- •Preface
- •Acknowledgments
- •Contents
- •1.1 Introduction
- •1.2 Normal Embryology
- •1.3 Abnormalities of the Kidney
- •1.3.1 Renal Agenesis
- •1.3.2 Renal Hypoplasia
- •1.3.3 Supernumerary Kidneys
- •1.3.5 Polycystic Kidney Disease
- •1.3.6 Simple (Solitary) Renal Cyst
- •1.3.7 Renal Fusion and Renal Ectopia
- •1.3.8 Horseshoe Kidney
- •1.3.9 Crossed Fused Renal Ectopia
- •1.4 Abnormalities of the Ureter
- •1.5 Abnormalities of the Bladder
- •1.6 Abnormalities of the Penis and Urethra in Males
- •1.7 Abnormalities of Female External Genitalia
- •Further Reading
- •2.1 Introduction
- •2.2 Pathophysiology
- •2.3 Etiology of Hydronephrosis
- •2.5 Clinical Features
- •2.6 Investigations and Diagnosis
- •2.7 Treatment
- •2.8 Antenatal Hydronephrosis
- •Further Reading
- •3.1 Introduction
- •3.2 Embryology
- •3.3 Pathophysiology
- •3.4 Etiology of PUJ Obstruction
- •3.5 Clinical Features
- •3.6 Diagnosis and Investigations
- •3.7 Management of Newborns with PUJ Obstruction
- •3.8 Treatment
- •3.9 Post-operative Complications and Follow-Up
- •Further Reading
- •4: Renal Tumors in Children
- •4.1 Introduction
- •4.2 Wilms’ Tumor
- •4.2.1 Introduction
- •4.2.2 Etiology
- •4.2.3 Histopathology
- •4.2.4 Nephroblastomatosis
- •4.2.5 Clinical Features
- •4.2.6 Risk Factors for Wilms’ Tumor
- •4.2.7 Staging of Wilms Tumor
- •4.2.8 Investigations
- •4.2.9 Prognosis and Complications of Wilms Tumor
- •4.2.10 Surgical Considerations
- •4.2.11 Surgical Complications
- •4.2.12 Prognosis and Outcome
- •4.2.13 Extrarenal Wilms’ Tumors
- •4.3 Mesoblastic Nephroma
- •4.3.1 Introduction
- •4.3.3 Epidemiology
- •4.3.5 Clinical Features
- •4.3.6 Investigations
- •4.3.7 Treatment and Prognosis
- •4.4 Clear Cell Sarcoma of the Kidney (CCSK)
- •4.4.1 Introduction
- •4.4.2 Pathophysiology
- •4.4.3 Clinical Features
- •4.4.4 Investigations
- •4.4.5 Histopathology
- •4.4.6 Treatment
- •4.4.7 Prognosis
- •4.5 Malignant Rhabdoid Tumor of the Kidney
- •4.5.1 Introduction
- •4.5.2 Etiology and Pathophysiology
- •4.5.3 Histologic Findings
- •4.5.4 Clinical Features
- •4.5.5 Investigations and Diagnosis
- •4.5.6 Treatment and Outcome
- •4.5.7 Mortality/Morbidity
- •4.6 Renal Cell Carcinoma in Children
- •4.6.1 Introduction
- •4.6.2 Histopathology
- •4.6.4 Staging
- •4.6.5 Clinical Features
- •4.6.6 Investigations
- •4.6.7 Management
- •4.6.8 Prognosis
- •4.7 Angiomyolipoma of the Kidney
- •4.7.1 Introduction
- •4.7.2 Histopathology
- •4.7.4 Clinical Features
- •4.7.5 Investigations
- •4.7.6 Treatment and Prognosis
- •4.8 Renal Lymphoma
- •4.8.1 Introduction
- •4.8.2 Etiology and Pathogenesis
- •4.8.3 Diagnosis
- •4.8.4 Clinical Features
- •4.8.5 Treatment and Prognosis
- •4.9 Ossifying Renal Tumor of Infancy
- •4.10 Metanephric Adenoma
- •4.10.1 Introduction
- •4.10.2 Histopathology
- •4.10.3 Diagnosis
- •4.10.4 Clinical Features
- •4.10.5 Treatment
- •4.11 Multilocular Cystic Renal Tumor
- •Further Reading
- •Wilms’ Tumor
- •Mesoblastic Nephroma
- •Renal Cell Carcinoma in Children
- •Angiomyolipoma of the Kidney
- •Renal Lymphoma
- •Ossifying Renal Tumor of Infancy
- •Metanephric Adenoma
