tag:blogger.com,1999:blog-168491692024-03-08T19:56:43.052+08:00babymakingThis blog is set up to chronological the long roller coaster ride of trying to concieve (TTC) in singaporebabymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.comBlogger100125tag:blogger.com,1999:blog-16849169.post-16157116863134925942008-11-30T05:47:00.000+08:002008-11-30T05:49:07.356+08:00Monitoring in IVF cycles - details<span style="font-family:verdana;font-size:85%;"><strong><span style="color:#66ffff;">MONITORING IN VITRO FERTILIZATION (IVF) CYCLES<br /><br />E. Tawfik, A. Mastrorilli and A. Campana<br />Infertility and Gynecologic Endocrinology Clinic,<br />Department of Obstetrics and Gynecology,<br />University Cantonal Hospital, 1211 Geneva 14, Switzerland<br /><br />The term " monitoring " means " close continuous observation ", so when we refer to monitoring an in vitro fertilization and embryo transfer (IVF-ET) cycle we mean close observation not only of a patient’s initial parameters and her own ovarian response to ovulation induction, but also events after completion of the therapy.<br /><br />Why monitor the patient? Monitoring serves two purposes. On the one hand, it helps the physician to choose the most suitable protocol, or to modify the dose and/or the approach for the protocol being applied in an attempt to obtain the best possible outcome and avoid complications of therapy or of the procedure as a whole. On the other hand, monitoring our patients adds to the common pool of information which increases our knowledge and understanding of human reproduction.<br /><br />In our opinion, monitoring IVF patients begins with the initial infertility work-up, and continues until after delivery. This chapter is concerned, however, with the time period of an IVF cycle which starts just before induction therapy and ends either by the establishment of a biochemical pregnancy, or failure of implantation. Before discussing different methods of monitoring, it is better to divide monitoring into three stages: before starting induction therapy, the period of induction and the period that follows completion of therapy.<br /><br /><br /><br />Before induction therapy<br /><br />During this period, one has to think about which protocol should be offered to the patient. This depends on many factors such as the patient’s endocrine profile and general health, her age and financial situation, and the physician’s previous experience.<br /><br />Clomiphene citrate<br /><br />Before prescribing clomiphene citrate (CC), the physician should be sure that the follicle stimulating hormone (FSH) is not abnormally elevated and that the patient is not hypoestrogenic. One should rule out disorders of the pituitary, adrenal and thyroid which require specific treatment. Liver function evaluation should precede CC therapy if history and physical examination findings suggest liver disease. Ultrasonography (US) should be done just before starting the therapy to exclude ovarian cysts.<br /><br />Gonadotropin therapy<br /><br />If gonadotropin therapy is chosen, it is of utmost importance to exclude ovarian incompetence because this type of treatment is very expensive and is not free of complications. Abnormally high serum levels of gonadotropins with low estrogen levels indicate ovarian failure which precludes induction of ovulation except in a few special cases. Non gynecological endocrine problems should be treated before starting the therapy. Hypogonadotropic function with galactorrhea requires evaluation for an intracranial lesion. It is important to know that hyperprolactinemia has no adverse effect on ovarian response to exogenous gonadotropin therapy (8). Ultrasonography should be done to exclude the presence of ovarian cysts and/or polycystic ovary disease (PCO) which require special care.<br /><br />Gonadotropin releasing hormone analogue (GnRHa) combined with exogenous gonadotropin therapy<br /><br />This approach is especially effective for women who either show no response to exogenous gonadotropins, or who develop premature spontaneous luteinizing hormone (LH) and progesterone rise. Indeed the major effect appears to be the prevention of premature luteinization which is a major reason for decreased success with other therapies. Patients with significant estrogen and gonadotropin levels, especially anovulatory women with PCO do not respond well to gonadotropins but the response can improve after GnRHa desensitization. Some protocols call for GnRHa use during the luteal phase of the preceding IVF cycle, others advocate its use during the follicular phase concomitantly with human menopausal gonadotropin (hMG) and/or pure FSH. At present there is no agreement as to which protocol is best, and the information available is rather conflicting.<br /><br />If it is decided to prescribe the long term GnRHa protocol, the patient should be monitored for the criteria of pituitary and ovarian suppression. Complete suppression is verified by the onset of menstruation associated with a serum LH <2>10 mm in diameter. If all these criteria are not met on day 12, GnRHa should be continued and the patient assessed at weekly intervals until suppression is complete, then induction can be started.<br /><br />Monitoring ovarian response to induction therapy<br /><br />Monitoring ovarian response to induction therapy depends mainly on the biophysical parameters of follicular growth, and hormonal parameters, principally E2 levels.<br /><br />Monitoring follicular growth<br /><br />Sonography can depict developing follicles, beginning at the time they measure between 3 and 5 mm. As follicles spontaneously reach maturity in the natural cycle their inner dimensions range from 17 to 25 mm (9). Within the same individual however, the size of a mature follicle is relatively constant. Intrafollicular echoes may be observed within mature follicles probably arising from clusters of granulosa cells that shear off the wall near the time of ovulation. After ovulation, the follicular wall becomes irregular. The fresh corpus luteum usually appears as an echogenic structure with a small hypoechoic center. Patients undergoing ovulation induction are usually examined every other day beginning at day 10, but those undergoing IVF–ET are examined earlier, usually starting between day 5 and 8 of their cycles, and daily thereafter.<br /><br />In CC-treated cycles, each follicle seems to develop at an individual rate, and at times may be accelerated or slowed down. Therefore the largest follicle on a given day may not be the same one that is the largest two days later, and it may not even be the one that is most mature. Furthermore, correlation of E2 and follicle size is poor and the maximum preovulatory diameter can range from 19 to 24 mm. However, the largest diameter in these cases estimated by Fossum et al. (12) ranged between 22 and 31 mm.<br /><br />In hMG-treated patients, there seem to be two distinct patterns of follicular development (35). In amenorrheic women with dormant ovaries, a small number of large follicles develops. The growth rate and E2 production are linear, correlate well and are of equal predictive value. A high pregnancy rate is achieved in this group. In contrast, stimulation of patients with estrogenic activity requires less hMG and usually results in the rapid recruitment of many follicles with different growth rates and E2 secretory capacity. The rate at which E2 increases is exponential, increasing the risk of hyperstimulation. The growth rate and functional maturity are asynchronous. In this group of women, both E2 and sonographic follicular monitoring are essential.<br /><br />The biophysical indicators that correlate best with the day of LH surge (12) have been found to be the follicular volume in spontaneous cycles (range: 3.4-5.6 ml), the cross-sectional area in GnRH stimulated cycles (range 1074-1382 mm2) and the largest diameter in CC-treated cycles (range: 22-31 mm). Because no significant difference was seen in the correlation among the various biophysical variables and the mid cycle LH peak however, it could be concluded that in women ovulating spontaneously, or in those induced to ovulate with CC or GnRH, any available biophysical index will have the same predictive value. In contrast, correlation analysis in cycles treated with hMG indicates that both the follicular diameter and E2 are required for optimal timing of human chorionic gonadotropin (hCG) administration.<br /><br />Sonographic delineation of follicle size is crucial because hCG is best administered once follicles reach 15 to 18 mm in size even in non-IVF cycles when ovulation is allowed to occur, as the LH surge is less frequent when hMG is used for stimulation. For IVF, follicles are typically aspirated when they reach 15 to 18 mm in average diameter and when the E2 level is approximately 400 pg/ml per large follicle (20). Another sonographic sign of mature follicles is the presence of low level intrafollicular echoes, as mentioned earlier. When follicles >15 mm are aspirated, oocytes are at all stages of maturity (23). Therefore one can rely on follicular diameters alone if the patient’s previous cycles and her E2 response are known.<br /><br />There is no difference in E2 production between follicles measuring 14 mm and those that are smaller, nor between follicles measuring 17 mm and those which are larger (32). The authors devised an equation to determine expected serum E2 levels depending on number and size of follicles in both ovaries. Thus the serum E2 level on the day of hCG injection is:<br /><br />E2 = 291 pg/ml + 180 (x) + 64 (y) + 18.7 (z)<br /><br />where x, y and z represent follicles measuring >17 mm, 15 to 16 mm and <14>9 mm thick) and group B (<9>300 pg/ml by day 8 of stimulation. Fast responders had their E2 levels >300 pg/ml by day 5 of stimulation. However because E2 levels can be augmented to comparable levels by increasing the dose of gonadotropins, a correlation between E2 levels and gonadotropin dose is needed. Ibrahim and co-workers (16) defined poor response in desensitization protocols as the need for 4 or more ampoules of hMG/day to induce ovulation.<br /><br />The dose of gonadotropin should not be changed as long as serial E2 levels rise between 50 and 100% every other day (32). Dirnfeld et al. (6), showed that very slow or very rapid estrogen growth rates (EGRs), calculated from the 4 days preceding oocyte aspiration in CC/hMG stimulated cycles, were associated with a reduced pregnancy rate. EGRs of 0.31 to 0.41 were associated with optimal pregnancy rates. EGR is calculated by the formula:<br /><br />EGR = e-B -1<br /><br />where B is the slope of the least square line corresponding to the semilogarithmic plot of E2 values versus time and e = 2.718.<br /><br />Using GnRHa and gonadotropin in a desensitization protocol, the ovarian response was evaluated in terms of E2 levels on the day of hCG injection, and 36 hours later at egg retrieval (23). Low responders, medium responders and high responders were those with E2 levels of <800>1500 pg/ml respectively on the day of hCG injection or <400>1000 pg/ml respectively at egg retrieval. There were no differences between the three groups in respect to development of mature oocytes and rapidly cleaving embryos. The pregnancy rate in the low responding group, however, was significantly lower than in the other two groups, despite replacement of an equivalent number of oocytes and cleaving embryos. Thus it seems that the receptivity of the endometrium depends at least partially on adequate E2 levels. It also seems that E2 levels do not directly correlate with oocyte maturity and embryonic growth.