Male Infertility: 155 Consecutive Cases
1990; King Faisal Specialist Hospital and Research Centre; Volume: 10; Issue: 1 Linguagem: Inglês
10.5144/0256-4947.1990.45
ISSN0975-4466
AutoresAdil Jamal, Mohammad S. Abomelha, Ketab El-Otaibi,
Tópico(s)Reproductive Health and Technologies
ResumoOriginal ArticlesMale Infertility: 155 Consecutive Cases Adil Jamal, FRCS(Glasgow) Mohammad S. Abomelha, and AF UROL Ketab El-OtaibiAF UROL Adil Jamal Address reprint requests and correspondence to Dr. Jamal: Consultant Urologist, King Khalid National Guard Hospital, P.O. Box 9515, Jeddah 21413, Saudi Arabia. From the Urology Department, Riyadh Armed Forces Hospital, Riyadh , Mohammad S. Abomelha From the Urology Department, Riyadh Armed Forces Hospital, Riyadh , and Ketab El-Otaibi From the Urology Department, Riyadh Armed Forces Hospital, Riyadh Published Online:1 Jan 1990https://doi.org/10.5144/0256-4947.1990.45SectionsPDF ToolsAdd to favoritesDownload citationTrack citations ShareShare onFacebookTwitterLinked InRedditEmail AboutAbstractThis paper reviews the first 155 cases of male infertility seen at the Riyadh Armed Forces Hospital during the three-year period, 1981 to 1983. There was a high incidence (46%) of primary testicular failure of unexplained etiology as well as idiopathic oligospermia (27%) and obstructive azoospermia (27%). Semen abnormalities were more profound than those seen in the West and a significant number of infertility cases were due to the male factor alone. The relationship between absent spermatogenesis on testicular biopsy and raised follicle stimulating hormone levels is confirmed. Scrotal varicoceles were associated with profound histologic testicular changes, and therefore varicocele surgery did not improve the chances of pregnancy, as reported in the West.IntroductionMale infertility represents a major contributor to the overall problem of infertility in Saudi Arabia.1 One hundred fifty-five male patients between the ages of 18 and 50 years were seen between 1981 and 1983 at our urology clinic. Most of the patients were young, healthy males presenting with infertility only. We will discuss the incidence and pattern of the problem and compare our findings with those from other centers. The various findings from semen analysis, hormonal status, and testicular biopsy are presented, and their value in the management or prognosis of such cases is summarized. The management of azoospermia and the problems of oligospermia are also discussed, especially in relation to hormonal analysis and the histologic picture found on testicular biopsy. The role and results of surgical intervention in the treatment of varicocele associated with subfertil-ity are also discussed.PATIENTS AND METHODSThe records of the first 155 consecutive patients with male infertility seen between 1981 and 1983 at the Riyadh Armed Forces Hospital were retrospectively reviewed. All investigations were carried out at the hospital.Various known contributory causes to infertility were sought, i.e., childhood cryptoorchidism or orchidopexy, or cases with a history of mumps orchitis, diabetes, testicular torsion, viral illnesses, or sexually transmitted diseases. Cases were also screened for history of exposure to occupational chemicals,2 drugs, and any hormonal treatment. The spouse's health was also assessed, and a full gynecology report requested if a female factor of subfertility was suspected.Investigations included the mean findings from two of three semen analysis samples and hormonal profile (serum follicle-stimulating hormone [FSH], luteinizing hormone [LH], prolactin, and testosterone). Testicular biopsy with hematoxylin-eosin staining was performed. Scrotal exploration with vasography was performed when indicated.RESULTSOf the 155 patients, 141 (90.9%) were Saudis and 14 (9%) were non-Saudis. Two hundred twenty-nine patients (83%) had primary infertility and 26 (17%) had secondary infertility. Our method of semen analysis (i.e., the mean of two of three analyses) follows that of MacLeod:3 the ejaculate volume should be 1.5 to 5.0 ml; sperm density, greater than 20 million per milliliter; motility, greater than 60%; and morphology, greater than 60% normal. There should also be no significant pyospermia or any hyperviscosity. Comparison of semen abnormalities in our patient group with those seen at the University of Pennsylvania study2 between 1974 and 1976 (Table 1) reveals that azoospermia and oligospermia are the most common disorders, indicating a high incidence of testicular dysfunction and disease. Sperm motility was the most common disturbance seen in an American study, and this could be related to the high incidence of varicoceles observed. Therefore, more profound semen abnormalities are seen in our patient population.Table 1. Distribution of semen abnormalities.Table 1. Distribution of semen abnormalities.Histopathologic examination of testicular tissue included assessment of all components, including seminiferous tubules and intertubular tissues. Testicular changes were reported as: normal histology, hypospermatogenesis, maturation arrest, Sertoli-cell-only syndrome, or fibrosis