- •Multilocular Cystic Renal Tumor
- •5.1 Introduction
- •5.2 Embryology
- •5.4 Histologic Findings
- •5.7 Associated Anomalies
- •5.8 Clinical Features
- •5.9 Investigations
- •5.10 Treatment
- •Further Reading
- •6: Congenital Ureteral Anomalies
- •6.1 Etiology
- •6.2 Clinical Features
- •6.3 Investigations and Diagnosis
- •6.4 Duplex (Duplicated) System
- •6.4.1 Introduction
- •6.4.3 Clinical Features
- •6.4.4 Investigations
- •6.4.5 Treatment and Prognosis
- •6.5 Ectopic Ureter
- •6.5.1 Introduction
- •6.5.3 Clinical Features
- •6.5.4 Diagnosis
- •6.5.5 Surgical Treatment
- •6.6 Ureterocele
- •6.6.1 Introduction
- •6.6.3 Clinical Features
- •6.6.4 Investigations and Diagnosis
- •6.6.5 Treatment
- •6.6.5.1 Surgical Interventions
- •6.8 Mega Ureter
- •Further Reading
- •7: Congenital Megaureter
- •7.1 Introduction
- •7.3 Etiology and Pathophysiology
- •7.4 Clinical Presentation
- •7.5 Investigations and Diagnosis
- •7.6 Treatment and Prognosis
- •7.7 Complications
- •Further Reading
- •8.1 Introduction
- •8.2 Pathophysiology
- •8.4 Etiology of VUR
- •8.5 Clinical Features
- •8.6 Investigations
- •8.7 Management
- •8.7.1 Medical Treatment of VUR
- •8.7.2 Antibiotics Used for Prophylaxis
- •8.7.3 Anticholinergics
- •8.7.4 Surveillance
- •8.8 Surgical Therapy of VUR
- •8.8.1 Indications for Surgical Interventions
- •8.8.2 Indications for Surgical Interventions Based on Age at Diagnosis and the Presence or Absence of Renal Lesions
- •8.8.3 Endoscopic Injection
- •8.8.4 Surgical Management
- •8.9 Mortality/Morbidity
- •Further Reading
- •9: Pediatric Urolithiasis
- •9.1 Introduction
- •9.2 Etiology
- •9.4 Clinical Features
- •9.5 Investigations
- •9.6 Complications of Urolithiasis
- •9.7 Management
- •Further Reading
- •10.1 Introduction
- •10.2 Embryology of Persistent Müllerian Duct Syndrome
- •10.3 Etiology and Inheritance of PMDS
- •10.5 Clinical Features
- •10.6 Treatment
- •10.7 Prognosis
- •Further Reading
- •11.1 Introduction
- •11.2 Physiology and Bladder Function
- •11.2.1 Micturition
- •11.3 Pathophysiological Changes of NBSD
- •11.4 Etiology and Clinical Features
- •11.5 Investigations and Diagnosis
- •11.7 Management
- •11.8 Clean Intermittent Catheterization
- •11.9 Anticholinergics
- •11.10 Botulinum Toxin Type A
- •11.11 Tricyclic Antidepressant Drugs
- •11.12 Surgical Management
- •Further Reading
- •12.1 Introduction
- •12.2 Etiology
- •12.3 Pathophysiology
- •12.4 Clinical Features
- •12.5 Investigations and Diagnosis
- •12.6 Management
- •Further Reading
- •13.1 Introduction
- •13.2 Embryology
- •13.3 Epispadias
- •13.3.1 Introduction
- •13.3.2 Etiology
- •13.3.4 Treatment
- •13.3.6 Female Epispadias
- •13.3.7 Surgical Repair of Female Epispadias
- •13.3.8 Prognosis
- •13.4 Bladder Exstrophy
- •13.4.1 Introduction
- •13.4.2 Associated Anomalies
- •13.4.3 Principles of Surgical Management of Bladder Exstrophy
- •13.4.4 Evaluation and Management
- •13.5 Cloacal Exstrophy
- •13.5.1 Introduction
- •13.5.2 Skeletal Changes in Cloacal Exstrophy
- •13.5.3 Etiology and Pathogenesis
- •13.5.4 Prenatal Diagnosis
- •13.5.5 Associated Anomalies
- •13.5.8 Surgical Reconstruction
