How will Gonal-f/Pregnyl affect thyroid function? Also, has it
been determined what TSH level works best for achieving pregnancy?
I'm 40 year old with
Hashimoto's diagnosed Nov '02. Currently taking Armour thyroid.
TSH level spring 2003 was 1.36/1.68. Early Dec '03, TSH was 2.46.
I began Gonal-f (150iu) 12.26.03 and completed course in eight
days. TSH increased to 4.53 on 1.8.04. My general MD has increased
my Armour to 90mg/day. As you know, the injectables are quite
costly and I want to maximize my chances during use. Thank you.
The gonadotropins will not affect Thyroid function. However, it
is important to keep your hypothyroidism under control by adequate
hormone replacement, as I am sure you are doing. Hashimoto's
disease is associated with the presence of antithyroid antibodies.
About 50% of women who have autoantibodies to their own thyroid
tissues (antithyroglobulin and/or antimicrosomal antibodies) regardless
of whether or not there are clinical signs or symptoms of reduced
thyroid hormone activity (hypothyroidism) have activated Natural
Killer cells (NKa+ and/or activated T-cells in their blood. Such
women often present with reproductive failure manifesting as infertility,
recurrent IUI and IVF failure or repeated pregnancy loss. The
antithyroid antibodies (antimicrosomal and/or antithyroglobulin
antibodies) do not cause the problem. They act as markers pointing
to an underlying immunologic implantation problem that occurs
when NKa or T-cell activation is present. Here, as soon as the
embryo starts to burrow into the uterine wall, "toxins"
are produced (locally) that impair implantation. In some cases,
the pregnancy is lost before a blood test can detect it, while
in other cases a miscarriage occurs. (Some pregnancies escape
the "toxic gauntlet" and proceed.)
One of the
most significant hints that a non symptomatic woman might have
antithyroid antibodies is a family history of hypothyroidism (under
performance of the thyroid gland requiring thyroid hormone therapy).
We were among
the first to demonstrate that women who have reproductive failure
associated with antithyroid antibodies and NKa+/T-cell activation
can have successful IVF outcomes following administration of intravenous
gammaglobulin (IVIG). Women who are antithyroid antibody positive
who do NOT have NKa+ and or T-cell activation do not require or
benefit from IVIG therapy.
I have been diagnosed with immunological problems. I have been trying
to have a baby for the past four years (after a tubal reversal).
I have gotten pregnant four times (last time was 1 1/2 years ago)
but cannot carry past 7.5 weeks. I have elevated Antinuclear,
AntiOvarian and Antiphospholipid antibodies.
My RE now
has me taking prednisone, 5mg cd 3 till trigger shot then 60 mg
for 4 days, then 10 mg's till pregnancy test, if positive then
20 mgs, if negative then stop. (This is along with my baby aspirin,
folic acid, Follistim and IUI treatment). My question is, does
this really work? What kind of chances does a 32 year old, with
children aged 12 and 14 who has lost her last 4 pregnancies have
of carrying a healthy baby to term? Thank you for your input.
National statistics indicate that only one out of four women under
the age of 40 achieves a live birth following treatment with in
vitro fertilization IVF). While most IVF laboratories report a
similar egg fertilization rate (I.e., 60-70%), program-to-program
IVF birth rates still range from below 10% to greater than 50%
per embryo transfer. To improve IVF success rates, the cause(s)
of this discrepancy, must be recognized and addressed.
evidence suggests that an abnormally functioning maternal immune
system often leads to poor reproductive performance (i.e., IVF
failure, recurrent abortion, poor intrauterine growth and even
fetal and that identification and selective immunotherapy results
in a significant improvement in IVF birth rates, intrauterine development
and fetal survival.
the board physicians who provide services in the field of Assisted
Reproductive Technology (ART) tend to attribute recurrent unexplained
treatment failures to sub-optimal embryo quality and then advise
such patients that the only way to improve their subsequent chance
of a successful outcome, is by changing clinical and laboratory
protocols involved in ovarian stimulation, gamete and embryo preparation
and/or the transfer of gametes or embryos to the woman's
reproductive tract. Such logic fails to take into account the
fact that it is "implantation failure" rather than poor
egg/embryo number or quality that is often the root of the problem.
