title: Oestrogen secreting Leydig cell tumour and GnRH agonist in-vivo and in-vitro studies.
abstract: OBJECTIVE
  The purposes of our study concerning two patients with oestrogen secreting Leydig cell tumour were to determine whether endogenous LH levels are involved in testicular tumour steroidogenesis and whether aromatase activity of oestrogen secreting Leydig cell tumours is directly or indirectly dependent on LH levels.
  
  
  METHODS
  E2 and T were evaluated after hCG injection (5000 IU) during 96 hours. Bio and immuno LH, T, E2, were determined at the basal state and after administration of D-Trp-6-GnRH agonist (3.75 mg) every 3 weeks. The abnormal testis was removed after the third injection and testicular venous blood was collected during the operation. Testicular tumour was incubated with 4-14C-T.
  
  
  RESULTS
  Oestradiol (E2) response to hCG injection (5000 IU) was prolonged and exaggerated while that of testosterone (T) was similar to that of the controls. The aromatase index (E2/T) remained elevated even 96 hours after hCG. Intramuscular injection of the GnRH agonist, D-Trp-6-GnRH (3.75 mg) resulted in a reduction of immunoreactive and bioactive LH. T was decreased to about 10% of baseline levels and E2 fell from 240 to 36 pmol/l. In the blood of the spermatic veins collected in the course of surgery, E2 levels were found to be lower in comparison with the controls. E2 was found to be twofold higher in the spermatic vein draining the tumoral side than in that of the contralateral testis. Incubation of the testicular tumours with 4-14C-T, displayed a reduced aromatase activity (conversion of T to E2: 0.3 and 0.1% in patients 1 and 2 respectively).
  
  
  CONCLUSIONS
  The kinetics of E2 response to hCG administration would suggest a modification of the regulation of the aromatase activity in this type of oestrogen secreting tumour. A certain endogenous LH level may be necessary to supply a sufficient quantity of T substrate, and to maintain aromatase activity of such Leydig cell tumours secreting oestrogens. These tumours seem to be responsive to endogenous LH levels.
authors.affiliation: Department of Endocrinology, University Bretagne Occidentale, Brest, France.
authors.forename: V
authors.initials: V
authors.lastname: Kerlan
authors.forename: K
authors.initials: K
authors.lastname: Nahoul
authors.forename: J H
authors.initials: JH
authors.lastname: Abalain
authors.forename: P
authors.initials: P
authors.lastname: Mangin
authors.forename: J P
authors.initials: JP
authors.lastname: Bercovici
mesh_terms: D000328:Adult; D000970:Antineoplastic Agents / Q000494:pharmacology; D001141:Aromatase / Q000378:metabolism*; D006063:Chorionic Gonadotropin / Q000494:pharmacology; D004958:Estradiol / Q000378:metabolism; D004967:Estrogens / Q000378:metabolism*; D006801:Humans; D007984:Leydig Cell Tumor / Q000378:metabolism*; D007986:Luteinizing Hormone / Q000378:metabolism*; D008297:Male; D013736:Testicular Neoplasms / Q000378:metabolism*; D013737:Testis / Q000098:blood supply / Q000201:enzymology; D013739:Testosterone / Q000378:metabolism; D017329:Triptorelin Pamoate / Q000494:pharmacology
chemical_list: D000970:Antineoplastic Agents; D006063:Chorionic Gonadotropin; D004967:Estrogens; D017329:Triptorelin Pamoate; D013739:Testosterone; D004958:Estradiol; D007986:Luteinizing Hormone; D001141:Aromatase