<br /><br />An upper limit of estradiol of 3800 pg/ml for anovulatory women (with polycystic ovaries) and 2400 for women with hypothalamic amenorrhea produces a risk of severe hyperstimulation of 5% in pregnant cycles and 1% in non conceptional cycles (14).<br /><br />Paltieli and colleagues (28) found that in hMG cycles in which ovulation was triggered by using hCG injections, at least 80% of pregnancies were achieved when the E2 rise (active phase) was 6±1 days, whereas only 15% of pregnancies were achieved when the active phase was >7 days. They attributed the high incidence of early abortion, when the active phase was >7 days, to be an expression of oocyte overexposure to hMG prior to hCG injection. Such overexposure may result in postmature oocytes and end in early abortion. The same group of investigators noted also that in good outcome cycles, E2 continued to rise until hCG was administered, but in nonpregnant cycles, E2 plateaued on the day before hCG administration, which suggests that luteinization or atresia of the more advanced follicles had commenced spontaneously.<br /><br />Monitoring special situations<br /><br />CC/hMG protocols<br /><br />Although adequate follicular development occurs with CC and hMG combination regimen, it is thought that one problem with that regimen is premature luteinization (13). In general, it is believed that the rise in serum progesterone occurs 12 hours before or on the day of the onset of a spontaneous LH surge in a natural cycle, or in a controlled ovarian hyperstimulation for IVF-ET program (36). Fleming and Coutts (10) defined the criteria for premature luteinization to be: serum progesterone >1.5 ng/ml associated with a rise in serum LH concentration before maturation of the developing follicles, together with a decline or plateauing of the serum E2 concentration despite continued hMG administration. However, there were reports that a significant rise in serum progesterone occurs in advance of the onset of the LH surge in regimens using a combination of CC and hMG (30).<br /><br />In 1992, Mio and colleagues (24) defined " subtle progesterone rise " as a fluctuation in the serum progesterone concentration of between 1 and 2 ng/ml from day 7 of the cycle until 24 hours before the hCG administration, or the onset of the LH surge. This is not coupled with a significant increase in the serum LH concentration, defined as an increase of <100%>17-18 mm in diameter. Patients with poor follicular development or with only one developing follicle are not given hCG. It is inadvisable to give hCG to patients in whom the serum estradiol level is seen to increase rapidly (i.e. doubling in 24 hours) in order to minimize the risk of the OHSS.<br /><br />Just prior to hCG injection, a serum LH can be drawn and compared to values earlier in the cycle. This helps to identify women who have initiated a premature LH surge (LH value 2.5 times baseline). However, without frequent sampling of LH (every 3 hours), the onset of the surge cannot be identified with precision (33). LH sampling is not required in patients who are treated with GnRHa. If a spontaneous LH surge occurs in a stimulated cycle, some centres cancel the treatment cycle, whereas others give hCG if there is a satisfactory estradiol response and adequate follicular growth has taken place (37). In these cases, it is necessary to adjust the timing of oocyte recovery.<br /><br />As a general rule, hyperstimulation is associated with the presence of many follicles. It is advisable that hCG not be administered if there are more than 3-4 follicles of 14 mm or more in diameter (33). Mild hyperstimulation has been associated with an increased number of intermediate size follicles and severe hyperstimulation with an increase in small follicles (2). A large number (11 or more) of small follicles should also preclude hCG administration.<br /><br />Check and colleagues (4) used hCG to trigger ovulation in their patients in whom ovulation was induced by hMG. The timing of injection of hCG was influenced by the serum progesterone level as follows: if the serum progesterone was >1.8 ng/ml, then 10,000 units of hCG would be given as long as there was at least one dominant follicle with serum estradiol >200 pg/ml, even if multiple follicles were present and the serum estradiol was <200>25 mIU/ml is diagnostic and is confirmed by a rising titre 3 days later. When pregnancy is diagnosed, it may be necessary to support it by exogenous hCG administration until 12 weeks gestation. The diagnosis of a clinical pregnancy is made when one or more gestational sacs can be identified by ultrasound image 4 to 6 weeks after oocyte retrieval. Embryonic viability is diagnosed when the heart beats can be detected on the screen.<br /><br />This is not the whole story. Pregnant patients still need close follow-up and special care in relation to an expensive precious pregnancy until after labour and delivery.<br /><br />References<br /><br />Belaisch-Allart, J., Testart, J., and Frydman, R. (1989): Hum. Reprod., 4:33-34.<br />Blankstein, J., Shalev, J., Saadon, T., Kukia, E.E., Rabinovici, J., Pariente, C., Lunenfeld, B., Serr, D.M., and Mashiach, S. (1987): Fertil. Steril., 47:597-602.<br />Channing, C.P., Kammerman, S. (1974): Biol. Reprod.,10:179-198.<br />Check, J.H., Adelson, H.G., Stern, J., and Lauer, C. (1992): Int. J. Fertil., 37:103-105.<br />deCrespigny, L., Cooper, D., and McKenna, M. (1988): J. Ultrasound Med., 7:7-10.<br />Dirnfeld, M., Lejeune, B., Camus, M., Vekemans, M., and Leroy, F. (1985): Fertil. Steril., 43:379-384.<br />Fakih, H., and Bello, S. (1992): Fertil. Steril., 58:829-832.<br />Farine, D., Dor, J., Lupovici, N., Lunenfeld, B., and Mashiach, S. (1985): Obstet. Gynecol., 65:658-660.<br />Fleischer, A.C., Daniell, J.F., Rodier, J., Lindsay, A.M., and James, A.E. (1981): J. Clin. Ultrasound, 9:275-280.<br />Fleming, R., and Coutts, J.R.T. (1986): Fertil. Steril., 45:226-230.<br />Forrest, T.S., Elyadereni, M.K., Muilenburg, M.I., Bewtra, C., Koble, W.T., and Sullivan, P. (1988): Radiology, 167:233-237.<br />Fossum, G.T., Vermesh, M., and Kletzky, O.A. (1990):Obstet. Gynecol., 75:407-411.<br />Hamori, M., Stuckensen, J.A., Rumpf, D., Kniewald, T., Kniewald, A., and Kurz, C.S. (1987): Hum. Reprod., 2:639-643.<br />Haning, R.V. Jr., Boehnlein, L.M., Carlson, I.H., Kuzma, D.L., and Zweibel, W.J. (1984): Fertil. Steril., 42:882-889.<br />Hodgen, G.D. (1989): Hum. Reprod., 4:37-46.<br />Ibrahim, Z.H., Matson, P.L., Puck, P., and Lieberman, B.A. (1991): Fertil. Steril., 55:202-204.<br />Kamrava, M.M., Seibel, M.M., Berger, M.J., Thompson, I., and Taymor, M.L. (1982): Fertil. Steril., 37:520-523.<br />Laufer, N., Reich, R., Braw, R., Shenker, J.G., and Tsafriri, A. (1982): Biol. Reprod., 27:463-470.<br />Leeton, J., Trounson, A., and Jessup, D. (1985): J. In Vitro Fert. Embryo Transf., 2:166-169.<br />Marrs, R.P., Vargyas, J.M., and March, C.M. (1983): Am. J. Obstet. Gynecol., 145:417-421.<br />Marut, E.L., and Hodgen, G.D. (1982): Fertil. Steril., 38:100-104.<br />McFaul, P.B., Traub, A.I., and Thompson, W. (1989): Acta Eur. Fertil., 20:157-161.<br />Mettler, L., and Tavmergen, E.N. (1989): Hum. Reprod., 4:59-64.<br />Mio, Y., Sekijima, A., Iwabe, T., Onohara, Y., Harada, T., and Terakawa, N. (1992): Fertil. Steril., 58:159-166.<br />Mizunuma, H., Andoh, K., Yamada, K., Takagi, T., Kamijo, T., and Ibuki, Y. (1992): Fertil. Steril., 58:46-50.<br />Muasher, S., Oehninger, S., Simonetti, S., Matta, J., Ellis, L.M., Liu, H.C., Jones, G.S., and Rosenwaks, Z. (1988): Fertil. Steril., 50:298-307.<br />Navot, D., Rosenwaks, Z., and Margalioth, E.J. (1987): Lancet, 2:645-647.<br />Paltieli, Y., Tal, J., Porat, N., Tesler, B., Abramovici, D., and Sharf, M. (1991): Int. J. Fertil., 36:94-98.<br />Schenken, R.S., and Hodgen, G.D. (1983): J. Clin. Endocrinol. Metab., 57:50-55.<br />Serafini, P., Stone, B., Kerin, J., Batzofin, J., Quinn, P., and Marrs, R.P. (1988): Fertil. Steril., 49:86-89.<br />Sher, G., Herbert, C., Maassarani, G., and Jacobs, M.H. (1991): Hum. Reprod., 6:232-237.<br />Silverberg, K.M., Olive, D.L., Burns, W.N., Johnson, J.V., Groff, T.R., and Schenken, R.S. (1991): Fertil. Steril., 56:296-300.<br />Speroff, L, Glass, R.H., and Kase, N.G. (1989): Clinical Gynecologic Endocrinology and Infertility, 4th ed. Williams & Wilkins, Baltimore.<br />Tanbo, T., Dale, P.O., Abyholm, T., and Stokke, K.T. (1989): Hum. Reprod., 4:647-650.<br />Tarlatizis, B.C., Laufer, N., and DeCherney, A.H. (1984): J. In Vitro Fert. Embryo Transf., 1:226-232.<br />Trounson, A.O., and Calabrese, R. (1984): J . Clin. Endocrinol . Metab., 59:1075-1080.<br />WHO, editor (1992): Recent advances in medically assisted conception. Geneva.</span></strong> </span>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com2tag:blogger.com,1999:blog-16849169.post-51178879156831895372008-11-30T05:31:00.003+08:002008-11-30T05:35:40.847+08:00Measuring estradiol levels before HCG to predict success of IVF treatment<span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>Found this article the other day while surfing the net - interesting read for those who are looking for quantitative methods to predict success rate of IVF treatment.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#66ffff;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#66ffff;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#66ffff;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#66ffff;"><strong>Association of estradiol levels on the day of hCG administration and pregnancy achievement in IVF: a systematic review Ioannis P. Kosmas, Efstratios M. Kolibianakis1 and Paul Devroey<br />Center for Reproductive Medicine, Dutch-speaking Brussels Free University, Laarbeeklaan 101, 1090 Brussels, Belgium<br />1 To whom correspondence should be addressed. Email: </strong></span><a href="mailto:stratis@easynet.be"><span style="font-family:verdana;font-size:85%;color:#66ffff;"><strong>stratis@easynet.be</strong></span></a><br /><span style="font-family:verdana;font-size:85%;color:#66ffff;"><strong>'//--><br /><br />BACKGROUND: Evaluation of the association between estradiol (E2) levels on the day of hCG administration and pregnancy achievement in IVF has so far yielded conflicting results. The purpose of the present study was to systematically review the above association in cycles down-regulated with GnRH analogues. METHODS: Literature search was performed using Medline, Embase (1978–2004) and the Cochrane Library. Additionally, references of retrieved articles were hand-searched. Only full articles published in peer-reviewed medical journals were considered for analysis. RESULTS: All the eligible studies (n=9) involved the use of GnRH agonists and were retrospective. Two studies (including 191 patients) suggested that the higher the E2 levels on the day of hCG administration, the higher the probability of pregnancy. However, five studies (including 1875 patients), did not support an association between E2 levels on the day of hCG administration and pregnancy rates. Moreover, two of the studies including (1286 patients) suggested that high E2 levels on the day of hCG administration are associated with a decreased probability of pregnancy. If we consider only studies in which criteria used for administering hCG include follicular development but not E2 levels (including 2687 patients), there is no study suggesting a positive association between E2 levels on the day of hCG administration and pregnancy achievement. CONCLUSIONS: Currently there is no high-quality evidence to support or deny the value of E2 determination on the day of hCG administration for pregnancy achievement in IVF cycles, where pituitary down-regulation is performed with GnRH agonists. Existing retrospective studies suggest that there is no positive association. However, in order to arrive at recommendations for clinical practice, there is a need to perform well-designed prospective studies in both agonist and antagonist cycles.