A role for sex steroids in the pathogenesis of AS is suggested by the male predominance, the peak age of onset in young adults, the increased number of first manifestations and flares after pregnancy, and the fact that sex steroids may modulate immune functions. There is a theoretic possibility that (normal levels of) androgens are indeed relevant in the male sex skew of AS. It has been reported that men with AS have higher than normal androgen levels; however, the evidence that serum testosterone levels are elevated in patients with AS is not robust. Elevated DHEAS and 17 alpha-hydroxyprogesterone levels have been reported in male AS patients; these may be secondary to inflammation and stress but may theoretically also be causally related to AS. These elevations might result from a partial late onset 11 beta- or 21-hydroxylase deficiency. Current data on sex steroid hormones provide no straightforward explanation for the male predominance in AS. It is fair to say that present data in patients with long-standing AS are too limited to suggest a role for androgens in the perpetuation of the disease, but a role in the initiation and the early stages of AS cannot be excluded. Such information can only be obtained from prospective studies. Cross-sectional studies cannot clearly distinguish causal relation from secondary disease effects, because blood sampling to test these hypotheses only takes place many years after the onset of disease. The impact of sex steroids on these features of AS is still unresolved. There is as yet no rationale for the use of medication that modifies sex steroid hormones in the management of AS. Alternative explanations for the higher male prevalence of AS may be found in the different chromosomal configuration and body composition of men and women.