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Bilateral Testicular Cancer J Am Board Fam Pract: first published as 10.3122/jabfm.7.6.516 on 1 November 1994. Downloaded from Bilateral Testicular Cancer Hdward F /3isch(!lJr., MD, Arthur H. Herold, MD, and Phillip]. Marty, PhD lesticular cancer is the most common cancer in but because of tumor vascular invasion, the pa­ men 15 to 35 years old. 1 The lifetime risk is 1 in tient received nearly 1 year of chemotherapy. 500.2 Furthermore, the annual incidence of tes­ Every 3 months for the next 3 years, the patient ticular cancer almost doubled between 1939 and was seen for a physical examination, a chest 1970 from 2.0 to 3.7 per 100,000,2 and the risk of roentgenography, and blood tests for beta human bilateral testicular cancer is increasing as well. 3 chorionic gonadotropin (beta-ReG) and alpha­ Because testicular cancer has become one of fetoprotein, all of which were within normal lim­ the most curable solid tumors 1 and its incidence its. The patient subsequently fathered 2 more is increasing, the primary care physician will be children. encountering patients with a history of testicular Twelve years after the patient's testicular cancer more frequently. This report presents a cancer was diagnosed, at the age of 41 years, he patient with unilateral mixed nonseminoma who noticed a left testicular mass on routine self­ subsequently developed a seminoma in the con­ examination despite previous normal physical tralateral testis 12 years later. Despite cure from examinations. The patient underwent a left or­ the highly malignant embryonal component of chiectomy and was found to have a pure semi­ the mixed nonseminoma, the patient was sub­ noma. The beta-HCG and alpha-fetoprotein jected to the further morbidity of a second can­ blood levels and findings on a computerized axial cer. This case emphasizes that to reduce further tomogram (CT) of the abdomen and pelvis and morbidity and mortality, proper management chest radiogram were normal. He received radia­ and an understanding of a patient's risk for tion therapy to the left pelvic and periaortic contralateral testicular cancer are required by the lymph nodes. At the present time follow-up ex­ primary care physician. aminations have shown no evidence of recur­ rence, and the patient, infertile but otherwise Case Report healthy, receives monthly intramuscular sus­ A 44-year-old man came to our clinic for tes­ tained-action testosterone injections. tosterone replacement 3 years after his second http://www.jabfm.org/ orchiectomy. Discussion The patient's history of testicular cancer began About 95 percent of testicular neoplasms are at age 29 years, when he complained to his physi­ germ cell tumors. Germ cell tumors are divided cian of a 2-month history of a nontender right into seminomas and nonseminomas because of testicular mass. The patient subsequently under­ differences in prognosis and responses to various went right orchiectomy, and the mass was identi­ treatment modalities, i.e., seminomas are radio­ on 26 September 2021 by guest. Protected copyright. fied as a teratoma containing embryonal and sensitive and nonseminomas usually require thera­ seminoma components with vascular invasion. peutic lymphadenectomy and chemotherapy.2 Clinical stage 1 disease was diagnosed and the Nonseminomas are further subdivided into em­ patient underwent retroperitoneallymphadenec­ bryonal cell carcinoma, teratoma, choriocarci­ tomy. His lymph nodes were negative for tumor, noma, and yolk sac tumor (endodermal sinus tumor). About 60 percent of germ cell tumors are a mixture of the above cell types and are classified as nonseminomas. Seminoma is the most com­ Submitted, revised, 21 Junc 1994. mon single histologic type in adults. Pure chorio- From the College of Medicine (EFB), the Departmcnt of . Family Medicine, College of Medicine (AHII), and the Depart­ carCInoma IS very rare. ment of Community and Family Health, College of Public Germ cell tumors produce the tumor markers Health (PJM), University of South Florida, Tampa. Address re­ alpha-fetoprotein and beta-HCG. The presence prints to Arthur I-I. Herold, MD, University of South Florida College of Medicine, 12901 Bruce B. Downs Boulevard, MDC of these markers in serum aid in the diagnosis of Box 13, 'Eunpa, FL 33612-3799. germ cell tumors, response to therapy, and the 516 JABFP Nov.