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Abstract
Androgen deprivation therapy (ADT) for prostate carcinoma (PCa) may cause cardiometabolic complications unless intermittent androgen blockade (IAB) is instituted. An 80-year-old caucasian man was diagnosed intermediate grade (Gleason 4 + 3) PCa and was treated with continuous ADT with triptorelin plus bicalutamide. After 6 months of treatment, he experienced an acute myocardial infarction and 1 month after hospitalization he came to our outpatient clinic for fatigue, weight gain, and hyperglycemia. Due to iatrogenic hypogonadism, we decided to proceed with IAB, but after 3 months ADT withdrawal his serum testosterone (T) was still 0.5 ng/mL. Due to very low concomitant PSA levels (0.1 ng/mL) he was then proposed intermittent T-gel supplementation (Tostrex®) which was initiated according to the following scheme: 6 months on and 3 months off. T-gel dose was titrated tri-weekly in order to achieve T plasma levels below 3.49 ng/mL. After 6 months on, his serum T raised to a mean value of about 2.0 ng/mL without increments in PSA. After overall 12 months on, his serum T peaked to a mean value of 3.0 ng/mL while a delay in PSA rise was seen after 24 months (0.6 ng/mL) but remained stable until the last observation carried forward (LOCF), at 45 months. No clinical and biochemical PCa progression were observed at LOCF. Reversion of iatrogenic metabolic syndrome started after 6 months of T supplementation without using any add-on treatment. This case provides support that once regression of PCa growth is attained, T supplementation may be administered in well differentiated PCa, especially if IAB is not successful in reverting iatrogenic hypogonadism and its associated cardiac and metabolic complications.
Highlights
Testosterone is the fundamental steroid hormone that drives prostate growth but there is no proven evidence that T treatment may convert subclinical prostate carcinoma (PCa) to clinically detectable PCa (Rhoden and Averbeck, 2009; Jannini et al, 2011)
DISCUSSION it is well documented that T administration in castrated men with advanced or metastatic PCa leads to progression of disease (Fowler and Whitmore Jr., 1981), this aspect has never been investigated in patients with localized PCa after Androgen deprivation therapy (ADT) withdrawal
As far as we are aware, this is the first report of intermittent T supplementation in the long-term (45 months) in a patient with non-invasive PCa after ADT withdrawal and persistent severe secondary hypogonadism
Summary
Testosterone is the fundamental steroid hormone that drives prostate growth but there is no proven evidence that T treatment may convert subclinical PCa to clinically detectable PCa (Rhoden and Averbeck, 2009; Jannini et al, 2011). We decided to proceed with IAB, but after 3 months ADT withdrawal his serum testosterone (T) was still 0.5 ng/mL.
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