- •13.5.9 Management of Urinary Incontinence
- •13.5.10 Prognosis
- •13.5.11 Complications
- •Further Reading
- •14.1 Introduction
- •14.2 Etiology
- •14.3 Clinical Features
- •14.4 Associated Anomalies
- •14.5 Diagnosis
- •14.6 Treatment and Prognosis
- •Further Reading
- •15: Cloacal Anomalies
- •15.1 Introduction
- •15.2 Associated Anomalies
- •15.4 Clinical Features
- •15.5 Investigations
- •Further Reading
- •16: Urachal Remnants
- •16.1 Introduction
- •16.2 Embryology
- •16.4 Clinical Features
- •16.5 Tumors and Urachal Remnants
- •16.6 Management
- •Further Reading
- •17: Inguinal Hernias and Hydroceles
- •17.1 Introduction
- •17.2 Inguinal Hernia
- •17.2.1 Incidence
- •17.2.2 Etiology
- •17.2.3 Clinical Features
- •17.2.4 Variants of Hernia
- •17.2.6 Treatment
- •17.2.7 Complications of Inguinal Herniotomy
- •17.3 Hydrocele
- •17.3.1 Embryology
- •17.3.3 Treatment
- •Further Reading
- •18: Cloacal Exstrophy
- •18.1 Introduction
- •18.2 Etiology and Pathogenesis
- •18.3 Associated Anomalies
- •18.4 Clinical Features and Management
- •Further Reading
- •19: Posterior Urethral Valve
- •19.1 Introduction
- •19.2 Embryology
- •19.3 Pathophysiology
- •19.5 Clinical Features
- •19.6 Investigations and Diagnosis
- •19.7 Management
- •19.8 Medications Used in Patients with PUV
- •19.10 Long-Term Outcomes
- •19.10.3 Bladder Dysfunction
- •19.10.4 Renal Transplantation
- •19.10.5 Fertility
- •Further Reading
- •20.1 Introduction
- •20.2 Embryology
- •20.4 Clinical Features
- •20.5 Investigations
- •20.6 Treatment
- •20.7 The Müllerian Duct Cyst
- •Further Reading
- •21: Hypospadias
- •21.1 Introduction
- •21.2 Effects of Hypospadias
- •21.3 Embryology
- •21.4 Etiology of Hypospadias
- •21.5 Associated Anomalies
- •21.7 Clinical Features of Hypospadias
- •21.8 Treatment
- •21.9 Urinary Diversion
- •21.10 Postoperative Complications
- •Further Reading
- •22: Male Circumcision
- •22.1 Introduction
- •22.2 Anatomy and Pathophysiology
- •22.3 History of Circumcision
- •22.4 Pain Management
- •22.5 Indications for Circumcision
- •22.6 Contraindications to Circumcision
- •22.7 Surgical Procedure
- •22.8 Complications of Circumcision
- •Further Reading
- •23: Priapism in Children
- •23.1 Introduction
- •23.2 Pathophysiology
- •23.3 Etiology
- •23.5 Clinical Features
- •23.6 Investigations
- •23.7 Management
- •23.8 Prognosis
- •23.9 Priapism and Sickle Cell Disease
- •23.9.1 Introduction
- •23.9.2 Epidemiology
- •23.9.4 Pathophysiology
- •23.9.5 Clinical Features
- •23.9.6 Treatment
- •23.9.7 Prevention of Stuttering Priapism
- •23.9.8 Complications of Priapism and Prognosis
- •Further Reading
- •24.1 Introduction
- •24.2 Embryology and Normal Testicular Development and Descent
- •24.4 Causes of Undescended Testes and Risk Factors
- •24.5 Histopathology
- •24.7 Clinical Features and Diagnosis
- •24.8 Treatment
- •24.8.1 Success of Surgical Treatment
- •24.9 Complications of Orchidopexy
- •24.10 Infertility and Undescended Testes
- •24.11 Undescended Testes and the Risk of Cancer
- •Further Reading
- •25: Varicocele
- •25.1 Introduction
- •25.2 Etiology
- •25.3 Pathophysiology
