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015PG Vasectomy Reversal and Male Infertility Treatment in the ICSI Era

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015PG Vasectomy Reversal and Male Infertility Treatment in the ICSI Era 015PG Vasectomy Reversal and Male Infertility Treatment in the ICSI Era Saturday, May 16, 2015 8:30 AM – 11:30 AM Faculty Peter N. Schlegel, MD - Course Director Sheldon H.F. Marks, MD Robert D. Oates, MD Vasectomy Reversal and Male Infertility Treatment in the ICSI Era Peter N. Schlegel, MD, Course Director, Professor & C hairm an, W Urologist-in-Chief, New York-Presbyterian/Weill Cornell, N e w Y o rk , N Y Sheldon H.F. Marks, MD Director, International Center for Vasectomy Reversal, PC, Tucson, AZ Robert D. Oates, MD Professor of Urology, Vice-Chair, Department of Urology Boston University School of Medicine B o s to n , M A Disclosures: Dr. Schlegel is a medical advisory board consultant to Theralogix, Inc. Drs. Marks and Oates have no disclosures at this time (updated information available at the AUA meeting.) Schedule: 8:30-8:35 Introduction Dr. Schlegel 8:35-9:20 Evaluation of azoospermic male Dr. Oates 9:20-9:30 Questions & Answers 9:30-10:15 Vasovasostomy & Vasoepididymostomy Dr. Marks 10:15-10:30 Questions & Answers 10:30-10:45 Break 10:45-11:05 Sperm retrieval techniques Dr. Schlegel 11:05-11:15 Evolving sperm genetic evaluation Dr. Schlegel 11:15-11:30 Cases, Questions & Answers All faculty The etiology and differential diagnosis of azoospermia will be discussed, emphasizing the differentiation of obstructive from non-obstructive causes. Microsurgical methods of vasovasostomy and vasoepididymostomy will be shown, including practical tips and video presentation with expected results according to the AUA Best Practice Policy committee recommendations. Objectives: After attending this course, participants should be able to: • describe the differential diagnosis of azoospermia, and the techniques and results of various methods of sperm retrieval from azoospermic men for IVF and ICSI • understand the importance of proper genetic testing before reconstructive or sperm retrieval procedures in azoospermic men • Identify novel tests that can be used to identify male factors for couples who have failed ICSI treatment • describe the surgical approaches, as well as the preoperative and intraoperative factors, that influence the results of vasovasostomy and vasoepididymostomy • discuss the effect of genetic abnormalities on the ability to retrieve sperm from men with non- obstructive azoospermia and the transmission of genetic abnormalities to offspring produced by sperm retrieval with IVF and ICSI 1 Evaluation of the azoospermic male Robert D. Oates, M.D. Evaluation of the azoospermic male: Azoospermia is defined as the absence of sperm in the ejaculate. It is imperative to examine at least two specimens before concluding the male is azoospermic. It is not unusual to have tiny numbers of sperm seen in the pellet after centrifugation that must be a part of the semen analysis protocol for azoospermic samples. In evaluating the azoospermic male, it is helpful to look at semen volume and pH, which allows a differentiation into low volume and normal volume azoospermia. The seminal vesicles contribute approximately 70% of the fluid to the normal ejaculate, which is alkaline (pH 8.0), and contains fructose. The vasa deliver approximately 10% and the acidic (pH 6.5) prostatic fluid component the remaining 20%. The seminal vesicle and vasal fluids are delivered to the prostatic urethra via the paired ejaculatory ducts. Therefore, if the seminal volume is normal (2.0cc) and the pH is alkaline (8.0), the seminal vesicles must be present and functional and the ejaculatory ducts must be patent. There is no need for a fructose assay since the volume and pH alone indicate the presence of seminal vesicle fluid and patency of the ejaculatory ducts. In normal volume azoospermia, the differential diagnosis does not, therefore, include Bilateral Ejaculatory Duct Obstruction (EDO) or Congenital Bilateral Absence of the Vas Deferens (CBAVD; vide infra). In both EDO and CBAVD, the semen volume is low and the pH is acidic as the seminal vesicles are normal but blocked in EDO and absent or atretic in CBAVD. However, the differential does include spermatogenic compromise or an obstructive process higher up than the ejaculatory ducts (most often in the scrotum at the level of the vas (e.g. prior vasectomy) or epididymis (prior inflammation). Prior history, physical examination, and hormonal assays can typically clarify these two possibilities in normal volume azoospermia. Physical examination cannot be overemphasized. In low volume, low pH azoospermia, there is no contribution to the ejaculate from seminal vesicle fluid and only prostatic fluid is present. No fructose assay is necessary as there is no seminal vesicle fluid present and the assay will be negative. The differential includes EDO and CBAVD. Physical examination will make the diagnosis in an instant – In EDO the vasa are present, palpable, and may feel “full” secondary to more distal obstruction. The testes will be