All anabolic/androgenic steroids when taken in doses sufficient to promote muscle gain are expected to suppress endogenous testosterone production. Without the intervention of testosterone-stimulating substances, testosterone levels should return to normal within 1-4 months of drug secession. Note that prolonged hypogonadotrophic hypogonadism can develop secondary to steroid abuse, necessitating medical intervention. Primobolan® is generally described as having a low impact on endogenous testosterone production. While this may be true in small clinical doses (20-25 mg daily), this may not be a major distinction when used for physique- or performance-enhancing purposes. In one study, more than half of the patients receiving only 30-45 mg per day noticed a 15-65% suppression of gonadotropin levels. 585 While this is far from having no hormonal impact, the suppression caused by methenolone acetate may still be less pronounced than with many other agents. If Primobolan® is used at moderate doses for less than 8 weeks, hormonal recovery should not be a protracted experience.
Metenolone acetate , or methenolone acetate , sold under the brand names Primobolan , Primobolan S , Primonabol , and Nibal , is a synthetic , orally active anabolic–androgenic steroid (AAS) and derivative of dihydrotestosterone (DHT) which is marketed in Europe , Australia , and Mexico .      It has been used in the treatment of bone marrow diseases and anemia .   Metenolone acetate is the C17β acetate ester and a prodrug of metenolone ,    and is the form of metenolone that is used orally; the form that is used via depot intramuscular injection is metenolone enanthate .   Along with the related AAS mesterolone , metenolone acetate is one of the few AAS that is orally active but is not 17α-alkylated .  
In a study of 1,685 patients treated with CPA, elevated liver enzymes were seen in 10% of patients at a dosage of 50 mg/day and in 20% of patients at a dosage of greater than 100 mg/day.  A study of 2,506 patients given 18–136 mg/day for less than 48 months per patient reported a rate of %.   In a trial of 89 prostate cancer patients who received high-dose CPA for 4 years, there were elevated liver enzymes in % of the patients.  Yet another study of 105 patients found a hepatotoxicity rate of %, with serious hepatic injury occurring in %.  In 2002, it was reported that there were 18 case reports of CPA-associated hepatitis in the medical literature, with 6 of the cases resulting in death.  In addition, a review article cited a report of 96 instances of hepatotoxicity that were attributed to CPA, and 33 of these instances resulted in death.  Moreover, a 2014 review found that 15 cases specifically of CPA-induced fulminant (sudden-onset and severe) liver failure had been reported to date, with only one of these cases not resulting in death.  As such, the prognosis of CPA-induced liver failure is death.