Complex Infertile Cases approach and management

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Complex Infertile Cases approach and management

• Dr. Anmar Nassir, FRCS(C)
• Canadian board in General Urology
• Fellowship in Andrology (U of Ottawa)
• Fellowship in EndoUrology and Laparoscopy
  (McMaster Univ)
• Assisstent Prof Umm Al-Qura
• Consultant Urology King Khalid National Guard
  Hospital

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• The hypothalamo-pituitary-gonadal axis provides
  pulsatile secretion of GnRH
• GnRH pulses are released every 90 to 120 minutes
• LH and FSH release from the pituitary to
  stimulate spermatogenesis and testosterone
  production.
• Diurnal variation of testosterone results in
  higher morning levels of testosterone

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Pituitary-Gonadal Axis

• LH
• Activate testicular T production from Leydig
  cells
• Feed back inhibition by testosterone
• FSH
• Stimulate Sertoli cells spermatogonial
  membranes
• The major stimulator of seminiferous tubule
  growth during development
• Feed back inhibition by inhibin from Sertoli cells

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• The seminiferous tubules have a combined length
  of approximately 250 meters.
• The rete testis coalesces to form the 6 to 12
  ductuli efferentes,
• They carry testicular fluid and spermatozoa into
  the caput epididymis.

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• The scrotal temperature is is 2C to 4C below
  rectal temperature due to counter-current
  mechanism
• Testosterone will initiate and maintain
  spermatogenesis
• Sperm fertility maturation, achieved at the level
  of the distal corpus or proximal cauda
  epididymis.

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• Patterns of tail movement in human epididymal
  spermatozoa.
• A, The pattern shown by spermatozoa taken from
  proximal regions of the epididymis is
  characterized by a high-amplitude, low-frequency
  beat producing little forward movement.
• B, In contrast, tail movement in a large
  proportion of spermatozoa from the cauda
  epididymis is characterized by low-amplitude,
  rapid beats that result in forward progression.

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• The oval sperm head consists principally of
• a nucleus that contains highly compacted
  chromatin material
• an acrosome that contains the enzymes required
  for penetration of the outer vestments of the egg.

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• ? The middle piece of the spermatozoon consists
  of
• helically arranged mitochondria surrounding
• outer dense fibers
• 9 2 microtubular structure of the sperm
  axoneme.
• ? The sperm tail has outer dense fibers, rich in
  disulfide bonds,
• provide the rigidity necessary for progressive
  motility.

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• Sperm fertility maturation in the human
  epididymis.
• Sperm fertilizing ability was assessed using zona
  pellucida-free hamster eggs and by changes in
  motility, which increases in the distal regions
  of the human epididymis.

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• The process of spermatogenesis and spermiogenesis
  takes approximately 64 days in humans and results
  in a haploid germ cell that acquires natural
  ability to fertilize oocytes during epididymal
  transport.
• Spermatogenesis is an androgen-dependent process
  that optimally occurs with very high
  intratesticular levels of testosterone .
• Spermatozoa exiting the testis are immotile and
  have limited capacity to fertilize an oocyte
  unless assisted reproductive techniques are
  applied.
• After epididymal transit (that takes 2 to 11
  days), sperm are typically motile and capable of
  fertilization without assistance.
• Immediately before emission, spermatozoa are
  rapidly and efficiently transported to the
  ejaculatory ducts from the distal epididymis.
• Spermatozoal function does not stop at the time
  of fertilization
• sperm-derived spindles even drive embryo
  development.

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Physiology

• Epididymis
• Maturation
• Transport
• Storage
• Vas
• Transfer of sperm
• Seminal vesicles
• (The main bulk of the ejaculate)
• Secretory products e.g.
• fructose, prostaglandin, clotting factors
• Ejaculation
• Coagulation of semen
• Prostate
• Liquifaction
• Zn antibacterial sperm stabilization

Seminal vesicles ? 1.5 to 2.0 mL. Prostate ? 0.5
mL, Cowper's glands ? 0.1 to 0.2 mL,
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• Before the ejaculation of the major portion of
  the ejaculate, a small amount of fluid from the
  glands of Littre and the bulbourethral glands is
  secreted.
• This is followed by a low viscosity opalescent
  fluid from the prostate containing a few sperm.
• The principal portion of the ejaculate contains
  the highest concentration of sperm, along with
  secretions from the testis, epididymis, and vas
  deferens, as well as some prostatic and seminal
  vesicle fluids.
• The last fraction of the ejaculate consists of
  seminal vesicle secretions.
• The majority of ejaculated sperm come from the
  distal epididymis, with a small contribution from
  the ampulla of the vas.