A rational approach to subsequent treatment requires that a clear
distinction be made between those factors that cause "true
infertility" (defined the absence of normal fertilization
and/or embryogenesis), and those that lead to "failed implantation,"
(namely; immunologic rejection of the embryo, local inflammation
and pathology involving the uterine cavity). Only treatment directed
at an identifiable probable cause of prior ART failure, can justify
providing patients with renewed hope of success in a subsequent
cycle of ART treatment.
process begins six or seven days after fertilization of the egg.
At this time, specialized embryonic cells (i.e., trophoblast),
which later becomes the placenta, begin growing into the uterine
lining. When the trophoblast and the uterine lining meet, they,
along with immune cells in the lining, become involved in a "cross
talk" through mutual exchange of hormone-like substances
called cytokines. Because of this complex immunologic interplay,
the uterus is able to foster the embryo's successful growth.
Thus, from the earliest stage, the trophoblast establishes the
very foundation for the nutritional, hormonal and respiratory
interchange between mother and baby. In this manner, the interactive
process of implantation is not only central to survival in early
pregnancy but also to the quality of life after birth.
its importance, it is not surprising that failure of proper function
of this immunologic interaction during implantation has been implicated
as a cause of recurrent miscarriage, late pregnancy fetal loss,
IVF failure and infertility. A partial list of immunologic factors
that may be involved in these situations includes: anti-phospholipid
antibodies (APA), antithyroid antibodies (ATA), and, perhaps most
importantly, activated natural killer cells (NKa). Presently,
these immunologic markers can be adequately measured by only a
few (less than a half dozen) highly specialized reproductive immunology
laboratories in the United States, from patient blood samples.
A large body
of literature has confirmed that patients who experience repeat
IVF failures often have increased levels of circulating APAs.
Compelling evidence has also demonstrated that up to 50% of women
with pelvic endometriosis and unexplained infertility harbor APAs
in their blood. Despite this information, the role of APAs in
reproductive outcome is still controversial. In 1995, we proposed
that in cases of non-male factor infertility, women who test positive
for APAs be treated with mini-dose heparin and low-dose aspirin
to improve IVF implantation and thus birth rates. This approach
was based upon research that suggested that heparin repels APAs
from the surface of trophoblast cells, thus enhancing their development.
Aspirin, by inhibiting platelets from adhering to the early trophoblast,
might prevent clot formation in the early utero-placental vasculature.
We subsequently demonstrated that heparin/aspirin therapy improved
IVF outcome only for women whose APA testing was positive for
antibodies other than those directed against two specific phospholipids,
i.e., phosphatidylethanolamine (PE) and phosphatidylserine (PS),
and that only women who had IgG/IgM-related anti-PE or anti-PS
antibodies experienced a significant improvement in IVF implantation
and birth rates when IVIG therapy, instead of heparin/aspirin,
was initiated more than one week prior to embryo transfer.
the above, the following recent observations suggest that
APA's rather than being causally linked to implantation failure,
might serve to identify a population at inordinate risk of implantation
failure and that NKa, through the unregulated release of embryo
toxins, are in fact the real culprits.
- The presence
of APAs in male factor cases appears to bear no relationship
to IVF outcome
- Only APA
positive women who also test positive for abnormal NK activity
appear to benefit from selective immunotherapy with IVIG.
- More than
75% of APA+ women who have increased NK cell activity also harbor
aPE and/or aPS antibodies
Killer Cell cytotoxicity
and during early pregnancy, NK cells comprise more than 80% of
the white blood cell population seen in the uterine lining. NK
cells produce a variety of local hormones known as TH-1 cytokines.
Uncontrolled, excessive release of TH-1 cytokines is highly toxic
to the trophoblast and endometrial cells, leading to their programmed
death (apoptosis) and, subsequently to failed implantation. In
the following situations these NK cells (and also T-cells) can
become abnormally activated (Nka+), and thereby over-produce these
patients that have both pelvic disease (especially endometriosis--regardless
of severity) and abnormal APA testing
- In about
half of the cases where the woman forms antibodies
her own thyroid gland (i.e., antithyroid antibodies.)