and atrophy.Seventy-one biopsies (41%) showed primary testicular failure and were associated with the diseases listed in Table 2. The morphologic pattern compared with that reported from Mount Sinai Hospital, Canada,4 is presented in Table 3. In our Saudi population, the majority showed testicular atrophy and Sertoli-cell-only syndrome, while the Canadian population showed hypospermatogenesis of posttesticular obstruction and a minority (12%) showed Sertoli-cell-only syndrome.Table 2. Primary testicular failure and associated diseases in 71 patients.Table 2. Primary testicular failure and associated diseases in 71 patients.Table 3. Comparative testicular biopsy results.Table 3. Comparative testicular biopsy results.The correlation between testicular histology and gonadotropin levels in our 71 patients was as follows: hypospermatogenesis, normal levels; maturation arrest, normal or elevated levels; Sertoli-cell-only syndrome, elevated FSH levels; and fibrosis and atrophy, elevated FSH and LH levels. Patients with Sertoli-cell-only syndrome and atrophy showed marked elevation of FSH, in keeping with failure of spermatogenesis. This is a well-recognized finding and is supported by findings from a recent study by Perry5 from Dammam as well as by two comprehensive studies conducted in British6 and American7 patients. LH and testosterone levels, when found in normally androgenized males, were of little help in determining treatment or prognosis, as corroborated by the British study.6With regard to semen analysis, hormonal assays, and testicular histology, our 155 patients fell into three groups: 71 patients (46%) had primary testicular failure, 42 patients (27%) had obstructive azoospermia, and 42 patients (27%) had idiopathic oligospermia. No pregnancy was achieved by the 71 patients with primary testicular failure.The 42 patients with obstructive azoospermia, who showed no sperm in two or more ejaculates, had normal gonadotropin hormone levels and showed satisfactory spermatogenesis on testicular biopsy. Associated diseases in these patients are shown in Table 4 and the most common infertility problems in our patient population are compared with the findings in a study from Texas7 in Table 5.Table 4. Associated diseases in 42 azoospermic patients.Table 4. Associated diseases in 42 azoospermic patients.Table 5. Comparison of common infertility conditions.Table 5. Comparison of common infertility conditions.Obstruction of the ejaculatory ducts and seminal vesicle dysfunction were ruled out by the presence of fructose in the semen. Clinically diagnosed abnormalities of the epididymis and vas deferens were confirmed at transscrotal exploration and vasography. Complete vas deferens block was found in five patients (12%) and congenital absence of the vas deferens, congenital atresia of the vas deferens, and partial aplasia of the vas deferens in 1 patient each (2%).Vasoepididymostomy was performed in 34 patients (bilateral in 23 and unilateral in 11) using the procedure of Turner.8 Our postoperative results, as compared to those in Cleveland, Ohio,9 and Hamburg, Germany,10 are shown in Table 6. Five patients manifested semen improvement; two showed the appearance of sperm at three months, and this occurred at four months, six months, and 18 months after surgery in the remaining three. In one report,9 sperm appeared as early as one month and as late as two years after operation. We considered vasoepididymostomy a failure in our patients if azoospermia persisted two years after surgery.Table 6. Comparison of vasoepididymostomy results.Table 6. Comparison of vasoepididymostomy results.We regarded as idiopathic oligospermics those patients who had a sperm count below 20 million per milliliter on two or more occasions and had a normal testicular biopsy, and whose wives had no female component of infertility. The 42 patients with idiopathic oligospermia had the coexisting diseases shown in Table 7.Table 7. Idiopathic oligospermia and coexisting diseases in 42 patients.Table 7. Idiopathic oligospermia and coexisting diseases in 42 patients.Recognizing the physiologic relationship of the hypothalamopituitary system to testicular function, we have used mesterolone, human chorionic gonadotropins, clomiphene citrate, and bromocriptine in an attempt to improve semen quality and production. Comparison of our results with other centers is shown in Table 8.11Table 8. Reported experience of treatment of idiopathic infertility.Table 8. Reported experience of treatment of idiopathic infertility.Mesterolone (a derivative of dihydrotestos-terone that is less likely to cause testicular atrophy) was given to 15 patients until azoospermia was achieved. The drug was then stopped with the hope that spermatogenesis would start anew, with a rebound to a higher level than existed prior to treatment. Four patients showed improvement in semen quality 6 to 18 months later, but no pregnancy was achieved. This testosterone rebound phenomenon was first described by Rowley and Heller,12 who reported a 41% pregnancy rate in 157 patients. This figure has not been equaled in other series. Therefore we are guarded