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• The chance of a normal couple conceiving is
  estimated to be
• 20 to 25 per month,
• 75 by 6 months
• 90 by 1 year.
• Fertility rates are at their peak in men and
  women at age 24.
• Studies of couples of unknown fertility status
  that are attempting to conceive within 1 year,
• 15 of couples are unable to do so.
• 20 of cases of infertility are due entirely to a
  male factor,
• 30 to 40 of cases involving both male and
  female factors.
• male factor is present in one half of infertile
  couples.

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• Of infertile couples without treatment,
• 25 to 35 will conceive at some time by
  intercourse alone
• 23 will conceive within the first 2 years,
• 10 will do so within 2 more years.
• (pregnancy rate of 1 to 3 per month )
• Infertility is often not considered to exist
  until after 12 months of attempted conception,
• With the advancing age of infertile couples, it
  is not recommend deferring an initial evaluation.
  
• A basic, simple, cost-effective evaluation of
  both the male and female partners should be
  initiated at the time of presentation.

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Evaluation ofInfertile patient
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Impairing Spermatogenesis

• Medications
• nitrofurantoin ,
• cimetidine ,
• sulfasalazine ,
• Anabolic steroid
• Substances
• cocaine
• marijuana
• Nicotine
• pesticides

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• Many of the genes that affect male reproduction,
  including the androgen receptor gene, are located
  on the X chromosome.
• Therefore, family history should focus on the
  phenotype of the maternal uncles

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• Pregnancy rates in normal fertile couples are 20
  to 25 per cycle compared with 1 to 3 in
  infertile couples.
• A thorough medical and reproductive history
  should be obtained on all men presenting with
  infertility.
• The female partner should be questioned about key
  aspects of her fertility evaluation.

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• Abnormalities in the woman are involved in
  approximately 75 of infertile couples.
• 30 Ovulatory disorders
• 25 fallopian tube abnormalities
• 4 endometriosis
• 4 cervical mucus abnormalities
• 4 hyperprolactinemia
• Conception rates drop more rapidly in the 35- to
  39-year-old age group.

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Physical Exam
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• This may be performed using calipers, an
  orchidometer, or sonography.
• The normal adult testis is
• greater than 4 3 cm in its greatest dimensions
  or
• greater than 20 mL in volume for whites and
  African Americans.
• Asian men normally have smaller testes.

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Laboratory Assessment

• Semen analysis X2
• Quantitation of leukocytes in semen
• Lab Baseline, gluc. , U/A
• Hormonal assay FSH, LH, Prol, TSH,
• Other tests
• Antisperm antibodies semen or blood
• Advanced sperm fertility tests

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Semen

• The WHO (1999) defines the following reference
  values

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rigid criteria
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• Small volume ejaculates may be produced in
  patients with
• obstruction of the ejaculatory ducts,
• retrograde ejaculation,
• sympathetic denervation,
• androgen deficiency
• drug therapy,
• absence of the vas deferens
• absence of seminal vesicles,
• bladder neck surgery.

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Hormonal Evaluation

• Although male reproductive function is critically
  dependent on endocrinologic control, less than 3
  of infertile men have a primary hormonal etiology
  
• endocrine abnormalities are rarely present when
  the sperm concentration is greater than 10
  million/mL

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Hormonal Evaluation
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• Most prolactin-secreting tumors in men are
  macroadenomas (tumors greater than 1 cm)
• Prolactin levels in these patients are typically
  higher than 50 ng/mL, and both gonadotropin and
  serum testosterone levels are depressed.
• In infertile patients
• Mild elevations of prolactin (lt50 ng/mL) are more
  frequently discovered,
• Their clinical significance is questionable.
• Imaging often fails to identify a tumor in these
  patients,
• They often have normal gonadotropin and
  testosterone levels.

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• Potential causes for mild prolactin elevation
  include
• stress,
• renal failure,
• medications,
• chest wall irritation,
• thyroid dysfunction.
• Treatment of isolated mild hyperprolactinemia
  doesnt improve spermatogenesis.
• pituitary tumor should be ruled out.

