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Reproductive health

THE MALE UROGENITAL TRACT

P. Graber
Urology Clinic, Department of Surgery,
University Cantonal Hospital, 1211 Geneva 14, Switzerland

Embryology

The male accessory genital organs are complex. Three different structures participate and each of them undergoes essential transformations:

  1. The wolffian ducts constitute the epididymis, the seminal vesicles, the ejaculatory ducts and the central part of the prostate.
  2. The müllerian ducts regress in the male and form occasionally the testicular appendices.
  3. The urogenital sinus forms the peripheral and transitional zones of the prostate.

The prostate

This complex organ contributes to urinary continence, produces a significant fraction of the seminal plasma, and closes the urinary pathway during ejaculation. It is attached to the pubic bones by solid ligaments and surrounded by a venous plexus. The anterior muscular envelope participates in the striated sphincter. The vesical trigone extends to the verumontanum and acts as a preprostatic sphincter. Its contraction allows anterograde ejaculation. The development of the prostate is androgen-dependent. The specific receptors respond to dihydrotestosterone after a transformation of testosterone by 5α-reductase.

Morphology

McNeal (11) established the current conceptualization of 4 different zones of the prostate:

  1. The central zone, which represents 20% of its mass. The glandular orifices are in contact with the ejaculatory ducts and end near the verumontanum.
  2. The peripheral zone (70% of the total mass). Its glandular ducts enter the urethra distal to the verumontanum.
  3. The transition zone (5 - 10% of the gland’s mass) forms two small lobes lateral to the proximal urethral segment. The tissue of this periurethral area will form the nodular hyperplasia.
  4. The periurethral segment which forms the preprostatic sphincter.

Physiology

Seminal plasma is a composite of secretions of the testes, epididymis, and the accessory sex glands. As an extremely rough approximation, it is estimated that 3% of the volume of the ejaculate consists of bulbourethral gland fluids, 20% of prostate gland secretions, 7% of spermatozoa, epididymal fluids, and ampullary fluids; and the rest (70% of secretions) originates from the seminal vesicles (16).

The prostate contributes to the seminal plasma by the secretion of electrolytes (zinc, magnesium, citric acid) and enzymes (acid phosphatase, proteases, and oxidase). The prostatic secretion exerts an inhibitory effect on microbial growth (10).

Pathology

Inflammatory conditions.

Acute prostatitis. The symptomatic patient presents with fever, pain, and dysuria. The infection mechanism is probably hematogenous. The prostate gland is swollen and painful on rectal examination. An antibiotic treatment of 3 weeks is normally effective and prevents relapse.

Chronic prostatitis. The term prostatitis is not a definite nosological entity. It includes various inflammatory and non-inflammatory conditions. The clinical classification system is based on a standardized bacteriologic localization technique, which includes a quantified analysis of expressed prostatic secretions for leukocytes and other inflammatory cells. No specific symptoms exist. The patient complains of pain in the lower abdomen and in the perineal region with irradiation to the tip of the penis. An emission of a clear liquid is occasionally reported. The inflammatory process is essentially located in the peripheral zone of the prostate. A possible trigger is the reflux of urine in the prostatic glands, especially in patients with poor relaxation of the urethral sphincter, or urethral stenosis.

Classification of the prostatitis syndrome according to bacteriological and cytological criteria:

  1. Chronic bacterial prostatitis.
  2. Non-bacterial prostatitis.
  3. Prostatosis.

There is no difference in the symptoms of the three different forms, and the diagnosis is based on biological criteria. In chronic bacterial prostatitis, the micro-organism (Gram-negative bacteria of intestinal origin, or Gram-positive saprophytic staphylococci) can be identified in a specimen voided after prostatic massage. In non-bacterial prostatitis the cultures are sterile, but the liquid contains significant inflammatory cells. Chlamydia, Mycoplasma, and possibly other micro-organisms may be implicated in its etiology. The diagnosis of a prostatosis is made by exclusion: the specimen is sterile and contains no inflammatory cells (9,13).

Treatment. Chronic bacterial prostatitis needs an antibiotic treatment for at least two months. The choice of the agent is important: the pH (6.4) of the prostatic liquid and the lipid membrane constitutes a barrier for most antibiotics. Only basic and liposoluble components, e.g. quinolones have a satisfactory intraprostatic penetration rate and a significant antibacterial effect.

