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Year : 2004  |  Volume : 20  |  Issue : 2  |  Page : 164-165

Virilising tumor of testis - a case report

Department of Urology, Government Royapettah Hospital, Chennai, India

Correspondence Address:
M G Rajamanickam
No.7 Anandan Street, T.Nagar, Chennai - 600 017
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Source of Support: None, Conflict of Interest: None

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Keywords: Leydic cell tumor, virilising tumor, Reinke′s crystals.

How to cite this article:
Sudhakar L, Anand C, Sri Ram K, Sivasankar G, Muthulatha N, Rajamanickam M G. Virilising tumor of testis - a case report. Indian J Urol 2004;20:164-5

How to cite this URL:
Sudhakar L, Anand C, Sri Ram K, Sivasankar G, Muthulatha N, Rajamanickam M G. Virilising tumor of testis - a case report. Indian J Urol [serial online] 2004 [cited 2022 Jul 6];20:164-5. Available from:

   Case Report Top

A 9-year-old boy presented with a sudden increase in height and weight of 6 months' duration, followed by a painless scrotal swelling. Patient also noticed change in voice for the same duration. On examination, the boy had an adult look with prominent facial hairs, acne vulgaris and well developed secondary sexual characters [Figure - 1]. His height was 5'1" and weighed 46 kg. Genital exami­nation revealed a penile length of 10.5 cm. Right testis was enlarged (4 x 3 cm), firm in consistency with dimin­ished testicular sensation. Left testis was normal (2 x 1 cm) for prepubertal age.

On evaluation, ultrasonogram of scrotum showed an irregular hypoechoeic lesion of 1.9 x 2.8 x 2.9 cm in the lower pole of right testis. Ultrasonogram and CT scan of the abdomen were normal. Endocrine evaluation with reference to prepubertal values revealed a raised testoster­one level of 18.3 ng/ml (Ref 2.7 - 10.7 ng/ml), LH was 2.23 mlU/ml (Ref 2-12 mIU/ml), FSH was 1.2 mIU/ml (Ref 3-15 mIU/ml), basal GH was 8.7 ng/ml (Ref 0-7 ng/ ml), cortisol was 9.83 mg/ml (Ref 8-9 mg/ml), DHEA was 80 mg/ml (Ref 80-560 mg/ml) and 17-OH progesterone was 10.88 ng/ml (Ref 0.4-3.6 ng/ml). (The reference val­ues mentioned are for the prepubertal age.) HCG and AFP levels were normal. Dexamethasone suppression test (DST) was negative, which rule out adrenal hyperplasia.

Bone age study was advanced to 14-16 years. A diag­nosis of a virilising tumor of the testis was made and right radical inguinal orchidectomy was done and histopatho­logical report was benign leydig cell tumor (LCT) [Figure - 2]A. Patient was followed up for 1 year and serum testo­sterone levels were normal. But the virilising features however were static.

   Comments Top

Precocious puberty in boys presents a diagnostic chal­lenge. A normal gonadotropin level indicates an extra-pituitary cause and LCT should be entertained. LCTs are the most common gonadal stromal tumors accounting for 1-3% of all testicular tumors and 6% of testicular tumors in children. [1] They occur predominantly in boys older than 4 years and in adults between 20-50 years of age. Child­hood LCTs usually are hormonally active and have a be­nign course. The tumor results in incomplete (peripheral) isosexual precocity accounting for 10% of all cases of pre­cocious puberty. The hallmark of the diagnosis of LCT is the triad of precocious puberty, testicular mass and elevated urinary 17 ketosteroid level. However a marked eleva­tion of 17 ketosteroid is characteristic of the 17-hydroxy­lase deficiency type of congenital adrenal hyperplasia (CAH). Thus it is mandatory to differentiate LCT from CAH. Testicular nodules in CAH often present in the sec­ond decade of life and are bilateral with a strong family history. [2] LCT should also be differentiated from leydig cell hyperplasia and tumors of adrenal rest tissue. Endo­crine evaluation should include serum testosterone, LH, FSH, GH, DHEA levels and DST. Ninety per cent of LCTs are benign. Macroscopically. LCTs appear well encapsu­lated with compression of adjacent testicular tissue. The pathognomonic histological feature characteristic of LCT is intracytoplasmic Reinke's crystals, which is present in only about 40% of tumors [Figure - 2]B. The absolute crite­rion for malignancy is metastases. The treatment of LCT is radical inguinal orchidectomy. In children in whom the diagnosis is suspected preoperatively, a testis sparing enu­cleation is acceptable provided histological confirmation of the lesion is obtained by frozen section. [3] The pro­nounced virilisation along with the hormonal profile and benign histology in this case are classical of childhood LCT.

   References Top

1.Ciftei AO. Bingol-Kologlu M, Senocak ME, Tanyel FC. Munevver Buyukpamukeu and Neibil Buyukpamukeu: Testicular tumors in children. J Pediatr Surg 2001; 36: 1800.  Back to cited text no. 1    
2.Cunnah D. Perry L, Dacie JA et al. Bilateral testicular tumors in congenital adrenal hyperplasia: a continuing diagnostic and thera­peutic dilemma. Clin Endocrinol (Oxf) 1989; 30: 141.  Back to cited text no. 2    
3.Klein EA. Levin HS. Non-germ cell tumors of the testis. In: Osterling JE, Richie JP. (eds.), Urologic Oncology, Philadelphia: WB Saunders: 1997: 496-514.  Back to cited text no. 3    


  [Figure - 1], [Figure - 2]


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