one month later

i am just so tired..tired of living, tired of life. it's not as if there is no laughter and light hearted moments...but just that life is a trial. maybe i just need a holiday and break from work.

even thinking about planning a holiday...is exhaustive..i wonder what is wrong with me.

Post IVF

It has been 2 weeks since the results are out. AF is already over and i am back at work, throwing myself into work which happens to be a busy period, enrolled in a gym and am going regularly *cross fingers* made plans to do more about the online shop and in fact met some pple over it. learning to write a biz plan, and figuring out the legal registration of the company.

i thought i was coping well with the failure.

on Sat, went for dinner at Yv, met a pregnant S and the whole bunch of kids and all of it came crashing back to me. looking at Yv younger boy and it came crashing to me that if my baby survive, he/she would be exactly that age.

Just why not me?

the pain is excrutiating. i wish i could cry and get rid of it once and forever, but no..it comes and goes..this empty feeling.

negative - THE END

been testing since 7DPET and gotten negative all along. Decided to bring forward the beta hcg blood test to Monday, got the results at 1pm, it's a very miserable 2.4. the nurse was still saying that it's early, and it may rise..but who the hell is she kidding?

all articles and all ivf centres in the world will concur that 2.4 is very NON PREGNANT. in fact any level below 5 is NON PREGNANT. I must admit that i am pretty annoyed at being 'entertained'

tried contact SF loh but was unable to get through to him as he was in OT all day. emailed him but didnlt get a reply either. it's frustrating, frustrating frustrating.

called kkh ivf again and was told to continue the progesterone jabs till thursday and then take another blood test on Friday. what the '1 quarter fish, 3 quarter duck' for?

hubby was optimistic, said why not....so we end up trudging to KKH early on tuesday. I then asked another the nurse manager if it's really necessary to continue on the progesterone jabs - she took a look at the chart and said ' let sf loh see you later and he will let you know'

that answers everything.

we waited 30 min to see as he's in OT (again). sf loh explained the figures and went through the egg retrival process, how many eggs retrieved (22), how many fertlised through IVF (final figure ?) and how many fertlised through ICSI. roughly half of the eggs retrieved was via IVF and ICSI.

total of 7 fertlised embroyos with 3 at grade 4 and treated with ICSI which was transferred this cycle.

The balance of 4 embroyos are frozen and mostly grade 3.

we discuss about the next cycle FET. And he still works on the premise that if so long the embroyo survives the thaw overnight, it should be transferrred, rather than waste it trying to grow it to blastocyst stage.

he said the chances that the embroyo will grow to blastocyst stage in the culture medium is so much lower than the chances that it will grow in the womb, that it is considered like wasting the embroyos.

i mentioned about the fact that if the embroyo doesn't survive till blastocysts stage after thawing , what makes him think that it will survive in the womb? he replied with some analogy about SAF men in camp training in the desert (which i so didn;t get) but anyways.....the idea is that the culture medium though the best that KKH uses is still not the real womb environment.

why did this cycle fail?
there is no specific reason. we can do only so much, the rest is still unexplained medically.

will the next cycle work?
no one can answer that question. FET has been known to have at least 10% chances lower than a fresh IVF cycle. But then there are also women who didn't get pregnant via a fresh cycle but gotten pregnant with FET. There's always hope!

Article in ST

Fertility clinics must disclose success rates by Andy HoThe Straits Times31 July 2007
A LOWER court had awarded a middle-age couple $32,000 for in-vitro fertilisation (IVF) treatment, but the High Court reversed this recently. The couple had lost both their teenage sons in a car accident and were asking for, among other things, IVF costs as replacement expenses in their effort to have a child.
The couple may appeal, so one may not comment on the case which involved, quite unusually, a motor vehicle insurer. But this tragic case does bring into focus the need for an IVF-specific law, which must address, if nothing else, two big issues.
First, given that Singapore needs more babies, it seems odd that there isn’t a law that requires (health) insurers to cover IVF treatment - or at least to offer coverage for it.
Insurers have argued that infertility is not an illness. Even if it were, they say, IVF does not treat the illness since it does not cure the underlying infertility. And, even if it did, coverage should be left to the market. After all, most plans here do not cover dental or psychiatric services.
Mandates to provide or offer coverage would distort markets, they say. That is, people who do not need IVF would have to bear part of the costs in higher premiums.
But I am pooled together with smokers anyway, so my insurance premium is already higher than it would be if my pool was smoker-free. After all, the essence of insurance is to socialise, or share out, risks.
Moreover, the lack of coverage means that health insurers are not helping to rein in IVF fees. It also means that IVF utilisation is probably less than that which would give Singapore more babies.
If so, instead of leaving it to the courts to decide piecemeal - someone must actually bring a suit for them to even consider the issue - Parliament should debate the question of coverage thoroughly.
And while Parliament is at it, it might also consider another issue, that is, how to regulate the sector.
Comprising mainly fee-forservice procedures, the sector is currently largely unregulated. Specifically, patients have no access to reliable information to help them choose service providers optimally, so they depend on word of mouth.
Most couples go through much pain for many years before they attain success, but many do not get that far.
IVF involves using drugs to urge a woman’s ovaries to produce eggs at each menstrual cycle, surgically retrieving the eggs, fertilising them with sperm in the lab to produce embryos, and then implanting the embryos into the woman’s womb. Women endure physical pain and couples are buffeted emotionally by the trials and tribulations the process puts people through. Moreover, each cycle of IVF treatment costs about $10,000.
Also, it is risky. Unlike most medical technologies, fertility treatments were introduced with little rigorous testing, except on animals. Most governments have simply left oversight of the sector to the medical profession’s self-regulation - and the courts.
Unsurprisingly then, it was merely five years ago that scientists were able to pin down the fact that IVF babies are six times more likely to have low or very low birth weights, and twice more likely to have major birth defects. Although clearer information has surfaced in the last dozen years, much is still unknown about the technology’s risks.
True, there is always some reluctance to regulate sectors where technology is rapidly evolving, since any law enacted today will have a hard time keeping up with the science tomorrow. But perhaps regulation can be targeted specifically to help with what customers really care about: results.
So whether we eventually pass a law to mandate insurance coverage or not, a law could be passed to mandate that providers report their individual success rates.
This is important because the infertile are very vulnerable and may persist in trying even when success is very unlikely. What they need is reliable data to make informed decisions that optimise their chances of getting a healthy baby.
However, providers in Singapore do not publicly report such statistics, so patients just go by word of mouth. And in jurisdictions where clinics do report their success rates, providers have been known to manipulate their data.
For example, some clinics count pregnancies rather than live births in their ’success’ rates, but some of those pregnancies end in miscarriages. Or, clinics may compare the number of live births to the number of embryos transferred, but this leaves out those cycles that are cancelled when eggs are harvested but cannot be fertilised.
However, the number of egg retrievals done does matter because the invasive procedure involved is painful and not risk-free. Any statistic that excludes failed cycles underplays the number of painful procedures (and risks) a woman might have to bear.
What to do?
We should pass a law to require service providers to disclose their success rates, specifying also how success-rate statistics are to be presented.
An unusually good model is that found in the American state of Virginia, where the law requires that before IVF treatment can commence, the clinic must give the patient a signed disclosure form detailing its success rates in specific ways. (This law specifies three statistics: First, the total number of live births, which is what couples care about most; second, the proportion of live births per menstrual cycle of retrieving eggs - which measures the true rate of success per attempt; and lastly, the numbers of both pregnancies and live births per retrieval cycle - which indicates the woman’s risk of miscarriage.)
The provider must also break down its data by age groups, since success rates drop as women age.
I urge Parliament to consider enacting a similar law. With uniform statistics among clinics, consumers can comparison shop and optimise the quest to make babies. And while Parliament is at it, mandate coverage of IVF services as well.

