scholarly journals Ovarian Leydig Cell Hyperplasia: An Unusual Case of Virilization in a Postmenopausal Woman

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.

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):  
Murat Atmaca ◽  
İsmet Seven ◽  
Rıfkı Üçler ◽  
Murat Alay ◽  
Veysi Barut ◽  
...  

Mild clinical signs of hyperandrogenism such as hirsutism may appear during the menopausal transition as part of the normal aging process, but the development of frank virilization suggests a specific source of androgen excess. We report a case of a 68-year-old woman with signs of virilization that had started 6 months before. Clinical analyses revealed high levels of serum testosterone for a postmenopausal woman. Pelvic MRI and abdomen CT showed no evidence of ovarian and adrenal tumor. 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 iatrogenic hyperandrogenism. This condition is 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 ◽  
...  

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Mohamed K M Shakir ◽  
Rinsha P V Sherin ◽  
Travis Weaver ◽  
David LaChance ◽  
Thanh Duc Hoang

Abstract Severe hyperandrogenism in post-menopausal women is rare. It may be caused by either benign or malignant neoplasms of the adrenal or ovary. We report a rare case of a post-menopausal woman with hirsutism associated with virilization due to Leydig cell tumors (LCT) of both ovaries. Case report 61 yo female presented for evaluation of hirsutism. She had also been experiencing increased facial hair growth, deepening of voice, clitoromegaly, alopecia, and acne. Physical examination: normal vital signs. Patient had signs of virilization, including coarse hair along her upper lip, chin, lower abdomen and inner thigh with Ferriman-Gallwey score of 8, acne, and clitoromegaly. She had no signs of acanthosis nigricans or Cushing syndrome. Base line labs: Hemoglobin 16.2 gm/dL (ref 12.0 to 15.5), total testosterone 803 ng/dL (ref 3–41), free testosterone 20.2 pg/mL (ref 0.0–4.2), estradiol 77 pg/mL (<6.0−54.7), estrone 148 pg/mL (ref 7–40), FSH 11.5 mIU/mL (ref 25.8 - 134.8), LH 6.90 mIU/mL (ref 7.7 - 58.5), androstenedione 28 ng/dL (ref 17–99), DHEAS 99.9 mcg/dL (ref 19–205), dehydroepiandrosterone 512 ng/dL (ref 31–701), inhibin A 2.3 pg/mL (ref <5), inhibin B <7.0 pg/mL (ref 00-16.9), 17-alpha hydroxyprogesterone 187 ng/dl (ref <51). Her other serum markers such as anti -Mullerian hormone, alpha-fetoprotein, and hCG were normal. A CT scan of adrenals: normal. Similarly a transvaginal US did not show any ovarian pathology, however MRI of the pelvis showed homogeneous ovarian enhancement bilaterally and based on this information a diagnosis of ovarian hyperthecosis was considered and patient underwent laparoscopic bilateral oophorectomy. Pathology confirmed: LCT in both ovaries. Laboratory values performed 3 months later showed the following values: hemoglobin 14.2 gm/dL, total testosterone 13 ng/dL, free testosterone 1.4 pg/mL, LH 124 mIU/mL, FSH 99mIU/mL, estradiol <5.0 pg/mL. In 6 months she had significant improvement in hirsutism and virilization. Discussion Hyperandrogenism, especially serum testosterone in the male range with rapidly progressive hirsutism or virilization signs in a female indicates tumor etiology. Androgen-secreting ovarian tumors are usually small and often embedded in the ovary. Transvaginal US is useful in the diagnosis of ovarian tumors. However, in our case, transvaginal US failed while MRI scan showed bilaterally enlarged ovaries and with this information patient underwent bilateral oophorectomy. Although 5 cases of bilateral LCT are reported in the literature, LCT is unilateral 95% of the time, the pathogenesis of Leydig cell proliferation and LCT is unclear. In conclusion, androgen secreting tumors should be considered in women (especially in post-menopausal state) with hyperandrogenism and hirsutism. In fact, diffuse stromal Leydig cell hyperplasia and small Leydig cell tumors may be missed on imaging and in some cases only pathology can confirm the result.


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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