NK cells (NKa) can spill over from the uterine lining into the
peripheral blood where their toxicity can be measured. IVIG therapy,
initiated more than 1 week prior to embryo transfer, can subdue
activated NK cells, thereby reducing the risk of implantation
A clear relationship
has been established between ATA and reproductive failure (especially
recurrent miscarriage and infertility). We have previously reported
on the ability to double IVF birth rates through the administration
of IVIG to ATA+ patients. IVIG therapy should be initiated prior
to initiation of treatment with fertility drugs, and should be
administered one more time after pregnancy is diagnosed. About
50% of women who harbor ATAs also test Nka-positive The risk of
implantation failure in ATA+ women appears to be confined to cases
where ATAs coexist with Nka. IVIG therapy should be confined to
There is compelling evidence that subcutaneous heparin (administration
at a dosage of 5000 U twice daily to women undergoing IVF for
female causes of infertility who test positive for APAs, but negative
for NK activation), significantly improves IVF birth rates. Heparin
administration is withheld on the day of egg retrieval until immediately
following embryo transfer, whereupon it is recommenced and continued
until the 8th week of pregnancy. Heparin is thought to act by
repelling APAs from the surface of the trophoblast (early "root
system" of the embryo). Provided that platelet counts are
normal, are checked on a regular basis and heparin is withheld
on the day of egg retrieval, its administration is virtually risk-free.
of aspirin in combination with heparin, offers no benefit over
treatment with heparin alone, for the management IVF patients
with immunologic implantation failure. As such, with the notable
exceptions of women with primary APA-related autoimmune diseases
(e.g., lupus erythematosis, rheumatoid arthritis, etc.) and cases
associated with recurrent pregnancy loss, we no longer prescribe
aspirin to women undergoing treatment for reproductive failure.
Immunoglobulin G (IVIG)
IVIG is a sterile protein preparation derived from human blood.
Every effort has been made to ensure that it is free of bacterial
and viral contamination. There are basically three ways in which
IVIG may offset or counter the anti-implantation effects associated
with reproductive immunologic deficiencies.
is a potent suppressor of activated (toxic) NK cells (see above).
Second, it contains anti-idiotype antibodies that combat the effects
of harmful antibodies, thereby protecting the embryo/fetus from
rejection. Third, IVIG deactivates activated T-cells and polyclonal
B-cells that may be involved in poor reproductive performance
associated with the presence of antithyroid antibodies (Sher,
et al, American Journal of Reproductive Immunology, 1998).
Unfortunately, IVIG has had some undeserved bad press. Since it
is a blood derivative, the thought of administering it in an era
where HIV is rampant, is frightening to most; but consider the
following: The IVIG products available in the United States and
the United Kingdom, according to the manufacturers, have not resulted
in a single HIV viral transmission in more than two million administrations.
Moreover, IVIG is derived from the very same blood pool used for
transfusion purposes, and since millions of units of blood have
been administered in the United States over the last 7 years without
any reports of HIV transmission, and since the product is thoroughly
tested in this country, it is safe to say that US produced IVIG
is untainted by viral contamination. IVIG therapy for increased
NK activity/APA positivity is initiated at least 10 days prior
to embryo transfer, and for ATA positivity is initiated 7 to 14
days prior to the initiation of gonadotropin therapy. The infusion
is repeated once pregnancy is diagnosed. We do not recommend repeating
IVIG administration subsequently during the pregnancy.
Therapy (Prednisone, Prenisilone and Dexamethazone)
is a mainstay of most IVF programs. Some programs use daily oral
methyl prednisilone while others prescribe oral Dexamethazone
commencing about ten days prior to initiating ovarian stimulation
with gonadotropins, and continuing until the diagnosis of pregnancy,
whereupon, in the event of a negative test (Beta HCG or ultrasound),
the dosage is tapered over a period of seven to ten days, and
then discontinued. Pregnant patients continue treatment through
the first trimester. Steroids are believed to act by inhibiting
the cellular immune response.
use of immunotherapy as outlined above has, on numerous occasions,
has enabled us to achieve successful pregnancies in-patients who
had previously suffered repeated IVF failures (4 or more). Many
such patients had previously been advised not to try again with
their own eggs. We are able to report IVF births occurring in
more than a dozen cases, after more than ten (10) prior IVF failures.
