A 53-year-old male patient presented to our clinic with a history of urinary hesitancy, intermittency and sense of incomplete voiding for the past 1-year duration. No other symptoms like hematuria or perineal pain were noted. Rectal examination revealed an ill-defined swelling in the left side of the pelvis in continuity with the prostate. External genitalia appeared normal. No clinical stigmata of von Recklinghausen's disease were noted. Transabdominal ultrasound showed a retrovesicular swelling with solid and cystic areas. Radiological examination using computerized tomography (CT) and magnetic resonance imaging (MRI) confirmed that the lesion was arising from the left seminal vesicle [Figure 1]. Bilateral upper urinary tracts appeared normal.
Figure 1.
Radiological features. (a) Axial, (b) coronal, and (c) sagittal T2W MRI images showing well-circumscribed heterogeneous hyperintense lesion with central hypointensity seen arising from the left seminal vesicle (target appearance). (d-f) Axial and coronal T1W fat-saturated MRI images showing well-defined heterogeneous hyperintense lesion in left rectovesical pouch extending posterior to pararectal space. No evidence of calcification or hemorrhage was noted
After thorough evaluation, he underwent diagnostic cystoscopy, and left retrograde pyelography (RGP). Cystoscopy was normal. Left RGP showed medially deviated left ureter due to the mass. A ureteric catheter was placed in the left ureter for its identification intraoperatively. Laparoscopic excision of the left seminal vesicle with mass was done.
The histopathology and immunohistochemistry showed features of neurofibroma arising from the left seminal vesicle [Figure 2]. The postoperative period was uneventful, and the patient voided well after catheter removal. At 3 years of follow-up, patient was doing well.
Figure 2.
Pathological features. (a) Gross examination showed well-encapsulated fleshy tan-colored tumor replacing the seminal vesicle. (b) H and E 10×; microscopically, the neoplasm was composed of elongated spindle-shaped cells along with abundant mucin, collagen bundles, and thin-walled blood vessels. (c) H and E 100×, showing spindle-shaped cells with elongated wavy nuclei. No evidence of mitosis was noted. (d-f) Immunohistochemical staining revealed that the tumor cells were positive for S-100 (40×) and vimentin (40×), and negative for CD34 (10×)
Primary tumors of the seminal vesicles are rare; however, secondary tumors are common.[1] Most common among the primary tumors are adenocarcinomas. Benign tumors like adenoma, leiomyoma, teratoma, schwannoma (neurilemoma), and cystadenoma arising from seminal vesicle have been reported.[1] The differentiation of primary and secondary tumor is only established by histopathological analysis after excision of the mass or after biopsy.[1]
Neurofibroma is a benign overgrowth having disorganization of normal nerve tissues with the accumulation of inflammatory cells and blood vessels.
Neurofibromas of urinary system may arise from pelvic, bladder, and prostatic nerve plexus. They commonly involve urinary bladder and, at times, prostate, urethra, spermatic cord, testis, penis, and ureter.[2,3] Solitary neurofibroma of spermatic cord has been reported earlier.[3,4,5] However, solitary neurofibroma of the seminal vesicle has not been reported so far.
Histologically, most neurofibromas are unencapsulated tumors and consist of elongated fibroblasts with bent, wavy, and serpentine nuclei separated by abundant fine collagen fibers and blood vessels.[6] Encapsulation of neurofibroma, as in our case, occurs in only 4% of the neurofibromas.[7] The tumor has strong immunoreactivity for vimentin and S-100.
To conclude, solitary neurofibroma of the seminal vesicle should be considered as a differential diagnosis in seminal vesicular lesions.
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