In non-bacterial chronic prostatitis an anti-inflammatory treatment with nonsteroidal anti-inflammatory drugs is advised. This treatment occasionally unmasks an underlying microbial contamination. Prostatosis is an affection with an important psychosomatic component. However the underlying conflict usually resists the psychiatric approach. The treatment of this very frequent affection is difficult and frustrating.

Benign hypertrophy of the prostate.

Small glandular and stromal nodules can be found in the periurethral region as early as the fourth decade. Their number increase in linear progression, but large nodules are uncommon until the seventh decade. The onset of the second phase, the expansion of the nodules, is probably the result of a hormonal influence: androgenic by an accumulation of dihydrotestosterone in the glandular compartment and estrogenic by a stimulation of the stroma. This transformation takes place exclusively in the periurethral transition zone. The central and peripheral zones are not involved in the " hypertrophy " (4,12). They are not removed in the surgical or endoscopic " prostatectomy " procedure and form the surgical capsule.

Treatment. Table 1 summarizes the therapies available for benign hypertrophy of the prostate (15).

Retrograde ejaculation is a possible complication of all prostatic surgery (6).

Prostatic carcinoma.

In contrast to benign hypertrophy of the prostate, carcinoma originates in the peripheral zone. Small dysplastic areas are detectable in 30% of men at the age of 50. Their prevalence increases to 80% at 70 years. Only a small number (1-5%) of these microscopic carcinomas will develop a clinically symptomatic tumour and only a minority (20-50%) of patients will die of their cancer. In the male population between 50 and 70 years, an early detection of the tumour yields a therapeutic benefit in the possibility of a curative treatment. The significant components of diagnosis are: digital rectal examination, prostate specific antigen (PSA), and transrectal ultrasound (14).

Treatment. Table 2 summarizes the therapies available for prostatic carcinoma (3).

Seminal vesicles

The seminal vesicles are lateral expansions of the vas deferens. They derive from the wolffian ducts, and their aspect is that of an irregular gland of 5-8 cm. The seminal vesicles are embedded in a muscular envelope, which expresses the liquid content during ejaculation. They contain no spermatozoa. The semen reservoir is the tortuous part of the ampulla of the vas deferens. Spermatozoa and the seminal plasma are ejaculated through the ejaculatory ducts which open to the urethra at the verumontanum.

Physiology

The liquid produced by the seminal vesicles contains essentially fructose, prostaglandins, and proteins. Vesicular proteins are involved in different physiological processes: formation of seminal coagulum, formation of the so-called " sperm-coat ", antimicrobial and immunosuppressive effects of seminal plasma (1).

Pathology

A number of cystic malformations exist, but their definition by morphological criteria is difficult. These malformations are often associated to ipsilateral renal or ureteral abnormalities. An irregular symptom of seminal vesicular malformation is reduced ejaculate volume. The diagnosis is made by suprapubic or transrectal ultrasound.

Inflammatory affections.

Historically, inflammation has been an important complication of gonorrhoea accompanied by abscess requiring surgical drainage. Currently the involvement of the seminal vesicles in bacterial prostatitis is probably very frequent. The revealing symptom is hematospermia with pain during ejaculation (7).

The epididymis

The epididymis is the organ of evacuation and maturation of the spermatozoa. They leave the testicle by the rete testis, enter the epididymis by its head and progress to the tail, which ends at the junction with the vas deferens. The epididymis consists of an extensive system of epithelium-lined canals. In the region of the head the epithelium is ciliar to help progression of spermatozoa, whereas in the caudal part this action is provided by a muscular sheath.

Physiology

The epididymis is the organ of maturation of spermatozoa. It has been shown by experiments in animals that the fertilizing quality of sperm varies from 1% in the head to 60% in the middle part and 90% if collected in the tail. Sperm maturation manifests itself by an increased mobility. The tail of the epididymis is a part of the sperm reservoir. During ejaculation the spermatozoa are actively transported by muscular contractions of the vas deferens.

The characteristic constituents of the epididymal plasma are glycerilphosphorylcholine, carnitine, certain mucoproteins and enzymes (10). Their action is incompletely known. Carnitine is used as a marker. Its concentration in the seminal plasma is a parameter of epididymal function and permeability of the deferens.

Pathology

There are different causes of epididymal obstruction, the most frequent being postinfectious obstruction. Other possible etiologies are: congenital abnormalities, epididymal cysts, and epididymal trauma.

Infections.

