A Novel Surgical Management for Male Infertility Secondary to Midline Prostatic Cyst

Gong Cheng; Bianjiang Liu; Zhen Song; Aiming Xu; Ninghong Song; Zengjun Wang

Disclosures

BMC Urol. 2015;15(18) 

In This Article

Discussion

MPC is previously thought to be Mullerian duct cyst, causing EDO and male infertility through oppressing ejaculatory duct.[4] Recent researches reveal that not all cystic lesions are located in the midline prostate originate from Mullerian duct remnant. Some cases are just the cystadenoma or the simple cyst of prostate.[5] Such cyst in the midline prostate should be termed as prostatic utricular cyst or cystic dilation of prostatic utricle, depending on whether an outlet to the urethra exists.

Despite the embryologic or histological origin, MPC is a surgically correctable disease. Many MPCs are asymptomatic, or have some non-specific symptoms such as perineal pain, hematospermia, and painful ejaculation. One of the most important and serious outcomes caused by cystic lesion oppression is EDO and male infertility. Semen analysis of these patients often showed low semen volume and pH level, reduced semen fructose, oligoasthenozoospermia, and even azoospermia.

Vasoseminal vesiculography is the golden standard for diagnosis. Percutaneous testicular sperm aspiration (PTSA) is helpful to identify the type of MPC. However, these methods are invasive and complicated. TURS is preferred for simple and noninvasive characteristics. It can offer greater details about the relationship of prostatic, seminal vesicle, and ejaculatory duct.[6] Pelvic MRI not only clearly shows the anatomy of prostatic, seminal vesicle, and ejaculatory duct, but also helps to judge the nature of cyst fluid.[7]

The treatment for MPC is still controversial. Some researchers claimed that treatment should only be performed on symptomatic or infertile patients since almost 60% of cases with MPC did not experience any cyst-related symptoms or fertility impairment.[8] Invasive procedures include transperineal or transrectal puncture and endoscopic section of the utricle meatu.[9] However, puncture therapy has a high recurrence rate while endoscopic incision faces persistent post-operative severe oligozoospermia or azoospermia.[10] We speculate that MPC may cause to seminal vesiculitis and further promote the abnormal semen quality through oppressing ejaculatory duct and causing semen stasis. Therefore, the dilation of ejaculatory duct and the irrigation of seminal vesicle using seminal vesiculoscope were performed after transurethral unroofing of the cyst in present study. A previous study achieved a better result for MPC with male infertility using transurethral endoscopic incision, in which a pregnancy rate was 30.8% (8/26).[10] However, other reports showed a poor efficacy of unroofing of the cyst.[11] The present study is delightful with a pregnancy rate of 41.7% (5/12) and an obviously improved semen quality of 75% (9/12). One patient with azoospermia had spermatozoa in the urine after ejaculation. For the two patients of poor efficacy, seminal vesicle impairment due to long term semen stasis might cause inadequate transfer of semen quality.[12] In conclusion, our data showed that the novel surgical management is effective, minimally invasive, and safe for male infertility secondary to MPC.

The followings are our endoscopic experiences. Sometimes, it is difficult to find the opening since the ejaculatory duct is oppressed by MPC or covered by inflammatory tissues.[3,13] Increasing the velocity of water perfusion and using a zebra guidewire as the guidance are helpful to find the openings. Otherwise, vas deferens puncture and injection of methylene blue, combined with the transurethral endoscope, are helpful to observe the ejaculatory duct openings. After observing the seminal vesicle lumen carefully, appropriate therapies can be implemented. Inflammatory semen can be treated with antibiotics irrigation into seminal vesicle. Stones can be removed through holmium laser lithotripsy and forceps.

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