<br />Key words: estradiol/GnRH agonist/IVF/pregnancy rate</strong></span>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com0tag:blogger.com,1999:blog-16849169.post-50720214762007854992008-11-13T08:22:00.003+08:002008-11-30T05:37:00.135+08:00Extension of lucin jabs<strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;">Wed 12 Nov 2008</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;">Did a estradiol bloodtest and scan today at 8am and was told to call back between 3pm and 4pm for the results.</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;">The results will determine whether i can start on puregon the next day or the lucrin jabs have to be extended.</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;">Time flew by as i was busy with reading up for my exams on Friday, before you know it, my mobile rang with Nurse Phua on the line.</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;">She said that i have to collect the puregon meds on Sat 22 Nov and continue with the lucrin jabs as "hormones are not properly suppressed". I ask her how did they know that by 22 Nov, hormones will bor perhaps i am just being sensitive...but .. but.. my questions still left hanging in my mind.</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;">I'm puzzled. there was no baseline test before i started on lucrin, so how did they know the hormones level is not suppressed properly? is there a fixed number that all women have to meet or is it subjective to indiv level?</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;">there is no planned bloodtest 11 days later - so how do they know that 11 days later, the hormones will be sufficiently suppressed?</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;">and how did they come up with 11 days, why not 7 days, 9 days or 12 days, it seems random to me since there is no blood test to test the level of estradoil again, how do they know that hormones will be suppressed by then?</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;">another question, does the extension of the lucrin mean that the lining of the womb will be thicker and hence reduce the success of implantation?</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;">so many questions and no answers.</span></strong>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com1tag:blogger.com,1999:blog-16849169.post-54200972847876398762008-11-05T21:05:00.003+08:002008-11-05T21:17:51.740+08:00Re start blogging again<span style="color:#cc33cc;"><strong><span style="font-family:Verdana;font-size:85%;">It has been quite some time since i last posted anything in here. In between Jan to Nov 2008, many things have occured.</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;">Milestones</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;">Feb: Quit FP after another failed FET cycle</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;">Mar: Join BMC as their centre manager</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;">May : Quit to start another FET cycle, decided to concentrate on IVF and continue my studies</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;">Jun : Accepted into 3 yr degree program, classes to start in July.</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;">Jul : FET Cycle 2 failed, started classes</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;">Aug : decide to close down online business and reconsider other options</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;">Sep : offered a couple of part time & freelance positions, but decided to re start IVF cycle</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;">Oct : started IVF Cycle 2, lucrin jabs end of Oct and accupunture @ raffles medical hospital</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;">Nov: prepare for exams, and 2nd stage of IVF: puregon</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#ff99ff;"></span></strong></span>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com1tag:blogger.com,1999:blog-16849169.post-79797740915583266512008-01-06T13:33:00.000+08:002008-01-06T14:04:09.101+08:00Life Cycle of an embroyo - From the start<strong><span style="font-family:verdana;font-size:85%;color:#66ffff;">Early Hours</span></strong><br /><strong><span style="font-family:verdana;font-size:85%;color:#ff99ff;">Fertilization begins when a sperm penetrates an oocyte (an egg) and it ends with the creation of the zygote. The fertilization process takes about 24 hours. A sperm can survive for up to 48 hours. It takes about ten hours to navigate the female productive track, moving up the vaginal canal, through the cervix, and into the fallopian tube where fertilization begins. Though 300 million sperm may enter the upper part of the vagina, only 1%, 3 million, enter the uterus.</span></strong><br /><strong><span style="font-family:verdana;font-size:85%;"></span></strong><br /><strong><span style="font-family:verdana;font-size:85%;color:#66ffff;">At 6 hours</span></strong><br /><strong><span style="font-family:verdana;font-size:85%;color:#ff99ff;">The sperm must make the penetration of the zona pellucida, a tough membrane surrounding the oocyte. Only one sperm needs to bind with the protein receptors in the zona pellucida to trigger an enzyme reaction allowing the zona to be pierced. Penetration of the zona pellucida takes about twenty minutes.</span></strong><br /><strong><span style="font-family:verdana;font-size:85%;"></span></strong><br /><strong><span style="font-family:verdana;font-size:85%;color:#66ffff;">At 1 - 5 days</span></strong><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>Within 11 hours following fertilization, the oocyte has extruded a polar body with its excess chromosomes. The fusion of the oocyte and sperm nuclei marks the creation of the zygote and the end of fertilization. The zygote now begins to cleave, with each division occurring into two cells called blastomeres. The zygote's first cell division begins a series of divisions, with each division occurring approximately every twenty hours. Each blastomere within the zona pellucida becomes smaller and smaller with each subsequent division. When cell division ungenerated about sixteen cells, the zygote becomes a morula (mulberry shaped). It leaves the fallopian tube and enters the uterine cavity three to four days after fertilization.</strong></span><br /><br /><span style="font-family:verdana;font-size:85%;color:#33ffff;"><strong>At 6 days</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>The blastocyst hatches from the zona pellucida around the sixth day after fertilization, as the blastocyst enters the uterus. The trophoblast cells secretes an enzyme which erodes the epithelial uterine lining and creates an implantation site for the blastocyst.In a cyclical process of hormonal stimulation, the ovary is induced to continue producing progesterone while human chorionic gonadotropin (hCG) is released by the trophoblast cells of the implanting blastocyst. Endometrial glands in the uterus enlarge in response to the blastocyst and the implantation site becomes swollen with new capillaries. Circulation begins - a process needed for the continuation of pregnancy.</strong></span><br /><strong></strong><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>At 12 days</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>Trophoblast cells engulf and destroy cells of the uterine lining creating blood pools, both stimulating new capillaries to grow and foretelling the growth of the placenta. The inner cell mass divides, rapidly forming a two-layered disc. The top layer of cells will become the embryo and amniotic cavity, while the lower cells will become the yolk sac. Ectopic pregnancies can occur at this time and sometimes continue for up to 16 weeks of pregnancy before being noticed. Diagnosed quickly, ectopic pregnancies can be treated pharmacologically without surgery, reducing danger to the mother, and preserving the site of the ectopic pregnancy.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>At 15 - 18 days</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>The formation of blood and blood vessels of the embryo begins. The blood system appears first in the area of the placenta surrounding the embryo, while the yolk sac begins to produce hematopoietic or non-nucleated blood cells. The embryo is attached by a connecting stalk (which will later become part of the umbilical cord), to the developing placenta. A narrow line of cells appears on the surface of the embryonic disc. This primitive streak is the future axis of the embryo and it marks the beginning of gastrulation, a process that gives rise to all three layers of the embryo: ectoderm, mesoderm and endoderm.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>At 19 - days</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>The embryonic area is now shaped like a pear, and the head region is broader than the tail end. The ectoderm has thickened to form the neural plate. The edges of this plate rise and form a concave area known as the neural groove. This groove is the precursor of the embryo's nervous system and it is one of the first organs to develop. The blood cells of the embryo are already developed and they begin to form channels along the epithelial cells which form consecutively with the blood cells</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>at 21 days</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>If you could look at the embryo from a top view, it would resemble the sole of a shoe with the head end wider than the tail end, and a slightly narrowed middle. Somites, which are condensations composed of mesoderm, appear on either side of the neural groove. The first pair of somites appear at the tail and progress to the middle. One to three pairs of somites are present. Every ridge, bump and recess now indicates cellular differentiation. A head fold rises on either side of the primitive streak. The primitive streak now runs between one-fourth to one-third of the length of the embryo. Secondary blood vessels now appear in the chorion/placenta. Hematopoietic cells appear on the yolk sac simultaneously with endothelial cells that will form blood vessels for the newly emerging blood cells. Endocardial (muscle) cells begin to fuse and form into the early embryo's two heart tubes.