- •25.4 Grading of Varicoceles
- •25.5 Clinical Features
- •25.6 Diagnosis
- •25.7 Treatment
- •25.8 Postoperative Complications
- •25.9 Prognosis
- •Further Reading
- •26.1 Introduction
- •26.2 Etiology and Risk Factors
- •26.3 Diagnosis
- •26.4 Intermittent Testicular Torsion
- •26.6 Effects of Testicular Torsion
- •26.7 Clinical Features
- •26.8 Treatment
- •26.9.1 Introduction
- •26.9.2 Etiology of Extravaginal Torsion
- •26.9.3 Clinical Features
- •26.9.4 Treatment
- •26.10 Torsion of the Testicular or Epididymal Appendage
- •26.10.1 Introduction
- •26.10.2 Embryology
- •26.10.3 Clinical Features
- •26.10.4 Investigations and Treatment
- •Further Reading
- •27: Testicular Tumors in Children
- •27.1 Introduction
- •27.4 Etiology of Testicular Tumors
- •27.5 Clinical Features
- •27.6 Staging
- •27.6.1 Regional Lymph Node Staging
- •27.7 Investigations
- •27.8 Treatment
- •27.9 Yolk Sac Tumor
- •27.10 Teratoma
- •27.11 Mixed Germ Cell Tumor
- •27.12 Stromal Tumors
- •27.13 Simple Testicular Cyst
- •27.14 Epidermoid Cysts
- •27.15 Testicular Microlithiasis (TM)
- •27.16 Gonadoblastoma
- •27.17 Cystic Dysplasia of the Testes
- •27.18 Leukemia and Lymphoma
- •27.19 Paratesticular Rhabdomyosarcoma
- •27.20 Prognosis and Outcome
- •Further Reading
- •28: Splenogonadal Fusion
- •28.1 Introduction
- •28.2 Etiology
- •28.4 Associated Anomalies
- •28.5 Clinical Features
- •28.6 Investigations
- •28.7 Treatment
- •Further Reading
- •29: Acute Scrotum
- •29.1 Introduction
- •29.2 Torsion of Testes
- •29.2.1 Introduction
- •29.2.3 Etiology
- •29.2.4 Clinical Features
- •29.2.5 Effects of Torsion of Testes
- •29.2.6 Investigations
- •29.2.7 Treatment
- •29.3 Torsion of the Testicular or Epididymal Appendage
- •29.3.1 Introduction
- •29.3.2 Embryology
- •29.3.3 Clinical Features
- •29.3.4 Investigations and Treatment
- •29.4.1 Introduction
- •29.4.2 Etiology
- •29.4.3 Clinical Features
- •29.4.4 Investigations and Treatment
- •29.5 Idiopathic Scrotal Edema
- •29.6 Testicular Trauma
- •29.7 Other Causes of Acute Scrotum
- •29.8 Splenogonadal Fusion
- •Further Reading
- •30.1 Introduction
- •30.2 Imperforate Hymen
- •30.3 Vaginal Atresia
- •30.5 Associated Anomalies
- •30.6 Embryology
- •30.7 Clinical Features
- •30.8 Investigations
- •30.9 Management
- •Further Reading
- •31: Disorders of Sexual Development
- •31.1 Introduction
- •31.2 Embryology
- •31.3 Sexual and Gonadal Differentiation
- •31.5 Evaluation of a Newborn with DSD
- •31.6 Diagnosis and Investigations
- •31.7 Management of Patients with DSD
- •31.8 Surgical Corrections of DSD
- •31.9 Congenital Adrenal Hyperplasia (CAH)
- •31.10 Androgen Insensitivity Syndrome (Testicular Feminization Syndrome)
- •31.13 Gonadal Dysgenesis
- •31.15 Ovotestis Disorders of Sexual Development
- •31.16 Other Rare Disorders of Sexual Development
- •Further Reading
- •Index
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27 Testicular Tumors in Children |
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•There is still insufficient data to quantify the risk, if any, of testicular cancer in boys or men incidentally found to have TM.