Implications of Blastocyst transfers

FEWER RISKS, NEW HOPE:
THE REALITY OF BLASTOCYST TRANSFERS
Mark Perloe, M.D.
Michael John Tucker, Ph.D.

Introduction
The first thing that usually comes to mind when people hear the term, "infertility treatment," is the risk of multiple births. This worry has been fueled by the recent highly publicized multiple births in Iowa and Texas. While such cases are rare, the incidence of triplets or higher-order births as a result of assisted reproductive technology is of great concern to all infertility practitioners and patients. For countless couples, deciding against treatment may mean abandoning their dream of having a child.

But what if there was a way to reduce or even eliminate the risk of multiples? Not only would that help more couples become parents, it would also decrease maternal and neonatal risks. That possibility is becoming a reality, thanks to a new technique known as blastocyst transfer. With blastocyst transfer, fewer embryos are transferred while maintaining and even increasing pregnancy rates. This technique virtually eliminates the risk of triplets or greater.

The Significance of Blastocyst Transfer
In a typical non-blastocyst in vitro fertilization (IVF) cycle, a woman's eggs are retrieved and fertilized. If all goes well, the embryos are transferred into the uterus three days later. Due to the fact that it is difficult to predict on day three which embryos are more likely to produce a pregnancy, four or more embryos are frequently transferred in hopes that at least one will result in a live birth. Until now, this has been a reasonable approach in order to achieve acceptable pregnancy rates.

The downside is that sometimes all the embryos become ongoing pregnancies and the result is high-order multiple gestations (triplets or greater). In such pregnancies, there are considerable medical risks as well as financial and emotional considerations. So the couple is faced with the agonizing decision of whether to opt for selective reduction (the removal of one or more embryos) or to continue with a risky pregnancy. Although everyone agrees that every possible safeguard should be in place to avoid such unfortunate situations, the distressing reality is that multiple pregnancies sometimes do occur.

However, with blastocyst transfer, only two or three embryos are transferred, practically eliminating the possibility of triplets or greater. And the same pregnancy rates are achieved as would be expected when four or more embryos are transferred on day three. Some centers report achieving even better pregnancy rates with blastocysts. Implantation rates of 48-50% and pregnancy rates of up to 66.3% have been reported in patients who responded well to gonadotropins.

What is 1 Blastocyst?
A blastocyst is a highly developed embryo that has divided many times to a point where it is nearly ready to implant on the walls of the uterus. A blastocyst has come a long way from its beginning as a single cell.

During maturation, an embryo rests inside a protective shell called a zona pellucida. You can think of this protective shell as being much like a chicken egg. But, unlike chicken eggs, human embryos do not remain inside a shell. Instead, the embryo hatches (breaks out of the shell) on the fifth or sixth day so it can attach to the uterine wall (implantation). Just prior to hatching, an embryo becomes a blastocyst.

Embryos developing to the critical blastocyst stage have a much greater chance of implanting successfully and resulting in an ongoing pregnancy. That is because these embryos have passed an important test. During the first few days, the embryo relies on the mother's egg for all its nutrients. However, in order to 15 survive past day three or four, the embryo must activate its own genes. Not all embryos are successful. In fact, only about one-third of the embryos become blastocysts. Yet these embryos are more highly-developed, healthier, and stronger, and have a higher rate of implantation when compared to day three embryos. Due to the higher probability of survival, we transfer fewer back into the uterus.

Getting to Day Five
For many years, infertility practitioners have known that day three transfers were too early when compared to what is physiologically normal. In naturally conceived pregnancies, a day three embryo resides in the fallopian tube, not in the uterus. The embryo does not even reach the uterus until the fifth or sixth day. Yet traditional IVF has always transferred on day three because, up until now, we have not been able to delay the transfer to day five. Previous laboratory culture media could only sustain an embryo's growth for three days. Now we have the ability to develop an embryo to the blastocyst (day five) stage.

What has made the difference is the recognition that the nutritional requirements of the embryo change as it develops. That knowledge led to the development of different laboratory culture media for the embryo's specific developmental stages. This so-called "sequential media" attempts to reproduce the natural environment of the maternal reproductive tract. The nutrients are designed to meet the requirements of the rapidly developing embryo and have led to the development of blastocysts with better viability and higher implantation rates.

Redefining Developmental Potential
The ability to develop embryos to the blastocyst stage allows clinicians to have greater certainty about which embryos are more likely to implant. Interestingly, no correlation has been found between what is traditionally considered a "good embryo" on day three and a "good blastocyst" on day five. Previously, Dr. Tucker reported a "significant disparity between the two stages in embryo viability estimates," meaning that even the best embryologists cannot tell which day three embryos have the potential to develop into a blastocyst.

While the quality of blastocysts is determined by examining morphology and development, it is important to point out that blastocyst grading standards are currently under development. Although the ability for the embryo to grow into a blastocyst is a milestone, other factors also play a role in its further development. In the near future, we believe we will be able to accurately predict which blastocysts are destined for success. When that happens, single blastocyst transfers will be considered the norm, and IVF will likely be considered the first-line infertility treatment.

Who Does it Help?
Determining who is a good candidate for blastocyst transfer is another rapidly evolving area. As more information becomes available and our knowledge base grows, guidelines based on actual clinical experience will be developed. Until then, we can offer some preliminary observations.

In general, blastocyst transfer is more advantageous for patients who develop a number of eggs and embryos. A significant correlation has been reported between the number of eggs and the number of blastocysts developed, as well as the number of day three embryos and the number of blastocysts developed. Other candidates for blastocyst transfer include those who would not consider fetal reduction or those in whom delivering multiple pregnancies would be of particular concern. Blastocyst transfer is probably not advantageous for patients who develop few eggs or embryos.

A side benefit of a blastocyst transfer is the fact that the ability to generate a blastocyst provides important information about the likelihood of pregnancy. In general, pregnancy rates are higher in those whose embryos grow to the blastocyst stage. Conversely, pregnancy rates are lower in those whose embryos do not develop into blastocysts.