in our opinion of testosterone rebound therapy, since the mechanism is only speculative. A few such patients have remained azoospermic for three years following treatment13 and a few have achieved pregnancy but without improvement in semen.Human chorionic gonadotropin hormone, which increases Leydig cell activity with consequential improvement in spermatogenesis and/or motility, has been used in four of our patients (1,500 IU twice per week for 12 months). Two achieved successful pregnancies. One successful pregnancy occurred after the wife was treated for pulmonary tuberculosis. Szollosi et al14 reviewed the cases of 160 men who all followed a similar regimen; they noted semen improvement in 34% and a 16% pregnancy rate in the wives of both hypogonadotropic and normal gonadotropic men. Thus our findings and those of others show that human chorionic gonadotropin therapy leads to improvement in the sperm count in some groups, but there is no evidence of an increased fertility rate.Clomiphene citrate is a nonsteroidal estrogen with minimal effect that has been shown to increase pituitary gonadotropin levels, and occasionally improves semen production. It is more beneficial when given to men with low to normal FSH and LH levels in the presence of oligospermia below 20 million per milliliter.15The patients in our study were given 50 mg of clomiphene once daily for three months, and this was repeated for up to nine months in 19 Oligospermic men. None achieved pregnancy. Five of the patients who had normal hormone levels, satisfactory testicular biopsy, and oligospermia below 15 million per milliliter responded to the therapy in that their semen production and quality increased; in two, sperm count increased to 25 million and 41 million per milliliter. The remaining 14 patients who had normal hormone levels and hypospermatogenesis showed reduced semen quality after clomiphene treatment. Schill16 reported a pregnancy rate of 20.7% in 367 patients treated with clomiphene. We found no evidence that clomiphene will improve the pregnancy rate though our number of patients was small and some positive responses were seen. Four of our patients had hyperprolactinemia and were given bromocriptine for three months (2.5 mg once daily). Two achieved successful pregnancies. The first patient had prolactin levels of 311 and 373 mIU/L (normal range, 70-290 mIU/L) and partial atrophy shown by testicular biopsy. After treatment, his prolactin level became normal and his wife got pregnant while he was still Oligospermic with a 4.0 million per milliliter sperm count. The second patient had a prolactin level of 359 mIU/L which became normal after treatment. His semen count increased from 20 million to 111 million per milliliter. The two patients who showed no improvement remained severely Oligospermic despite normal prolactin levels after treatment.Scrotal varicocele with its well-recognized decrease in testicular function has been mentioned as the major cause of male infertility. Greenberg and Lipshultz17 cited a rate of 30 to 50% in their study from the U.S. and Hendry et al18 quoted a rate of 21% in their study from England. It was only 8% in our study (one of 12 patients).In our small series of 12 patients with varicoceles, eight (66%) were oligospermics and four (33%) were azoospermics. In contrast, MacLeod19 reported a 65% oligospermia rate and no azoospermia or testicular atrophy. However, in our varicocele study, 42% of our patients showed testicular atrophy. It is unlikely that varicocele alone is the cause of atrophy or azoospermia; more likely the varicocele coexisted with a primary testicular disease. Because of this high rate of testicular atrophy and azoospermia, we have seen poor improvement in semen quality and the pregnancy rate after varicocelectomy compared with the rates given in other studies (Table 9).Table 9. Changes in semen quality and pregnancy rate after varicocelectomy.Table 9. Changes in semen quality and pregnancy rate after varicocelectomy.In all our patients with varicocele, both sperm counts and stress cytology have shown some improvement. Only one patient (8%) produced a successful pregnancy, and two patients (16%) showed good improvement in semen quality, which allowed the respective wives to undergo artificial insemination.DISCUSSIONWe found that infertility in a significant number of Saudis is due to the male factor alone. The more profound semen abnormalities in our patients and a high incidence (46%) of testicular atrophy and Sertoli-cell-only syndrome of unknown etiology explain our poor results from treatment.The report from the King Faisal Specialist Hospital20 about the deposition of IgG in the basement membrane of 13 of 30 Saudi patients, causing an antibody directed against specific antigens in the basement membrane of seminiferous tubules, in part explains the testicular damage seen in Saudi patients.A high FSH level in our study indicates total germinal cell failure which corroborates similar findings in Britain,6 the U.S.,7 and Dammam.5 Therefore testing of the FSH level has replaced testicular biopsy as a diagnostic aid for male infertility, especially