•Studies suggest that TM may be most significant when it occurs in conjunction with other risk factors for testicular cancer, such as men with infertility or a history of contralateral testicular cancer.
27.16 Gonadoblastoma
•While rare, certain disorders of sexual development (DSD) harbor a very significant risk for the development of gonadal tumors.
•Some disorders, such as complete androgen insensitivity syndrome, have an increased risk comparable to that of other patients with testicular maldescent.
•But unique to patients with DSD are the risks of tumor formation in dysgenetic or streak gonads. This risk seems to exist almost exclusively in patients with Y chromatin.
•For example, patients with Turner syndrome and any portion of a Y chromosome in their karyotype have an approximately 12 % risk of tumor development; while patients with traditional Turner syndrome and a 45 XO karyotype are at no significant risk for gonadal tumors.
•Similarly the gonads of patients with pure gonadal dysgenesis and Y chromatin as well as the “streak” gonad of patients with mixed gonadal dysgenesis are at a 15–30 % risk for tumor development.
•The tumors arising in the setting of gonadal dysgenesis are usually gonadoblastomas.
•While gonadoblastomas are benign, they are prone to the development of malignant degeneration and overt malignant behavior is seen in 10 % of cases.
•While most cases of malignancy occur after puberty, there have been cases reported in children as well.
•Prophylactic removal of dysgenetic gonads should be undertaken early in life in patients with at-risk karyotypes.
•Gonadectomy is sufficient treatment for gonadoblastoma.
•If malignant degeneration has occurred, then further therapy may be warranted.
•When malignancies occur, dysgerminoma is the most common histological type.
•These tumors are very radiosensitive and the outlook for these patients is generally favorable.
•These occurs in association with disorders of sexual development (intersex).
•About 80 % of cases involve phenotypic females with intra-abdominal testes or streak gonads.
•The putative gonadoblastoma gene is on the Y chromosome, and the tumor almost always develops in a child with a Y chromosome. The streak gonads in patients with mixed gonadal dysgenesis often develop gonadoblastomas.
•The incidence peaks at puberty, and early gonadectomy is recommended in patients at risk for gonadoblastoma.
•Metastatic spread of a gonadoblastoma occurs in 10 % of patients.
•These tumors may elevate serum levels of betahuman chorionic gonadotropin (beta-HCG).
27.17 Cystic Dysplasia of the Testes
•This is a benign lesion that is often associated with ipsilateral renal agenesis or dysplasia.
•This association, along with a characteristic ultrasonographic appearance (i.e., hypoechoic lesions), permits preoperative diagnosis and possible treatment with testicular-sparing surgery.
27.18 Leukemia and Lymphoma
•These are the most common secondary malignancies to affect the testis.
•These tumors can present bilaterally, and, because the blood-testis barrier protects the intratesticular cells, the testis may be the site
27.19 Paratesticular Rhabdomyosarcoma |
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of residual tumor in children after chemotherapy.
•Metastatic disease to the testes should be considered in a child presenting with bilateral testicular tumors.
•Paratesticular structures can give rise to various benign (lipoma, leiomyoma, hemangioma, or fibroma) and malignant tumors; however, these are extremely rare.
27.19Paratesticular Rhabdomyosarcoma
•This is the most common malignant tumor (17 %) and may arise from the distal spermatic cord and appear as a scrotal mass or hydrocele.
•These tumors have a bimodal distribution and occur in boys aged 3–4 months and in teenagers.
•Up to 70 % of cases involve the retroperitoneal lymph nodes at presentation.
•About 90 % of paratesticular rhabdomyosarcomas demonstrate a favorable embryonal pattern on histology.
•Paratesticular rhabdomyosarcomas usually present with an enlarging painless scrotal mass.
•By the time of presentation distinction from a primary testicular tumor is usually not possible on physical examination, though the extratesticular nature of the tumor is usually apparent on ultrasound
•The initial management for paratesticular rhabdomyosarcomas is an inguinal excision of the tumor and testis.
