Dr Eric Daiter has served Monmouth and Middlesex Counties of New Jersey as an infertility expert for the past 20 years. Dr. Daiter is happy to offer second opinions (at the office or over the telephone) or new patient appointments. It is easy, just call us at 908 226 0250 to set up an appointment (leave a message with your name and number if we are unable to get to the phone and someone will call you back).
Availability
"I always try to be available for my patients since I do understand the pain and frustration associated with fertility problems or endometriosis."
Cost
"I understand that the economy is very tough and insurance companies do not cover a lot of the services that might help you. I always try to minimize your out of pocket cost while encouraging the most successful and effective treatments available."
Azoospermia (detailed)
Azoospermia is the complete absence of sperm in the seminal ejaculate.
Azoospermia is uncommon but not rare, occurring in about 2% of
men in the general population and 10-20% of men receiving care
in infertility centers. Aspermia is an absence of ejaculate (semen).
The finding of azoospermia often comes as a surprise for a couple
since there often are no symptoms (there frequently is an ejaculate
and a normal ejaculation process). The approach to this difficult
situation looks at categories of causes for azoospermia (such
as pre testicular, testicular and post testicular), with the goal
being to identify the treatable causes. In general, the pre and
post testicular causes are more readily treatable than the testicular
causes.
(1) Pre testicular azoospermia includes
* ejaculatory dysfunctions, which may be due to such
diverse issues as psychosexual dysfunction, prior urologic surgery,
medications, and neurologic disease. Some of these are treatable.
* hormonal abnormalities such as hypogonadotropic hypogonadism
(pituitary FSH and LH deficiency). This is often treatable. If
a structural lesion or elevated prolactin concentration is discovered
then these are treated. If there is destruction of the pituitary
gland or a CNS-hypothalamic cause, then treatment with menotropins
is often useful.
* anabolic steroid hormone abuse (such as for muscle
building), which is associated with marked impairment of spermatogenesis
that may recover once the drugs are stopped.
* hemochromatosis, which is a rare condition involved
in azoospermia by means of iron overload of the pituitary gland
occasionally causing isolated gonadotropin deficiency and possibly
testicular atrophy.
(2) Testicular azoospermia includes
* cryptorchidism (undescended testes), which is the
most common congenital abnormality associated with azoospermia.
The testes normally descend in the 8th month of gestation, with
3-4% of term male infants having cryptorchid testes at birth that
will descend within the first year of life. The prevalence in
adults is less than 1% in the general population but up to 6%
in the infertile population. If the failure of descent is due
to an obstruction then the prognosis in terms of fertility is
much higher than if no obstruction is present. The degree of spermatogenic
dysfunction is proportional to the duration of time the testes
are outside the scrotum so most pediatric urologists suggest repair
by the end of the second year of life. Cryptorchid testes have
a greater chance of malignancy (cancer) and require appropriate
followup with a urologist.
* androgen resistance syndromes due to the inability
of cells to adequately respond to circulating androgens, either
due to an androgen receptor deficiency or an androgen receptor
dysfunction. This syndrome has a wide range in degrees of severity,
with more severe forms resulting in azoospermia and less severe
forms resulting in oligospermia. The most severe of these syndromes
has been referred to as "testicular feminization" where
the external genitalia are female.
* 5 alpha reductase deficiency, which is the enzyme
that converts testosterone to dihydrotestosterone (its more active
form for many cells in the body). A deficiency can result in azoospermia
and is usually associated with multiple major congenital abnormalities
of the reproductive tract.
* congenital anorchia (lack of testes) is a rare condition
in which the testes are present and functioning at 8-14 weeks
gestation (since the external and internal genitalia are male)
and for some unknown reason are lost after this point in development.
* infection involving the testes (orchitis), including
mumps (associated with a thickening and nodularity of the epididymis)
and bacterial infections, which can result in azoospermia
* Sertoli only syndrome, which is associated with relatively
normal appearing seminiferous tubules except for an absence of
germ cells from which spermatozoa are developed. It is postulated
that this is due to abnormal migration of the germ cells in early
embryonic life. This is associated with an increased FSH concentration,
slightly decreased size of the testes, and a normal (or mildly
suppressed) testosterone.
* vascular insult with resulting spermatogenic arrest
possibly due to trauma, torsion (twisting) or varicocele (uncommon
cause of azoospermia). Occasionally, repair surgically can improve
spermatogenesis.
* gonadotoxins including radiation, chemotherapy, excessive
heat, and some medications
(3) Post testicular cause of azoospermia include
* obstructive lesions of the epididymis, vas deferens
or ejaculatory ducts. These may be associated with medical conditions
such as cystic fibrosis.
* vasectomy with or without attempted reversal
* retrograde ejaculation with the seminal fluid traveling
the path of least resistance, which is back into the bladder in
certain postoperative conditions or with impaired nerve function.
