Archive for the ‘Learning More’ Category
Testosterone Deficiency
November 9th, 2008 | 
Author: Hypogonadism may be present at birth (congenital) or may develop later (acquired). Causes of the condition are classified according to their location along the hypothalamic-pituitary-gonadal axis:
- Primary, disruption in the testicles
- Secondary, disruption in the pituitary gland
- Tertiary, disruption in the hypothalamus
The most common congenital cause is Klinefelter syndrome. This condition, which is caused by an extra X chromosome, results in infertility, sparse facial and body hair, abnormal breast enlargement (gynecomastia), and smaller than normal testes.
Congenital hormonal disorders such as leutenizing hormone-releasing hormone (LHRH) deficiency and gonadotropin-releasing hormone (GnRH) deficiency (e.g., Kallmann syndrome) also may cause testosterone deficiency.
Other congenital causes include absence of the testes (anorchism; may also be acquired) and failure of testicles to descend into scrotum (cryptorchidism).
Acquired causes for testosterone deficiency include the following:
- Chemotherapy
- Damage to the pituitary gland, hypothalamus, or testes
- Glandular malformation
- Head trauma affecting the hypothalamus
- Infection (e.g., meningitis, syphilis, mumps)
- Isolated LH deficiency (e.g., fertile eunuch syndrome)
- Radiation
- Testicular trauma
- Tumors of the pituitary gland, hypothalamus, or testicles
To learn more about testosterone deficiency including symptoms, diagnosis, and treatment, see details on testosterone deficiency.
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Asherman’s Syndrome and Fertility
Asherman’s Syndrome Silently Blocks Conception
See a fertility specialist now
If you are trying to get pregnant and suspect ovulation or infertility problems time is important. Don’t wait, see a specialist (reproductive endocrinologist) for a consultation. All our specialists treat Asherman’s Syndrome.
Susan Kunin had no reason to suspect she was infertile. She’d become pregnant the first time she and her husband attempted conception, and had no other conditions or symptoms of anything amiss. Sadly, that first pregnancy miscarried and a D&C (dilatation and curretage, a common procedure in which the cervix is entered and the uterine lining is scraped) was performed. Susan didn’t realize that this relatively simple procedure resulted in a severe case of Asherman’s Syndrome, a cause of female infertility.
Dr. Alan Copperman, Director of the Division of Reproductive Endocrinology at the Mount Sinai Medical Center in New York and physician with Reproductive Medicine Associates of New York, is an expert in the diagnosis and treatment of Asherman’s Syndrome, a condition in which the walls of the uterus adhere together to an extent where the uterine cavity itself is diminished. It is defined by uterine inflammation, adhesions, and scarring.
While the actual occurrence rate is hard to determine, Copperman says, “Any time there’s a surgical procedure performed inside the uterus, there’s a chance for scarring to occur.” It typically results from common surgeries such as D&C following miscarriage or birth, as well as intrauterine procedures for fibroid removal, to correct structural abnormalities of the uterus, or cesarean section. Additionally, inflammation and infection from any foreign object within the uterus, such as an IUD (intrauterine device for contraception), may result in Asherman’s.
The varying severity of scarring can have different levels of impact on a woman’s ability to conceive and then successfully carry a pregnancy. Copperman describes, “With mild scarring, the walls of the uterus will stick to each other and the result is literally less room for menstruation and pregnancy to occur. In the case of severe scarring, all of the normal endometrium (lining of the uterus) has been removed, leaving no normal tissue in which an embryo can implant.”
Women with Asherman’s generally experience no uncomfortable symptoms, and in fact, may have very light or even no menstrual periods. Often, they first learn about this possible cause of infertility after speaking with a reproductive specialist.
Susan began to worry when she still had not begun menstruating several months following her miscarriage and related D&C. Eventually she was diagnosed with Asherman’s and told to consider surrogacy as an option for parenthood.
