Leydigcelhyperplasie: een zeldzame oorzaak van hyperandrogenisme bij een menopauzale vrouw

Author(s):  
M. BEKAERT ◽  
H. SONNEMANS ◽  
G. PEETERS ◽  
L. KEULEN ◽  
N. WILLERS ◽  
...  

Leydig cell hyperplasia: an atypical cause of postmenopausal hyperandrogenism We present a case of a 64-year old postmenopausal patient with new onset hirsutism, acne and clitoromegaly. Her medical history includes a non-secreting adrenal incidentaloma. Biochemical evaluation withheld an elevated testosterone with normal dehydroepiandrosterone sulphate (DHEAS). Other adrenal biochemical tests were normal and adrenal imaging was unaltered. Imaging of the ovaries was unremarkable. Due to the normal DHEAS, ovarian etiology was suspected, for which a bilateral oophorectomy was performed. Pathological examination showed bilateral Leydig cell hyperplasia, a benign though rare cause of postmenopausal hyperandrogenism. Postmenopausal hyperandrogenism is caused by of a group of gynaecological and endocrinological disorders. In case of rapid onset and severe symptoms of hirsutism or virilization an androgen-secreting neoplastic disorder should be suspected. Normal DHEAS is suggestive for an ovarian etiology. Imaging is necessary to differentiate between adrenal and ovarian causes, though normal imaging of the ovaries does not rule out ovarian pathology. Definitive diagnosis is often based on pathological examination after oophorectomy.

2014 ◽  
Vol 2014 ◽  
pp. 1-4
Author(s):  
Jaya M. Mehta ◽  
Jeffrey L. Miller ◽  
Anthony J. Cannon ◽  
Stacey K. Mardekian ◽  
Lawrence C. Kenyon ◽  
...  

Objective. To report an unusual case of ovarian Leydig cell hyperplasia resulting in virilization in a postmenopausal woman.Methods. Patient’s medical history and pertinent literature were reviewed.Results. A 64-year-old woman presented with virilization with worsening hirsutism, deepening of her voice, male musculature, and male pattern alopecia. Her pertinent past medical history included type 1 diabetes, hyperlipidemia, and hypertension. Her pertinent past surgical history included hysterectomy due to fibroids. On further work-up, her serum total testosterone was 506 ng/dL (nl range: 2–45) and free testosterone was 40 pg/mL (nl range: 0.1–6.4). After ruling out adrenal causes, the patient underwent an empiric bilateral oophorectomy that showed Leydig cell hyperplasia on pathology. Six weeks postoperatively, serum testosterone was undetectable with significant clinical improvement.Conclusion. Postmenopausal hyperandrogenism can be the result of numerous etiologies ranging from normal physiologic changes to ovarian or rarely adrenal tumors. Our patient was found to have Leydig cell hyperplasia of her ovaries, a rarely reported cause of virilization.


2000 ◽  
Vol 75 (3) ◽  
pp. 288-292 ◽  
Author(s):  
Harris C. Taylor ◽  
Indira Pillay ◽  
Sebouh Setrakian

2001 ◽  
Vol 138 (6) ◽  
pp. 949-951 ◽  
Author(s):  
Ellen Werber Leschek ◽  
Wai-Yee Chan ◽  
David A. Diamond ◽  
Martin Kaefer ◽  
Janet Jones ◽  
...  

Endocrinology ◽  
2013 ◽  
Vol 154 (10) ◽  
pp. 3900-3913 ◽  
Author(s):  
Stacey R. McGee ◽  
Prema Narayan

The LH receptor (LHR) is critical for steroidogenesis and gametogenesis. Its essential role is underscored by the developmental and reproductive abnormalities that occur due to genetic mutations identified in the human LHR. In males, activating mutations are associated with precocious puberty and Leydig cell hyperplasia. To generate a mouse model for the human disease, we have introduced an aspartic acid to glycine mutation in amino acid residue 582 (D582G) of the mouse LHR gene corresponding to the most common D578G mutation found in boys with familial male-limited precocious puberty (FMPP). In transfected cells, mouse D582G mLHR exhibited constitutive activity with a 23-fold increase in basal cAMP levels compared with the wild-type receptor. A temporal study of male mice from 7 days to 24 weeks indicated that the knock-in mice with the mutated receptor (KiLHRD582G) exhibited precocious puberty with elevated testosterone levels as early as 7 days of age and through adulthood. Leydig cell-specific genes encoding LHR and several steroidogenic enzymes were up-regulated in KiLHRD582G testis. Leydig cell hyperplasia was detected at all ages, whereas Sertoli and germ cell development appeared normal. A novel finding from our studies, not previously reported in the FMPP cases, is that extensive hyperplasia is commonly found around the periphery of the testis. We further demonstrate that the hyperplasia is due to premature proliferation and precocious differentiation of adult Leydig cells in the KiLHRD582G testis. The KiLHRD582G mice provide a mouse model for FMPP, and we suggest that it is a useful model for studying pathologies associated with altered LHR signaling.


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