The 5 Minute Urology Consult 3rd Ed.

TESTIS, SERTOLI CELL TUMOR

Tariq A. Khemees, MD

Ahmad Shabsigh, MD, FACS

BASICS

DESCRIPTION

• Sertoli cell tumor is a rare sex cord stromal tumor; 90% are benign

– No reliable criteria for malignancy

– Presence of metastasis indicate malignancy

• 3 different subtypes has been described with distinctive clinical, histologic, and prognostic characteristics:

– Classic “tumors that are not otherwise specified”

– Large-cell calcifying Sertoli cell tumor (LCCSCT)

– Sclerosing

EPIDEMIOLOGY

Incidence

• Comprise <1% of testicular neoplasms

• Majority are sporadic

• Classic and sclerosing subtypes are mainly reported in young adult with rare occurrence in prepubertal boys

• LCCST has bimodal age incidence:

– Early onset: Prepubertal

– Late onset: Adulthood

Prevalence

< 1/1,000,000

RISK FACTORS

Usually arise in normal intrascrotal testes; however, may occur in cryptorchid or maldescended testes

Genetics

• 40% of LCCSCT are hereditary and are associated with multiple neoplasia syndromes (MNSs) namely:

– Carney complex (CNC): Autosomal dominant; often caused by PRKAR1A gene mutations and characterized by

Spotty skin pigmentation

Myxomas (cardiac, cutaneuos, and mucosal)

Primary pigmented nodular adrenocortical disease

Thyroid tumors

Acromegaly due to growth hormone-producing adenoma

LCCSCTs

– Peutz–Jeghers syndrome (PJS): Autosomal dominant; mainly caused by STK11 gene mutations and characterized by

Multiple hamartomatous polyps along the whole gastrointestinal tract

Mucocutaneous hyperpigmented macules

– Tuberous sclerosis (TS) (possible): Autosomal dominant caused by TSCI and TSC2 mutations and characterized by

Mental retardation

Cutaneuos lesions

Nonmalignant brain tumors

Malformation of internal organs

PATHOPHYSIOLOGY

• Sertoli cells are supporting cells of the testis

– During fet al development: Secrete anti-Mullerian hormone, which lead to regression of Mullerian ducts.

– During adulthood: Promote differentiating of spermatocyte.

• Normally, Sertoli cells do not have aromatase activity (the enzyme that converts testosterone to estradiol); however, neoplastic Sertoli cells may express aromatase.

• Excess estrogens in prepubertal boy will lead to accelerated skelet al maturation and gynecomastia

ASSOCIATED CONDITIONS

• Gynecomastia

• Carney complex (CNC)

• Peutz–Jeghers syndrome (PJS)

• Tuberous sclerosis (TS)

GENERAL PREVENTION

In familial cases and in those who present with bilateral testicular Sertoli cell tumor, periodic screening for other tumors and associated conditions with MNS is highly recommended

DIAGNOSIS

HISTORY

• Painless or painful testicular mass/enlargement

• Breast pain and/or gynecomastia

• Growth spurt

• Family history of MNS

• Fertility

PHYSICAL EXAM

• General physical exam: Look for

– Feminization, hair pattern, and other signs of estrogen access

– Stigmata of MNS

• Testicular exam: Look for

– Mass

Bilateral in 20% of LCCSCT with occasional coarse irregularities due to macrocalcifications

• Breast exam: Look for

– Tenderness

– Gynecomastia

DIAGNOSTIC TESTS & INTERPRETATION

Lab

• Sex steroid: Check for age-appropriate levels of

– FSH

– LH

– Androgens

– Estrogen

– Progesterone

• Tumor markers:

– AFP is usually negative

– β-hCG is usually negative.

– Placental alkaline phosphatase is usually negative.

