**4. Androgen deprivation therapy (ADT) and its side effects**

ADT is increasingly attained through the use of luteinizing hormone-releasing hormone (LHRH) agonists, which down-regulate anterior pituitary receptors and lead to therapeutic hypogonadism, or directly by inhibiting pituary receptors by LHRH antagonists. The standard castration level is < 50 ng/dL. Prostate cells are physiologically dependent on androgens which stimulate its growth, function and proferation. TST, although not tumorigenic, is essential for the growth and perpetuation of tumor cells (36).

Prostate cancer (PCa) displays a range of clinical behavior, from slow-growing tumors of no clinical significance to aggressively metastatic and lethal disease. Most PCa cases diagnosed with present diagnostic techniques fall into the moderately differentiated group (grade 2, Gleason 6), of which the cancer-specific 10–15-year mortality is 18–30%. This is even lower in the group of PCa diagnosed with grade 1 and 2 or Gleason 4–6, and there are subgroups of patients who are not at risk of dying from PCa even within 15years. Overall mortality is then determined by comorbidity (37). While both short- and long-term ADT are effective for treating PCa, it can often have significant side-effects. It is important that these complications are recognized and managed appropriately so that adverse effects on the patient's quality of life (QoL) are minimized. There has been an increase in the use of ADT at all stages of PCa in recent years. The extensive use of ADT is raising concerns about adverse effects – loss of BMD being the most prominent.