Maternal Age and Blastocyst Development
Does maternal age have any bearing on the production of blastocysts? Although some studies have shown advanced maternal age to be a factor in blastocyst production, Schoolcraft found "no correlation between percentage of blastocyst formation and increasing maternal age" in a population of women who responded well to gonadotropins. However, implantation rates and pregnancy rates in this study decreased with maternal age, with women over 40 faring the worst.

What Happens When Embryos Do Not Become Blastocysts?
Because only a few embryos develop to the blastocyst stage, it is possible to have no embryos survive to day five to transfer. This is especially true if the cycle begins with only a few fertilized eggs. When no embryos survive to become blastocysts, it is a tremendous disappointment. The looming question then becomes, "Would the embryos that did not survive to become blastocysts have implanted if transferred at day three?" Unfortunately, we simply do not have enough clinical data at this time to answer that question. In our opinion, pregnancy would have been unlikely in that situation. But since that outcome is not a certainty, day three transfers may still be a reasonable option for some patients.

Genetic Testing And Blastocysts
Another benefit of blastocyst transfer is the ability to perform biopsies on a more highly-developed embryo in order to test for genetic diseases. In the future, immunofluorescent testing techniques will allow practitioners to remove a few cells from the blastocyst, stain them, and examine them under the microscope to detect any genetic anomalies. While that type of testing is not currently available on a day-to-day basis, we believe it will be considered routine within the next two to five years.

Frozen Blastocyst Cycles
Blastocysts tend to have a very good survival rate after cryopreservation (freezing). Menezo and his colleagues have reported that "the recovery after thawing is equivalent, if not superior to, that of thawing of earlier embryonic stages."

Because blastocysts are superior to earlier stage embryos in terms of development, they are easier to freeze, store, and thaw. Additionally, because blastocysts have higher implantation rates, it is possible for a couple to go through IVF once and have enough blastocysts for the current cycle as well as any future cycles.

The Future
We are just beginning to understand the implications of blastocyst transfer for both practitioners and patients. ,We believe infertility treatment centers will soon be able to reliably grow blastocysts and accurately assess which embryos are destined to implant and develop into an ongoing pregnancy. When that happens, the transfer of a single blastocyst will become the norm. And today's risk of high-order multiples will become a memory. The future holds much hope, much promise, and considerably fewer risks.

trigger shot and HPT

How long does it take synthetic hCG (trigger shot) to leave my body before I can test for pregnancy?

Every woman's metabolism is different, but as a general rule of thumb, you should allow 1 day for every 1,000 units of hCG you injected. The standard hCG dose is 10,000 units; thus, 10 days after the shot, the synthetic hCG should be gone and you should be able to test for pregnancy without detecting the shot. However, you should ask your doctor what the recommended protocol for your dosage is.
Some women choose to test daily to monitor the presence of the hCG in their bodies; once the synthetic hCG is gone, the tests become negative. If the hCG "comes back" and the HPT's turn positive again, it's likely due to a pregnancy and not the leftover hormone shot.

7 days post embryo transfer [7DPET]

Tuesday 14 August 2007

just had p4 bloodtest yesterday, result is 92.5nmol. a level sufficient enough not to increase the dosage of progesterone jabs. thank goodness for small favours.

i am feeling so much better now. i got my appetite back on Sunday. had fried bee hoon for breakfast and pizza for a very late lunch/dinner. and i didn't throw up.

yet on the other hand, the bloatedness has gone away and i feel back to normal. too normal - hiaks - got symptoms also worry, got no symptoms also worry.

i read somewhere that the earliest one can test for HPT is 10DPET - can't wait to rec the strips HPT i bought online.

painful ER, drama ET, hospitalised

Wednesday 8 August 2007

was hospitalised after ER on Monday, vomitting non stop , plus bloatedness, my belly grew like 8 cm within one day but it turned out not to be OHSS but sore ovaries, disturbed lining in the abdomen area due to the ER procedure.

ET was jeopardised and it was only this morning at 6.30am when Dr SF loh gave the go ahead for ET. and even so, he warned of the risk of going ahead with ET, increased risk of OHSS etc.

very drama, in the end ET went thru at almost 10am. it went smoothly and i was discharged from hospital at about 230pm. but it's a trying 3 days from mon to today - i snapped on monday night and bloody shouted everyone at the hosptial ward as i had to wait 5 hours in excruitating pain before the attending doctor saw me at 11pm.

all in all, i realised that the response from doctors in KKH is very subjective to which doctor is available. it so happens that SF loh was not around and he has already left the hospital on Monday evening.

so a piece of advise, when facing any emergency during the course of treatment, call ahead and make arrrangements to have your doctor waiting for you before you head down to the a & e dept. right now i am crossing fingers and toes that my 2www will go on smoothly.

p/s: today at KKH IVF, i saw a couple of gals who went thru ER at the same time as i did, they all look very healthy and painfree...guess it's just my bad luck to be the 1% that suffer through like crazy after the procedure.

My love will get you home - Christine Glass

If you wander off too far, my love will get you home.
If you follow the wrong star, my love will get you home.
If you ever find yourself, lost and all alone,
get back on your feet and think of me, my love will get you home.
Boy, my love will get you home.
If the bright lights blinds your eyes, my love will get you home.
If your troubles break your stride, my love will get you home.
If you ever find yourself, lost and all alone,
get back on your feet and think of me, my love will get you home.
Boy, my love will get you home.
If you ever feel ashamed, my love will get you home.
When there's only you to blame, my love will get you home.
If you ever find yourself, lost and all alone,
get back on your feet and think of me, my love will get you home.
Boy, my love will get you home.
If you ever find yourself, lost and all alone,
get back on your feet and think of me, my love will get you home.
Boy, my love will get you home,
Boy, my love will get you home.

When does implantation happen in IVF?

When does implantation actually occur in IVF or normal cycles? (We're not focusing on the "window" anymore, but on when real implantation does occur)

A very good study of implantation was published in 1992 by Bergh & Navot.
They studied 33 pregnancies from ovum donation or frozen-thawed cycles with serial HCG levels on the mothers to find the time of "first embryonic signal". The HCG assay used can detect very low levels.
Average first detection was at an embryonic age of 7.1 +/- 0.28 days (range 6.6-7.4 days).
This correlates with the studies of Hertig and Rock in the 1950's (hysterectomy studies) that showed the day of implantation to be day 6.
They did not find any evidence to support the concept of an embryonic diapause in humans.

IVF - Puregon - 2nd scan

Friday 03 Aug 2007

2nd scan done today - right ovary - 13 follicles ranging from 7.5 to 14mm. left ovary - 6 follicles ranging from 9.5 to 14.5mm. was told to do ER on Tuesday and ET on Thursday

Then rec call from KKH IVF in the afternoon that ER have to be done on Monday instead, as the doc will be away on Thursday., so ET will be on Wednesday.

