA-B27 prevalence in New Zealand Caucasians is consistent with that of Northern European populations and did not decline with increasing age. In Māori with AS who were HLA-B27 positive, 76.9% were positive for HLA-B*2705, suggesting that genetic susceptibility to AS in Māori is primarily due to admixture with Caucasians.