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DIAGNOSTIC ALGORITHMS BASED ON THE INITIAL
EVALUATION
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Azo
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• Patients with small (atrophic) testes have either
  primary or secondary testicular failure. Serum
  hormone testing including testosterone , LH,
  FSH, and prolactin is done to differentiate
  between the two as well as to identify both
  functioning and nonfunctioning pituitary tumors.
  Patients with small testes and FSH concentrations
  greater than two to three times normal have
  severe germ cell failure, and the prognosis for
  natural conception is poor. A testicular biopsy
  should only be performed in these patients if
  testicular sperm retrieval combined with IVF is
  being considered, and this is often performed in
  conjunction with egg retrieval in the spouse.

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• Patients with azoospermia due to testicular
  failure should be offered genetic testing to rule
  out chromosomal abnormalities such as
  Klinefelter's syndrome and microdeletions of the
  Y chromosome. Patients with secondary testicular
  failure may be treated with hormone therapy,
  whereas primary testicular failure is almost
  always irreversible.

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Oligo

• Oligospermia refers to sperm densities of less
  than 20 million sperm/mL. Isolated oligospermia
  with normal motility and morphology parameters is
  uncommon.
• In cases with less than 10 million sperm/mL,
  testosterone and FSH levels should be
  determined.

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Asthenospermia

• Defects in sperm movement (asthenospermia) refer
  to low levels of motility or forward progression,
  or both. Spermatozoal structural defects,
  prolonged abstinence periods, genital tract
  infection, antisperm antibodies, partial ductal
  obstruction, varicoceles, and idiopathic causes
  may be responsible for these cases

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• Complete absence of sperm motility or cases with
  motilities less than 5 to 10 should be
  evaluated by a sperm viability assay.
  Necrospermia exists when the nonmotile sperm are
  not viable. The finding of a high fraction of
  viable sperm in the presence of low or absent
  sperm motility suggests an ultrastructural
  abnormality, such as that found in primary
  ciliary dyskinesia (PCD, formerly called immotile
  cilia syndrome) and Kartagener's syndrome (PCD
  associated with situs inversus).

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vasography and seminal vesiculography

• .A, Normal vasogram note contrast agent in
  bladder.
• B, Vasogram depicting left ejaculatory duct
  obstruction.
• C, Normal seminal vesiculogram, again note
  contrast agent in bladder.
• D, Seminal vesiculogram demonstrates complete
  left ejaculatory duct obstruction.

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Multiple Defects in Seminal Parameters

• oligoasthenoteratospermia (OAT)
• varicocele
• cryptorchidism,
• heat,
• drugs, or
• environmental toxins, or
• idiopathic causes.

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Normal Semen Parameters

• antisperm antibodies.
• direct assay
• indirect in the female
• sperm penetration assay or
• acrosome reaction

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TREATMENT OVERVIEW
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Endocrine Causes

• Endocrine causes of male infertility are often
  referred to as pretesticular causes.
• Impairment of fertility in these cases is
  secondary to either hormone deficiency, hormone
  excess, or receptor abnormality.
• Pituitary Disease
• Isolated Hypogonadotropic Hypogonadism
• Fertile Eunuch Syndrome
• Isolated FSH Deficiency
• Other Congenital Syndromes
• The Prader-Willi syndrome.
• Androgen Excess
• Congenital adrenal hyperplasia is the most common
  cause of endogenous androgen excess.
• Estrogen Excess
• Prolactin Excess
• Thyroid Abnormalities
• Glucocorticoid Excess
• Abnormalities of Androgen Action
• Androgen abnormalities may involve a deficiency
  in androgen synthesis, a deficiency in conversion
  of testosterone to dihydrotestosterone
  (5a-reductase deficiency) or androgen receptor
  abnormalities.