“I was completely devastated,” she remembers. “I cried non-stop. I was also extremely angry. I had no fertility issues a few months before, and now I was completely infertile.”
Fortunately, before she had fully pursued surrogacy to have a child, Susan learned about an educational website called simply “Asherman’s Syndrome” (http://www.ashermans.org) through which she joined a related support group. It was through this group that she met Dr. Copperman. While he concurred that, indeed, Susan’s case was severe — her diagnostic hysterosalpingogram (HSG) should virtually no uterine cavity because of the extent of scar tissue — he disagreed that she needed to make arrangements for surrogacy.
While HSG is one method of diagnosing Asherman’s Syndrome, Copperman states a preference for the use of hysteroscopy and 3-D ultrasound. He explains that these methods allow the physician to see adhered areas that simply aren’t visible via HSG. In hysteroscopy, the patient is sedated and a tiny telescopic viewer is inserted through the cervix into the uterus, allowing the physician to have an almost direct view of the uterine interior.
Hysteroscopy is also the preferred manner for treating Asherman’s, through which the physician carefully removes any scar tissue within the uterus. In some cases, a balloon catheter is placed in the uterine cavity for one to two weeks following hysteroscopy, and estrogen supplement and infection-preventing antibiotics are administered during that period of time.
The goal of treatment is not merely to remove scar tissue, but to help the uterus re-build it’s endometrial lining. Inadequate endometrial lining, for any reason, can be a cause of implantation difficulty and resulting infertility.
While most women who seek treatment for Asherman’s are likely doing so in order to conceive and have a baby, some women may instead be concerned about the syndrome’s possible connection to the development of endometriosis, thought to be caused by retrograde (in effect, backward) menstrual flow.
In Susan’s case, treatment by hysteroscopy and balloon catheter was successful — she became pregnant several months following, and her daughter was born in May 2003. Copperman states that chances of conception after treatment for Asherman’s Syndrome are related to the severity of disease. If a woman’s uterus has only a few wispy bands of scar tissue, she’ll likely do well in attempts to conceive after treatment. Her chances are less if the maximum endometrial thickness achieved is less than six millimeters.
Because of the unpredictable and possibly devastating results from commonly performed uterine surgeries, experts and patient advocates alike emphasize the importance of finding physicians with extensive experience in the diagnosis and, especially, treatment of Asherman’s Syndrome.
See a fertility specialist now
If you are trying to get pregnant and suspect ovulation or infertility problems time is important. Don’t wait, see a specialist (reproductive endocrinologist) for a consultation. All our specialists treat Asherman’s Syndrome.
Article Source: Integramed.com
Determining Ovarian Reserve
Ovarian Reserve: When the News is Bad The results of ovarian reserve testing are often viewed by patients as either good news or bad. The bad news is that, for patients with low ovarian reserve, implantation rates are generally poor and the possibility of successful pregnancy is very limited. When faced with such information, couples are often devastated. They may have a variety of reactions – including, anger, denial or depression, all of which are normal and natural expressions of grief.
When couples receive a diagnosis of poor ovarian reserve, it is often helpful for them to spend time talking to each other, examining their parenting needs. They may want to ask themselves, “What is the most important thing to us about having a family? Is it the opportunity to provide love and guidance to a child? Is the genetic link essential? Is it important to experience pregnancy and childbirth? Is childfree living a realistic alternative?” By answering such questions, the couple will be in a better position to assess other options. Many patients have enlisted the aid of support groups, therapists, or compassionate physicians to help them through this crucial time. Whatever the outcome, patients receiving such shocking news will need time to mourn their loss and find a way toward acceptance.
What is Ovarian Reserve? As a woman ages, her supply of eggs gradually declines over time until the eggs are depleted at menopause. Although we expect the ovary to age in a certain way, there are times when it doesn’t behave as predicted. That’s why screening for ovarian reserve is a fundamental part of the initial evaluation for infertility patients of any age.