One such case involved a 42-year-old woman who had a baby (using
her own eggs) following 22 consecutive prior IVF failures. It
is indisputable that such results would not have been achieved
without access to selective immunotherapy. In a recent study,
we were able to show that Nka+ women who do not receive IVIG/heparin
therapy have a 10 times lower chance of successful IVF.
problems may lead to implantation failure, it is important to
properly evaluate women with risk factors such as:
or recurrent IVF failures
(about 30% of cases are associated with increased Nka+ activity
following recurrent miscarriage
- A positive
personal or family history of autoimmune disorders such as Rheumatoid
arthritis, Lupus erythematosis and hypothyroidism (Hashimoto's
disease) which is rather common in women.
relating to the use of selective immunotherapy in IVF has been
spawned by issues other than those related to science. Political
one upmanship, the competitive nature of the ART field and lack
of understanding with regard to the complex issue of reproductive
immunology, has led a lot of misinformation. This issue will be
laid to rest by a large randomized and controlled study we have
been able to undertake due to a >1 million dollar grant given
to us by a large pharmaceutical company.
The immunologic contribution to successful reproduction is
a complex puzzle that is still being assembled one piece at a
time. Clear evidence now exists to support the view that women
with non-male factor related infertility, who harbor IgG/IgM,
APAs, can selectively benefit from immunotherapy with heparin
or IVIG. Rather than being causally linked to implantation failure,
APAs, probably serve as markers that point to a population at
risk and that this risk is greatly increased when such antibodies
are specifically directed against PE and/or PS are present and/or
when Nka are detected. APA positive/Nka negative women should be
treated with heparin, while all Nka positive women, regardless
of their APA/ATA status should receive IVIG.
I am a 35 year old woman who has been trying to conceive my second
baby for a year. I have had two miscarriages, one before my son
and one after. My TSH was a bit high (one at 6.4 and the other
4.5) at the time of my miscarriages. My TSH at the time of my
only successful pregnancy was .06. Did my TSH play a factor here?
What is your opinion on TSH levels and successful pregnancy outcomes?
Gina, raised TSH levels may point to Thyroid dysfunction . . . either
hyperthyroidism or Hypothyroidism. Both may have an immunologic
basis and increase the risk of immunologic implantation failure.
Please read my responses above. Best of luck.
Is there any link between IF tx and pre-eclampsia? I had a successful
IUI with a vanishing twin. Horrible morning sickness and I threw
up the whole pregnancy. I started getting Pre-eclampsia symptoms at 24 weeks
and delivered at 26 weeks 3 days with eclampsia, HELLP, Kidney Failure,
Liver Failure and a Grand Mail seizure. I just wondered if there
have been any links to IF tx with my problems. Thank you.
Limber, because we now are beginning to see a link between pregnancy
induced complications such as pre-eclampsia and abruptio placentae
and perhaps hyperemesis on the one hand and immunologic implantation
problems and thrombophylia on the other.
Most women with
a thrombophylia have healthy pregnancies. However, the thrombophylias
can contribute to a number of pregnancy complications, including
pregnancy loss in the second or third trimester (i.e., stillbirths),
placental abruption (when the placenta separates from the uterine
wall, partially or completely, before delivery), and poor fetal
growth. The thrombophylias also may cause pre-eclampsia, a pregnancy-related
disorder characterized by high blood pressure and protein in the
urine that can pose serious risks for mother and baby. Several of
these problems are believed to result from blood clots in placental
blood vessels that lead to changes in the placenta and reduced blood
flow to the fetus.
is the inherited tendency to develop blood clots too easily.
Thrombophylias are due either the presence of too much of certain
blood-clotting factors or too little of anti-clotting proteins
in the blood. As many as one in five people in the United States
has a thrombophylia.
women in general are more likely than non-pregnant women to develop
a venous thrombotic episode (VT), or development of a blood clot
in a vein. This is due to normal pregnancy-related changes in
blood clotting in order to limit blood loss during labor and delivery.
And pregnant women with a thrombophylia are at a higher risk than
other pregnant women of developing a VTE. Studies suggest that
more than half of pregnant women who develop a VTE have an underlying
women who have had a blood clot should be offered testing for
hereditary thrombophylias. In addition, women with a family history
of blood clots, pulmonary embolism (blood clot in the lung), or
strokes that occurred prior to age 60; or a history of pregnancy
complications, including stillbirth, early or severe pre-eclampsia,
placental abruption, or poor fetal growth due to undetermined
causes may be considered for testing.
women with thrombophylia are treated with one or more daily injections
of low dose heparin, a blood-thinning drug, which does not cross
the placenta and is safe for the baby. In some cases, physicians
may recommend low doses of aspirin along with heparin. Low-dose
aspirin with the B vitamins folic acid, B6 and B12 can be given
to women who have one of the milder thrombophylias and a history
of pregnancy complications, but not a history of blood clots.