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Kallmanns syndrome

• 1- 10,000 to 60,000
• x-linked ,no (GnRH)
• C/P
• delayed puberty
• cryptorichedism
• micropenice
• congenital defense
• anosmia
• color blind
• FSH ,LH,Testosterone all are low.
• Hypogonadotrophic hypogonadism
• Rx LH and FSH analogue

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Prader willi syndrome

• Abnormal chromosome 15q11-q13
• lack of GnRH secretion
• C/F
• Obesity
• infantile hypotonia
• mental retardation
• cryptorichdism
• hypogonadism hypogonadotrphic
• Rx Kallmann

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Androgen Excess

• Anabolic
• Testicular tumor
• CAH

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Estrogen Excess

• Testicular Sertoli cell tumors or interstitial
  cell (Leydig cell) tumors may produce estrogen.
  Excess peripheral estrogens may also result from
  hepatic dysfunction or obesity.

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Prolactin Excess

• Caused by
• pituitary tumor,
• stress,
• medications,
• medical illness,
• idiopathic causes
• S/S ED, infertility
• Ix Hormonal, MRI
• Rx bromocriptine and cabergoline

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Abnormalities of Androgen Action

• Androgen abnormalities may involve
• a deficiency in androgen synthesis,
• a deficiency in conversion of testosterone to
  dihydrotestosterone
• 5a-reductase deficiency
• androgen receptor abnormalities.

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Disorders of Spermatogenesis

• Genetic Disorders
• Cryptorchidism
• Testicular Torsion
• Orchitis
• Varicocele
• Sertoli Cell-Only Syndrome
• Chemotherapy
• Radiation Exposure
• Heat
• Environmental Toxins and Occupational Exposures
• Drugs, Medications, and Other Gonadotoxins
• Idiopathic Infertility

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Genetic causes of infertility

• 1- Structural chromosomal disorder
• 2-Syndromes affecting the HPGAxis.
• 3- Syndromes affecting the androgen biosynthesis
  and /or action.
• 4-Syndromes affecting function of the ductal
  system
• 5- Syndromes affecting sperm transportation.
• 6- Syndromes with variable RSAxis effects.

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Klinefelters syndrome

• 14 of azoospermia.
• 90 XXY
• 1-600 live male birth.
• Clinical presentation
• increase height,Dec intelligence
• azoospermia,gynacomastia, small firm testis
• ? Cancers breast or nonseminoma extragonadal.
• DM, CVD
• Hormones
• FSH markedly elevated
• LH elevated or normal.
• Testosterone decreased in 50 of pts

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Klinefelters syndrome

• Pathology
• tubular hyalinization.
• leyding cell hyperplasia.
• azoospermia.
• Rx
• No therapy to improve spermatogenesis
• Paternity has been documented
• IVF, ICSI

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XX male

• 1-20000 live birth
• C/F
• phenotype normal
• azospermia
• sporadic ?AR.
• Ambiguous genitalia
• hypospadies
• FSH (high)
• No sperm on TESA

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XYY male

• 1 - 4 / 1000 live birth
• C/F
• Dec intelligence
• phenotype normal
• Inc height
• LH,Testosterone are normal
• FSH may be normal or increase
• Azo or sever oligo
• may be fertile

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XYY male

• Risks
• leukemia
• antisocial behavior
• Pathology
• germinal cell aplasia
• maturation arrest
• tubular sclerosis
• No treatment to improve spermatogenesis,
• Candidates for ART

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Noonans syndrome

• Phenotype (Turners)
• Mostly sporadic, familial transmission. ?
  chromosome 12.
• Occur both in male female.
• No obvious chromosomal anomalies yet found (XY
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• FSH (high) due to spermatogenies dysfunction
• No treatment for the fertility
• androgens may be given to complete virilization.

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The Y Chromosome

• Contain Genes for gonadal Differentiation Into a
  Testis
• Gene Required for Full Spermatogenesis

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• The majority of Y chromosome microdeletions that
  have been associated with azoospermia or severe
  oligospermia occur in one of three nonoverlapping
  regions of the long arm of the Y chromosome
  designated as AZFa (proximal), AZFb (middle), and
  AZFc (distal)
• The vast majority of these deletions occur de
  novo and are not inherited from the parents. Rare
  vertical transmission from father to son has been
  reported

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• Although most studies have examined patients with
  idiopathic azoospermia or severe oligospermia, a
  7 prevalence of Y chromosome microdeletions has
  been reported in patients with nonidiopathic
  severe male factor infertility
• Deletions in AZFc are the most frequently
  identified microdeletions in azoospermic and
  severely oligospermic men. The deletion in the
  azoospermia gene (DAZ) is thought to be
  responsible for spermatogenic defects in patients
  with deletions in this interval
• A gene called RBMY (RNA-binding motif, Y
  chromosome also called RBM for RNA-binding
  motif) is thought to be the candidate
  spermatogenic gene in the AZFb region.

