Horm Metab Res 2003; 35(5): 324-329
DOI: 10.1055/s-2003-41310
Original Clinical
© Georg Thieme Verlag Stuttgart · New York

An Oestrogen-Producing Seminoma Responsible for Gynaecomastia

C.  Duparc 1 , G.  Boissiere-Veverka1 , H.  Lefebvre 1 , A.  Laquerriere 2 , P.  Vuillermet 1 , A.  Landreat 2 , R.  Ivell 3 , N.  DeRoux 4 , J.  M.  Kuhn 1
  • 1 European Institute for Peptide Research (IFRMP 23), Department of Endocrinology, INSERM U 413, University Hospital of Rouen, France
  • 2 Laboratory of Anatomopathology, University Hospital of Rouen, France
  • 3 Institute for Hormone and fertility research, University of Hamburg, Hamburg, Germany
  • 4 Laboratory of Hormonology and molecular Biology, University Hospital Bicêtre, Le Kremlin-Bicêtre, France
Further Information

Publication History

Received 15 July 2002

Accepted after Revision 3 December 2002

Publication Date:
13 August 2003 (online)

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Abstract

In feminising testicular tumours, oestrogens can be either secreted by the tumour itself or produced by normal Leydig cells in response to paracrine and/or endocrine stimulation by hCG. Typical hormonal Leydig cell tumour patterns include: plasma oestradiol levels > 300 pmol/l on day 3 following an hCG injection, reduced plasma testosterone, and normal plasma hCG and gonadotrophin levels. Except for elevated plasma oestradiol levels, opposite results are observed in seminomas. We report a case of oestrogen-secreting seminoma mimicking a Leydig cell tumour. A 24-year-old Caucasian patient had complained of gynaecomastia for 6 months before admission. Hormonal pattern was typical of Leydig cell tumour. A 1.4 cm tumour was found in the left testis and confirmed on sonography. Considering the likely diagnosis of Leydig cell tumour, the patient was treated by tumourectomy. Surprisingly, pathological examination revealed a pure seminoma. Perifusion experiments showed that the tumour was able to secrete significant amounts of oestradiol. In addition, hCG induced a two-fold increase in oestradiol production from perifused tumour explants. Immunohistochemistry revealed that the tumour was composed of nests of seminoma cells intermingled with lymphoid infiltrates. Tumour cells also expressed aromatase, the hCG/LH receptor and the Leydig cell marker relaxin-like factor, but were βhCG-negative. These results demonstrate that a pure seminoma of the testis is able to synthesise and secrete oestrogens. They also illustrate that the body of proof favouring the diagnosis of feminising Leydig cell tumour of the testis is not rigorously specific.

References.

J. M. Kuhn, Pr.

IFRMP 23 · Department of Endocrinology · INSERM U 413 · Boisguillaume Hospital · CHU de Rouen

76031 Rouen cedex · France

Phone: + 33 (232) 88 90 82

Fax: + 33 (232) 88 91 54 ·

Email: jean-marc.kuhn@chu-rouen.fr