IVF - 1st scan after stimulation

After being on Puregon for 7 days, I had my first scan, manage to see 9 follicles on right side from 7.5mm to 9mm, and 3 follicles on right side from 9mm to 12mm. Hope to see more follicles on Friday, I rather risk OHSS than not have enough eggs to fertillise.

although having said that the doc did advise that with the no of follicles so far and the nausea, there's a high tendency of 20-30% that the cycle have to be cancelled due to OHSS. the reasoning is that although it may be beareable now...after ET, the OHSS will worsen.

Costing of IVF

i'm supposed to do a costing here but never got round to doing it.

total i estimated so far we have forked out more than $2000, excluding out of pocket expenses such as taxi fares to and from the hospital.

will do a break down later.

Start of Puregon stage

Finally got the go ahead to start with stimulations stage. need to jab 200 units of puregon every day for next 7 days before heading for scan to check growth of follicles.

in the meantime, suppose to continue with lucrin as well, that means 2 jabs every morning. oh great!

the puregon injection pen takes some taking use to - i still prefer the old fashion syringe but then since puregon cost like $120 per jab, it's better to have a mechanised measurement. oh yeah, due to the longer time to jab lucrin, i had to get a new bottle of lucrin as well.

calculating ER should be on 3rd or 6th Aug....cross fingers, follicles grow well otherwise it's going to get expensive if need to increase puregon dose.

Am i doing too much?

Am i having too much on my plate at this point in time? going through IVF cycle is tough enough, having to work full time and trying to run a business and expanding, geting new manufacturers, having to do the housework etc etc...

i can't give up any of the above, already outsource the housework...work brings in money, business is sucking up money as fast as i could earn it. i really hope that it will work out in the end, if it does..i can quit and work from home and look after the pregnancy. worse case scenario ..if both doesn't work out, at least i have my work to fall back upon.

Lucrin or Lupron as called in the US

Clinical Policy Bulletin:Gonadotropin-Releasing Hormone Analogs (Lupron/Zoladex) and Antagonists (Plenaxis)