Not all pregnant
women with a thrombophilia need heparin treatment during pregnancy..
Regular heparin can be supplanted with a newer form of heparin,
called low-molecular-weight heparin, that appears to pose a lower
risk of side effects such as bone loss and can be injected once
instead of twice daily (as with regular heparin) and which reduces
the risk of local bruising, significantly.
treatment is not recommended for most pregnant women with one
of the less severe thrombophilias (such as factor V Leiden or
prothrombin mutation) and no history of blood clots or pregnancy
complications. This is because the risk of blood clots or pregnancy
complications due to thrombophilia appears to be less than 1 percent
in these women. However, treatment may be recommended for about
six weeks after birth, when the risk of blood clots may be highest,
if the woman has a strong family history of blood clots or if
she has had a cesarean delivery.
is recommended throughout pregnancy and the postpartum period
for women who have one of the more severe thrombophylias ( e.g
MTHFR genetic mutations and factor II G20210A) , even if they
have not experienced any blood clots or pregnancy complications.
Women with a thrombophilia (regardless of severity) who have a
past history of blood clots are usually treated with heparin during
pregnancy and the postpartum period. Warfarin (also a blood-thinning
drug) may be used safely in addition to, or instead of, heparin
in the post-partum period and during breast feeding. However,
it is not recommended during pregnancy because it can cause birth
As yet, no
proven cause and effect relationship has been shown to exist between
thrombophilia on the one hand and failed embryo implantation,
poor IVF outcome, and/or early recurrent miscarriages, on the
I have been charting for 8 months now and my LP is never any longer
than 10 days. That is the average. What can I do to lengthen this
in order to sustain a pregnancy? Here are my charts for your perusal.
you very much.
Jane, you could have luteal phase defect.
ovulation, the remainder of the dominant follicle transforms itself
into a structure called the Corpus Luteum (CL) which produces
progesterone. The purpose of progesterone is to prepare the uterus
to accept and support an early pregnancy until it is able to sustain
itself at around 8-10 weeks of gestation.
The life span
of the CL is predetermined to be 12-13 days, unless rescued by
a signal from the early pregnancy. If no pregnancy occurs, the
CL stops making progesterone and menses ensues 1-2 days later.
For most women the length of the second half of the menstrual
cycle (the luteal phase) is constant at 14 days. A small percentage
of infertile women (3-4%) have a shortened luteal phase. This
may result in the loss of pregnancy support before the budding
pregnancy has a chance to signal the ovary that it is there.
of the uterus (the endometrium) has a specific appearance that
changes throughout the menstrual cycle, such that a biopsy of
the lining a few days prior to expected menstruation, can accurately
date endometrial development. A three or more day difference between
endometrial dating by biopsy and cycle day as determined by the
start of the next menstrual period is indicative of a luteal phase
defect (LPD). Sequential mid luteal progesterone levels < 10
ng/dl can also be used to diagnose a LPD. Luteal phase defect
can be treated with Clomiphene Citrate, Progesterone supplementation
or hCG injections.
husband and I have a 3.5 year old that was conceived on our "first
try." We now want to add another baby to our family, but
we have tried for nine months now without any luck. Since we have
one child we know that we can have children, but I want to ask
you what some of the reasons for me not getting pregnant again
could be. Thank you!
There could be many possible reasons for secondary infertility.
You need to see an RE and have a thorough evaluation as outlined
I am 36 year old and have been ttc for 2.5 years. Lap in August
revealed asymptomatic endometriosis on uterus which was removed. Also fibroids
within uterine walls which were not removed. Having a less than
great response to follistim, should I move on to IVF or try one
more cycle at six vials/night? Should fibroids within the uterine
wall be removed? Thank you for your time!
With endometriosis at 36, IVF is probably the best alternative. Read
question has to do with male infertility. I am really curious
on your opinion regarding the lack of research on this cause for
infertility. The "solution" seems to be IVF with ICSI
which is not actually a solution but a work-around. Male infertility
seems to be so far behind female infertility. Do you have any
thoughts as to why this is the case? Insurance will often pay
for treatment of the causes, but in the case of male infertility,
there are seldom such treatments available! I am just curious
on your thoughts or experiences. Thank you.