normal size and consistency. In CBAVD, the vasa will not be palpable, there will always be at least a caput epididymis present and the testes will be of normal size and consistency. Sperm aspiration is almost always successful and the sperm can be used for ICSI. A preliminary differential diagnosis can be formulated just based on knowledge of the semen volume and pH. History and physical examination then direct the work-up from that point. It is also necessary to determine whether the azoospermia is secondary to blockage of sperm produced by normal testes (obstructive azoospermia; OA) as may happen in EDO, CBAVD, a post- inflammatory epididymal blockage, etc, or whether the azoospermia is due to inadequate or absent spermatogenesis with a normal ductal system (non-obstructive azoospermia; NOA). In OA, the testes will be normal size and consistency as spermatogenesis is adequate (the bulk of the testis mass is comprised of the seminiferous tubules). No testis biopsy is necessary as the histological pattern will only confirm what is already suspected – spermatogenesis is not the problem. Conversely, in NOA, the testes are typically smaller and softer than normal as spermatogenesis is compromised and the total mass of the seminiferous tubules is reduced. The epididymis and vasa are normal to palpation. No testis biopsy is necessary as the histological pattern will only confirm what is already suspected – spermatogenesis is the problem. History may also direct one to the diagnosis: prior chemotherapy would suggest NOA, prior inguinal hernia repair might be a clue to obstruction, etc. Finally, hormonal data will be additive and, possibly, definitive if the history and physical examination are not diagnostic. Follicle stimulating hormone is released by the pituitary and is regulated by a negative feedback loop involving inhibin, the two subunits of which are secreted by Sertoli cells and germ cells. When spermatogenesis is normal, the hypothalamic-pituitary-gonadal axis works without strain and the FSH level will typically be in the lower aspects of the reported reference range. For an assay with a reference range – not to be interpreted as a “normal range” – of 2 – 20, for example, the value in a patient with normal sperm production will be roughly 2-5. When spermatogenesis is compromised, less inhibin is secreted, there is less negative feedback on the hypothalamus/pituitary and the output of FSH rises. The old adage that the FSH must be “2-3 times the upper limit of normal” to be indicative of spermatogenic failure is not true. As the FSH steadily climbs out of the lowest aspects of whatever that particular assay’s reference range, the more likely the spermatogenic process is flawed and dysfunctional. In a patient with normal volume azoospermia, slightly small and soft testes and palpably normal ductal structures, even an FSH of 7 or 8 suggests compensatory output due to spermatogenic compromise and, therefore, NOA. Finally, the question of whether an azoospermic male is taking anabolic steroids / testosterone supplementation is a critical one. Men are being prescribed testosterone (gels or injections) in increasing numbers and the body building culture is growing as well (they may be taking a variety of anabolic agents). It is necessary for testosterone to be produced within the testis, otherwise spermatogenesis will be disrupted. If testosterone (or any anabolic) is coming from an exogenous source, the pituitary does 2 not need to release LH (or FSH as well) and, as a result, the Leydig cells within the testis will not be stimulated to produce testosterone (as far as the body knows, there is plenty around) and, consequently spermatogenesis will be reduced/stopped. In an azoospermic male in whom you suspect this to be occurring (and who does not admit to taking anabolics), his testosterone values will be high while his LH and FSH will be very suppressed. The treatment is to have the patient stop the testosterone/anabolic use and let his own system restore itself which it typically will do over a week or so (the hypothalamic pituitary axis) and a few months later there will be sperm in the ejaculate (quite variable, however). Measurement of Estradiol is important in these cases as well since not all of the anabolic compounds taken are easily measured by the assays we have. In the case where a man is taking one of these preparations, his FSH and LH will be suppressed, his Testosterone will be low or not detectable but his Estradiol (arising from conversion of androgen via aromatase) will be normal or high – proof of anabolic use. Genetic testing in the azoospermic male: Genetic studies, as described below, are necessary to obtain prior to any surgical intervention in men with NOA (no definable, obvious cause such as prior chemotherapy) or CBAVD. Darwinian evolution speaks about genetic change that allows improved survival and adaptation. The many branches of the evolutionary tree are now being refined with increased genetic knowledge, a supplement to form and function which have been the determinants so far as to where a species was located on that tree.
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