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>at 23 - 26 days</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>Rapid growth and change as the embryo becomes longer and the yolk sac expands. On each side of the neural tube, between four and twelve pairs of somites can exist by the end of this stage. The cells which become the eyes appear as thickened circles just off of the neural folds. The cells of the ears are also present. Neural folds are rising and fusing at several points along the length of the neural tube concomitant with the budding somites which appear to zipper the neural tube closed. Neural crest cells will eventually contribute to the skull and face of the embryo. The two endocardial tubes formed in before fuse here to form one single tube derived from the roof of the nueral tube, which becomes S-shaped and makes the primitive heart asymmetric. As the S-shape forms, cardiac muscle contraction begins.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>at 28 - 31 days</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>Thirteen to twenty pairs of somites are present and the embryo is shaped in a modified S curve. The embryo has a bulb-like tail and a connecting stalk to the developing placenta. A primitive S-shaped tubal heart is beating and peristalsis, the rhythmic flow propelling fluids throughout the body, begins. However, this is not true circulation because blood vesel development is still incomplete. At this stage, the neural tube determines the form of the embryo. Although the primary blood vessels along the central nervous system are connecting, the central nervous system appears to be the most developed system. If twenty somites are present in the embryo, the forebrain is completely closed.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>at 32 days</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>The brain differentiates into the three main parts: the forebrain, midbrain and hindbrain. The forebrain consists of lobes that translate input from the senses, and will be responsible for memory formation, thinking, reasoning, problem solving. The midbrain will serve as a relay station, coordinating messages to their final destination. The hindbrain will be responsible for regulating the heart, breathing and muscle movements.Thyroid continues to develop and the lymphatic system, which filters out bacteria, starts to form. Otic placode invaginates and forms the otic vesicle, which will develop into the structures needed for hearing and maintenance of equilibrium. Retinal disc presses outward and touches the surface ectoderm. In response the ectoderm proliferates forming the lens disc. Specific parts of the eye, such as the retina, the future pigment of the retina and the optic stalk are identifiable. Primitive mouth with a tongue is recognizable. Thyroid continues to develop and the lymphatic system, which filters out bacteria, starts to form. Heart chambers are filled with plasma and blood cells making the heart seem distended and prominent. The heart and liver combined are equal in volume to the head by this stage. Blood circulation is well established, though true valves are not yet present.. The villous network is in place to accommodate the exchange of blood between the woman and the embryo. Aortic arches 4 and 6 develop and 5 may appear. Lung buds continue to form. Gall bladder, stomach, intestines, pancreas continue to form and the metanephric bud appears in the chest cavity. The stomach is in the shape of a spindle and the pancreas may be detected at the intestinal tube. The developing liver receives blood from the placenta via the umbilical cord. The amnion encloses the connecting stalk helping to fuse it with the longer and more slender umbilical vesicle (the remnant of the yolk sac). Upper limb buds are visible as ridges and the lower limb buds begin to develop. Folding is complete and the embryo is now three-dimensional and is completely enclosed in the amniotic sac. The somites will be involved in building bones and muscles. The first thin surface layer of skin appears covering the embryo.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>at 35 days</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>The brain and head grow rapidly. The mandibular and hyoid arches are noticeable. Ridges demarcate the three sections of the brain (midbrain, forebrain and hindbrain). The spinal cord wall at this stage contains three zones: the ventricular, the mantle and the marginal. The ventricular zone will form neurons, glial cells and ependymal cells, the intermediate mantle will form neuron clusters and the marginal zone will contain processes of neurons. Adenohypophyseal pouch, which will develop into the anterior pituitary, is defined. Lens vesicle opens to the surface and is nestled within the otptic cup. Otic vesicle increases its size by approximately one-fourth and its endolymphatic appendage is more defined. Nasal plate can be detected by thickened ectoderm. Esophagus, the tube through which food is swallowed, forms from a groove of tissue that separates from the trachea, which is also visible. Semilunar valves begin to form in the heart. Four major subdivisions of the heart (the trabeculated left and right ventricles, the conus cords and the truncus arteriosus) are clearly defined. Two sprouts, a ventral one from the aortic sac and a dorsal one from the aorta, form the pulmonary (sixth aortic) arch. Right and left lung sacs lie on either side of the esophagus. Ureteric bud appear. Metanephros, which will eventually form the permanent kidney, is developing. Upper limbs elongate into cylindrically-shaped buds, tapering at tip to eventually form hand plate. Nerve distribution process, innervation, begins in the upper limbs.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>at 42 days</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>s the brain has increased in size by one-third since the last stage, it is still larger than the trunk. Rostral neuropore is closed and four pairs of pharyngeal arches are visible now, though the fourth one is still quite small. The maxillary and mandibular prominence of the first arch are clearly delineated. The stomodeum, the depression in the ectoderm which will develop into the mouth and oral cavity, appears between the prominent forebrain and the fused mandibular prominence.Swellings of the external ear begin to appear on both sides of the head, formed by the mandibular arch. Lens pit has closed, retinal pigment may appear in the external layer of the optic cup and lens fibers form the lens body. Two symmetrical and separate nasal pits may appear as depressions in the nasal disc. Esophagus lengthens. Blood flow through the atrioventricular canal is divided into left and right streams, which continue through the outflow tract and aortic sac. The left ventricle is larger than the right and has a thicker wall. Lobar buds appear in the bronchial tree. The intestine lengthens. Ureteric bud lengthens and its tip expands, thus beginning the formation of the final and permanent set of kidneys. Distinct regions of the handplate, forearm, arm and shoulder may be discerned in the upper limb bud. Lower limb bud begins to round at top and tip of its tapering end will eventually form the foot. Innervation, the distribution of nerves, begins in the lower limb buds. The relative width of the trunk increases from the growth of the spinal ganglia, the muscular plate and the corresponding mesenchymal tissues.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>at 44 days</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>Brain is well marked by its cerebral hemispheres. The hindbrain, which is responsible for heart regulation, breathing and muscle movements, begins to develop. Future lower jaw, the first part of face to be established, is now visible while future upper jaw is present, but not demarcated. Mesenchymal cells originating in the primitive streak, the neural crest and the prechordal plate, continue to form the skull and the face. External retina pigment is visible and the lens pit has grown into a D shape. Nasal pits are still two separate plates, but they rotate to face ventrally as head widens. Primary cardiac tube separates into aortic and pulmonary channels and the ventricular pouches deepen and enlarge, forming a common wall with their myocardial shells. Mammary gland tissue begins to mature. The mesentery, which attaches the intestines to the rear abdominal wall, holds them in position and supplies them with blood, nerves and lymphatics, is now clearly defined. Ureter, the tube that will convey urine from the kidney to the bladder, continues to lengthen. Proliferation of the coelomic epithelium indicates the gonadal primordium. Hand region of upper limb bud differentiates further to form a central carpal part and a digital plate. The thigh (rostrolateral part), leg (the caudomedial part) and foot areas can be distinguished in the lower limb buds. </strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>at 46 days</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>Jaw and facial muscles are now developing. The nasofrontal groove becomes distinct and an olfactory bulb (sense of smell) forms in the brain. Auricular (ear) hillocks become recognizable. The dental laminae or teeth buds begin to form. The pituitary, which is the master gland responsible for growth of hormones that regulate other glands, such as the thyroid, adrenal glands, gonad) begins to form.Trachea, the larynx and the bronchi begin to form. The heart begins to separate into four chambers. The diaphragm, the tissue that separates the chest cavity from the abdomen, forms. Intestines begin to develop within the umbilical cord and will later migrate into the abdomen when the embryo's body is large enough to accommodate them. Primitive germ cells arrive at the genital area and will respond to genetic instructions to develop into either female or male genitals. Digital rays in appear in the foot plates and finger rays are more distinct. Trunk becomes straighter.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>at 51 days</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ff99ff;"><strong>Nerve plexuses begin to develop in the region of the scalp. Eyes are pigmented and eyelids begin to develop and may fold. Within the heart, the trunk of the pulmonary artery separates from the trunk of the aorta. Nipples appear on the chest. Body appears more like a cube. Kidneys begin to produce urine for the first time. Genital tubercle, urogenital membrane and anal membrane appear. The critical period of arm development ends, and the arms are at their proper location, roughly proportional to the embryo. However, the hand plates are not finished, but develop further in the next two days. The wrist is clearly visible and the hands already have ridges or notches indicating the future separation of the fingers and the thumbs. Ossification of the skeleton begins.</strong></span><br /><span style="font-size:85%;"></span><br /><span style="font-size:85%;"></span><br /><span style="font-size:85%;"></span><br /><strong><span style="font-size:85%;"></span></strong><br /><span style="font-size:85%;"></span>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com1tag:blogger.com,1999:blog-16849169.post-18474601077215675562008-01-06T04:34:00.000+08:002008-01-06T04:43:27.707+08:00FET day 3<span style="font-family:verdana;font-size:85%;color:#ffccff;"><strong>After what it seems like months on OCP and progynova (oestradiol), finally got the go ahead for FET on last friday.