Schlosstein and colleagues tested whether the frequencies of 24 HL‑A antigens in ankylosing spondylitis, rheumatoid arthritis and gout differ from those of normal controls.
Case‑control typing study of Caucasian patients from two Los Angeles centers (ankylosing spondylitis 40, rheumatoid arthritis 119, gout 66) vs 906 controls, May 1971 to October 1972.
Methods
Design
Case‑control antigen frequency comparison
Typed May 1971 to October 1972
Data source
Wadsworth VA Hospital arthritis and gout clinics
UCLA Arthritis Clinic
Patients
40 with ankylosing spondylitis (Rome criteria)
119 with definite rheumatoid arthritis (ARA criteria)
66 with typical primary gout
906 Caucasian controls
Spondylitis with IBD, Reiter's disease, psoriasis or juvenile RA excluded
Exposure
24 HL‑A specificities
Microdroplet lymphocyte cytotoxicity test
W27 defined by 4 serum specimens from 3 donors
Outcomes
Antigen phenotype frequency vs controls
Chi‑square with p multiplied by 24 for the number of antigens tested
Key Findings
W27 was present in 88% of patients with ankylosing spondylitis (35 of 40), vs 8% of 906 controls (p < 0.0001).
None of the 24 antigens differed significantly from controls in rheumatoid arthritis or in gout.
Among 10 Black patients with ankylosing spondylitis, 8 carried W27, although its control frequency among American Black people is 4%.
Homozygosity was not required, because a large proportion of patients were clearly heterozygous for W27 and only 4 were possibly homozygous.
The authors estimated that 10.6 per 2000 W27 carriers are susceptible, vs 1 per 2000 in the general population, a risk about 10 times higher.
Board pearl
Assuming close linkage, the authors calculated W27 penetrance at only about 0.5%, because 8% of the population carries W27 but 0.05% has ankylosing spondylitis.
Authors' conclusion
This association between W27 and ankylosing spondylitis is so marked that it is possible to assume either very close genetic linkage of a specific immune responsiveness gene to the disease or perhaps a strong immunologic cross-reaction between W27 and the etiologic agent involved.
Schlosstein and colleagues tested whether the frequencies of 24 HL‑A antigens in ankylosing spondylitis, rheumatoid arthritis and gout differ from those of normal controls.
Case‑control typing study of Caucasian patients from two Los Angeles centers (ankylosing spondylitis 40, rheumatoid arthritis 119, gout 66) vs 906 controls, May 1971 to October 1972.
Methods
Design
Case‑control antigen frequency comparison
Typed May 1971 to October 1972
Data source
Wadsworth VA Hospital arthritis and gout clinics
UCLA Arthritis Clinic
Patients
40 with ankylosing spondylitis (Rome criteria)
119 with definite rheumatoid arthritis (ARA criteria)
66 with typical primary gout
906 Caucasian controls
Spondylitis with IBD, Reiter's disease, psoriasis or juvenile RA excluded
Exposure
24 HL‑A specificities
Microdroplet lymphocyte cytotoxicity test
W27 defined by 4 serum specimens from 3 donors
Outcomes
Antigen phenotype frequency vs controls
Chi‑square with p multiplied by 24 for the number of antigens tested
Key Findings
W27 was present in 88% of patients with ankylosing spondylitis (35 of 40), vs 8% of 906 controls (p < 0.0001).
None of the 24 antigens differed significantly from controls in rheumatoid arthritis or in gout.
Among 10 Black patients with ankylosing spondylitis, 8 carried W27, although its control frequency among American Black people is 4%.
Homozygosity was not required, because a large proportion of patients were clearly heterozygous for W27 and only 4 were possibly homozygous.
The authors estimated that 10.6 per 2000 W27 carriers are susceptible, vs 1 per 2000 in the general population, a risk about 10 times higher.
Board pearl
Assuming close linkage, the authors calculated W27 penetrance at only about 0.5%, because 8% of the population carries W27 but 0.05% has ankylosing spondylitis.
Authors' conclusion
This association between W27 and ankylosing spondylitis is so marked that it is possible to assume either very close genetic linkage of a specific immune responsiveness gene to the disease or perhaps a strong immunologic cross-reaction between W27 and the etiologic agent involved.