A 76-year-old woman with androgenic alopecia of frontal predominance, grade IV of the Ludwig scale, with two years of evolution, associated with facial hirsutism, more aggressive behavior and exacerbation.
No history compatible with hyperisolism.
Menopause at age 54 and absence of posterior red flows.
No history of hormone replacement therapy.
Endocrine evaluation confirmed hyperandrogenism.
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Her past medical history included hypertension controlled with the use of amikacin 5 mg/day and hydrochlorothiazide 25 mg/day associated with triamterene 50 mg/day, mixed dyslipidemia treated with diet and bezafibrate 400 mg
Her physical examination revealed androgenic alopecia, Ferriman-Gallway score of 7 (VN < 6), increased muscle spasm and mucosa, vaginal untututeness x mild estrogen deficiency.
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The initial biochemical study showed polyglobulia (hemoglobin increased from 12.5 g/dL in 2004 to 17.8 at the time of the study in 2009), plasma testosterone increased from 711 ng/dL (high serum estradiol 48 mIU/dL
Urinary free cortisol was normal.
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Magnetic resonance imaging (MRI) of the abdomen and pelvis showed diffuse hepatic steatosis, normal adrenal glands, uterine adenomyosis, right ovary of 20 x 10 mm and left ovary of 35 x 20 mm with a small 17 mm post-pumen cyst.
Transvaginal gynecologic ultrasound confirmed these findings and detected endometrial thickening of 11 mm (VN < 5 in postmenopausia)3.
Endometrial biopsy yielded scarce material reported as mucus, scattered endocervical cells and few polymorphonuclear cells.
Since there was no clinical, laboratory or imaging evidence compatible with an adrenal origin of hyperandrogenism, bilateral salpingo oophorectomy was performed laparoscopically.
The right ovary weighed 6.6 g and measured 28 x 25 mm, presenting an irregular cystic lesion, and the left ovary measured 3 g and measured 32 x 20 mm presenting an opaque surface.
Microscopy showed a Leydig cell tumor hiliar in the right ovary, which compromised a large part of this gonad, formed by polygonal cells with clear eosinophilic cytoplasm or thinly granular chromatin nuclei, with 1
The left ovary showed stromal hyperplasia and cystic lesion.
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The patient was discharged on the third postoperative day.
One week after surgery, the patient reported decay, decreased libido and vasomotor symptoms.
Examinations one month post-surgery showed normalization of hyperandrogenism (total testosterone 19 ng/dl, SH > 30.7 nmol/L and free androgen index 2.0).
Seven months after surgery, androgenetic alopecia significantly reversed and vasomotor symptoms resolved spontaneously.
Plasma hemoglobin was normalized (14.2 gr/%) and HOMA was 3.9, total cholesterol 235 mg/dl, LDL 132 mg/dl, HDL 39 mg/dl, triglycerides 321 mg/dl total FSH 123.8 ng/dl.