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ffccff;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ffccff;"><strong>It took only one scan on wed to reveal that the lining is primed sufficiently at 8mm to proceed with FET in 2 days time. - a lot less hassle than a fresh cycle.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ffccff;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ffccff;"><strong>was put on cylogest suppositories but had very bad bloatededness, and some nausea. switched to im progesterone instead for luteal support. the jabs are really painful. somehow though having gone thru the same jabs for a fresh cycle, this time round, the oil based jabs are less tolerable. :(</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ffccff;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ffccff;"><strong>got to just grin and bear! perhaps it's the oestradiol acting as well, cause every pain seem to be magnified and am really super short fused. husband got the brunt of that..</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ffccff;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ffccff;"><strong>what we did different this time - we did accupunture 3 days continuously before the FET (inluding on the day of the FET itself). and am taking 14 days of twice a day sachets of some TCM powder.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ffccff;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ffccff;"><strong>also avoiding all cold water and raw food. and taking chicken essence once or twice a day. trying to drink lots of warm water.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ffccff;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ffccff;"><strong>I have good feelign about this cycle, the law of averages should be on my side this time.</strong></span><br /><strong><span style="color:#ffccff;"></span></strong><br /><strong><span style="color:#ffccff;"></span></strong>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com2tag:blogger.com,1999:blog-16849169.post-34688678452636700312007-10-13T09:41:00.000+08:002007-10-13T09:46:06.819+08:00one month later<span style="font-size:85%;">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.</span><br /><span style="font-size:85%;"></span><br /><span style="font-size:85%;">even thinking about planning a holiday...is exhaustive..i wonder what is wrong with me.</span>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com4tag:blogger.com,1999:blog-16849169.post-50893529907478320392007-09-10T14:03:00.000+08:002007-09-10T14:11:13.204+08:00Post IVF<span style="font-family:verdana;font-size:85%;">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.</span><br /><span style="font-family:verdana;font-size:85%;"></span><br /><span style="font-family:Verdana;font-size:85%;">i thought i was coping well with the failure. </span><br /><span style="font-family:Verdana;font-size:85%;"></span><span style="font-family:Verdana;font-size:85%;"></span><br /><span style="font-family:verdana;font-size:85%;">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. </span><br /><span style="font-family:verdana;font-size:85%;"></span><br /><span style="font-family:verdana;font-size:85%;">Just why not me?</span><br /><span style="font-family:Verdana;font-size:85%;"></span><br /><span style="font-family:Verdana;font-size:85%;">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.</span><br /><span style="font-family:Verdana;font-size:85%;"></span><br /><br /><span style="font-family:Verdana;font-size:85%;"></span><br /><span style="font-family:Verdana;font-size:85%;"></span>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com4tag:blogger.com,1999:blog-16849169.post-45703301375012379612007-08-23T11:09:00.000+08:002007-08-23T11:24:31.000+08:00negative - THE END<span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>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?</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>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'</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>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.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>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?</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>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'</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>that answers everything.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>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. </strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>total of 7 fertlised embroyos with 3 at grade 4 and treated with ICSI which was transferred this cycle.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>The balance of 4 embroyos are frozen and mostly grade 3.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>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.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>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.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>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.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>why did this cycle fail?</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>there is no specific reason. we can do only so much, the rest is still unexplained medically.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>will the next cycle work?</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>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!</strong></span><br /><span style="font-family:Verdana;font-size:85%;"></span><br /><span style="font-family:Verdana;font-size:85%;"></span><br /><span style="font-family:Verdana;font-size:85%;"></span>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com0tag:blogger.com,1999:blog-16849169.post-56309292403300770142007-08-23T11:06:00.000+08:002007-08-23T11:07:44.430+08:00Article in ST<span style="font-family:verdana;font-size:85%;color:#cccccc;"><strong>Fertility clinics must disclose success rates by Andy HoThe Straits Times31 July 2007<br />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.<br />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.<br />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.<br />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.<br />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.<br />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.<br />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.<br />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.<br />And while Parliament is at it, it might also consider another issue, that is, how to regulate the sector.<br />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.<br />Most couples go through much pain for many years before they attain success, but many do not get that far.<br />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.<br />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.<br />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.<br />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.<br />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.<br />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.<br />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.<br />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.<br />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.<br />What to do?<br />We should pass a law to require service providers to disclose their success rates, specifying also how success-rate statistics are to be presented.<br />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.)<br />The provider must also break down its data by age groups, since success rates drop as women age.<br />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.</strong></span>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com0tag:blogger.com,1999:blog-16849169.post-8714691572913431482007-08-19T18:59:00.000+08:002007-08-19T19:00:39.104+08:00Implications of Blastocyst transfers<span style="font-family:verdana;font-size:85%;color:#ffff66;"><strong>FEWER RISKS, NEW HOPE:<br />THE REALITY OF BLASTOCYST TRANSFERS<br />Mark Perloe, M.D.<br />Michael John Tucker, Ph.D.<br /><br />Introduction<br />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.<br /><br />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.<br /><br />The Significance of Blastocyst Transfer<br />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.<br /><br />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.<br /><br />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.<br /><br />What is 1 Blastocyst?<br />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.<br /><br />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.<br /><br />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.<br /><br />Getting to Day Five<br />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.<br /><br />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.<br /><br />Redefining Developmental Potential<br />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.<br /><br />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.<br /><br />Who Does it Help?<br />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.<br /><br />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.<br /><br />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.<br /><br />Maternal Age and Blastocyst Development<br />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.<br /><br />What Happens When Embryos Do Not Become Blastocysts?<br />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.<br /><br />Genetic Testing And Blastocysts<br />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.<br /><br />Frozen Blastocyst Cycles<br />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."<br /><br />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.<br /><br />The Future<br />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.<br /></strong></span>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com1tag:blogger.com,1999:blog-16849169.post-58816249250983161762007-08-15T06:43:00.000+08:002007-08-15T06:44:20.548+08:00trigger shot and HPT<span style="font-family:verdana;font-size:85%;color:#ffffcc;"><strong>How long does it take synthetic hCG (trigger shot) to leave my body before I can test for pregnancy? </strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ffffcc;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#ffffcc;"><strong>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.<br />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. </strong></span>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com1tag:blogger.com,1999:blog-16849169.post-18886366832604272242007-08-14T09:42:00.000+08:002007-08-14T09:49:36.656+08:007 days post embryo transfer [7DPET]<span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>Tuesday 14 August 2007</strong></span><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;"></span></strong><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>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.</strong></span><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;">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. </span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;">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.