Number: 0501
Policy
Lupron
Aetna considers Lupron (leuprolide) medically necessary for the following indications subject to the specified limitations:
Endometriosis (see appendix)
To decrease fibroid size prior to surgery (see appendix).
To decrease endometrial thickness prior to endometrial ablation (see appendix).
For palliative treatment of members with advanced (Stage III or Stage IV) prostate cancer that has metastasized or has recurred after treatment, or member refuses orchiectomy (see appendix).
For true (central) precocious puberty, defined as sexual maturation before age 8 in girls and age 10 in boys, and tumor has been ruled out by lab tests, CT, MRI, or ultrasound (see appendix).
Infertility (used in conjunction with urofollitropin or menotropins) to suppress luteinizing hormone (LH) production in members with documented premature LH surge, or used in “super-ovulation” regimens associated with in vitro fertilization (see appendix).
For treatment of metastatic breast cancer, when the member is pre-menopausal and the disease has progressed or recurred after a trial of at least 3 months of tamoxifen (see appendix).
To suppress onset of puberty in cases where the adolescent meets medical necessity criteria for growth hormone supplementation and has early onset of puberty and is not within target growth range (within 1 standard deviation of mean height for age and sex) (see appendix).
For the treatment of women with chronic refractory pelvic pain (see appendix).
Aetna considers Lupron experimental and investigational for all other indications, including any of the following conditions, since limited information has been published and further research including randomized, controlled trials is required to determine its efficacy:
Precocious pubarche alone, or pseudoprecocious puberty (gonadotropin independent precocious puberty); or
Polycystic ovarian disease; or
Pre-menstrual syndrome; or
Endometrial cance; or
Ovarian cancer; or
Preservation (suppression) of ovarian function during chemotherapy; or
Preservation (suppression) of testicular function during chemotherapy.
Zoladex
Aetna considers Zoladex (goserelin) medically necessary for any of the following indications:
Advanced (metastatic) prostatic carcinoma; or
Advanced (metastatic) breast cancer in pre-menopausal members; or
Endometriosis, Stage III or IV; or
Uterine fibroids (leiomyoma uteri) (preoperative adjunct to surgical treatment) (short-term (less than 6 months) use); or
Endometrial ablation or hysterectomy (preoperative adjunct) (short-term (less than 6 months) use). (See also CPB 091 - Endometrial Ablation.)
Aetna considers Zoladex (goserelin) experimental and investigational for preservation of ovarian or testicular function during chemotherapy and for all other indications because its effectiveness for these indications has not been established.
Plenaxis
Aetna considers Plenaxis (abarelix) medically necessary for the treatment of the symptoms of men with advanced prostate cancer who cannot take other hormone therapies and who have refused surgical castration. Abarelix is considered experimental and investigational for all other indications. This policy is based on the FDA-approved indications for Plenaxis.
For gonadotropin-releasing hormone antagonists for infertility, see CPB 327 - Infertility.
Background
Lupron:
Leuprolide (Lupron) is a gonadotropin-releasing hormone analog, which may be indicated for treatment of certain conditions, which are hormonally regulated.
Leuprolide may be indicated in advanced cancer (palliative treatment) in patients who have inoperable prostate tumor, or refuse orchiectomy. The available literature suggests combined therapy with leuprolide and an anti-androgen (e.g., megestrol, flutamide) appears to produce additive effects and to be more effective than leuprolide therapy alone in the treatment of advanced prostate cancer. According to established guidelines, recommended dosing of leuprolide for palliative treatment of advanced prostate cancer is 1 mg given subcutaneously daily. According to established guidelines, if patient is receiving leuprolide acetate suspension (Lupron depot) dosing is 7.5 mg IM once monthly.
Leuprolide has been used in the treatment of true (central) precocious puberty, defined as sexual maturation less than age 8 in girls, and sexual maturation less than age 10 in boys. The available literature suggests tumors should be ruled out by lab tests, CT, MRI, or ultrasound. Leuprolide is not indicated for precocious pubarche alone or pseudoprecocious puberty (gonadotropin-independent precocious puberty). According to established guidelines, recommended starting doses are: Lupron Depot Ped: 0.3 mg/kg every four weeks (minimum 7.5 mg), or Lupron injection: 50 mcg/kg daily. Doses may be titrated upwards in order to achieve hormonal down-regulation.
Studies of leuprolide for endometriosis indicate that six months is an appropriate length for therapy. Because of lack of safety data with long-term use, and because of concerns expressed in the available literature regarding effects on bone density, treatment after six months is typically not recommended. According to established guidelines, recommended dosing of leuprolide for endometriosis is 3.75 mg as a single monthly IM injection.
Leuprolide has been studied for the treatment of uterine fibroids (leiomyoma uteri), as a preoperative adjunct to surgical treatment. Clinical studies have demonstrated the benefit of leuprolide in reducing vascular and surgical complications secondary to obstructive fibroid size. In tests, GnRH agonists have effectively reduced the fibroid size, but their use was accompanied by a rapid regrowth following discontinuation. The available literature states Leuprolide therapy does not prevent or replace the eventual need for surgery. If used as a pre-operative adjunct, the available literature states short-term treatment only is recommended (i.e., 1-3 months).
Leuprolide also has been shown to be an effective preoperative adjunct to decrease endometrial thickness prior to endometrial ablation. If used as a pre-operative adjunct, short-term treatment only (i.e., 1-2 months) is indicated.
Leuprolide is used in conjunction with urofollitropin or menotropins in patients with infertility. It has been used to suppress LH production in patients with documented premature LH surge. In addition, it has been used in “super-ovulation” regimens associated with in vitro fertilization. Treatment of infertility may be subject to limitations under some benefit plans. Some HMO contracts, with or without a separate infertility benefit such as the Advanced Reproductive Technology (ART) Rider, specifically exclude injectable infertility drugs.
Leuprolide has been shown to be useful in the treatment of metastatic breast cancer in pre-menopausal patients whose disease has progressed or recurred despite a 3 or more month trial of tamoxifen.
Leuprolide has been used as treatment for various other conditions (e.g., polycystic ovarian disease, hypermenorrhea, premenstrual syndrome, paraphilias, endometrial cancer, and ovarian cancer). At this time limited information has been published to show efficacy for conditions other than those mentioned in the clinical criteria above. Further research with randomized, controlled trials is required to determine efficacy in these other conditions.
The American Society of Clinical Oncology's recommendations on fertility preservation in cancer patients (Lee, et al., 2006) stated that sperm and embryo cryopreservation are considered standard practice. On the other hand, the use of GNRH analogs or antagonists for testicular or ovarian suppression is considered investigational. ASCO guidelines state: “At this time, since there is insufficient evidence regarding the safety and effectiveness of GnRH analogs and other means of ovarian suppression on female fertility preservation, women interested in ovarian suppression for this purpose are encouraged to participate in clinical trials.” The guidelines also noted that there is insufficient evidence of the effectiveness of GnRH analogues in preventing chemotherapy-induced gonadal damage in men: “The efficacy of gonadoprotection through hormonal manipulations has only been evaluated in very small studies in cancer patients.”
In a review of the literature, Sonmezer and Oktay (2006) explained that there are a limited number of prospective studies of GNRH analogues in preventing chemotherapy-induced gonadal damage, “which are flawed because of short-term follow-up and/or because of lack of control subjects.” The review notes that “[i]n addition to the lack of consistent support from clinical studies, there is currently no biological explanation for who GNRHa [GNRH analogues] can affect ovarian reserve.” The authors concluded that “[i]n the absence of a prospective randomized study with sufficient power, we do not rely on ovarian suppression as an effective means of fertility preservation.”
Zoladex:
Goserelin (Zoladex) is a gonadotropin releasing hormone (GnRH) (also known as gonadorelin and luteinizing hormone releasing hormone or LHRH) analog, which is indicated in certain conditions requiring suppression of estrogen or testosterone secretion. At this time it is available only in a continuous-release subcutaneous implant which releases drug over a period of about 28 days.
Goserelin is approved by the FDA for treatment of advanced metastatic prostate cancer and advanced endometriosis. Goserelin has also been shown to be effective for treatment or palliation of breast cancer in pre-menopausal patients.
Goserelin has been studied for the treatment of uterine fibroids. Clinical studies have demonstrated the benefit of leuprolide in reducing vascular and surgical complications secondary to obstructive fibroid size. In tests, GnRH agonists have effectively reduced the fibroid size, but their use was accompanied by a rapid regrowth following discontinuation. Therefore, the literature states that goserelin therapy does not prevent or replace the eventual need for surgery. If used as a pre-operative adjunct, the literature recommends short-term treatment (six months or less).
Goserelin has been shown to be effective for the short-term (less than 6 months) preoperative adjunct to endometrial ablation or surgery for leiomyomata uteri (uterine fibroids).
Goserelin is under investigation as a method of prevention of chemotherapy-induced gonadal damage. In a prospective pilot study (n = 5), Franke, et al. (2005) explore the effects of goserelin acetate in women with Hodgkin's disease (HD) receiving chemotherapy while taking a continuous combined estrogen-progestin preparation as add-back on the prevention of premature ovarian failure (POF). Pre-menopausal women with HD received goserelin and add-back until polychemotherapy was completed. Every 4 weeks during treatment and thereafter, a hormonal profile (follicle-stimulating hormone (FSH), LH, 17beta-estradiol, progesterone and inhibin B) was measured until resumption of menstruation or the development of a hyper-gonadotropic state (2 x FSH greater than 30 U/l). All patients reached pre-pubertal status during treatment. Following cessation of goserelin therapy, 1 patient developed a hyper-gonadotropic state and 4 patients resumed menstruation. One of those patients became pregnant and delivered a healthy son. These investigators concluded that the effectiveness of GnRH agonist plus add-back on the prevention of POF during polychemotherapy in women with HD needs further elucidation in randomized controlled trials.
Del Mastro, et al. (2006) noted that standard methods to prevent chemotherapy-induced early menopause in young, breast cancer patients are unavailable to date. Pre-clinical data has suggested that LHRH analogs given during treatment can decrease the gonado-toxicity induced by chemotherapy. In a phase II clinical trial, these investigators evaluated the activity of such a method in young, breast cancer patients undergoing adjuvant chemotherapy. Pre-menopausal patients received goserelin 3.6 mg every 4 weeks before and during chemotherapy. According to 2-stage optimal phase II Simon design, treatment was considered clinically interesting if it was able to prevent menopause in 19 out of 29 patients of the study population. The resumption of ovarian function was defined by a resumption of menstrual activity or by a FSH value less than or equal to 40 IU/l within 12 months after the last cycle of chemotherapy. A total of 30 patients were enrolled and 29 were evaluable. Median age was 38 years (range 29 to 47 years). All but one patient received CEF regimen (cyclophosphamide, epirubicin, 5-fluorouracil). Resumption of menstrual activity was observed in 21 patients (72%; 95% CI 52 to 87%) and a FSH value less than or equal to 40 IU/l in 24 patients (83%; 95% CI 63 to 93%). Menses resumption was observed in 16 out of 17 patients (94%) with age less than 40 years and in 5 out of 12 patients (42 %) with age 40 years or over. These researchers concluded that goserelin given before and during chemotherapy may prevent premature menopause in the majority of patients. However, the different success rate by age indicates the need of a prospective evidence of the effectiveness of such a strategy.
Plenaxis:
Plenaxis (abarelix) is a gonadotropin-releasing hormone antagonist approved by the FDA in November 2003. It is indicated for the treatment of the symptoms of men with advanced prostate cancer who cannot take other hormone therapies and who have refused surgical castration. Plenaxis is marketed under a voluntary risk management program agreed to and administered by the sponsor that will restrict the use of Plenaxis to patients with advanced prostate cancer, who have no alternative therapy, because of an increased risk of serious, and potentially life-threatening, allergic reactions associated with its use.
In a phase III clinical study (n = 269), McLeod et al (2001) evaluated the levels of testosterone and other hormones in men with prostate cancer treated with abarelix versus leuprolide acetate. The authors concluded that treatment with abarelix produced a higher percentage of patients who avoided a testosterone surge and had a more rapid time to testosterone suppression with a higher rate of medical castration 1 day after treatment and greater reductions in testosterone, LH, follicle-stimulating hormone, and dihydrotestosterone during the first 2 weeks of treatment compared with leuprolide acetate. The achievement and maintenance of castration was comparable between the two groups.
In another phase III clinical trial (n = 255), Trachtenberg et al (2002) reported that abarelix as monotherapy achieved medical castration significantly more rapidly than combination therapy (LHRH agonist and a non-steroidal anti-androgen) and avoided the testosterone surge characteristic of agonist therapy. Both treatments were equally effective in reducing serum prostate specific antigen, and achieving and maintaining castrate levels of testosterone.
Koch, et al. (2003) stated that abarelix provided a safe and effective medical alternative to surgical castration in symptomatic patients (n = 81) with advanced prostate cancer without the risk of the clinical flare associated with LHRH agonists.

