Clinical History
A 22-year-old male patient presented to our hospital with pelvic pain and infertility. He was referred to our department for ultrasound, computed tomography (CT) and magnetic resonance imaging (MRI) examinations.
Imaging Findings
Firstly, transrectal ultrasound showed that the prostate gland was normal, but the seminal vesicle (SV) was not evaluated optimally because of his pain. The CT examination showed absence of the right kidney, and an approximately 80x40mm hypodense lesion with macrolobulated contour in the retrovesical area. The MRI demonstrated that there were multiple cysts and dilated ducts in both seminal vesicles, which were obvious in the right side. The lesion was hyperintense on T2-weighted (T2-W) and T1-W VIBE image due to haemorrhagic or proteinaceous content. Also, on the MRI and CT, a thin-walled tubular structure which lined upward on the cystic lesions was shown and was thought to be a remnant ureteric bud. The patient underwent an operation where stenosis of ejaculatory ducts was discovered. No haemorrhagic component was seen in the ejaculatory ducts during the operation. In diffusion-weighted image (DWI) cysts were hyperintense in both ADC map and b800 images.
Discussion
The embryological development of seminal vesicle (SV) and vas deferens is closely related with the urinary system, for this reason developmental anomalies of SV are often associated with renal or ureteral anomalies. Pronephros is composed of the mesoderm at the 3rd week of life and pronephros differentiates to mesonephros at the end of the 4th week [1]. The ureteric bud, which will grow upward to constitute the primitive kidneys at the 6th week, arises from the lower end of the mesonephric duct at the 5th week of life [1, 2]. In addition, a bulbous structure of the distal mesonephric duct gives rise to the SV and the distal segments of mesonephric ducts become vas deferens [2]. SV is responsible for the production and secretion of seminal fluid. Disruption of the development of distal mesonephric ducts results in atresia of ejaculatory ducts and abnormal ureteric bud. SV cysts and tubulary dilatations develop due to ejaculatory duct obstruction. An abnormal ureteric bud leads to renal agenesis or dysplasia. Zinner syndrome, which was described by Zinner in 1914, has a triad of "unilateral ejaculatory duct obstruction, SV cysts and ipsilateral renal agenesis" [3]. The cysts are symptomatic during the 3th-4th decade of life [3]. Clinical findings of SV cysts are pelvic pain, infertility, painful ejaculation, haemospermia, recurrent epididymitis or prostatitis [2, 3]. SV cysts show high signal intensity on T2-W image and low signal intensity on T1-W image. If cysts contain haemorrhage or proteinaceous content, they are seen hyperintense on T1-W image. Cysts are thin-walled and do not show contrast enhancement unless they are infected. A remnant ureteric bud may also accompany the classical triad. Diagnosis of Zinner syndrome is important for treatment of recurrent urinary symptoms.
Differential Diagnosis List
Zinner syndrome
Seminal vesiculitis
SV abscess
SV neoplasms
Other cystic lesions which mimic SV cysts