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• There is currently no treatment to improve
  spermatogenesis in patients with Y chromosome
  microdeletions however, these patients are
  candidates for IVF with ICSI.
• Sperm from semen may be used in oligospermic
  patients, whereas attempts at testicular sperm
  extraction may be employed in azoospermic
  patients. It is important to realize that these
  deletions will be transmitted to male offspring
• Couples in whom the husband has Y-chromosome
  microdeletions should be offered genetic
  counseling before embarking on a course of ART

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The azoospermia factor gene

• Located on the long arm of Y chromosome.

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Varicocele

• Semen samples from infertile men with varicoceles
  have demonstrated decreased motility in 90 of
  patients and sperm concentrations less than 20
  million sperm/mL in 65 of patients.

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• Improvement in seminal parameters is demonstrated
  in approximately 70 of patients after surgical
  varicocele repair.
• Improvements in motility are most common,
  occurring in 70 of patients, with improved sperm
  densities in 51 and improved morphology in 44
  of patients.
• Conception rates have averaged 33 to 50
  compared with 16 in the control group

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Sertoli Cell-Only Syndrome
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Orchitis
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Chemotherapy

• Permanent sterility occurs in 80 to 100 of
  patients with Hodgkin's disease treated with MOPP
  and COPP regimens
• fertility rates of patients treated with
  alkylating agents were 60 lower than controls

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• During chemotherapy, most patients demonstrate
  elevations of serum FSH levels that correlate
  with the development of azoospermia. Those
  patients in whom FSH levels decline demonstrate a
  return of spermatogenesis, whereas those in whom
  FSH levels remain elevated are unlikely to
  recover

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• Preexisting spermatogenic defects in the
  contralateral testis are found in 25 of
  testicular cancer patients
• Although many patients have transient
  azoospermia, resumption of spermatogenesis occurs
  in 50 to 60 of these patients with the use of
  chemotherapeutic agents such as PVB, PVP-16, and
  POMP/ACE
• With cisplatin-based chemotherapy, most patients
  will become azoospermic however, the majority
  will recover spermatogenesis within 4 years
• There appears to be no increased risk of birth
  defects in children born to patients after
  chemotherapy
• Thus, patients should bank sperm before but not
  during chemotherapy. In addition, contraception
  should be used during and for a period of time (6
  to 24 months) after chemotherapy

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Radiation Exposure

• Because of the high rate of cell division, the
  germinal epithelium is very radiosensitive.
• Spermatids are more resistant than spermatogonia
  or spermatocytes.
• Leydig cells are reasonably radioresistant
  therefore, testosterone levels usually remain
  normal after radiation exposure.
• Serum FSH levels increase after irradiation but
  may revert to normal after a return of
  spermatogenesis.
• Azoospermia usually results from doses of over 65
  cGy.
• After dosages less than 100 cGy, recovery takes 9
  to 18 months
• with doses of 200 to 300 cGy, recovery may take
  30 months
• and at dosages of 400 to 600 cGy, more than 5
  years may be required for spermatogenesis to
  return

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• Semen quality will usually return to baseline
  within 2 years after radiation therapy for
  seminoma.
• Approximately one fourth of patients may become
  permanently infertile from such radiation
  treatment.
• After radiation therapy most patients are advised
  to avoid conception a minimum of 6 to 24 months.
• Pregnancies after treatment have revealed no
  evidence of an increase in the prevalence of
  congenital anomalies in the offspring of these
  patients

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Idiopathic Infertility

• 25 of patients exhibit abnormal semen analyses
  for which no cause can be identified
• the vast majority of these patients have
  abnormalities of all semen parameters or
  oligoasthenoteratospermia (OAT).
• In the absence of an identifiable or correctable
  etiology, patients with idiopathic male
  infertility are managed with either empirical
  medical therapy or assisted reproductive
  technology.