Appendix
Medically Necessary Indications for Lupron
Limitations
Endometriosis
Up to six months - because of lack of safety data with long-term use, and concerns in available peer-reviewed medical literature regarding effects on bone density.
Lupron dosages greater than 3.75 mg per month or 11.25 mg per 3 months are subject to medical necessity review.
To decrease fibroid size prior to surgery
Up to three months - under accepted guidelines, does not prevent or replace the eventual need for surgery except in peri-menopausal women.
Lupron dosages greater than 3.75 mg per month or 11.25 mg per 3 months are subject to medical necessity review.
To decrease endometrial thickness prior to endometrial ablation
Up to two months.
Lupron dosages greater than 3.75 mg per month or 11.25 mg per 3 months are subject to medical necessity review.
For palliative treatment in members with advanced prostate cancer, defined as Stage III or Stage IV, that has metastasized or recurred after treatment, or patient refuses orchiectomy
1 mg given subcutaneously daily. If receiving leuprolide acetate suspension (Lupron Depot), dosing is 7.5 mg IM once monthly.
For true (central) precocious puberty, defined as sexual maturation before age 8 in girls and age 10 in boys, and tumor has been ruled out by lab tests, CT, MRI, or ultrasound
Lupron Depot Ped: 0.3 mg/kg every four weeks (minimum 7.5 mg).
Lupron injection: 50 mcg/kg daily. It may be medically necessary to titrate dosages upwards in order to achieve hormonal down-regulation.
Infertility (used in conjunction with urofollitropin or menotropins) to suppress luteinizing hormone (LH) production in members with documented premature LH surge, or used in “super-ovulation” regimens associated with in vitro fertilization
Note: Treatment of infertility may be subject to specific limitations under some benefit plans. Most HMO plans exclude injectable infertility drugs from coverage.
For treatment of metastatic breast cancer
Indicated where member is pre-menopausal and the disease has progressed or recurred after a trial of at least 3 months of tamoxifen
To suppress onset of puberty in adolescents with early onset of puberty on growth hormone therapy
Adolescent must meet medical necessity criteria for growth hormone supplementation, have early onset of puberty, and be below target growth range (within 1 standard deviation of mean height for age and sex)
For the treatment of women with chronic refractory pelvic pain
Indicated where attempts at medical therapy with analgesics and oral contraceptive have been unsuccessful.

