A systematic search of published evidence was performed using Medline (1969 to September 2010).
RESULTS:
Androgen-dependency of prostate growth is evident only in the hypogonadal condition, but not in the eugonadal state (the "saturation hypothesis"). There is unequivocal evidence that reducing
androgen signaling to the hypogonadal range can reduce PC growth and patient symptoms. At physiological
testosterone concentration there is no link between
androgen levels and PC risk. In addition, different strategies of
androgen deprivation (ADT) for advanced PC are only palliative and rarely cure patients. Preliminary evidence indicates that a low
androgen milieu is associated with
tumor aggressiveness. Transition to
androgen-independence is complex and involves both selection and outgrowth of preexisting
androgen resistant clones, as well as adaptative upregulation of genes that help the
cancer cells to survive and grow after ADT. Because
androgens are essential for the regulation of fat distribution,
insulin sensitivity, and
lipid and bone metabolism, recent publications have highlighted the concept that ADT may also be involved with an increase in overall, as well as cardiovascular, morbidity and mortality.
CONCLUSIONS: While ADT still represents a cornerstone for the
palliative therapy of a small fraction of aggressive PC, a "misuse and/or abuse" of ADT should be avoided.