Well, I can't answer to how the patients for the study were chosen, but I can say that many of them would have been the doctors' own patients.
That said, am I the only one who finds it exciting that somebody, somewhere, has bothered to try to figure out what's going on with the gender-based differences in this disease? Am I the only one who gets that maybe the reason for the lag in diagnosis in women could be based in this variance:
In this study of the association of ANKH genetic markers with AS, including 201 AS multiplex families, we found that ANKH variants located in two different regions of the ANKH gene were associated with AS. A more striking finding was that the genetic association for men and women with AS differed. In men, AS was associated with genetic markers at the 3' end of the ANKH gene, whereas in women AS appeared to be associated with genetic markers at the 5' end of the ANKH gene. As expected, when the genders of AS patients were analyzed separately, we observed more than one SNP in each region (within the same haplotype block) showing significant association with AS. Haplotype analyses appeared to confirm the results of the single-marker tests (FBAT analyses), indicating that the predisposing polymorphism(s) for men with AS probably lies at the 3' end of the ANKH gene, whereas those for affected women are probably at the 5' end of the gene. After Bonferroni correction for the number of haplotypes and models, the haplotype combination of rs26307 [C] and rs27356 [C] was significantly associated with men with AS; and the haplotype combination of rs28006 [C] and rs25957 [C] was significantly associated with women with AS. However, in both cases, the significance level was modest. We attribute this to the fact that we have not identified the aetiological variants in the men/women with AS. Despite the modest P values (which are a function of sample size), the calculated 'odds ratios' for increased risk (which provide estimates of the magnitude of the effect) were close to 2 for the transmission of rs26307 [C] rs27356 [C] to affected men, and close to 3 for the transmission of rs28006 [C] rs25957 [C] to affected women in the subset of families with affected individuals of both genders.
A test of interaction identified the region that was associated in men with AS (rs26307) as showing a difference in the strength of the association by gender. The region associated with AS in women only showed significance of the test of interaction among the subset of families with affected individuals of both genders. Our current efforts are to identify and analyze more common SNPs in these two regions, ultimately finding the predisposing polymorphisms in men and women.Sorry if I sound frustrated, but the ratio of men:women is not the point of this article and it frustrates the crap out of me that women and the progression of AS in women are constantly (apparently) being ignored. Does this genetic difference
make a difference? I don't know, but it is proof positive (to me) that there is a difference. And if more GPs and PCPs and rheumies knew about these things, if researchers bothered to do studies on women, maybe women like our Karen and Sue wouldn't be lost in diagnosis limbo. It has to start somewhere and this seems a pretty good start - figuring out that there is a genetic difference in where the disease sits in men and women (if that's what this article indeed says - my brain twitch activates automatically after a point). Why does it appear that AS is severe in different ways in both genders? Why does it appear that severe kyphosis is more common in men? Why does it appear that fusing doesn't occur in women until later in life? I don't know about anyone else, but I want to know these things and this is the first time I've seen anything beyond Dr. Monika Østensen and Dr. Harald Østensen's research of over 10 years ago that even talks about women with AS in a research capacity. One other article I've found (one dating back to 1959) acknowledge that women get it more frequently than was generally thought and noted differences in progression, but again, nobody actually bothered to look into the whys, the wherefors, and the hows. And nobody was actually listening in this particular case either, because this doctor felt in 1956 (the year the research was done) that the ratio was closer to 5:1 and for another 40 odd years, the mainstream medical community still believed the 10:1 crap.
By the way, for our moms to be out there, here's an article on their research:
Ankylosing Spondylitis: The Female Aspect OK, I'm going to get off my soapbox now. grumble grumble grouch. I need more coffee.
Warm hugs,