CPT Codes / HCPCS Codes / ICD-9 Codes
Lupron (suspension and implant):
HCPCS codes covered if selection criteria are met:
J1950
Injection leuprolide acetate (for depot suspension), per 3.75 mg
J9217
Leuprolide acetate (for depot suspension), 7.5 mg
J9219
Leuprolide acetate implant, 65 mg
ICD-9 codes covered if selection criteria are met:
174.0 - 175.9
Malignant neoplasm of breast
185
Malignant neoplasm of prostate
218.0 - 218.9
Uterine leiomyoma
233.0
Carcinoma in situ of breast
233.4
Carcinoma in situ of prostate
259.1
Precocious sexual development and puberty, not elsewhere classified
617.0 - 617.9
Endometriosis
Lupron prior to endometrial ablation (see CPB 91):
ICD-9 codes covered if selection criteria are met:
626.2
Excessive or frequent menstruation
626.3
Puberty bleeding
627.0
Premenopausal menorrhagia
627.1
Postmenopausal bleeding
2 week Lupron kit:
HCPCS codes covered if selection criteria are met:
J9218
Leuprolide acetate, per 1 mg
Other HCPCS codes related to the CPB:
J3355
Injection, urofollitropin, 75 IU
S0122
Injection, menotropins, 75 IU
S0187
Tamoxifen citrate, oral, 10 mg
ICD-9 codes covered if selection criteria are met:
185
Malignant neoplasm of prostate
233.4
Carcinoma in situ of prostate
259.1
Precocious sexual development and puberty, not elsewhere classified
628.0 - 628.9
Infertility, female
ICD-9 codes not covered for indications listed in the CPB:
140.0 - 239.9
Neoplasms [when used for preservation of ovarian or testicular function during chemotherapy]
182.0
Malignant neoplasm of corpus uteri, except isthmus
183.0
Malignant neoplasm of ovary
198.6
Secondary malignant neoplasm of ovary
218.0 - 218.9
Uterine leiomyoma
256.4
Polycystic ovaries
625.4
Premenstrual tension syndromes
V58.11 - V58.12
Encounter for antineoplastic chemotherapy and immunotherapy [when used for preservation of ovarian or testicular function during chemotherapy]
Zoladex (Goserelin):
HCPCS codes covered if selection criteria are met:
J9202
Goserelin acetate implant, per 3.6 mg
ICD-9 codes covered if selection criteria are met:
174.0 - 175.9
Malignant neoplasm of breast
185
Malignant neoplasm of prostate
218.0 - 218.9
Uterine leiomyoma
233.0
Carcinoma in situ of breast
233.4
Carcinoma in situ of prostate
617.0 - 617.9
Endometriosis
625.3
Dysmenorrhea
628.0 - 628.9
Infertility, female
Zoladex prior to endometrial ablation (see CPB 91):
ICD-9 codes covered if selection criteria are met:
626.2
Excessive or frequent menstruation
626.3
Puberty bleeding
627.0
Premenopausal menorrhagia
627.1
Postmenopausal bleeding
ICD-9 codes not covered for indications listed in the CPB:
140.0 - 239.9
Neoplasms [when used for preservation of ovarian or testicular function during chemotherapy]
V58.11 - V58.12
Encounter for antineoplastic chemotherapy and immunotherapy [when used for preservation of ovarian or testicular function during chemotherapy]
Plenaxis (abarelix):
Other CPT codes related to the CPB:
54520 - 54535, 54690
HCPCS codes covered if selection criteria are met:
C9216
Injection, Abarelix for injectable suspension, per 10 mg (deleted 12-31-04)
J0128
Injection, abarelix, 10 mg
ICD-9 codes covered if selection criteria are met:
185
Malignant neoplasm of prostate
Other ICD-9 codes related to the CPB for Lupron, Zoladex, and Plenaxis:
253.3
Pituitary dwarfism
625.8 - 625.9
Other and unspecified symptoms associated with female genital organs
V58.11 - V58.12
Encounter for antineoplastic chemotherapy and immunotherapy
V66.0
Convalescence and palliative care following surgery
V66.1
Convalescence and palliative care following radiotherapy
V66.2
Convalescence and palliative care following chemotherapy
V66.7
Encounter for palliative care The above policy is based on the following references:
Lupron:
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Dodson WC, Hughes CL, Whitesides DB, et al. The effect of leuprolide acetate on ovulation induction with human menopausal gonadotropins in polycystic ovary syndrome. J Endocrin Metab. 1987;65(1):95-100.
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Precocious Puberty
Brenner PE. Precocious puberty in the female. In: Reproductive Endocrinology, Infertility and Contraception. DR Mishell, VC Davajan, eds. Philadelphia, PA: FA Davis Co.; 1979.
Partsch CJ, Sippell WG. Treatment of central precocious puberty. Best Pract Res Clin Endocrinol Metab. 2002;16(1):165-189.
Mul D, Wit JM, Oostdijk W, et al. The effect of pubertal delay by GnRH agonist in GH-deficient children on final height. J Clin Endocrinol Metab. 2001;86(10):4655-4656.
Cara JF, Kreiter ML, Rosenfield RL. Height prognosis of children with true precocious puberty and growth hormone deficiency: Effect of combination therapy with gonadotropin releasing hormone agonist and growth hormone. J Pediatr. 1992;120(5):709-715.
Pelvic Pain
ACOG Committee on Practice Bulletins -- Gynecology. ACOG Practice Bulletin No. 51. Chronic pelvic pain. Obstet Gynecol. 2004;103(3):589-605.
Royal College of Obstetricians and Gynaecologists (RCOG). The initial management of chronic pelvic pain. RCOG Guideline No. 41. London, UK: RCOG; April 2005.
Infertility
Albuquerque LE, Saconato H, Maciel MC. Depot versus daily administration of gonadotrophin releasing hormone agonist protocols for pituitary desensitization in assisted reproduction cycles. Cochrane Database Syst Rev. 2005;(1):CD002808.
Al-Inany H, Aboulghar M. Gonadotrophin-releasing hormone antagonists for assisted conception. Cochrane Database Syst Rev. 2001;(4):CD001750.
Nugent D, Vandekerckhove P, Hughes E, et al. Gonadotrophin therapy for ovulation induction in subfertility associated with polycystic ovary syndrome. Cochrane Database Syst Rev. 2000;(3):CD000410.
Prostate cancer
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Seidenfeld J, Samson DJ, Aronson N, et al. Relative effectiveness and cost-effectiveness of methods of androgen suppression in the treatment of advanced prostate cancer. Evidence Report/Technology Assessment No. 4. Prepared for the Agency for Healthcare Policy and Research (AHCPR) by the Blue Cross and Blue Shield Association Technology Evaluation Center. AHCPR Pub. No. 99-E0021. Rockville, MD: AHCPR; May 1999.
Seidenfeld J, Samson DJ, Hasselblad V, et al. Single-therapy androgen suppression in men with advanced prostate cancer: A systematic review and meta-analysis. Ann Intern Med, 2000;132(7):566-577.
Prostate Cancer Trialists' Collaborative Group. Maximum androgen blockade in advanced prostate cancer: An overview of the randomised trials. Lancet, 2000;355:1491-1498.
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Leiomyomas
Lefebvre G, Vilos G, Allaire C, et al. The management of uterine leiomyomas. SOGC Clinical Practice Guidelines. No. 128. Society of Obstetricians and Gynaecologists of Canada. J Obstet Gynaecol Can. 2003;25(5):396-405.
Vollenhoven BJ. Uterine fibroids: A clinical review. Br J Obstet Gynecol. 1990;97:285-298.
Friedman AJ. Treatment of leiomyomata uteri with short-term leuprolide followed by leuprolide plus estrogen-progestin hormone replacement therapy for 2 years: A pilot study. Fertil Steril. 1988;51(3):526-528.
Farquhar C, Arroll B, Ekeroma A, et al. An evidence-based guideline for the management of uterine fibroids. Working Party of the New Zealand Guidelines Group. New Zealand Guidelines Group; November 1999.
Lethaby A, Vollenhoven B, Sowter M. Pre-operative GnRH analogue therapy before hysterectomy or myomectomy for uterine fibroids. Cochrane Database Syst Rev. 2001;(2):CD000547.
Breast cancer
Olin BR. Drug Facts and Comparisons. St. Louis, MO: J.B. Lippincott Company; 1992.
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Dowsett M, Jacobs S, Aherne J, et al. Clinical and endocrine effects of leuprorelin acetate in pre- and postmenopausal patients with advanced breast cancer. Clin Ther. 1992;14 Suppl A:97-103.
Manni A, Santen R, Harvey H, et al. Treatment of breast cancer with gonadotropin-releasing hormone. Endocr Rev. 1986;7(1):89-94.
Harvey HA, Lipton A, Max DT, et al. Medical castration produced by the GNRH analogue leuprolide to treat metastatic breast cancer. J Clin Oncol. 1985;3(8):1068-1072.
Sunderland MC, Osborne CK. Tamoxifen in premenopausal patients with metastatic breast cancer: A review. J Clin Oncol. 1991;9(7):1283-1297.
No authors listed. Tamoxifen. In: Drug Evaluation Subscriptions. DR Bennett, ed. Chicago, IL: American Medical Association; 1993;5:5.
Endometriosis
Henzl MR, Corson SL, Moghissi K, et al. Administration of nasal nafarelin as compared with oral danazol for endometriosis. N Engl J Med. 1988;318(8):485-489.
Letassy NA, Thompson DF, Britton ML, et al. Nafarelin acetate: A gonadotropin-releasing hormone agonist for the treatment of endometriosis. DICP. 1990;24:1204-1209.
Lemay A, Maheux R, Quesnel G, et al. LH-RH agonist treatment of endometriosis. Contr Gynec Obstet. 1987;16:247-253.
Souney PF, Rossiter A. Focus on naferelin acetate: GnRH agonist for the management of endometriosis. Hosp Formul. 1990;25:1041-1054..
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Gerhard I, Schindler AE, Bruhler K, et al. Treatment of endometriosis with leuprorelin acetate dept: A German multicenter study. Clin Ther.1992;14(Suppl A):3-16.
Crosignani PG, Gastaldi A, Lombardi PL, et al. Leuprorelin acetate depot versus danazol in the treatment of endometriosis: Results of an open multicenter trial. Clin Ther. 1992;14 (Suppl A):29-36.
Tummon IS, Pepping ME, Binor Z, et al. A randomized, prospective comparison of endocrine changes induced with intranasal leuprolide or danazol for treatment of endometriosis. Fertil Steril. 1989;51(3):390-394.
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Premenstrual syndrome
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Zoladex
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baseline scan and bloodtest

Tues 17 July 2007

went for baseline scan and bloodtest today. results out about 4pm. was told to conitnue with lucrin for another 7 days before going back for another scan and bloodtest. was also told that the endometrium is thick at 8mm.

normally by this time of the cycle, (day 5 of the cycle after AF), the endometrium shd be about 2mm only. yet mine is 8mm, not sure how this will affect the IVF cycle.

