Clinical Presentation - Testicular Cancer

Because this disease affects a younger age group not generally aware of the possible diagnosis, a 4 to 6 month delay in diagnosis is not uncommon. The most common symptom is a painless testicular mass. In some series, however, pain has been associated with almost one half of the presentations. Between 5 and 25 percent of patients may be initially misdiagnosed and treated for epididymitis. Gynecomastia can be present and is secondary to the effect of tumor estradiol synthesis. This is classically associated with Leydig cell tumors. Cough, abdominal mass, back pain, and supraclavicular or other a lymphadenopathy can present in cases of advanced disease.

  • Diagnosis
    • Transcrotal ultrasound can confirm the presence of an intraparenchymal testicular mass, rule out benign processes such as a hydrocele or epididymitis, and effectively evaluate the contralateral gonad.
    • Inguinal (radical) orchiectomy. The primary lesion is best handled by early clamping of the spermatic cord near the internal ring and complete removal of the gonad. Only in very rare circumstances is exploration and frozen biopsy performed. The extent of the tumor, any vascular invasion, and the subtype composition of the lesion (i.e., mixed germ cell) should be noted. A scrotal approach should not be employed as this may theoretically increase the risk of inguinal nodal metastasis and recurrence. Nevertheless, there is no need for a hemiscrotectomy or prophylactic inguinal lymph node dissection in the rare patient who has undergone a scrotal orchiectomy for testicular cancer.
    • Imaging is best conducted with a standard chest x-ray and a CT scan of the retroperitoneum. There is a 20 to 30 percent chance of understaging lesions by this method. Chest CT detects many small nodes, which are usually benign. Pedal lymphangiography is no longer performed on a regular basis.
  • Tumor markers
    • Human chorionic gonadotropin (hCG). hCG is a heterodimeric protein with immunologically distinct chains. Circulating levels are extremely low (1 ng/mL) in normal males. The syncytiotrophoblastic tissue of some germ cell tumors produces this substance. It can, therefore, be detected in almost all choriocarcinomas, 40 to 60 percent of embryonal cell carcinomas, and 5 to 10 percent of pure seminomas. In seminoma, the level is rarely elevated above twice-normal. The half-life for this substance ranges between 24 and 36 hours, but the beta subunit alone has a half-life of 1 hour. Since beta-hCG shares structural homology with luteinizing hormone, spurious elevations can occur in patients with inadequate testosterone production from the contralateral testis (thus higher LH).
    • Alpha -fetoprotein. AFP is an oncofetal protein detected in testis and liver tumors. It is produced by yolk sac elements that may or may not be histologically recognized. This substance is not produced in purechoriocarcinoma or pure seminoma. The presence of elevated AFP in a patient with histologic seminoma precludes the diagnosis of pure seminoma. The half-life of AFP is 5 to 7 days.
    • Lactate dehydrogenase. This general cellular enzyme is not particularly specific for testicular lesions but provides a correlation to tumor bulk. It may have some role in monitoring patients with advanced seminoma and in marker-negative patients with NSGCT and persistent disease.
    • Placental alkaline phosphatase. This substance can be elevated in patients with advanced stage testicular cancer. It can be spuriously raised by tobacco use.
    • Over all stages, 90 percent of patients with nonseminomatous tumors will have an elevation of one or both markers. Fifty to 70 percent will display an elevation of AFP and 40 to 60 percent will have an elevation of B-hCG In stage I lesions, two thirds of patients will have an elevation of one or both major markers. After therapy, tumor markers should display a logarithmic pattern of decrease in accordance with their half-lives. Sustained elevation of markers or slower decrease after orchiectomy or retroperitoneal lymph node dissection (RPLND) suggests residual disease. Normalization of markers is not definite evidence of complete surgical cure.

References

  • Baniel J, Foster RS, Rowland RG, Bihrle R, Donahue JP: Testis cancer: Complications of post-chemotherapy retroperitoneal lymph node dissection. J Urol 153:976-980, 1995.
  • Donohue JP, Thornhill JA, Foster RS, Bihrle R, Rowland RG, Einhorn LH: The role of retroperitoneal lymphadenectomy in clinical stage B testis cancer: The Indiana University experience (1965 to 1989). J Urol 153:85-89, 1995.
  • Einhorn LH: Salvage therapy for germ cell tumors. Semin Oncol 21:47-51, 1994.
  • Einhorn LH, Donohue JP: Advanced testicular cancer: Update for urologists. J Urol 160:1964-1969. 1998.
  • Moller H, Skakkeback NE: Testicular cancer and cryptorchidism in relation to prenatal factors: Case control studies in Denmark. Cancer Causes Control 8:904-12, 1997.
  • Nichols C, Loehrer P Sr: The story of second cancers in patients cured of testicular cancer: Tarnishing success of burnishing irrelevance. J Natl Cancer Inst 89:1304-1305, 1997.
  • Wegner HEH, Hubotter A, Andresen R, Miller K: Testicular microlithiasis and concomitant testicular intraepithelial neoplasia. Int Urol Nephrol 30:313-315, 1998.

 

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