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Primary hypogonadism associated with o,p' DDD (mitotane) therapy
1Medical and Research Services, Veterans Administration Hospital, Hines, Illinois 60141.
Abstract:
Mitotane is a drug which is concentrated largely in adipose tissue and the adrenal glands. It has a remarkable specificity for the adrenal cortex and can produce necrosis of that organ; consequently, it has been used as a therapeutic agent for adrenocortical carcinoma. Because of the similarity between adrenocortical and testicular tissue, mitotane could be expected to cause testicular damage; however, there is sparse support for this in the literature. We recently studied a patient who developed impotency due to primary testicular failure at the time that he was treated with mitotane. A testicular biopsy, performed about four months after the drug was discontinued, showed normal appearing Leydig cells and atrophy of the seminiferous tubules with the picture of a maturation arrest. In the four and one half years since he last received mitotane, the patient's libido has slowly improved and his plasma testosterone, gonadotropins and LH response to gonadotropin-releasing hormone have become essentially normal. We propose that mitotane can be cytotoxic to the testis as it is to the adrenal cortex.
Insights
Mitotane, used for adrenocortical carcinoma, may harm the testes, causing impotence and testicular failure. Recovery of testicular function is possible after discontinuing the drug.
Area of Science:
- Endocrinology
- Oncology
- Pharmacology
Background:
- Mitotane is a drug primarily used for treating adrenocortical carcinoma due to its cytotoxic effects on the adrenal cortex.
- Adrenocortical and testicular tissues share similarities, suggesting potential testicular toxicity from mitotane, though literature support is limited.
Observation:
- A patient treated with mitotane for adrenocortical carcinoma developed impotence attributed to primary testicular failure.
- Testicular biopsy revealed seminiferous tubule atrophy and maturation arrest, with normal Leydig cells, four months post-mitotane discontinuation.
Findings:
- The patient experienced gradual improvement in libido and normalization of testosterone, gonadotropins, and LH response to GnRH over 4.5 years after mitotane cessation.
- These observations suggest mitotane may possess cytotoxic properties affecting testicular function, similar to its known effects on the adrenal cortex.
Implications:
- Mitotane's potential testicular toxicity warrants further investigation and consideration in patients undergoing treatment for adrenocortical carcinoma.
- Understanding mitotane's effects on testicular function is crucial for managing potential side effects and monitoring patient recovery.