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Androgens and ankylosing spondylitis: a role in the pathogenesis?
E J Giltay1, D van Schaardenburg, L J Gooren
1Institute of Endocrinology, Reproduction and Metabolism, Hospital Vrije Universiteit, Amsterdam, The Netherlands. giltay@dds.nl
Annals of the New York Academy of Sciences
|July 23, 1999
Summary
Serum testosterone levels are not elevated in ankylosing spondylitis (AS) patients, suggesting testosterone does not perpetuate the condition. Further research is needed to fully understand the role of sex steroids in AS pathogenesis.
Area of Science:
- Endocrinology
- Immunology
- Rheumatology
Background:
- Ankylosing spondylitis (AS) predominantly affects males, with early hypotheses implicating androgenic steroids.
- Conflicting reports exist regarding serum androgen and estrogen levels in AS patients compared to controls.
Purpose of the Study:
- To investigate the role of sex steroids, including testosterone and dehydroepiandrosterone (DHEA), in the etiology and pathogenesis of ankylosing spondylitis.
- To evaluate the impact of hormonal imbalances on the immune response in AS.
Main Methods:
- Review of existing literature on serum hormone levels (testosterone, 17 beta-estradiol, androstenedione, 17 alpha-hydroxyprogesterone, DHEA sulfate) in AS patients and controls.
- Analysis of in vitro, animal, and human studies on the immunomodulatory effects of sex steroids.
- Examination of clinical outcomes following hormonal therapies (oral estrogen, human chorionic gonadotrophin) in AS patients.
Main Results:
- Recent studies show no significant difference in serum testosterone, 17 beta-estradiol, or androstenedione levels between AS patients and controls.
- Elevated levels of 17 alpha-hydroxyprogesterone and dehydroepiandrosterone (DHEA) sulfate were observed in AS patients, potentially due to hydroxylase deficiencies or stress response.
- DHEA enhances, while 17 beta-estradiol and progesterone inhibit, cell-mediated immune responses, suggesting a role in AS pathogenesis.
Conclusions:
- Serum testosterone levels are not elevated in AS patients, indicating it likely does not perpetuate long-standing disease or warrant antiandrogenic treatment.
- The role of sex steroids in AS pathogenesis remains incompletely understood due to the inability of cross-sectional studies to distinguish etiological factors from secondary effects.