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The pituitary causes for ovulatory dysfunctions include:
* (1) hypothyroidism
The mechanism for the ovulatory dysfunction associated with hypothyroidism
has not been entirely worked out.
Hypothyroidism probably interferes with ovulation via an increase
in circulating active estrogen. Increased bioactive estrogen may
be due to decreased metabolism of estrogen in the liver (seen
with both hypothyroidism and hyperthyroidism) or due to decreased
levels of the protein that binds estrogen in the circulation.
Sex hormone binding globulin (SHBG) decreases the bioactivity
of bound hormones by reducing the "free" (bioactive)
fraction of the hormone. Persistent elevations of bioactive estrogen
can interfere with follicular growth and can disrupt the midcycle
preovulatory LH and FSH surges that are required for normal ovulation.
Hypothyroidism may also interfere with ovulation through an elevation
in TRH. With decreased circulating thyroid hormone there is enhanced
secretion of hypothalamic thyrotropin releasing hormone (TRH)
which acts on the brain's pituitary gland to release thyrotropin
or thyroid stimulating hormone (TSH). This TSH then stimulates
the synthesis and release of thyroid hormone in a normal thyroid
gland. Elevated TRH can "crosstalk" within the pituitary
gland to release other pituitary hormones such as prolactin. Elevated
prolactin levels are known to interfere with ovulation .
* (2) hyperthyroidism
The mechanism for the ovulatory dysfunction associated with hyperthyroidism
is not entirely clear.
There may be elevated bioactive estrogen concentrations either
due to decreased liver metabolism of estrogens or due to an increase
in the activity of the enzyme that forms estrogens (called aromatase).
Persistent elevations of estrogen interfere with follicular growth
and can disrupt the midcycle LH and FSH surges.
* (3) excessive circulating prolactin
The mechanism for the association between excess prolactin concentration
and ovulatory dysfunction is not entirely clear.
Increased prolactin released from the pituitary gland can increase
the brain's dopamine levels (which will then normally feedback
to decrease the prolactin secretion) and increased dopamine can
inhibit GnRH release from the hypothalamus to in turn decrease
pituitary FSH and LH secretion. A decrease in FSH may be the basis
for most prolactin associated ovulatory problems.
There are prolactin receptors on the adrenal glands. The adrenal
glands may respond to increased prolactin by increasing their
own androgenic hormones. The adrenal androgenic hormones are known
to interfere with ovulation.
Prolactin can decrease progesterone production by granulosa cells
(the cells that line ovarian follicles) when grown in culture.
If there is a direct effect of prolactin on granulosa cell progesterone
production in vivo (in a woman's ovaries) then this could also
lead to an ovulatory dysfunction, called a luteal phase defect.
* (4) non-prolactin secreting pituitary tumors
These are uncommon but included for completeness sake. The more
common of these are ACTH secreting tumors (resulting in Cushing's
syndrome) and Growth Hormone secreting tumors (resulting
in acromegaly). Also, there are gonadotropin
secreting tumors of the pituitary that secrete excess amounts
of FSH (and rarely LH) that may result in an ovulatory dysfunction
but rarely amenorrhea (these frequently go undetected due to the
difficulty in finding these tumors with the relative lack of identifiable
symptoms).
* (5) pituitary damage
Thrombosis or hemorrhage around the pituitary gland can result
in permanent pituitary destruction and amenorrhea. This is rare,
but possibly due to a hypotensive episode occurring during a severe
postpartum hemorrhage, called "Sheehan's syndrome."
In the situation where pituitary damage is the cause of the ovulatory
dysfunction, it is very important to evaluate the non reproductive
pituitary hormones as well since they may also be insufficient.
Adrenal insufficiency due to a deficiency of pituitary ACTH can
be life threatening.
* (6) empty sella syndrome
The sella turcica is a depression in the spenoid bone (a bone
at the base of the skull) that contains the pituitary gland. The
sphenoid bone is covered by a "diaphragm" of dura mater (a tough fibrous
membrane). The empty sella syndrome is a disorder characterized
by a congenital imperfection in the sellar diaphragm that allows
for the herniation of both the subarachanoid space and cerebrospinal
fluid into the sella turcica to flatten the enclosed pituitary
gland. This may result in increased prolactin and decreased FSH
and LH secretion. Amenorrhea and galactorrhea (milky discharge
from the breasts) are associated. Some women have a nasal cerebrospinal
fluid discharge or headaches. On radiologic imaging the sella
turcica looks empty, to give the condition its name.
* (7) medications
Progesterone or progestagenic medications can inhibit ovulation.
An excess circulating progesterone concentration just prior to
the LH surge will possibly inhibit the LH surge and thereby prevent
ovulation.. This is one of the mechanisms of the progesterone
only birth control pills. If progesterone supplementation for
luteal support is (accidentally) taken during the follicular phase
of the cycle, this can also inhibit ovulation
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