•The excision should be performed just as for a testicular malignancy.
•Trans-scrotal biopsies of solid scrotal masses should be avoided due to the risk of seeding of the incision if the mass is indeed a rhabdomyosarcoma.
•All children with rhabdomyosarcoma require vincristine, Adriamycin, and dactinomycin (VAC) chemotherapy or treatment with a combination of these drugs. Patients with evidence
of metastatic disease may require radiation therapy.
•Routine dissection of the retroperitoneal lymph nodes is recommended in all patients aged 10 years or older (regardless of the imag-
ing results) and in patients younger than 10 years whose images show retroperitoneal disease.
•Children younger than 10 years have a survival rate of nearly 95 %. Children older than 10 years have a worse prognosis and an increased risk for involvement of the retroperitoneal lymph nodes; therefore, an aggressive approach with dissection of the retroperitoneal lymph nodes is recommended.
•Paratesticular rhabdomyosarcoma should be evaluated for metastasis including:
–CT of the chest, abdomen, and pelvis.
–The most common sites of metastases are the retroperitoneum and lungs.
•Patients with retroperitoneal metastases undergo a modified unilateral nerve-sparing retroperitoneal lymph node dissection.
•All patients are treated with chemotherapy and those with positive retroperitoneal nodes receive radiation therapy as well.
•Younger children with a normal abdominal CT may be treated with chemotherapy alone without a staging retroperitoneal lymph node dissection.
•The role of staging RPLND in patients with clinical stage 1 disease is based on experience in the Intergroup Rhabdomyosarcoma Studies (IRS).
–IRS-III (from 1984 to 1991) required a staging unilateral RPLND for all clinical stage 1 patients.
–In IRS-IV (from 1991 to 1997) patients with a negative CT scan did not undergo staging RPLND (and did not receive radiation to the retroperitoneum).
•This approach resulted in a worrisome decrease in the percentage of patients diagnosed with metastatic disease in IRS-IV, particularly among adolescents.
•Furthermore, adolescents with clinical stage 1 disease in IRS-IV had a 3-year event-free
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27 Testicular Tumors in Children |
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survival (EFS) of only 68 % compared to a 100 % survival for patients with recognized lymph node involvement (who received radiation and more intense chemotherapy) presumably due to under-staging and under-treatment of those stage 1 patients with occult retroperitoneal disease.
•Such discrepancies were not seen in the prepubertal patients.
•Based on these data, patients over 10 years of age with or without radiographic evidence of retroperitoneal disease should undergo a staging RPLND and receive radiation in addition to chemotherapy if the lymph nodes are positive.
•Younger children with a normal abdominal CT may be treated with chemotherapy alone without a staging RPLND.
•These tumors are highly aggressive and spread via the blood, lymphatics, or direct extension to the lungs, the cortical bone, or to the bone marrow in 20 % of patients at the time of diagnosis.
•Radical inguinal orchiectomy followed by retroperitoneal lymph node dissection is recommended for all children older than 10 years and for those younger than 10 years with retroperitoneal disease.
•Patients with positive lymph nodes are treated with multimodal therapy (chemotherapy and radiation).
•The overall survival rates for patients with paratesticular rhabdomyosarcoma is currently about 90 %.
27.20 Prognosis and Outcome
•In the past, the survival rates from testicular cancer were low.
•Perhaps the greatest advance in the management of testicular cancer was the introduction of platinum-based chemotherapy.
•Survival for both prepubertal and adult tumors has increased dramatically since its introduction.
•Multiagent chemotherapy has become the standard therapy for virtually all metastatic prepubertal testicular malignancies.
•Since the introduction of adjuvant chemotherapy, chiefly platinum-based drugs like cisplatin and carboplatin, the outlook has improved substantially.
•The survival rates have improved markedly and currently the cure rates are over 95 %.
•With recent advances in radiologic staging, serum tumor marker surveillance, and platinum-based chemotherapy for advanced disease, overall survival rates for patients with seminoma have increased to more than 90 %.
•Nearly 100 % of patients with stage I testicular seminoma are cured.