Jodi, the amount
of research and knowledge on MF infertility is growing exponentially.
Can you share more about your opinion about Viagra assisting
with blood flow to the uterus and lining thickness? Is it similar
to baby aspirin or more effective? How can one introduce the idea
to an RE who may be unaware of this treatment option? Thank you!
It is far more
effective. BUT alas "there are none so blind as those that
will not see!"
In 1989, we
were among the first to show that in normal and "stimulated"
cycles, pre-ovulatory endometrial thickness and ultrasound appearance,
is predictive of embryo implantation (pregnancy) potential following
In Vitro Fertilization/Embryo Transfer (IVF/ET). With conventional
IVF (where the woman receives fertility drugs and has her own
fresh embryos transferred to her uterus), here needs to be a 9mm
sagital thickness (Grade 2) and a triple line appearance (Grade
A) accordingly, a Grade 2A lining is optimal in such cases. Anything
less is associated with about a five- (5) fold reduction in live
birth rate per ET. An exception to this rule seems to apply for
third party embryo Recipients (Ovum donation, IVF-Surrogacy) and
in cases of frozen embryo transfers (i.e., where the recipient
receives supplementary estrogen/progesterone and not gonadotropins,
to prepare the uterine lining. Here, a lining of 8mm thickness
seems to be adequate.
endometrial lining most commonly occurs in women with a history
of unexplained recurrent IVF failures or early recurrent miscarriages
and is usually attributable to: 1) inflammation of the uterine
lining (endometrium), i.e., endometritis (occurring following
a septic delivery, abortion or miscarriage, 2) adenomyosis (gross
invasion of the uterine muscle by endometrial glandular tissue),
3) multiple fibroid tumors of the uterine wall) 3) prenatal exposure
to the synthetic hormone, diethylstilbestrol ( DES) and, 4) in
women who have received clomiphene citrate (Clomid, Serophene)
for at least 3 months in a row without a resting cycle (this effect
is self-reversible within 4-6 weeks of discontinuing clomiphene).
attempts to augment endometrial growth in women with poor endometrial
linings by bolstering circulating estrogen blood levels (through
the administration of increased doses of fertility drugs, aspirin
administration and by supplementary estrogen therapy) yielded
we began to recognize that it was possible to improve endometrial
development in women who had "poor uterine linings,"
by the daily application of nitroglycerine skin patches during
ovarian stimulation with fertility drugs. We believed that the
therapeutic effect was probably attributable to the local action
of nitric oxide (NO) on the uterine vasculature, leading to improved
endometrial blood flow and enhanced delivery of estrogen to the
uterine lining. About 75% of our IVF patients with compromised
uterine linings so treated with nitroglycerine skin patches, showed
a marked improvement in estrogen-induced endometrial growth and
many went on to achieve viable pregnancies. Unfortunately the
lack of access to ultrasound color flow Doppler (UCFD) to measure
uterine blood flow at the time precluded us from confirming that
the observed enhancement in endometrial development was directly
attributable to enhancement of uterine blood flow. Accordingly
we did not publish these findings.
The high incidence
of unpleasant side effects associated with nitroglycerine therapy
(e.g. severe headaches, nausea, and light-headedness brought about
by fluctuations in blood pressure) resulted in poor patient tolerance.
Accordingly, when Sildenafil (Viagra) was shown to facilitate
penile erection through increasing penile blood flow, without
eliciting bothersome side effects, we decided to investigate whether
this drug could replace nitroglycerine for the improvement of
endometrial development. This time, with ready access to UCFD,
we set out to examine for a cause and effect relationship between
Viagra-induced enhancement of uterine blood flow and improved
endometrial growth in women with poor endometrial development.
to incorporate Viagra into vaginal suppositories in an attempt
to improve local uterine absorption and minimize the incidence
of systemic side effects .To this end, we enlisted the services
of a compound pharmacist and began testing the effect of vaginally
administered Viagra on uterine blood flow and on estrogen-induced
endometrial development. Four women with chronic histories of
poor endometrial development and failure to conceive following
several advanced fertility treatments were evaluated for a period
of 4-6 weeks and then underwent IVF with concomitant Viagra therapy.