in cost-conscious centers. We limit use of testicular biopsy to azoospermic patients with normal sized testes and normal hormone levels to distinguish between primary testicular failure and obstructive azoospermia. The use of testicular biopsy in cases of oligospermia is controversial, and some practitioners have found results noncontributory. We have found it useful in predicting prognosis in patients brought to us for second opinion consultation. Successful counseling of oligospermics can be given only if its etiology is better understood, including the associated phenomena of sperm autoantibodies, female cervical mucous hostility, and sperm chromosomal abnormalities, for it is well known that oligospermics have fathered children successfully.21 The wives of our patients whose semen count increased to 4 million per milliliter motile spermatozoa were referred for artificial insemination.The lack of good results from vasoepididymostomy (6% pregnancy rate despite positive sperm presence in epididymal smears) could be due to scar tissue formation, sperm granuloma, vas ileus, agglutinating sperm antibodies found in 60% of obstructive azoospermics,7 and most notably poor microsurgical technique.The incidence of varicocele in this study was small and the results suggest that varicocele is a coincidental finding rather than the cause of testicular atrophy or azoospermia. After high-ligation varicocelectomy, semen quality and production improved in 16% of patients, resulting in 8% pregnancy.ARTICLE REFERENCES:1. Kubb A, Lautsch EV, Perry W. "Male subfertility in Saudi Arabia" . Proceedings of the 6th Saudi Medical Conference, Jeddah, Saudi Arabia, 1981. Google Scholar2. Lipshultz LI. "Evaluation of the subfertile male" . Presented at the 77th Annual Meeting of the American Urological Association, Kansas City, Missouri, 1982;23–41. Google Scholar3. MacLeod J. "The male factor in fertility and infertility" . J Urol. 1951; 66: 436. Google Scholar4. Gottesman IS, Bain J. "Subfertility and infertility in the male: a persistent dilemma" . Clin Androl. 1980; 4: 79–92. Google Scholar5. Perry W. "Endocrine assessment of the subfertile male in Saudi Arabia" . Proceedings of the 7th Saudi Medical Conference, Dammam, Saudi Arabia, 1982. Google Scholar6. Wu FCW, Edmond P, Raab G, Hunter WM. "Endocrine assessment of the subfertile male" . Clin Endocrinol. 1981; 14: 493. Google Scholar7. Lipshultz LI. "The varicocele in infertility" . Presented at the 77th Annual Meeting of the American Urological Association, Kansas City, Missouri, 1982;35–52. Google Scholar8. Turner TT. "On the epididymis and its function" . Invest Urol. 1979; 16: 311–21. Google Scholar9. Thomas AJ. "The medical and surgical management of male infertility" . Presented at the 77th Annual Meeting of the American Urological Association, Kansas City, Missouri, 1982;71–89. Google Scholar10. Wagenknecht LV. Obstruction in the male reproductive tract. In: Bain J, Schill WB, Swhwarzstein L, eds. Treatment of male infertility, ed 1. New York: Springer Verlag; 1982;221–32. Google Scholar11. Sherins RJ, Howard SS. Male infertility. In: Harrison JH, Gittes RF, Perlmutter AD, et al., eds. Campbell's Urology, ed 4. Philadelphia: Saunders, 1978;715–76. Google Scholar12. Rowley MJ, Heller CG. "The testosterone rebound phenomenon in the treatment of male infertility" . Fertil Steril. 1972; 23: 498–504. Google Scholar13. Lamensdorf H, Compere H, Begley G. "Testosterone rebound therapy in treatment of male infertility" . Fertil Steril. 1975; 1-26, 469–72. Google Scholar14. Szollosi J, Apro G, Falkay G, Sas M. "Choriogonin treatment of patients with pathospermia" . Int Urol Nephrol. 1978; 10: 65. Google Scholar15. Paulson DF. "Clomiphene citrate in the management of hypofertility: predictors for treatment selection" . Fertil Steril. 1977; 28: 1226. Google Scholar16. Schill WB. "Recent progress in pharmacological therapy for male subfertility" . Rev Androl. 1979; 11: 77. Google Scholar17. Greenberg SH, Lipshultz LI. Varicocele and male sub-fertility. In: Sciarra JJ, ed. Gynaecology and Obstetrics, ed 5. Hagerstown: Harper and Row, 1977;53–61. Google Scholar18. Hendry WF, Sommerville IF, Hall RR, Pugh RCB. "Investigation and treatment of the subfertile male" . Br J Urol. 1973; 45: 684–92. Google Scholar19. MacLeod J. "Further observations on the role of varicocele in human male infertility" . Fertil Steril. 1969; 20: 545–63. Google Scholar20. Woodhouse NJY, Akhtar M, Fredrickson M, Bissada NK. "Testicular immunoglobulin deposition as a possible cause of male infertility" . King Faisal Specialist Hosp J. 1983; 3: 25–9. Google Scholar21. Barker GH. Male infertility. In: New infertility. Adam-son Books Ltd. London, 1986;44–69. Google Scholar Previous article Next article FiguresReferencesRelatedDetailsCited byHaddad F (2019) Male Infertility, Annals of Saudi Medicine , 11:4, (478-479), Online publication date: 1-Jul-1991. Volume 10, Issue 1January 1990 Metrics History Accepted27 June 1989Published online1 January 1990 InformationCopyright © 1990, Annals of Saudi MedicinePDF download
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