Imaging

• Testicular US

– Usually appear as solid, well-circumscribed, and hypervascularized mass

– Bilateral increase in testicular volume

– Occasionally cysts are seen

– Calcifications: Microcalcifications within the tumor mass

Christmas tree–like appearance of multiple calcifications in syndromic LCCSCT is almost always pathognomonic for this tumor

• Metastatic workup: Includes

– Chest x-ray

– CT pelvis and abdomen

– Bone scan

Diagnostic Procedures/Surgery

• Excisional biopsy usually by radical orchiectomy, can be curative

• Fine needle biopsy or nonexcisional biopsy of mass should never be done due to the risk of spread of the more common malignant tumors such as embryonal cell carcinoma or seminoma

• Partial orchiectomy, inguinal approach for patient with familial syndrome

Pathologic Findings

• Gross: Generally well circumscribed, yellow-gray, and lobulated on cut-surface

• Histologically:

– Solid, tubular, or cord-like growth pattern of stromal epithelial tumor cells

– Ovoid or spindle-shaped nuclei

– Eosinophilic or clear cytoplasm

– Variably scanty, edematous, hyalinized, or sclerotic connective tissue stroma

– Call-Exner-like bodies sometimes seen

• Immunopathology:

– Positive for vimentin, cytokeratin, and epithelial membrane antigen stains

– Negative or focally positive for CD30, OCT3/4, and placental alkaline phosphates

• Histologic subtypes:

– Classic or tumors that are not otherwise specified:

Low malignant potential (around 10–20%)

Mean age of 45 yr

No hereditary or MNS association

Occasionally causes access estrogen

Medium-size cells, scanty stroma with no calcifications

– LCCSCT:

Mostly have benign clinical course, but malignancy can occur especially in older ages

Bimodal age: Early and late onset

Frequently associated with MNS

Occasionally causes access estrogen

Bilateral in 20% of reported cases, especially in syndromic disease

Often multifocal

Large eosinophilic cells surrounded by myxoid to collagenous stroma with occasional neutrophilic infiltrate

Necrosis and calcifications are common

– Sclerosing:

Malignancy has never been reported

Affects young adults mainly

No hereditary association

Unilateral affection only

No hormonal imbalances

Usually small in size, <4 cm

Small pale cells with scanty cytoplasm surrounded by dense fibrous stroma

DIFFERENTIAL DIAGNOSIS

• Always rule out precocious puberty in any child who present with testicular enlargement and accelerated growth pattern

• Adult/pediatric painful mass:

– Epididymitis/orchitis; bacterial, STD, mumps, TB

– Fournier gangrene

– Henoch–Schönlein purpura (usually no mass)

– Incarcerated/strangulated hernia

– Postvasectomy syndrome (usually no mass)

– Testicular trauma: Usually blunt; contusion, rupture; usually associated hematocele

– Torsion (testicle, testicular, or epididymal appendage)

– Tumor (infrequent unless traumatized or rapidly growing; see below)

• Adult painless mass:

– Adenomatoid tumor of testis or epididymis

– Adrenal rest tumors

– Adenocarcinoma of the rete testis

– Chylocele: Usually associated with filariasis

– Fibrous pseudotumor of the tunica albuginea

– Hydrocele, primary or due to trauma, torsion, tumor, epididymitis; hydrocele of the cord

– Lipoma of the cord

– Mesothelioma of tunica vaginalis

– Polyorchidism

– Paratesticular sarcomas: Rhabdomyosarcoma, fibrosarcoma, leiomyosarcoma, liposarcoma

– Scrotal edema (insect bite, nephritic syndrome, acute idiopathic scrotal edema)

– Scrotal wall: Sebaceous and inclusion cysts, idiopathic calcinosis, fat necrosis, malignancy

– Sperm granuloma following vasectomy

– Spermatocele (epididymal cyst)

– Testicular cysts (simple, tunica albuginea, epidermoid)

– Testicular tumor:

Germ cell tumors (95% of testicular malignancies): Seminoma, embryonal cell carcinoma, choriocarcinoma, yolk sac carcinoma teratoma (1–5%), teratocarcinoma

Gonadal stromal tumors: Leydig tumor, granulosa cell tumors

Metastatic tumors: Prostate, lung, and GI tract; rare kidney, malignant melanoma, pancreas, bladder, and thyroid

Mixed germ cell and stromal tumor (gonadoblastoma)

