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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

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complex infertile cases approach and management

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

slide2

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
pituitary gonadal axis
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
slide5

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.
slide7

The scrotal temperature is is 2°C to 4°C 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.
slide9

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.

slide10

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.
slide11

▪ 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.
slide12

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.

slide13

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.
physiology
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,

slide16

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.
slide18

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.
slide19

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.

impairing spermatogenesis
Impairing Spermatogenesis
  • Medications:
    • nitrofurantoin ,
    • cimetidine ,
    • sulfasalazine ,
    • Anabolic steroid
  • Substances:
    • cocaine
    • marijuana
    • Nicotine
    • pesticides
slide24

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
slide25

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.
slide26

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.
slide29

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.
laboratory assessment
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

semen
Semen
  • The WHO (1999) defines the following reference values:
slide36

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.
hormonal evaluation
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
slide39

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 (<50 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.
slide40

Potential causes for mild prolactin elevation include

    • stress,
    • renal failure,
    • medications,
    • chest wall irritation,
    • thyroid dysfunction.
  • Treatment of isolated mild hyperprolactinemia doesn’t improve spermatogenesis.
  • pituitary tumor should be ruled out.
slide45

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 testesand 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.

slide46

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.

oligo
Oligo
  • Oligospermiarefers 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.
asthenospermia
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 beresponsible for these cases
slide50

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).

vasography and seminal vesiculography
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.

multiple defects in seminal parameters
Multiple Defects in Seminal Parameters
  • oligoasthenoteratospermia (OAT) :
    • varicocele
    • cryptorchidism,
    • heat,
    • drugs, or
    • environmental toxins, or
    • idiopathic causes.
normal semen parameters
Normal Semen Parameters
  • antisperm antibodies.
    • direct assay
    • indirect in the female
  • sperm penetration assay or
  • acrosome reaction
endocrine causes
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 (5α-reductase deficiency) or androgen receptor abnormalities.
kallmann s syndrome
Kallmann’s 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
prader willi syndrome
Prader willi syndrome
  • Abnormal chromosome 15q11-q13
  • lack of GnRH secretion
  • C/F:
    • Obesity
    • infantile hypotonia
    • mental retardation
    • cryptorichdism
    • hypogonadism hypogonadotrphic
  • Rx = Kallmann
androgen excess
Androgen Excess
  • Anabolic
  • Testicular tumor
  • CAH
estrogen excess
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.
prolactin excess
Prolactin Excess
  • Caused by:
    • pituitary tumor,
    • stress,
    • medications,
    • medical illness,
    • idiopathic causes
  • S/S: ED, infertility
  • Ix: Hormonal, MRI
  • Rx: bromocriptine and cabergoline
abnormalities of androgen action
Abnormalities of Androgen Action
  • Androgen abnormalities may involve
    • a deficiency in androgen synthesis,
    • a deficiency in conversion of testosterone to dihydrotestosterone
      • 5α-reductase deficiency
    • androgen receptor abnormalities.
disorders of spermatogenesis
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
genetic causes of infertility
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.

klinefelter s syndrome
Klinefelter’s 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
klinefelter s syndrome69
Klinefelter’s syndrome
  • Pathology
      • tubular hyalinization.
      • leyding cell hyperplasia.
      • azoospermia.
  • Rx
    • No therapy to improve spermatogenesis
    • Paternity has been documented
      • IVF, ICSI
xx male
XX male
  • 1-20000 live birth
  • C/F
      • phenotype normal
      • azospermia
      • sporadic ?AR.
      • Ambiguous genitalia
      • hypospadies
      • FSH (high)
  • No sperm on TESA
xyy male
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
xyy male73
XYY male
  • Risks
      • leukemia
      • antisocial behavior
  • Pathology
      • germinal cell aplasia
      • maturation arrest
      • tubular sclerosis
  • No treatment to improve spermatogenesis,
    • Candidates for ART
noonan s syndrome
Noonan’s syndrome
  • Phenotype (Turner’s)
  • Mostly sporadic, familial transmission. ? chromosome 12.
  • Occur both in male & female.
  • No obvious chromosomal anomalies yet found (XY 46)
  • FSH (high) due to spermatogenies dysfunction
  • No treatment for the fertility
    • androgens may be given to complete virilization.
the y chromosome

The Y Chromosome

Contain Genes for gonadal Differentiation Into a Testis

Gene Required for Full Spermatogenesis

slide78

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
slide79

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 calledRBMY(RNA-binding motif, Y chromosome; also calledRBMfor RNA-binding motif) is thought to be the candidate spermatogenic gene in the AZFb region.
slide80

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
the azoospermia factor gene
The azoospermia factor gene
  • Located on the long arm of Y chromosome.
varicocele
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.
slide83

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
chemotherapy
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
slide87

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

slide88

Preexisting spermatogenic defects in the contralateral testis are found in 25% of testicular cancer patients

  • Although manypatients 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
radiation exposure
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
slide90

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
idiopathic infertility
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.
slide92

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.
slide93

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.
slide94

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
sperm delivery disorders
Sperm Delivery Disorders
  • Ductal Obstruction
  • Ejaculatory Problems
ductal obstruction
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.
ejaculatory problems
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 (<1.0 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
slide98

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)
slide99

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.
sperm function disorders
Sperm Function Disorders
  • Immunologic Infertility
  • Ultrastructural Abnormalities of Sperm
immunologic infertility
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.
ultrastructural abnormalities of sperm
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
immotile cilia syndrome
immotile cilia syndrome
  • AR
  • 1/20,000
  • 50% with situs inversus =Kartagener’s
  • Kartagener’s 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.