The term “ovarian reserve” refers to a woman’s current supply of eggs, and is closely associated with reproductive potential. In general, the greater the number of remaining eggs, the better the chance for conception. Conversely, low ovarian reserve greatly diminishes a patient’s chances for conception.
Methods of Assessing Ovarian Reserve Since a woman’s chronological age is the single most important factor in predicting a couple’s reproductive potential, age has often guided infertility treatment choices. However, age alone doesn’t tell the whole story. Consequently, researchers have developed (and are continuing to develop) more refined methods of predicting a couple’s response to infertility treatment. Some of the more sophisticated tools for assessing fertility potential include the measurement of FSH, LH, estradiol, and inhibin-B [Table 1]. Additionally, because patients should not be subjected to all tests, decisions regarding which method(s) to use are guided by practitioner experience.
Even though several sophisticated tools exist for measuring ovarian reserve, most fall short of what we consider ideal sensitivity and specificity. Also, how best to interpret ovarian reserve tests is controversial, since clinical experience with these tests is still evolving. Even so, most infertility patients should be periodically evaluated for the possibility of impaired ovarian reserve before pursuing any advanced fertility treatment.
Finite Supply of Eggs Even before birth, a woman’s eggs begin to diminish in number. During the 20th gestation week, a female embryo contains about seven million eggs. At birth, the number of eggs has already dropped to about 200,000. The number of eggs continues to decline as the woman ages, until no eggs remain (menopause).
Fortunately, women are naturally equipped with an ample supply of extra eggs. The number of eggs a woman has at birth far exceeds the average number of menstrual cycles she will have during her lifetime. Therefore, when women undergo fertility treatment to boost egg production, the risk for premature menopause is no different than it would be for other women [1].
The Effects of Maternal Age on Ovarian Reserve, Part 1 Menstrual cycles that occur near the end of the ovaries’ lifetime are associated with older eggs of poorer quality [2]. In general, ovarian age parallels chronological age. But since that is not always the case, it is vitally important for clinicians to assess an infertility patient’s ovarian reserve. This is particularly true for women over the age of 35.
Conception and childbirth in women of advanced age has always been uncommon. This fact was recognized from the beginning of recorded human history [3]. Later, studies looking at communal societies found solid evidence of reduced fertility associated with older women [4]. More recent work has validated these findings [5,6]. The father’s age, however, appears to have only a marginal influence on fertility [7].
The Effects of Maternal Age on Ovarian Reserve, Part 2 The effect of maternal age on fertility has been the subject of considerable research. In one such study, pregnancy success rates as a result of timed therapeutic insemination (intrauterine insemination; IUI) were evaluated in terms of maternal age. The poorest outcomes were consistently seen among women 36 years of age or older [8]. This observation was confirmed by research in an in vitro fertilization (IVF) setting, where women 37 years of age or older had a 9% ongoing pregnancy rate compared to a 26% ongoing pregnancy rate in patients younger than 30 [9].
Our experience with donor-egg cycles offers further evidence that infertility and live birth rates are strongly influenced by the age of oocytes. Younger oocytes from donors under the age of 35 are typically used in donor-egg cycles. This greatly improves the reproductive outcome[13,14]. While the recipient’s age does have some negative impact on implantation rates, the effects appear limited. In fact, even if the recipient is over 40, clinical pregnancy rates approaching 59% have been achieved when donor (younger) oocytes are used [15].
Passive Ovarian Reserve Testing: Measuring FSH and LH, Part 1
The methods for assessing ovarian reserve are classified into two groups: passive testing and dynamic testing. The goal of both approaches is to provide information regarding oocyte (egg) quality and quantity. We’ll begin this section by examining passive testing methods.
As clinicians gained experience with IVF in the 1980′s, it became apparent that early follicular-phase FSH levels played an important role in pregnancy outcomes. We soon discovered that day 3 FSH (measured by a blood test) could be very useful in predicting response to ovulation induction and IVF.
