Authors: Robert Brannigan, MD and James Kashanian, MD
Testicular reserve is based on reproductive and androgenic function. Males may have a congenital or acquired defect in either reproductive function/spermatogenesis, androgenic function/testosterone, or both. Causes of testicular dysfunction are vast, and can include; cryptorchidism, disorders of sexual development (DSD), trauma, infection, iatrogenic, or medication use. Moreover, cancer treatment has been shown to affect all aspects of testicular function in a largely dose dependent and treatment dependent manner.
It has been well proven that spermatogenesis can be affected by chemotherapy in a dose dependent manner.  It is also known that prior chemotherapy is associated with an increase in post treatment LH and FSH levels . Likewise, radiation therapy can affect spermatogenic function by permanently damaging gonadal germ cells and at high enough doses can also affect Leydig cell function/testosterone production. Transient effects on spermatogenesis have been seen in very low doses of RT with cumulative doses as low as 2 Gy causing transient or even permanent azoospermia . Doses of RT in excess of 20Gy have also been shown to affect testosterone production with ensuing primary Hypogonadism .
The baseline parameters required to properly assess testicular reserve in the male cancer survivor are testosterone and FSH blood levels and a semen analysis.