</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;">i read somewhere that the earliest one can test for HPT is 10DPET - can't wait to rec the strips HPT i bought online.</span></strong>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com0tag:blogger.com,1999:blog-16849169.post-59708796811338969842007-08-14T09:40:00.000+08:002007-08-14T09:58:52.409+08:00painful ER, drama ET, hospitalised<span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>Wednesday 8 August 2007</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>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. </strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>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. </strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>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. </strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>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. </strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong>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.</strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong></strong></span><br /><span style="font-family:verdana;font-size:85%;color:#cc33cc;"><strong> 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.</strong></span>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com0tag:blogger.com,1999:blog-16849169.post-978913698622086302007-08-14T09:38:00.000+08:002007-08-14T09:40:03.774+08:00My love will get you home - Christine Glass<span style="font-family:verdana;font-size:85%;color:#66ffff;"><strong>If you wander off too far, my love will get you home.<br />If you follow the wrong star, my love will get you home.<br />If you ever find yourself, lost and all alone,<br />get back on your feet and think of me, my love will get you home.<br />Boy, my love will get you home.<br />If the bright lights blinds your eyes, my love will get you home.<br />If your troubles break your stride, my love will get you home.<br />If you ever find yourself, lost and all alone,<br />get back on your feet and think of me, my love will get you home.<br />Boy, my love will get you home.<br />If you ever feel ashamed, my love will get you home.<br />When there's only you to blame, my love will get you home.<br />If you ever find yourself, lost and all alone,<br />get back on your feet and think of me, my love will get you home.<br />Boy, my love will get you home.<br />If you ever find yourself, lost and all alone,<br />get back on your feet and think of me, my love will get you home.<br />Boy, my love will get you home,<br />Boy, my love will get you home.</strong></span>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com0tag:blogger.com,1999:blog-16849169.post-55025811730304161612007-08-11T09:48:00.000+08:002007-08-11T09:49:35.066+08:00When does implantation happen in IVF?<span style="font-family:verdana;font-size:85%;color:#ffff00;"><strong>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)</strong></span><br /><br /><span style="font-family:verdana;font-size:85%;color:#ffff00;"><strong>A very good study of implantation was published in 1992 by Bergh & Navot.<br />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.<br />Average first detection was at an embryonic age of 7.1 +/- 0.28 days (range 6.6-7.4 days).<br />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.<br />They did not find any evidence to support the concept of an embryonic diapause in humans. </strong></span>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com0tag:blogger.com,1999:blog-16849169.post-51831800543712384472007-08-03T21:10:00.000+08:002007-08-03T21:14:26.454+08:00IVF - Puregon - 2nd scan<strong><span style="font-family:verdana;font-size:85%;color:#cc33cc;">Friday 03 Aug 2007</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;">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</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;">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.</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;"></span></strong>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com0tag:blogger.com,1999:blog-16849169.post-68035149372616075592007-08-01T22:04:00.000+08:002007-08-01T22:09:10.455+08:00IVF - 1st scan after stimulation<strong><span style="font-family:verdana;font-size:85%;color:#cc33cc;">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.</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;">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.</span></strong>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com0tag:blogger.com,1999:blog-16849169.post-13794600569088707432007-07-26T11:07:00.001+08:002007-07-26T11:09:05.624+08:00Costing of IVF<strong><span style="font-family:verdana;font-size:85%;color:#ff9966;">i'm supposed to do a costing here but never got round to doing it.</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#ff9966;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#ff9966;">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.</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#ff9966;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#ff9966;">will do a break down later.</span></strong>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com0tag:blogger.com,1999:blog-16849169.post-49575345878113447352007-07-26T11:02:00.000+08:002007-07-26T11:06:43.102+08:00Start of Puregon stage<strong><span style="font-size:85%;color:#cc33cc;">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.</span></strong><br /><strong><span style="font-size:85%;color:#cc33cc;"></span></strong><br /><strong><span style="font-size:85%;color:#cc33cc;">in the meantime, suppose to continue with lucrin as well, that means 2 jabs every morning. oh great!</span></strong><br /><strong><span style="font-size:85%;color:#cc33cc;"></span></strong><br /><strong><span style="font-size:85%;color:#cc33cc;">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.</span></strong><br /><strong><span style="font-size:85%;color:#cc33cc;"></span></strong><br /><strong><span style="font-size:85%;color:#cc33cc;">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.</span></strong>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com0tag:blogger.com,1999:blog-16849169.post-58164773622306129922007-07-22T10:32:00.000+08:002007-07-22T10:39:14.280+08:00Am i doing too much?<strong><span style="font-family:verdana;font-size:85%;color:#cc33cc;">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...</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;">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.</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;"></span></strong>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com0tag:blogger.com,1999:blog-16849169.post-7199990615528134622007-07-18T22:09:00.000+08:002007-07-18T22:10:56.635+08:00Lucrin or Lupron as called in the US<span style="font-family:verdana;font-size:85%;color:#66ff99;"><strong>Clinical Policy Bulletin:Gonadotropin-Releasing Hormone Analogs (Lupron/Zoladex) and Antagonists (Plenaxis)<br /><br /><br />Number: 0501<br />Policy<br />Lupron<br />Aetna considers Lupron (leuprolide) medically necessary for the following indications subject to the specified limitations:<br />Endometriosis (see appendix)<br />To decrease fibroid size prior to surgery (see appendix).<br />To decrease endometrial thickness prior to endometrial ablation (see appendix).<br />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).<br />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).<br />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).<br />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).<br />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).<br />For the treatment of women with chronic refractory pelvic pain (see appendix).<br />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:<br />Precocious pubarche alone, or pseudoprecocious puberty (gonadotropin independent precocious puberty); or<br />Polycystic ovarian disease; or<br />Pre-menstrual syndrome; or<br />Endometrial cance; or<br />Ovarian cancer; or<br />Preservation (suppression) of ovarian function during chemotherapy; or<br />Preservation (suppression) of testicular function during chemotherapy.<br />Zoladex<br />Aetna considers Zoladex (goserelin) medically necessary for any of the following indications:<br />Advanced (metastatic) prostatic carcinoma; or<br />Advanced (metastatic) breast cancer in pre-menopausal members; or<br />Endometriosis, Stage III or IV; or<br />Uterine fibroids (leiomyoma uteri) (preoperative adjunct to surgical treatment) (short-term (less than 6 months) use); or<br />Endometrial ablation or hysterectomy (preoperative adjunct) (short-term (less than 6 months) use). (See also </strong></span><a href="http://www.aetna.com/cpb/medical/data/1_99/0091.html" target="_blank"><span style="font-family:verdana;font-size:85%;color:#66ff99;"><strong>CPB 091 - Endometrial Ablation</strong></span></a><span style="font-family:verdana;font-size:85%;color:#66ff99;"><strong>.)<br />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.<br />Plenaxis<br />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.<br />For gonadotropin-releasing hormone antagonists for infertility, see </strong></span><a href="http://www.aetna.com/cpb/medical/data/300_399/0327.html" target="_blank"><span style="font-family:verdana;font-size:85%;color:#66ff99;"><strong>CPB 327 - Infertility</strong></span></a><strong><span style="color:#33ff33;"><span style="font-family:verdana;font-size:85%;color:#66ff99;">.<br />Background<br />Lupron:<br />Leuprolide (Lupron) is a gonadotropin-releasing hormone analog, which may be indicated for treatment of certain conditions, which are hormonally regulated.<br />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.<br />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.<br />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.<br />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).<br />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.<br />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.<br />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.<br />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.<br />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.”<br />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.”<br />Zoladex:<br />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.<br />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.<br />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).<br />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).<br />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.<br />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.<br />Plenaxis:<br />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.<br />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.<br />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.<br />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.<br /><br />Appendix<br />Medically Necessary Indications for Lupron<br />Limitations<br />Endometriosis<br />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.<br />Lupron dosages greater than 3.75 mg per month or 11.25 mg per 3 months are subject to medical necessity review.