I am so diasppointed by the extension of the lucrin jabs and to top that now the point about the thickened endometrium..i wonder all thse additional hurdles is some omen that i should consider ending the cycle.

the side effects of lucrin/lupron is really beyond my control..it made me tempermental, frustrated at the slightest thing and short tempered, not to mentioned fatigue and nausea. I am not sure if it's the stress adding or the meds, but it seems to have triggered off a fibromyglia flare as well, my ribs, hips and knee hurts like hell.

lucrin side effects

the days are getting harder to cope - perhaps it's the side effect of lucrin/lupron. been feeling moody, teary, and super tired. and guess what AF come by today which is only Day 25 of the cycle.

so far been on 11 days of lucrin jabs with baseline scanning next Tuesday. Hoping to be able to start puregon ASAP. i can't wait for it to end.

IVF Start of Lucrin cycle

Finally 3rd July 2007 came around, today is Day 16 of the IVF cycle and officially i got started on Lucrin. I was pretty worried about the jabs, who wouldn;t be? it turn out to be less painful and less complicated.

will start to jab myself tomorrow.

IVF Status

AF finally showed up, 6 days after the end of the 5 days course of duphaston. called KKH IVF and made an appointment to start Lucrin 16 days later on 3rd July 2007.

at the same time, made an appointment with Caroline for counselling.

in the meantime, suppose to start on Microgyon for the next 21 days.

looking eagerly to start the program.

KKH IVF - Pre IVF cycle Day 6

Time seems to be crawling. so far completed the course of duphaston for 5 days at 2 tabs daily. now just waiting for AF to start. normally after a course of progesterone, AF will start like 3-5 days later. Let's hope this holds true again.

i wonder if it's the effects of the progesterone - i have been feeling teary, fatigue and unable to sleep well at nights. I am trying to relax but arghs....the lack of sleep is making me so tired. i worry if this continues that it will trigger of fibromyglia.

today is also the second day after hubby had his 2 teeth; 1 wisdom and 1 molar taken out. needless to say he is in excruitating pain and milking it completely. how i wish i am home looking after him now.

my mind is 1/4 at work, 1/4 in IVF and 1/2 at home.

KKH IVF

Friday 08 June 2007 3pm

WE had an appointment with KKH IVF at 3pm. Staff Nurse Tan CK went through the details of the program. Basically it's more or less what we expected, except that the jabs went on longer than expected. I will be on lucrin for almost 21 days, in addition to Puregon for up to16 days. That's like 37 days of self inflicted pain.

a night jab of IM pregnyl and 4 days of HCG if egg collection is less than 15, or 17 days of IM progesterone if number of eggs collected is more than 15.

i really cannot imagine 17 days of progesterone jabs. last time we did alternate days and it was damn painful to the extent of numbed butts.

The actual schedule as follows:

Day 1 : start of menses - call KKH IVF
Day 2 - Day 16 : Microgyon (birth control pills) x 16 days
Day 16 - Day 21 : Microgyon 5 days + subcut Lucrin 10 units x 5 days Total Microgyon 21 days
Day 21 - Day 30 : subcut Lucrin 10 Units 9 days Total 14 days Lucrin - baseline scan & bloodtest for E2
Day 31 - Day 37 : subcut Lucrin 10 units x another 7 days
Day 38 - Day 44 : subcut Puregon 200 IU x 7 days + Lucrin 10 units
Day 45 (8th day of puregon)- Day 53 (16th day of puregon): subcut Puregon + Lucrin 10 units (dosage depends on growth of follicles) - 1st scan on 8th day of puregon; 2nd scan betwen 9th -12th days; 3rd scan between 13th - 15th day. When follicles reach 16mm, STOP Lucrin. Total 16 days puregon
Day 54 : IM pregnyl at night , ER 2 days later
Day 56 : Egg Retrieval
Day 57 - Day 58 : wait for fertilisation
Day 59 : Egg transfer / balance embroyo to freeze
Day 60 - Day 76 - return for progesterone blood tests (x3) - if more than 15 eggs collected, got to return for IM progesterone daily for 17 days. If less than 15 eggs collected, 4 x HCG jabs.
Day 77 : 17 days later, pregnancy test

Now the challenge is to put the estimated dates in

Day 1 : Mon 18 Jun
Day 16 : Tue 3 Jul - start of lucrin + appt at KKH + counselling session with Caroline
Day 30 : Tue 17 Jul - baseline scan & blooodtest
Day 38 : Wed 25 Jul - Start Puregon
Day 45: Wed 1 Aug - 1st Scan
Day 48 : Sat 4 Aug - 2nd scan
Day 51 : Tue 7 Aug - 3rd scan
Day 54 : Fri 10 Aug - IM pregnyl jab
Day 57 : Mon 13 Aug - ER
Day 59 : Wed 15 Aug - ET
Day 77 : Sat 1 Sep - pregnancy test

starting on IVF

Starting on IVF is daunting - not just about the physical aspects, but also the emotional and financial aspects, not to mention how it will affect my work.

but then if we don't get started, nothing will happen.

after all the reserach done in the past 2 years, we decided the best place to do IVF would be KKH IVF

reasons as follows:
1) the medical team headed by SF Loh. His approachability via emails is huge factor in our decision, not to mention that he helped me get over the ectopic pregnancy. btw he's now the head of the reproductive dept in KKH and the director of the IVF program.
2) the success rate in KKH IVF exceeds the rest of the centres
3) the convenience of early morning clinics for scans and blood test - which means less time off work
4) the financial cost factor.

Our first appt at Clinic D didn't start of very well. the appt was at 430pm but we only got to see the doctor close to 6pm. and it was a very rush consultation as there are still quite a few patients after me.

the decision was made so swiftly by Dr Loh that we didn;t have a chance to absorb it. half an hour later while we were waiting to make payment, the doc happened to walk past us and he made an effort to talk to us about the rough time scheduling of this IVF cycle. that help to reliev some of our doubts about chosing KKH.

The next appointment will be on Friday at the IVF clinic for registration, counselling by the doctor, required blood tests, and counselling by the phychologist.

Start of a new cycle - this time IVF

We tried 3 cycles of serophene in NUH but nothing happened. we thought that with the better HSG results and the successful ovulation, we will be able to achieve a baby by now, but no nothing happen.

i started a new job and am now in my 3rd month, wasn't planning to start TTC again so soon..except that MIL announce that SIL is pregnant.

That brought back a lot of memories, and not all good. It was all i could to control myself and not break out in tears on the spot.

life is so unfair.