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Pituitary hyperplasia after goserelin (LHRH-analogue) therapy
Neuropathology and Applied Neurobiology
|February 1, 1991
Summary
Goserelin (Zoladex) treatment for prostate cancer may cause pituitary gland hyperplasia in humans. This condition involves the abnormal growth of hormone-producing cells in the pituitary gland.
Area of Science:
- Endocrinology
- Oncology
- Pathology
Background:
- Prostate carcinoma treatment often involves androgen deprivation therapy.
- Goserelin (Zoladex), a luteinizing hormone-releasing hormone (LHRH) analogue, suppresses testosterone production to castration levels, mimicking orchidectomy.
- This mechanism involves down-regulation of pituitary receptors, reducing follicle-stimulating hormone (FSH) and luteinizing hormone (LH).
Observation:
- Autopsy revealed diffuse, partially nodular hyperplasia of growth hormone (GH) and adrenocorticotropin (ACTH) producing cells in the anterior pituitary gland of a patient treated with goserelin.
- The patient had received goserelin for 16 months for metastasizing prostate carcinoma.
Findings:
- Goserelin's down-regulation of pituitary receptors may lead to increased hypothalamic releasing hormone (RH) secretion.
- This increased RH secretion could be responsible for the observed ACTH- and GH-cell hyperplasia.
- The findings suggest goserelin might induce pituitary hyperplasia in humans, similar to pituitary adenomas observed in rats.
Implications:
- This case highlights a potential, previously unconfirmed side effect of goserelin therapy in humans.
- Further investigation is warranted to understand the mechanism and clinical significance of goserelin-induced pituitary hyperplasia.
- Clinicians should be aware of this potential pituitary complication when managing patients with prostate cancer using LHRH analogues.