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Oestrogen secreting Leydig cell tumour and GnRH agonist in‐vivo and in‐vitro studies
Author(s) -
Kerlan Véronique,
Nahoul Khalil,
Abalaln JeanHervé,
Mangln Philippe,
Bercovici JeanPierre
Publication year - 1992
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1992.tb02314.x
Subject(s) - medicine , leydig cell , endocrinology , agonist , testosterone (patch) , aromatase , basal (medicine) , testicle , gonadotropin , in vivo , estrogen , biology , receptor , luteinizing hormone , hormone , cancer , breast cancer , microbiology and biotechnology , insulin
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. MEASUREMENTS E 2 and T were evaluated after hCG Injection (5000IU) during 96 hours. Bio and Immuno LH, T, E 2 , 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‐ 14 C‐T. RESULTS Oestradiol (E 2 ) 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 (E 2 /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 bloactive LH. T was decreased to about 10% of baseline levels and E 2 fell from 240 to 36 pmol/l. In the blood of the spermatic veins collected in the course of surgery, E 2 levels were found to be lower in comparison with the controls. E 2 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‐ 14 C‐T, displayed a reduced aromatase activity (conversion of T to E 2 :0.3 and 0.1% in patients 1 and 2 respectively). CONCLUSIONS The kinetics of E 2 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.