Abstract
Endometriosis is a common condition affecting up to 10% of women of reproductive age. Despite being described nearly 150 years ago its aetiology remains unclear. In addition there is a clear lack of knowledge of the natural history of the condition if left untreated. Numerous medical treatments have been described and are in common use, however the evidence for their efficacy at causing disease regression is limited at best. For endometriotic implants to continue to grow they need to develop additional blood supply and their angiogenic potential has been demonstrated. Vascular endothelial growth factor and prostaglandin E2 are, at least in part, believed to be responsible for this. Both of these require cyclooxygenase 2 for their production. Oestrogen is also essential for the growth of endometriosis and high levels have been demonstrated in endometriotic lesions. Local oestrogen production is predominantly the result of aromatase activity which is potently induced by prostaglandin E2. It is thus hypothesised that if the action of cyclooxygenase 2 is inhibited, endometriosis will regress as a consequence of both inhibition of angiogenesis and reduction in local oestrogen concentration. Based on this theory a randomised double blind placebo controlled trial was undertaken to test the hypothesis that valdecoxib (a cyclooxygenase 2 inhibitor) will cause regression of peritoneal endometriosis in patients with minimal or mild disease over a twelve week period. No significant change in disease quantity was demonstrated compared to placebo. There was a consistent (but statistically insignificant) improvement in pain symptoms in those subjects taking valdecoxib compared to placebo. It is concluded that valdecoxib is ineffective at causing disease regression in minimal and mild endometriosis.