Angioma, fibroma, leiomyoma, hamartoma, carcinoid, mesothelioma, and neurofibroma

Malignant fibrous histiocytoma (most common soft tissue sarcoma in late adult life)

Leukemia or lymphoma

– Varicocele

• Pediatric painless mass:

– Similar to adult list; most/more common are: Hydrocele, hernia, varicocele, testicular teratoma, adrenal rest tumors, rhabdomyosarcoma

TREATMENT

GENERAL MEASURES

• Radical inguinal orchiectomy is the primary procedure of choice as these rare tumors are usually thought to be a more common malignancy of the testicle

• LCCSCT in the setting of CNC in children and young adults are typically benign and can be treated with pharmacotherapy for symptomatic relief of gynecomastia and/or advanced puberty

MEDICATION

First Line

• Platinum-based chemotherapy

– Used in metastatic disease, but unproven benefit

Second Line

N/A

SURGERY/OTHER PROCEDURES

• Radical inguinal orchiectomy

• In prepubertal boys, testis-sparing local excision has been reported (none are malignant) after frozen-section biopsy confirms the diagnosis

• Testis-sparing (partial orchiectomy) inguinal approach for patient with familial syndrome

• Retroperitoneal lymph node dissection: Reported but unproven efficacy

ADDITIONAL TREATMENT

Radiation Therapy

No proven role

Additional Therapies

Aromatase inhibitors may be an effective mode of therapy for patients with increased aromatization; currently, only limited number of patients has been treated and no definite recommendations can be made

Complementary & Alternative Therapies

Used in metastatic disease, but unproven benefit

ONGOING CARE

PROGNOSIS

• Benign, completely excised: Excellent

• Malignant, poor

COMPLICATIONS

• Recurrence: Rare

• Metastasis: Uncommon

• Infertility/subfertility

– Bilateral LCCSTs can gradually increase in size, block the seminiferous tubules, and decrease fertility

– Effect of treatment

– Inhibin: Has been proposed as marker for LCCST cell activity and can inhibit FSH, but larger studies are needed to confirm the finding

FOLLOW-UP

Patient Monitoring

• Benign tumors: Periodic scrotal exam

• Malignant tumors: Imaging for metastasis

• Periodic screening for conditions associated with MNS is necessary in syndromic LCCSCT

Patient Resources

MedlinePlus: Sertoli-Leydig cell tumor. http://www.nlm.nih.gov/medlineplus/ency/article/001172.htm

REFERENCES

1. Gourgari E, Saloustros E, Stratakis CA. Large-cell calcifying Sertoli cell tumors of the testes in pediatrics. Curr Opin Pediatr. 2012;24:518–522.

2. Giglio M, Medica M, De Rose AF, et al. Testicular Sertoli cell tumours and relative sub-types. Analysis of clinical and prognostic features. Urol Int. 2003;70:205–210.

3. Young RH. Testicular tumors–some new and a few perennial problems. Arch Pathol Lab Med. 2008;132:548–564.

4. Lodish MB, Stratakis CA. Endocrine tumours in neurofibromatosis type 1, tuberous sclerosis and related syndromes. Best Pract Res Clin Endocrinol Metab. 2010;24(3):439–449.

ADDITIONAL READING

Brunocilla E, Pultrone CV, Schiavina R, et al. Testicular sclerosing Sertoli cell tumor: An additional case and review of the literature. Anticancer Res. 2012;32(11):5127–5130.

See Also (Topic, Algorithm, Media)

• Gynecomastia

• Testis Cancer, Adult General Considerations

• Testis Cancer, Pediatric, General Considerations

• Testis, Tumor and Mass, Adult, General

• Testis, Tumor and Mass, Pediatric, General

CODES

ICD9

222.0 Benign neoplasm of testis

ICD10

• D29.20 Benign neoplasm of unspecified testis

• D29.21 Benign neoplasm of right testis

• D29.22 Benign neoplasm of left testis

CLINICAL/SURGICAL PEARLS

• Consider hereditary syndromes.

• Most Sertoli cell tumors are benign.



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