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• A meta-analysis of all controlled studies for
  idiopathic male infertility has failed to reveal
  significant efficacy of currently available
  treatments
• There is a significant background pregnancy rate
  (26) for untreated couples with abnormal semen
  parameters independent of treatment
• If empirical pharmacologic therapy is going to be
  used, it should be administered for a minimum of
  a 3- to 6-month period so that at least one full
  spermatogenic cycle will be incorporated.

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• Therefore, we do not recommend GnRH therapy in
  patients with idiopathic infertility owing to its
  high cost and lack of efficacy.
• The two gonadotropins FSH and LH stimulate
  spermatogenesis and steroidogenesis,
  respectively.
• As with GnRH, these treatments are expensive and
  of limited efficacy. We do not currently
  recommend these therapies in men without a
  demonstrable hormonal abnormality.
• Clomiphene Citrate and Tamoxifen
• However, the majority of investigators have found
  pregnancy rates lower than 30.
• Antiestrogens are relatively inexpensive and safe
  oral medications for the treatment for idiopathic
  male infertility, which explains their
  popularity. Because their efficacy is in doubt,
  prolonged courses of empirical therapy should not
  be used as a substitute for more effective modes
  of management.

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• Testolactone
• Testosterone rebound therapy
• There is currently no role for it, because there
  are other methods that are equally good or better
  and because some patients have persistent
  azoospermia after treatment.
• Miscellaneous Treatments
• Thyroxine, arginine, corticosteroids,
  antibiotics, zinc, methylxanthines,
  bromocriptine, and vitamins A, E, and C
• L-carnitine and L-acetyl-carnitine are now
  available as an over-the-counter nutritional
  supplement
• all of these therapies must be considered
  "empirical" and have not been shown to be
  efficacious in controlled studies

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Sperm Delivery Disorders

• Ductal Obstruction
• Ejaculatory Problems

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Ductal Obstruction

• Obstruction of the ductal system is found in 7
  to 12 of all infertile men and is much more
  common in azoospermic men
• Congenital bilateral absence of the vas deferens
  is the most common cause of obstructive
  azoospermia in patients who have not undergone
  elective sterilization
• The currently recommended management of couples
  with infertility due to CBAVD is sperm retrieval
  combined with IVF using ICSI after appropriate
  genetic testing and counseling of the couple
  regarding the risk of cystic fibrosis.

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Ejaculatory Problems

• Any process that interferes with the peristaltic
  function of the vas deferens and closure of the
  bladder neck may result in either failure of
  emission or retrograde ejaculation.
• Ejaculatory dysfunction should be suspected in
  any patient with low volume (lt1.0 mL) or absent
  ejaculate and should be distinguished from
  anorgasmia
• positive post-ejaculate urinalysis, the finding
  of greater than 10 to 15 sperm/HPF confirms the
  presence of retrograde ejaculation

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• divided into anatomic and functional
• Pharmacologic therapy for retrograde ejaculation
  is only likely to be effective in patients who do
  not have surgical changes of the bladder neck and
  for patients with failure of emission.
• Rx
• Phenylpropanolamine (75 mg bid),
• ephedrine (25 to 50 mg qid),
• pseudoephedrine (60 mg qid),
• imipramine (25 mg bid)

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• These medications are more effective if given for
  a period of at least 7 to 10 days before planned
  ejaculation,
• tolerance may develop if administered
  continuously over several cycles.
• Success is unlikely if no effect is observed
  within 2 weeks of treatment.

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Sperm Function Disorders

• Immunologic Infertility
• Ultrastructural Abnormalities of Sperm

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Immunologic Infertility

• Rx
• Corticosteroid
• intermediate-cyclic corticosteroid regimen
• Consider the success and adverse effects
• IUI
• chymotrypsin-processed sperm
• ICSI
• if their semen is of adequate quality.

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Ultrastructural Abnormalities of Sperm

• Defects in this pattern are commonly found in
  patients with immotile but viable sperm.
• The most common of these defects involves defect
  of both inner and outer dynein arms.
• commonly associated with identical defects in the
  cilia of the respiratory tract.
• This condition is known as the primary ciliary
  dyskinesia or immotile cilia syndrome

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immotile cilia syndrome

• AR
• 1/20,000
• 50 with situs inversus Kartageners
• Kartageners triad
• situs inversus, bronchiectesis, ch sinusitis
• Rx
• no cure for these ultrastructural conditions,
• the sperm may be used for IVF with ICSI.
• but genetic basis.

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