Acute epididymitis is the most frequent inflammatory disease of the male urogenital tract. The underlying micro-organisms tend to be coliform bacteria in the age group >35 and Chlamydia in younger men (<35 years) (5). The contamination is normally canalicular, but hematogenous and lymphatic infections cannot be excluded.

Diagnosis. Swollen, red and painful testicle. Palpation is not always conclusive. The transillumination is normally positive.

Complementary examination: Ultrasound, possibly combined with a Doppler to exclude a torsion or the possibility of a (rare) epididymal tumour.

Bacteriology: Urine voided in 2 fractions. Urethral swab for the detection of Chlamydia trachomatis. Possibly prostatic massage or direct epididymal aspiration. A positive culture is found in 50% of cases, and a positive serology in 30% of chlamydial infections (8).

Treatment. A problem of decision: overtreat 50% of patients (with negative cultures) or undertreat a potentially dangerous condition for its possible effect on fertility.

Compromise: treat young patients at risk for chlamydial infections together with their partners for 3-6 weeks. This treatment is supposed to prevent the formation of anti-sperm antibodies which have been identified in up to 30% of acute epididymitis cases.

Varicocele

Varicocele and its effect on fertility have been discussed for a long time. This abnormal dilatation of the pampiniform plexus within the spermatic cord is diagnosed in one third of men being evaluated for infertility. Nevertheless, incidence of varicocele in the male population is 15% compared to an overall 5% incidence of male infertility: not all those with varicocele are infertile and need to be treated. Elevated scrotal temperatures, reflux of adrenal metabolites, stagnation and hypoxia are possible etiologic factors for varicocele-induced infertility (2). There is not yet a semen analysis profile that is pathognomonic for varicocele. The surgical treatment of infertile patients with varicocele however, offers the most encouraging results among all therapeutic options, with a rate of improvement in semen quality in 60% of cases, and a pregnancy rate in 40% of affected couples. In conclusion, adolescents and infertile men with varicocele should be treated if the testicular mass is decreased, or if they are symptomatic.

References

  1. Balerna, M., Leonardi, D., Campana, A., and Colpi, G.M. (1985): Progr. Reprod. Biol. Med., 12:36-63.
  2. Biase, J.N., Nagler M.N. (1992): Current Op. Urol., 2:463-466.
  3. Crawford, E.D. (1990): Cancer, 66(Suppl. 5):1035-1038.
  4. Farnsworth, W.E. (1980): In: Male Accessory Sex Glands, edited by E. Spring-Mills, and E.S.E. Hafez, pp. 155-182. Elsevier/North-Holland Biomedical Press, Amsterdam.
  5. Gerris, J., Schoysman, R., and Piessens-Denef (1985): Acta Eur. Fertil., 179-182.
  6. Hellinga, G. (1976): Clinical Andrology. William Heinemann Medical Books Ltd., London.
  7. Hermabessière, J. (1989): In: Andrologie II, edited by G. Arvis, pp. 1145-1152. Maloine, Paris.
  8. Ingerslev, H.J., Walter, S., Andersen, J.T., Brandenhoff, P., Eldrup, J., Geerdsen, J.P., Scheibel, J., Tromholt, N., Jensen, H.M., and Hjort, T. (1986): J. Urol., 136:162-164.
  9. Krieger, J.N. (1984): Sex. Transm. Dis., 11:100-112.
  10. Mann, T., and Lutwak-Mann, C. (1981): Male Reproductive Function and Semen. Springer Verlag, Berlin.
  11. McNeal, J.E. (1968): Am. J. Clin. Pathol., 49:347-357.
  12. McNeal, J.E. (1978): Invest. Urol., 15:340-345.
  13. Pfau, A., and Caine, M. (1980): In: Male Accessory Sex Glands, edited by E. Spring-Mills, and E.S.E. Hafez, pp. 357-372. Elsevier/North-Holland Biomedical Press, Amsterdam.
  14. Schmidt, J.D. (1992): Cancer, 70 (Suppl. 1):221-224.
  15. Swerdloff, R.S., Wang, C., and Bhasin, S. (1992): Baillieres Clin. Endocrinol. Metab., 6:451-483.
  16. Zaneveld, L.J.D., and Polakoski, K.L. (1977): In: Techniques of Human Andrology, edited by E.S.E. Hafez, pp. 147-172. Elsevier/North-Holland Biomedical Press, Amsterdam.

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