As a woman ages, FSH becomes elevated in an attempt to force the aging ovary to respond. However, the exact mechanism responsible for this adaptive response remains unknown. A rise in early follicular-phase FSH is also accompanied by a decline in oocyte quality, and some investigators have linked such FSH elevations to fetal abnormalities [18]. In fact, it has been theorized that subtle but measurable increases in FSH precede menopause by approximately five years in some women [19].
Passive Ovarian Reserve Testing: Measuring FSH and LH, Part 2 Since FSH has such high predictive value, should FSH always be measured? And if so, what values are important? It is difficult to establish absolute values that define how high an FSH level can be and still achieve pregnancy due to variations in laboratory assessments and treatment methods. Adding to this uncertainty is the fact that no data exists which describes FSH patterns in a “control” population of fertile women [20].
Arbitrarily applying day 3 FSH tests to all women (even those with no infertility history) is controversial, and can offer confusing results. Some clinicians have therefore questioned the usefulness of widespread FSH screening [21]. It is our opinion that ovarian reserve screening should be an integral part of every infertility patient’s workup.
Passive Ovarian Reserve Testing: Measuring FSH and LH, Part 3 While it is unwise to rely on a single test to fully assess ovarian reserve, considerable data exists that provides some general guidelines about which FSH values are most significant. In one center, women undergoing IVF with a day 3 FSH of less than 15 mIU/ml were twice as likely to conceive than women with FSH values between 15 and 24.9 mIU/ml [22]. Other investigators confirmed these results, and FSH values emerged as superior to maternal age as a method for determining reproductive outcome in IVF [23]. Indeed, one series reported that when day 3 FSH levels exceed 20 IU/L, conception rates fell sharply [24].
Passive Ovarian Reserve Testing: Measuring FSH and LH, Part 4 Traditionally, clinicians have relied on cycle day 3 FSH test results to help assess ovarian function. However, since FSH fluctuates only slightly during cycle days 2 through 5, testing does not have to be done exactly on cycle day 3. More flexible FSH testing may be done over a range of dates [25].
While FSH values may not change significantly from days 2 through 5 within a given cycle, fluctuations of day 3 FSH from cycle to cycle are more important to detect. When FSH does fluctuate, subsequent menstrual cycles will likely produce oocytes of varying quality. This principle has emerged as a fundamental belief in human reproductive physiology [26]. Patients with low FSH values (suggesting satisfactory ovarian reserve) generally show the least fluctuation, while those with elevated FSH levels have broader ranges. Wide FSH fluctuations from month to month present a difficult “moving target” for laboratory assessment. In such cases, it is difficult to precisely estimate ovarian reserve.
Passive Ovarian Reserve Testing: Measuring FSH and LH, Part 5 A single measurement of day 3 FSH may not represent actual ovarian reserve. When testing reveals elevated FSH, this result should be confirmed in a later cycle. However, interpretation of fluctuations across multiple cycles is controversial. Among patients with a series of day 3 FSH values that include at least one unfavorable (elevated) FSH test, a low response to ovulation induction has been observed [27]. Another analysis revealed that patients with both high and low FSH values across multiple cycles performed as low responders during IVF [28]. However, other investigators regard variable FSH results differently. Some consider relatively low day 3 FSH values permissive for IVF or other fertility treatments during that cycle. Preliminary data suggest that if FSH returns to a “normal” level after an abnormal (high) test in a previous month, conception rates for IVF may be approximately 35% for patients under the age of 40 [29].
Passive Ovarian Reserve Testing: Measuring FSH and LH, Part 6 LH measurement may also have predictive value for ovarian reserve, but FSH is considered a better marker since as menopause approaches, FSH rises sooner and more dramatically than LH [30,31]. There may be a place for combined FSH+LH testing to estimate ovarian reserve, as some investigators have suggested an increased FSH:LH ratio may predict an elevation in FSH alone [32].