<br />To decrease fibroid size prior to surgery<br />Up to three months - under accepted guidelines, does not prevent or replace the eventual need for surgery except in peri-menopausal women.<br />Lupron dosages greater than 3.75 mg per month or 11.25 mg per 3 months are subject to medical necessity review.<br />To decrease endometrial thickness prior to endometrial ablation<br />Up to two months.<br />Lupron dosages greater than 3.75 mg per month or 11.25 mg per 3 months are subject to medical necessity review.<br />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<br />1 mg given subcutaneously daily. If receiving leuprolide acetate suspension (Lupron Depot), dosing is 7.5 mg IM once monthly.<br />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<br />Lupron Depot Ped: 0.3 mg/kg every four weeks (minimum 7.5 mg).<br />Lupron injection: 50 mcg/kg daily. It may be medically necessary to titrate dosages upwards in order to achieve hormonal down-regulation.<br />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<br />Note: Treatment of infertility may be subject to specific limitations under some benefit plans. Most HMO plans exclude injectable infertility drugs from coverage.<br />For treatment of metastatic breast cancer<br />Indicated where member is pre-menopausal and the disease has progressed or recurred after a trial of at least 3 months of tamoxifen<br />To suppress onset of puberty in adolescents with early onset of puberty on growth hormone therapy<br />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)<br />For the treatment of women with chronic refractory pelvic pain<br />Indicated where attempts at medical therapy with analgesics and oral contraceptive have been unsuccessful.<br /><br />CPT Codes / HCPCS Codes / ICD-9 Codes<br />Lupron (suspension and implant):<br />HCPCS codes covered if selection criteria are met:<br />J1950<br />Injection leuprolide acetate (for depot suspension), per 3.75 mg<br />J9217<br />Leuprolide acetate (for depot suspension), 7.5 mg<br />J9219<br />Leuprolide acetate implant, 65 mg<br />ICD-9 codes covered if selection criteria are met:<br />174.0 - 175.9<br />Malignant neoplasm of breast<br />185<br />Malignant neoplasm of prostate<br />218.0 - 218.9<br />Uterine leiomyoma<br />233.0<br />Carcinoma in situ of breast<br />233.4<br />Carcinoma in situ of prostate<br />259.1<br />Precocious sexual development and puberty, not elsewhere classified<br />617.0 - 617.9<br />Endometriosis<br />Lupron prior to endometrial ablation (see CPB 91):<br />ICD-9 codes covered if selection criteria are met:<br />626.2<br />Excessive or frequent menstruation<br />626.3<br />Puberty bleeding<br />627.0<br />Premenopausal menorrhagia<br />627.1<br />Postmenopausal bleeding<br />2 week Lupron kit:<br />HCPCS codes covered if selection criteria are met:<br />J9218<br />Leuprolide acetate, per 1 mg<br />Other HCPCS codes related to the CPB:<br />J3355<br />Injection, urofollitropin, 75 IU<br />S0122<br />Injection, menotropins, 75 IU<br />S0187<br />Tamoxifen citrate, oral, 10 mg<br />ICD-9 codes covered if selection criteria are met:<br />185<br />Malignant neoplasm of prostate<br />233.4<br />Carcinoma in situ of prostate<br />259.1<br />Precocious sexual development and puberty, not elsewhere classified<br />628.0 - 628.9<br />Infertility, female<br />ICD-9 codes not covered for indications listed in the CPB:<br />140.0 - 239.9<br />Neoplasms [when used for preservation of ovarian or testicular function during chemotherapy]<br />182.0<br />Malignant neoplasm of corpus uteri, except isthmus<br />183.0<br />Malignant neoplasm of ovary<br />198.6<br />Secondary malignant neoplasm of ovary<br />218.0 - 218.9<br />Uterine leiomyoma<br />256.4<br />Polycystic ovaries<br />625.4<br />Premenstrual tension syndromes<br />V58.11 - V58.12<br />Encounter for antineoplastic chemotherapy and immunotherapy [when used for preservation of ovarian or testicular function during chemotherapy]<br />Zoladex (Goserelin):<br />HCPCS codes covered if selection criteria are met:<br />J9202<br />Goserelin acetate implant, per 3.6 mg<br />ICD-9 codes covered if selection criteria are met:<br />174.0 - 175.9<br />Malignant neoplasm of breast<br />185<br />Malignant neoplasm of prostate<br />218.0 - 218.9<br />Uterine leiomyoma<br />233.0<br />Carcinoma in situ of breast<br />233.4<br />Carcinoma in situ of prostate<br />617.0 - 617.9<br />Endometriosis<br />625.3<br />Dysmenorrhea<br />628.0 - 628.9<br />Infertility, female<br />Zoladex prior to endometrial ablation (see CPB 91):<br />ICD-9 codes covered if selection criteria are met:<br />626.2<br />Excessive or frequent menstruation<br />626.3<br />Puberty bleeding<br />627.0<br />Premenopausal menorrhagia<br />627.1<br />Postmenopausal bleeding<br />ICD-9 codes not covered for indications listed in the CPB:<br />140.0 - 239.9<br />Neoplasms [when used for preservation of ovarian or testicular function during chemotherapy]<br />V58.11 - V58.12<br />Encounter for antineoplastic chemotherapy and immunotherapy [when used for preservation of ovarian or testicular function during chemotherapy]<br />Plenaxis (abarelix):<br />Other CPT codes related to the CPB:<br />54520 - 54535, 54690<br />HCPCS codes covered if selection criteria are met:<br />C9216<br />Injection, Abarelix for injectable suspension, per 10 mg (deleted 12-31-04)<br />J0128<br />Injection, abarelix, 10 mg<br />ICD-9 codes covered if selection criteria are met:<br />185<br />Malignant neoplasm of prostate<br />Other ICD-9 codes related to the CPB for Lupron, Zoladex, and Plenaxis:<br />253.3<br />Pituitary dwarfism<br />625.8 - 625.9<br />Other and unspecified symptoms associated with female genital organs<br />V58.11 - V58.12<br />Encounter for antineoplastic chemotherapy and immunotherapy<br />V66.0<br />Convalescence and palliative care following surgery<br />V66.1<br />Convalescence and palliative care following radiotherapy<br />V66.2<br />Convalescence and palliative care following chemotherapy<br />V66.7<br />Encounter for palliative care The above policy is based on the following references:<br />Lupron:<br />Olin BR, ed. Drug Facts and Comparisons. St. Louis, MO: JB Lippincott Company; 1992.<br />Conn MP, Crowley WF. Gonadotropin-releasing hormone and its analogues. N Engl J Med. 1991;324(2):93-103.<br />Higham JM. The medical management of menorrhagia. Br J Hosp Med. 1991;45:19-21.<br />Schriock ED. Practical aspects of pulsatile gonadotropin-releasing hormone administration. Am J Obstet Gynecol. 1990;163(5):1765-1770.<br />Gompel A, Mauvais-Jarvis P. Induction of ovulation with pulsatile GnRH in hypothalamic amenorrhoea. Hum Reprod. 1988;3(4):473-477.<br />Macdonald R. Modern treatment of menorrhagia. Br J Obstet Gynecol. 1990;97:3-7.<br />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.<br />Adamson GD. Treatment of uterine fibroids: Current findings with gonadotropin-releasing hormone agonists. Am J Obstet Gynecol. 1992;166(2):746-751.<br />Brooks PG, Serden SP. Preparation of the endometrium for ablation with a single dose of leuprolide acetate depot. J Reprod Med. 1991;36(7):477-478.<br />Shaw RW, Fraser HM. Use of a superactive luteinizing hormone releasing hormone agonist in the treatment of menorrhagia. Br J Obstet Gynecol. 1984;91:913-916.<br />Schrlock ED. GnRH agonists. Clin Obstet Gynecol. 1989;32(3):550-563.<br />Hodgen GD. General applications of GnRH agonists in gynecology: Past, present and future. Obstet Gynecol Surv. 1989;44(5):293-296.<br />McEvoy GK, ed. American Hospital Formulary Service Drug Information 92. Bethesda, MD: American Society of Hospital Pharmacists, Inc.; 1992.<br />Bennett DR, ed. AMA Drug Evaluations Subscription. Chicago, IL: American Medical Association; Winter 1992.<br />Schrlock ED. GnRH agonists. Clin Obstet Gynecol. 1989;32(3):550-563.<br />Bucci KK, Carson DS. Contraception and infertility. In: Pharmacotherapy: A Pathophysiological Approach. JT Dipiro, RL Talbert, PE Hayes, et al, eds. Norwalk, CT: Appleton & Lange; 1993:1211-1130.<br />U.S. Pharmacopeial Convention, Inc. (USPC). USP Dispensing Information. Volume I -- Drug Information for the Healthcare Professional. 18th ed. Rockville, MD: USPC; 1998.<br />Medical Economics, Inc. Physicians' Desk Reference. 52nd ed. Montvale, NJ: Medical Economics Data Production; 1998.<br />Mosby-Year Book, Inc. Mosby's GenRx: The Complete Reference for Generic and Brand Drugs. 8th ed. St. Louis, MO: Mosby; 1998.<br />American Hospital Formulary Service (AHFS). AHFS Drug Information 98. Bethesda, MD: American Society of Health-System Pharmacists; 1998.<br />Levitsky AM. Pharmacologic treatment of hypersexuality and paraphilias in nursing home residents. J Am Geriatr Soc. 1999;47(2):231-234.<br />Vilos GA, Lefebvre G, Graves GR, et al. Guidelines for the management of abnormal uterine bleeding. SOCG Clinical Practice Guidelines No. 106. J Obstet Gynaecol Can. 2001;23(8):704-709.<br />Duckitt K. Menorrhagia. In: Clinical Evidence, Issue 9. London, UK: BMJ Publishing Group, Ltd.; June 2003.<br />Lethaby A, Hickey M. Endometrial destruction techniques for heavy menstrual bleeding. Cochrane Database Syst Rev. 2002;(2):CD001501.<br />Sowter MC, Lethaby A, Singla AA. Pre-operative endometrial thinning agents before endometrial destruction for heavy menstrual bleeding. Cochrane Database Syst Rev. 2002;(3):CD001124.<br />Rao GG, Miller DS. Hormonal therapy in epithelial ovarian cancer. Expert Rev Anticancer Ther. 2006;6(1):43-47.<br />Lee SJ, Schover LR, Partridge AH, et al. American Society of Clinical Oncology recommendations on fertility preservation in cancer patients. J Clin Oncol. 2006;24(18):2917-2931.<br />Sonmezer M, Oktay K. Fertility preservation in young women undergoing breast cancer therapy. Oncologist. 2006;11(5):422-434.<br />Precocious Puberty<br />Brenner PE. Precocious puberty in the female. In: Reproductive Endocrinology, Infertility and Contraception. DR Mishell, VC Davajan, eds. Philadelphia, PA: FA Davis Co.; 1979.<br />Partsch CJ, Sippell WG. Treatment of central precocious puberty. Best Pract Res Clin Endocrinol Metab. 2002;16(1):165-189.<br />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.<br />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.<br />Pelvic Pain<br />ACOG Committee on Practice Bulletins -- Gynecology. ACOG Practice Bulletin No. 51. Chronic pelvic pain. Obstet Gynecol. 2004;103(3):589-605.<br />Royal College of Obstetricians and Gynaecologists (RCOG). The initial management of chronic pelvic pain. RCOG Guideline No. 41. London, UK: RCOG; April 2005.<br />Infertility<br />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.<br />Al-Inany H, Aboulghar M. Gonadotrophin-releasing hormone antagonists for assisted conception. Cochrane Database Syst Rev. 2001;(4):CD001750.<br />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.<br />Prostate cancer<br />Wojciechowski NJ, Carter CA, Skoutakis VA, et al. Leuprolide: A gonadotropin-releasing hormone analog for the palliative treatment of prostate cancer. Drug Intell Clin Pharm. 1986;20:746-751.<br />Debruyne F. Hormonal therapy of prostate cancer. Semin Urol Oncol. 2002;20(3 Suppl 1):4-9.<br />National Institutes of Health. The management of clinically localized prostate cancer. National Institutes of Health Consensus Development Conference 1987 June 15-17. NCI Monogr. 1988;(7):1-174.<br />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.