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Radiologic-Pathologic Conference of the University of Arizona |
1 Both authors: Department of Radiology, University of Arizona, PO Box 245067, 1501 N Campbell Ave., Tucson, AZ 85724-5067.
Received November 23, 2006; accepted after revision March 28, 2007.
Address correspondence to S. L. Shin.
Keywords: large cell calcifying Sertoli cell tumor • oncologic imaging • pediatric imaging • radiologic-pathologic correlation • Sertoli cell tumor • testis
A14-year-old boy noticed a painless left testicular mass. Physical
examination revealed neither gynecomastia nor abnormal skin pigmentation.
Serum 
-fetoprotein and ß-HCG levels were normal. Sonography
depicted an intratesticular diffusely hyperechoic lesion with acoustic
shadowing and hypervascularity (Fig.
1A). CT showed an enhancing left testicular lesion with dense
central calcification (Fig. 1B)
and no evidence of metastases. The patient underwent surgical excision.
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Tumors may be associated with genetic abnormalities such as Carney's complex (cardiac myxomas, skin pigmentation, and endocrine hyperactivity) and Peutz-Jeghers syndrome (gastrointestinal polyposis, muco-cutaneous pigmentation) [2].
In the past decade in the literature, certain features of LCCSCT have been associated with benign histology. Benign tumors are more commonly small (mean, 1.4 cm), occur in younger patients (mean age, 17 years old), and are multifocal or bilateral (28% vs 0% of malignant tumors). Nevertheless, 72% of benign tumors are unilateral and unifocal [1]. Malignant tumors tend to be large (> 4 cm); to occur in older patients (mean age, 39 years old); and to show extratesticular extension, hemorrhage, necrosis, lymphovascular invasion, frequent mitosis, or cellular atypia. Malignant tumors metastasize to the retroperitoneal lymph nodes, with less common hematogenous spread to the lungs, liver, and bone [1].
LCCSCTs are characterized histologically by large tumor cells, abundant eosinophilic cytoplasm, tubular and trabecular differentiation, and extensive calcified debris. Immunohistochemical reactivity for the S-100 calcium-binding protein ß subunit excludes from the differential diagnosis more common Leydig cell tumors that can have a similar appearance on H and E stains [3].
Visualization on imaging of a well-circumscribed diffusely hyperechoic intratesticular mass with heavy acoustic shadowing and moderate hypervascularity is suggestive of LCCSCT [4]. These imaging findings allow differentiation of LCCSCT from other causes of intratesticular calcifications, such as old infarct or hematoma; nonseminomatous germ cell tumors, epidermoid tumor, or "burnt out" tumor; granulomatous disease; and microlithiasis [5]. Of note, testicular microliths, which have been associated with testicular carcinoma, are hypothesized to result from Sertoli cell dysfunction [6].
A small (< 2 cm) intratesticular mass with the described features suggestive of an LCCSCT in a prepubescent boy, especially if multifocal or bilateral, has a high likelihood of benign histology. Testis-sparing surgery could be considered in these situations, with completion orchiectomy performed if pathology proves malignancy.
Recognizing the unique imaging characteristics of LCCSCT of the testis also has important implications regarding clinical workup. Patients with LCCSCT should be evaluated for Carney's syndrome, particularly considering possible sudden death secondary to cardiac myxoma.
Acknowledgments
We thank Robert R. Hattery and Jonathan Greenfeld for their help with this manuscript.
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