Further Reading
1. Agarwal PK, Palmer JS. Testicular and paratesticular neoplasms in prepubertal males. J Urol. 2006;176(3): 875–81.
2. Bujons A, Sfulcini JC, Pascual M, Feu OA, Garat JM, Villavicencio H. Prepubertal testicular tumours and efficacy of testicular preserving surgery. BJU Int. 2011;107(11):1812–6.
3. Carver B, Al-Ahmadie H, Sheinfeld J. Adult and pediatric testicular teratoma. Urol Clin N Am. 2007;34: 245–51.
4. Cornejo KM, Frazier L, Lee RS, Kozakewich HP, Young RH. Yolk sac tumor of the testis in infants and children: a clinicopathologic analysis of 33 cases. Am J Surg Pathol. 2015;39(8):1121–31.
5. Cortez J, Kaplan G. Gonadal stromal tumors, gonadoblastomas, epidermoid cysts, and secondary tumors of the testis in children. Urol Clin North Am. 1993;20:15–26.
6.Cost NG, Lubahn JD, Adibi M, Romman A, Wickiser JE, Raj GV, et al. Risk stratification of pubertal chil-
dren and postpubertal adolescents with clinical stage I testicular nonseminomatous germ cell tumors. J Urol. 2014;191(5 Suppl):1485–90.
7. Cushing B, Giller R, Cullen J, et al. Randomized comparison of combination chemotherapy with etoposide, bleomycin, and either high-dose or standarddose cisplatin in children and adolescents with high-risk malignant germ cell tumors: a pediatric intergroup study – Pediatric Oncology Group 9049 and Children’s Cancer Group 8882. J Clin Oncol. 2004;22:2691–700.
8. Furness PD, Husman DA, Brock JW, et al. Multiinstitutional study of testicular microlithiasis in childhood: a benign or premalignant condition? J Urol. 1998;160:1151–4.
9.Hisamatsu E, Takagi S, Nakagawa Y, Sugita Y, Yoshino K, Ueoka K, et al. Prepubertal testicular tumors: a 20-year experience with 40 cases. Int J Urol. 2010;17(11):956–9.
Further Reading |
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10. Kao CS, Cornejo KM, Ulbright TM, Young RH. Juvenile granulosa cell tumors of the testis: a clinicopathologic study of 70 cases with emphasis on its wide morphologic spectrum. Am J Surg Pathol. 2015;39(9):1159–69.
11. Mann J, Raafat F, Robinson K, et al. The United Kingdom Children’s Cancer Study Group’s second germ cell tumor study: carboplatin, etoposide, and bleomycin are effective treatment for children with malignant extracranial germ cell tumors, with acceptable toxicity. J Clin Oncol. 2000;18:3809–18.
12.Metcalfe PD, Farivar-Mohseni H, Farhat W, McLorie G, Khoury A, Bagli DJ. Pediatric testicular tumors: contemporary incidence and efficacy of testicular preserving surgery. J Urol. 2003;170(6 Pt 1):2412–5.
13.Petkovic V, Salemi S, Vassella E, et al. Leydig-cell tumour in children: variable clinical presentation, diagnostic features, follow-up and genetic analysis of four cases. Horm Res. 2007;67:89–95.
14.Petterson A, Richiardi L, Nordenskjold A, et al. Age at surgery for undescended testis and risk of testicular cancer. NEJM. 2007;356:1835–41.
15. Ross J, Rybicki L, Kay R. Clinical behavior and a contemporary management algorithm for prepubertal testis tumors: a summary of the Prepubertal Testis Tumor Registry. J Urol. 2002;168:1675–9.
16. Ross JH, Rybicki L, Kay R. Clinical behavior and a contemporary management algorithm for prepubertal testis tumors: a summary of the Prepubertal Testis Tumor Registry. J Urol. 2002;168(4 Pt 2):1675–8.
17.Rushton H, Belman A, Sesterhenn I, et al. Testicular sparing surgery for prepubertal teratoma of the testis: a clini-
cal and pathological study. J Urol. 1990;144:726–30. 18. Schneider D, Calaminus G, Koch S, et al.
Epidemiologic analysis of 1,442 children and adolescents registered in the German germ cell tumor protocols. Pediatr Blood Cancer. 2004;42:169–75.
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