Sertoli cell tumor
Testicular tumors are common in dogs and humans. They account for 90% of all cancers arising from the canine male genitalia and primarily affect geriatric patients. Primary testicular tumors may be derived from three specialized testicular elements: interstitial Leydig cells, sustentacular Sertoli cells and spermatic germinal epithelium. Malignant transformation of these elements occurs with equal frequency, giving rise to interstitial cell tumors (ICT), Sertoli cell tumors (SCT), and seminomas (SEM) respectively. De novo formation of multiple testicular tumors in the same patient is common; roughly 40% of dogs diagnosed with testicular cancer have more than one primary testicular tumor.
Several factors are believed to influence the development of testicular tumors, including cryptorchidism, age, breed, and exposure to environmental carcinogens. Boxers, German shepherd dogs, Afghan hounds, Weimaraners and Shetland sheepdogs appear to have an increased risk of developing primary testicular tumors. Both Sertoli cell tumors and seminomas are associated with intra-abdominal or inguinal cryptorchidism. The incidence of SCT is more than 20 times higher in cryptorchid than in scrotal testes. One study revealed 54% of SCT diagnosed in intact male dogs developed in cryptorchid testes.
Most primary testicular tumors in dogs remain locally confined, with a rate of metastasis less than 15%. When seen, metastatic lesions typically involve regional lymph nodes, skin, liver, lungs, and spleen. Although metastasis is uncommon, it may result from the chronicity of the mass or its anaplastic nature. Removal of such a substantial mass inherently involves removal of a large percentage of the patient’s blood volume, which contributes to the patient’s anemia, hypovolemia, and hypotension. Large abdominal masses also place pressure on the caudal vena cava, impairing venous return and contributing to hypotension. Aggressive resuscitation with blood products, synthetic colloids, and crystalloids is often necessary. Surgical removal of these tumors can result in a loss of more than 16% of total blood volume. Subsequent hypotension is often responsive to dopamine and dobutamine.
Sertoli cells normally aid in the formation of the blood-testis barrier and produce hormones, including estrogen and inhibin. Estradiol- 17β concentrations are significantly higher in dogs with SCTs, and these dogs have lower levels of testosterone than normal. Reductions in the testosterone/estradiol ratio are attributed to clinical feminization. Clinical signs hyperestrogenism include symmetric alopecia and hyperpigmentation, gynecomastia, galactorrhea, and atrophic penis. Less common clinical signs associated with primary testicular tumors include hematuria, spermatic cord torsion, and hemoperitoneum.
Testicular tumors are usually diagnosed by palpation during routine physical examination or ultrasound. Clinical staging should include a complete blood count to screen for anemia, leukopenia, and thrombocytopenia as well as comprehensive thoracic radiographs and abdominal ultrasound to check for metastases.
Localized disease is often cured with orchiectomy and scrotal ablation. Dogs with bone marrow hypoplasia secondary to hyperestrogenism have a guarded prognosis. The efficacy of chemotherapy and radiation for treatment of metastatic testicular disease is limited. In a small case study, cisplatin (which is used for the treatment of testicular cancer in humans) was reported effective as a single agent in the treatment of 2 of 3 dogs with testicular tumors (SCT and SEM).
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