Late Effects

Given the high cure rates for testicular cancer, the long-term impact of surviving cancer and its treatment has gained importance. While undergoing treatment, fear of cancer, sleep disturbances, and cognitive dysfunction occur frequently ([21]. After therapy, a minority of patients (10-15%) report continued fear of cancer, sleep disturbances, and inability to concentrate, complete tasks, or think clearly. Symptoms of anxiety or depression persist in 30% of survivors at an average of 9 years after therapy compared to 5% of controls [22]. Conversely, other investigators have found no difference in the level of psychological functioning of long-term survivors versus normal controls [23]. Some have even reported improvement in areas such as personal optimism, family relationships, perceived quality of life, and self respect [24].

Sexual function has been studied extensively in survivors. During treatment and soon thereafter, approximately one-third of survivors report sexual dysfunction and/or dissatisfaction with level of sexual activity. However, this effect does not seem to be permanent in the majority of cases and studies indicate the level of dysfunction returns to baseline by 3 years after completion of therapy. The sexual dysfunction of some patients at the time of diagnosis, due to testicular atrophy and to the presence of disease, must be taken into account. The complications of RPLND and ejaculation have been well documented and have decreased with improved surgical techniques.

Late or prolonged toxicities of chemotherapy are agent- and dose-specific. Early studies showed high rates of bleomycin-induced pulmonary toxicity ranging from 34 to 46%. In a recent EORTC study, BEP induced a 20% decrease in carbon monoxide diffusing capacity versus 2% in the EP group [25]. Efforts to reduce this toxicity by decreasing the dose of bleomy-cin (three cycles vs. four) or administering bleomycin only on the 1st day of each cycle rather than weekly (decreasing the total dose by 66.6%) may ameliorate this toxicity without decreasing survival in selected patients.

Cisplatin causes proximal renal tubule defects with hypomagnesemia, hypokalemia, and hypocalcemia. Acute decreases in glomerular filtration also occur. Some studies report persistence of these abnormalities, while others report gradual improvement. The late occurrence of hypertension has also been reported.

Ototoxicity is related to the total dose of cisplatin, is permanent, and occurs in 20-40% of patients. It begins as a high-frequency loss and progresses to involve frequencies in the speech range with continued exposure to the drug. The concurrent exposure to ototoxic environmental factors (e.g., rock concerts, airplanes, jack hammers) by adolescents and young adults may increase their risk of hearing loss. Appropriate anticipatory guidance and monitoring of audiograms may lessen the impact of ototoxicity. The delivery of only three cycles of cisplatin, when appropriate, will decrease the incidence of severe toxicity.

Peripheral neurotoxicity is characterized by pares-thesias and dysesthesias. It is induced in 30-40% of patients who receive cisplatin and persists over time [26, 27]. Vascular toxicities reported with cisplatin include Raynaud's phenomenon, venous thrombosis, and myocardial infarctions.

An increased risk of second malignant neoplasms has been reported for survivors of testicular tumors. Cancer in the contralateral testis is the most common finding and is probably not treatment related. Patients who receive irradiation therapy have an increased risk of stomach cancer (van Leeuwen et al. 1993). Leukemia and myelodysplasia also occur in testicular tumor patients. These complications are usually associated with total doses of etoposide in excess of 2 g/M2 and are often characterized by an 11q23 or 21q22 translocation [28]. Some secondary leukemias appear to be related to the germ-cell tumor and not the treatment.

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