<br />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.<br />Prostate Cancer Trialists' Collaborative Group. Maximum androgen blockade in advanced prostate cancer: An overview of the randomised trials. Lancet, 2000;355:1491-1498.<br />Wilt T, Nair B, MacDonald R, Rutks I. Early versus deferred androgen suppression in the treatment of advanced prostatic cancer. Cochrane Database Syst Rev. 2001;(4):CD003506.<br />Schmitt B, Bennett C, Seidenfeld J, et al. Maximal androgen blockade for advanced prostate cancer. Cochrane Database Syst Rev. 1999;(2):CD001526.<br />Leiomyomas<br />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.<br />Vollenhoven BJ. Uterine fibroids: A clinical review. Br J Obstet Gynecol. 1990;97:285-298.<br />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.<br />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.<br />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.<br />Breast cancer<br />Olin BR. Drug Facts and Comparisons. St. Louis, MO: J.B. Lippincott Company; 1992.<br />McEvoy GK, ed. Leuprolide. In: AHFS Drug Information. Bethesda, MD: American Society of Hospital Pharmacists; 1993:606-612.<br />McGuire T. Breast cancer. In: Pharmacotherapy: A Pathophysiologic Approach. 2nd ed. J Dipiro, RL Talbert, PE Hayes, et al, eds. Norwalk, CT: Appleton & Lange; 1993:1930-1945.<br />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.<br />Manni A, Santen R, Harvey H, et al. Treatment of breast cancer with gonadotropin-releasing hormone. Endocr Rev. 1986;7(1):89-94.<br />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.<br />Sunderland MC, Osborne CK. Tamoxifen in premenopausal patients with metastatic breast cancer: A review. J Clin Oncol. 1991;9(7):1283-1297.<br />No authors listed. Tamoxifen. In: Drug Evaluation Subscriptions. DR Bennett, ed. Chicago, IL: American Medical Association; 1993;5:5.<br />Endometriosis<br />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.<br />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.<br />Lemay A, Maheux R, Quesnel G, et al. LH-RH agonist treatment of endometriosis. Contr Gynec Obstet. 1987;16:247-253.<br />Souney PF, Rossiter A. Focus on naferelin acetate: GnRH agonist for the management of endometriosis. Hosp Formul. 1990;25:1041-1054..<br />Wheeler JM, Knittle JD, Miller JD. Depot leuprolide versus danazol in the treatment of women with symptomatic endometriosis. Am J Obstet Gynecol. 1992;167(1):283-291.<br />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.<br />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.<br />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.<br />Fayez JA, Collazo LM, Vernon C. Comparison of different modalities of treatment for minimal and mild endometriosis. Am J Obstet Gynecol. 1988;159:927-932.<br />Moghissi KS, Hull ME, Magyar DM, et al. Comparison of different treatment modalities of endometriosis in infertile women. Controversies Gyncec Obstet. 1987;16:236-240.<br />Olive DL, Schwartz LB. Endometriosis. New Engl J Med. 1993;328(24):1759-1767.<br />Saltiel E, Garabedian-Ruffal SM. Pharmacologic management of endometriosis. Clin Pharm. 1991;10:518-531.<br />Olin BR. Drug Facts and Comparisons. St. Louis, MO: JB Lippincott Company; 1992.<br />Schmidt CL. Endometriosis: A reappraisal of pathogenesis and treatment. Fertil Steril. 1985;44(2):157-173.<br />Buckman RW. Endometriosis: Pharmacologic alternatives to surgery. J Pract Nurs. 1994;44(3):47-56.<br />Rebar RW. The ovaries. In: Cecil Textbook of Medicine. 19th ed. JB Wyngaarden, LH Smith, JC Bennett, eds. Philadelphia, PA: WB Saunders Co.; 1992.<br />Segraves R, Letassy NA. Gynecologic disorders. In: Applied Therapeutics. 5th ed. MA Koda-Kimble, LY Young, eds. Vancouver, BC: Applied Therapeutics, Inc.; 1992:70-77.<br />Winkel CA, Scialli AR. Medical and surgical therapies for pain associated with endometriosis. J Womens Health Gend Based Med. 2001;10(2):137-162.<br />Howard FM. An evidence-based medicine approach to the treatment of endometriosis-associated chronic pelvic pain: Placebo-controlled studies. J Am Assoc Gynecol Laparosc, 2000;7(4):477-488.<br />Yap C, Furness S, Farquhar C. Pre and post operative medical therapy for endometriosis surgery. Cochrane Database Syst Rev. 2004;(3):CD003678.<br />Hughes E, Fedorkow D, Collins J, Vandekerckhove P. Ovulation suppression for endometriosis. Cochrane Database Syst Rev. 2003;(3):CD000155.<br />Premenstrual syndrome<br />Hussain SY, Massil JH, Matta WH, et al. Buserelin in premenstrual syndrome. Gynecol Endocrinol. 1992;6(1):57-64.<br />Blackstrom T, Hammarback S. Premenstrual syndrome--psychiatric or gynaecological disorder? Ann Med. 1991;23(6):625-633.<br />Mortola JF, Girton L, Fischer U. Successful treatment of severe premenstrual syndrome by combined use of gonadotropin-releasing hormone agonist and estrogen/progestin. J Clin Endocrinol Metab. 1991;72(2):252A-252F.<br />Hammarback S, Backstrom T. Induced anovulation as treatment of premenstrual tension syndrome. A double-blind cross-over study with GnRH-agonist versus placebo. Acta Obstet Gynecol Scand. 1988;67(2):159-166.<br />Bancroft J, Boyle H, Warner P, et al. The use of an LHRH agonist, buserelin, in the long-term management of premenstrual syndromes. Clin Endocrinol (Oxf). 1987;27(2):171-182.<br />Muse KN, Cetel NS, Futterman LA, et al. The premenstrual syndrome. Effects of 'medical ovariectomy'. N Engl J Med. 1984;311(21):1345-1349.<br />Zoladex<br />No authors listed. Endocrine drugs: Drugs used for gynecologic indications. In: Drug Evaluations Subscription. DR Bennett, ed. Chicago, IL: American Medical Association; 1993; II/ENDO-6:11-12.<br />No authors listed. Oncolytic drugs: Antineoplastic agents: Hormonal agents. In: Drug Evaluations Subscription. DR Bennett, ed. Chicago, IL: American Medical Association; 1993; III/ONC-5:12-15.<br />United States Pharmacopeial Convention, Inc. (USPC). Goserelin (Systemic). In: USP Dispensing Iinformation. Volume 1 - Drug Information for the Healthcare Professional, 15th ed. Rockville, MD:,USPC; 1995:1410-1411.<br />United States Pharmacopeial Convention, Inc. (USPC). Additional products and indications In: USP Dispensing Information. Volume 1 - Drug Information for the Healthcare Professional. 15th ed. Rockville, MD: USPC; 1995:2849.<br />Lu PY, Ory SJ. Endometriosis: Current management. Mayo Clin Proc. 1995;70:453-463.<br />Goldhirsch A, Wood WC, Senn HJ, et al. Meeting highlights: International consensus panel on the treatment of primary breast cancer (commentary). J Natl Cancer Inst. 1995;87(19):1441-1445.<br />Vercellini P, Fedele L, Maggi R, et al. Gonadotropin releasing hormone agonist for chronic anovulatory uterine bleeding and severe anemia. J Reprod Med. 1993;38(2):127-129.<br />DeVita VT, Hellman S, Rosenberg SA, eds. Cancer: Principles and Practice of Oncology. 4th ed. Philadelphia, PA: JB Lippincott Co.; 1993.<br />United States Pharmacopeial Convention, Inc (USPC). USP Dispensing Information. Volume I -- Drug Information for the Health Care Professional. Rockville, MD: USPC; 1998.<br />American Society of Health-System Pharmacists, Inc. American Hospital Formulary Service Drug Information 98. Bethesda, MD: American Society of Health-System Pharmacists; 1998.<br />Medical Economics, Inc. Physicians' Desk Reference. 52nd ed. Montvale, NJ: Medical Economics; 1998.<br />Mosby-Year Book, Inc. Mosby's GenRx: The Complete Reference for Generic and Brand Drugs, 8th ed. St. Louis, MO: Mosby; 1998.<br />Korman LB. Treatment of prostate cancer. Clin Pharm. 1989;8:412-424.<br />Furr BA, Woodburn JR. Luteinizing hormone-releasing hormone and its analogues: A review of biological properties and clinical uses. J Endocrinol Invest. 1988;11:535-537.<br />Hughes E, Collins J, Vandekerckhove P. Gonadotropin releasing hormone analogue as an adjunct to gonadotropin therapy for clomiphene-resistant PCOS. Cochrane Database of Systematic Reviews. Oxford, U.K.: Update Software; 1998.<br />Franke HR, Smit WM, Vermes I. Gonadal protection by a gonadotropin-releasing hormone agonist depot in young women with Hodgkin's disease undergoing chemotherapy. Gynecol Endocrinol. 2005;20(5):274-278.<br />Del Mastro L, Catzeddu T, Boni L, et al. Prevention of chemotherapy-induced menopause by temporary ovarian suppression with goserelin in young, early breast cancer patients. Ann Oncol. 2006;17(1):74-78.<br />Plenaxis<br />Cook T, Sheridan WP. Development of GnRH antagonists for prostate cancer: New approaches to treatment. Oncologist. 2000;5(2):162-168.<br />McLeod D, Zinner N, Tomera K, et al. A phase 3, multicenter, open-label, randomized study of abarelix versus leuprolide acetate in men with prostate cancer. Urology. 2001;58(5):756-761.<br />Trachtenberg J, Gittleman M, Steidle C, et al. A phase 3, multicenter, open label, randomized study of abarelix versus leuprolide plus daily antiandrogen in men with prostate cancer. J Urol. 2002;167(4):1670-1674.<br />Koch M, Steidle C, Brosman S, et al. An open-label study of abarelix in men with symptomatic prostate cancer at risk of treatment with LHRH agonists. Urology. 2003;62(5):877-882.<br />Reddy GK. Abarelix (Plenaxis): A gonadotropin-releasing hormone antagonist for medical castration in patients with advanced prostate cancer. Clin Prostate Cancer. 2004;2(4):209-211.</span> </span></strong>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com2tag:blogger.com,1999:blog-16849169.post-52425545781237468622007-07-18T21:42:00.000+08:002007-07-18T21:51:20.181+08:00baseline scan and bloodtest<strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;">Tues 17 July 2007</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;">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.</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;">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.</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;">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.</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc33cc;">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. </span></strong>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com1tag:blogger.com,1999:blog-16849169.post-71090377508024777642007-07-13T13:23:00.000+08:002007-07-13T13:27:03.851+08:00lucrin side effects<strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;">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.</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;"></span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;">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.</span></strong><br /><strong><span style="font-family:Verdana;font-size:85%;color:#cc66cc;"></span></strong>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com0tag:blogger.com,1999:blog-16849169.post-25085899901224158932007-07-03T21:59:00.000+08:002007-07-03T22:05:09.192+08:00IVF Start of Lucrin cycle<span style="font-size:85%;color:#cc33cc;"><strong><span style="font-family:verdana;">Finally 3rd July 2007 came around,</span></strong> <strong>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.</strong></span><br /><strong><span style="font-size:85%;color:#cc33cc;"></span></strong><br /><strong><span style="font-size:85%;color:#cc33cc;">will start to jab myself tomorrow.</span></strong><br /><strong><span style="font-size:85%;color:#cc33cc;"></span></strong>babymakinghttp://www.blogger.com/profile/11790062934370723907noreply@blogger.com0