Hormonal pattern and testicular histology in patients with prostatic cancer after long-term treatment with a gonadotropin-releasing hormone agonist analogue

Eur Urol. 1988;15(1-2):125-7. doi: 10.1159/000473411.

Abstract

Seven patients suffering from prostatic cancer were treated with a depot form of D-Trp-6-luteinizing hormone-releasing hormone (LH-RH), a LH-RH agonist analogue (3 mg i.m. every 28 days) for a period of 24-32 months. The peptide induced a sharp and long-lasting inhibition of both gonadotropin and testosterone secretion. A sustained suppression of pituitary and testicular function was observed 40 days after the treatment was suspended. Testicular biopsies performed in all patients showed a marked impairment of Leydig cell mass and a complete spermatogenic arrest with a tubular derangement and fibrosis. Results indicate that the long-term continued gonadotropin-releasing hormone agonist analogue therapy induces not only a functional inhibition of testicular androgenesis but also anatomical testicular damage whose reversibility does not seem to be probable.

MeSH terms

  • Aged
  • Aged, 80 and over
  • Antineoplastic Agents / adverse effects
  • Antineoplastic Agents / therapeutic use*
  • Follicle Stimulating Hormone / metabolism*
  • Gonadotropin-Releasing Hormone / adverse effects
  • Gonadotropin-Releasing Hormone / analogs & derivatives*
  • Gonadotropin-Releasing Hormone / therapeutic use
  • Humans
  • Leydig Cells / drug effects
  • Luteinizing Hormone / metabolism*
  • Male
  • Middle Aged
  • Prostatic Neoplasms / drug therapy*
  • Spermatogenesis / drug effects
  • Testis / pathology*
  • Testosterone / metabolism*
  • Time Factors
  • Triptorelin Pamoate

Substances

  • Antineoplastic Agents
  • Triptorelin Pamoate
  • Gonadotropin-Releasing Hormone
  • Testosterone
  • Luteinizing Hormone
  • Follicle Stimulating Hormone