Bilateral Seminal Vesicle Hypoplasia




Cabrero, Daniel
Butson, Carter
Brown, Kerrie
Costello, Kathryn
Fisher, Cara L.


0000-0003-0257-3614 (Fisher, Cara L.)

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Background: Seminal vesicles, two coiled sacs located posteriorly to the male bladder and lateral to the ampulla of the ductus deferens, play a vital role in male fertility. The duct of the seminal vesicle joins with the ampulla of the ductus deferens forming the ejaculatory duct, which then opens into the prostatic urethra. Producing about 70% of male semen, the seminal gland secretes alkaline fluid that contains fructose, prostaglandins, proseminogelin, and other substances that aid in successful fertilization. Contraction of the seminal vesicles releases seminal fluid into the ejaculatory duct where it mixes with spermatozoa from the ductus deferens. Little to no secretions from the seminal vesicles would likely result in male infertility due to the absence of fructose, the primary energy source for motile spermatozoa. Seminal vesicles can be affected by infection, cysts, tumors, hypoplasia, and congenital disease, but isolated seminal vesicle abnormalities are a very uncommon occurrence. There are a few disease states in which seminal vesicle abnormalities do occur. For example, Zinner syndrome is associated with renal agenesis and seminal vesicle hypoplasia or cysts. A Hoxa 13 gene mutation is associated with reduced seminal vesicle size and abnormal morphology, diminished dorsolateral ductal branching of the prostate, and agenesis of the bulbourethral gland. The complete bilateral absence of seminal vesicles can occur following a radical prostatectomy, where the prostate and seminal vesicles are excised together. Case Information: A pelvic dissection of an 82-year-old male donor during a first-year medical anatomy course revealed bilateral seminal vesicle hypoplasia. The seminal vesicle tissue was abnormally tough and embedded within enlarged prostatic tissue. The ductus deferens appeared normal and bilaterally intact. No other significant abnormalities in the reproductive tract nor the kidneys were noted. Conclusions: Based on our current research and ideas, seminal vesicle hypoplasia with no other concurrent reproductive abnormalities is unusual. Apart from the small seminal vesicles, our cadaver had a complete, bilateral set of male internal reproductive organs and an enlarged prostate with no signs of cancer treatment, ruling out the possibility of radical prostatectomy. Due to the presence of an intact urinary tract, Zinner syndrome is unlikely. The most promising possibility for this abnormality is a mutation of the Hoxa 13 gene based on the similarities between this mutation's presentation and our findings.