-Dec.1994 Vol. 7 No.6 J Am Board Fam Pract: first published as 10.3122/jabfm.7.6.516 on 1 November 1994. Downloaded from detection of recurrence. For patients with non­ be the universal precursor of germ cell testicular 5 seminomas about 50 to 70 percent will have el­ cancer. evated alpha-fetoprotein levels, and 40 to 60 per­ Bilateral inguinal hernias have been associated cent will have elevated beta-HCG. About 10 in some studies with an increased risk of testicular 6 percent of seminomas will produce beta-HCG cancer. Our patient had a history of bilateral in­ levels, but alpha-fetoprotein is uniformally ab­ guinal hernias as a young adult. Ideally, clinicians sent. Patients who initially test negatively for would like to be able to predict who might de­ tumor markers can become positive if they have velop contralateral cancer. Studies have shown tumor recurrence, progression with treatment, or that patients with a family history of testicular a new primary tumor. cancer, a personal history of cryptorchidism, in­ Germ cell tumors are highly malignant, metas­ fertility, or a testicular volume less than 12 mL tasizing when the tumor is still small. Seminomas have a higher risk of developing contralateral tes­ are the least malignant of germ cell tumors. ticular cancer than do patients without these risk 9 About 50 to 70 percent of patients with nonsemi­ factors.7- A more accurate method, however, of nomas have metastasis at the time of diagnosis distinguishing patients at risk for contralateral compared with 20 to 30 percent of patients with testicular cancer is by testicular biopsy. seminomas. Germ cell tumors spread first It is believed that carcinoma in situ (CIS) is the through the lymphatic channels to the retroperi­ universal precursor of both seminomas and non­ toneallymph nodes (not inguina!), where they are seminomas and can be accurately detected by ran­ disseminated, although hematogenous spread to dom testicular biopsy.l0 As a result of their study the lungs and other viscera occurs early if chorio­ of patients with unilateral testicular carcinoma, a carcinoma or embryonal cell carcinoma is group of Scandinavian researchers estimated that present. Vascular invasion at the site of the pri­ those with CIS of the contralateral testis have a mary tumor portends early hematogenous meta­ 40 percent risk of developing invasive cancer in static spread. The clinician must be aware that the 3 years and a 50 percent risk in 5 years. In the patient might initially complain of signs and same study, 473 patients without contralateral symptoms produced by metastases (weight loss, CIS did not develop invasive cancer during a 12- back pain, supraclavicular node) or the effect of to 96-month follow-up period. 11 the tumor markers (gynecomastia) rather than Although detecting patients with CIS before discovery of the primary tumor (mass in the testis). invasive cancer develops has not proved to affect Patients with unilateral testicular cancer have overall mortality, 11 it can reduce morbidity. If http://www.jabfm.org/ up to a 5 percent chance of developing contralat­ CIS is found in the contralateral testis, it can be eral testicular cancer. Their relative risk for this treated effectively with radiation while preserving disease is 23. The second tumor usually occurs the Leydig cells and, hence, endogenous tes­ within 20 years after the first tumor, with a me­ tosterone froduction, although the patient will be 1 dian time of 4.2 years.4 Because these contralat­ infertile. Detecting and treating CIS, therefore, eral tumors commonly occur when the patient is prevent the morbidity associated with taking life­ on 26 September 2021 by guest. Protected copyright. no longer being cared for by the oncologist or long exogenous testosterone, such as gynecomas­ 13 urologist, the primary care physician must know tia, water retention, and behavioral changes. how to care for these patients and educate them Fertility is usually not an issue, because most pa­ about their risk of contralateral testicular cancer. tients with contralateral CIS are infertile as a re­ 9 Contrary to some theories, most contralateral sult of decreased spermatogenesis. The patient testicular cancers are believed to be a second pri­ in the case described here is interesting because mary, not metastatic, disease, becau~e (1) ther~ is he fathered 2 children between his first and sec­ little anatomic evidence of lymphatlc connectlon ond testicular cancers. between the testes; (2) cancer in the contralateral Physicians in Denmark, where the incidence of testicle occurs without evidence of other me­ testicular cancer is one of the highest in the world tastases' (3) tumors that are histologically differ­ and where many studies on testicular cancer have ent oft~n occur, as in the case described; and been done,14 support the policy of performing a (4) carcinoma in situ frequently occurs independ­ biopsy on all patients who have a history of unilat­ ently in the contralateral testis and is believed to eral testicular cancer. In the United States this Bilateral Testicular Cancer 517 J Am Board Fam Pract: first published as 10.3122/jabfm.7.6.516 on 1 November 1994. Downloaded from policy has not been accepted. 15 Some physicians Although continuing care with the primary choose to focus on only high-risk subgroups for care physician is important to discuss risks and biopsy, such as those who have a history of crypt­ options, the primary care physician is unlikely to orchidism, decreased testicular volume, or infer­ be the one to detect a contralateral tumor.
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