Viagra vaginal suppositories were administered four times daily
for 8-11 days and were discontinued 5-7 days prior to embryo transfer
in all cases.
on our findings in a preliminary study, published in the prestigious
journal, "Human Reproduction" (April 2000). The findings
clearly demonstrated that vaginal Viagra produced a rapid and
profound improvement in uterine blood flow and that this was followed
by enhanced endometrial development in all four cases. While three
of the four women subsequently conceived, the study is too small
to prove that these pregnancies can be attributed to the Viagra
therapy. Larger independent and controlled studies will be needed
to demonstrate this.
In a manuscript
which appeared in "Fertility & Sterility" (The official
journal of The American Society of Reproductive Medicine) in October
2002, we reported on the administration of vaginal Viagra to 105
women with repeated IVF failure due to persistently thin endometrial
linings. All of the women had experienced at least two (2) prior
IVF failures attributed to intractably thin uterine linings. About
70% of these women responded to treatment with Viagra suppositories
with a marked improvement in endometrial thickness and 45% of
these achieved live IVF- births following a single cycle of treatment
with Viagra. 9% miscarried. None of the women who had failed to
achieve an improvement in endometrial thickness following Viagra
subsequently and underwent embryo transfers in the same cycle
during which Viagra was administered, achieved viable pregnancies.
Our very first
patient (Rene Danford)to achieve a live birth following Viagra
treatment subsequently again conceived following IVF where Viagra
was administered and has since delivered a healthy baby (a girl
this time), at full term.
My husband and I got pregnant back in 1995 but miscarried at 11
weeks, and we have been trying ever since. I have gone to a few
doctors and had tests done and they seem to come back fine. Could
my weight be what the problem is? I have been heavy all my life
but what is the largest some one can weigh and still get pregnant?
Weight should not be a major factor in getting pregnant, but it
can cause problems in pregnancy. Diabetes of pregnancy, pre-eclampsia,
prolonged/dysfunctional labor, large babies, obstructed labour,
post partum hemorrhage and infection etc are all more common.
My husband and I have been trying to conceive for almost 2 years
now. I am 28 and he is 30. We've had many fertility tests done
(SA, HSG, hormone levels drawn, and PCT) and they all are normal
(besides a low LP progesterone). I'm normally anovulatory, so
my doctor put me on Clomid eight months ago. After five months
on Clomid, we moved onto injectables (Bravelle-FSH) and HCG trigger.
After eight months of medicated cycles (five which were ovulatory
and three which were anovulatory), I never became pregnant. I'm
wondering, do you suggest I get a laparoscopy done before we move
onto IUI? I have no symptoms of endometriosis, but I know that
many women who have it don't. Thanks in advance for taking time
out of your busy day to chat with us here on StorkNet!
You probably will be best advised to consider IVF. Call Sharon
Benzel at 800-780-743 and set up a free medical telephone consultation
with me so we can talk.
I am a 35 year old woman (divorced and recently remarried) who
already has two children ages 12 & 8. My new husband and I
want to have a baby, however, in the last couple of years, my
menstrual cycles have become either extremely irregular, short
or non-existent. My former OB-GYN diagnosed it as just stress
based the results of a laparoscopy, hysteroscopy, and a D&C.
My new OB-GYN has decided to try some medication to get me back
on track. Does this mean that I have stopped ovulating completely
or just that the time that I am ovulating is drastically shortened?
Is there hope for us to conceive a child? Explain to me the different
medications used to resume ovulation? Side effects? Thank you
so very much, Dr. Sher.
Could be stress, abnormal hormone balance, or you may be moving
more quickly to a menopause ( hopefully not). Either way it sounds
a s if you are not ovulating functionally or at all. You need
to be properly evaluated ASAP and then move on to the most appropriate
Hi, Dr. Sher, I appreciate you being available for questions!
My question is what is the probability of infertility after giving
birth to one child (via c-section)? We have been actively trying
for six months now and haven't gotten pregnant. We didn't try
at all for our first child. I visit a family doctor and he said
he won't intervene until we'd been trying for a year. I guess
I'm impatient and I just want to make sure everything is okay.
I know when I'm ovulating and so we plan sex for that time and
I'm still not getting pregnant. Any suggestions on what we can
do? Should I see an ob/gyn about this problem? Thanks so much for
any help! Amy
Amy, by definition infertility is the inability to conceive after
1 year of regular trying . You may indeed be best advised to give
it another six months. Try not to stress out; it only makes
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