In a population of IVF patients without pre-treatment GnRH-a (i.e., Lupron) suppression, cycle day 3 E2 and FSH were compared to reproductive outcome. The researchers observed that even when FSH values were less than 20mIU/mL, no pregnancy occurred when day 3 E2 was greater than 75pg/mL [33]. This result was supported by others who observed better outcomes for women aged 38-42 when day 3 E2 was less than 80pg/mL and FSH was normal [34]. From these studies it seems that evaluating both E2 and FSH was a better predictor of ovarian reserve than using either measurement alone.
Passive Ovarian Reserve Testing: Measuring Estradiol, Part 2 Low day 3 E2 levels, combined with normal FSH, have been associated with improved stimulation response, higher pregnancy rates [35], and lower cycle cancellation rates [36]. Interestingly, researchers reported that measurement of E2 one day earlier (on cycle day 2) did not enhance the predictive value of ovarian response [37].
High levels of E2 early in the menstrual cycle suggest an inappropriately advanced stage of follicular development. This may occur as the ovary ages, or when ovarian follicular cysts remain from a prior menstrual cycle. The follicular cysts can interfere with egg “recruitment” in the treatment cycle, naturally leading lead to a poor response to fertility treatment.
Passive Ovarian Reserve Testing: Measuring Progesterone A decline in ovarian reserve has also been associated with a short follicular phase, early LH surge, and premature elevation of progesterone (P4) [38]. Initially, it was though P4 might be a useful tool for ovarian screening. However, daily E2 and P4 testing performed in volunteers with ovulatory cycles revealed no differences in E2 or P4 as a function of age [31]. Researchers then turned their attention from “static” P4 assessment to the study of P4 patterns in the context of dynamic testing (see next section). In that setting, some investigators found high P4 levels (*1.1 ng/mL) on day 10 of clomiphene citrate challenge tests (CCCT) to be associated with short follicular phases, diminished ovarian reserve, and reduced potential to achieve pregnancy. [39].
Passive Ovarian Reserve Testing: Measuring Inhibin-B, Part 1 Inhibin-B is an ovarian hormone that inhibits FSH release [40]. Although present in ovulating women, it is not normally found in postmenopausal women. As early as 1932, researchers suspected that a non-steroidal regulator of FSH secretion might exist [41], but it was not until 1976 that this hypothesis was actually confirmed [42].
Unfortunately, the initial enthusiasm for inhibin-B as an ovarian reserve screening tool was tempered by the lack of a satisfactory way to study it. If measured by standard FSH-release methods, more than seven active forms of inhibin, as well as inactive inhibin constituents, are found in human serum [46]. Studies are currently underway to uncover more information about inhibin-B [47,48].
Although measuring inhibin-B is still considered investigational as a way to screen ovarian reserve, a number of advances have helped make measurement of inhibin-B a clinical reality. Nevertheless, it is critical for clinicians using inhibin-B in ovarian reserve testing to understand exactly which assay is being used, and acknowledge limitations in measurement methods.
Passive Ovarian Reserve Testing: Measuring Inhibin-B, Part 2 Inhibin-B may prove to be a beneficial marker for ovarian reserve assessment because it fluctuates during the menstrual cycle, and is significantly reduced in women over the age of 35 [51]. One center observed that when day 3 inhibin-B was less than 45pg/mL, the response to fertility treatment was lower, the cancellation rate was higher, the number of retrieved oocytes was less, and the pregnancy rate was significantly reduced when compared to subjects with day 3 inhibin-B values greater than or equal to 45pg/mL [52]. In an effort to broaden the diagnostic capability of inhibin-B, some researchers have proposed including this test as an experimental component of the clomiphene citrate challenge test (see next section) [53].
Although these early reports confirm that inhibin-B can enhance current tools that measure ovarian reserve, more data are needed before meaningful normal ranges for inhibin-B can be routinely applied in clinical practice [54,55].
Passive Ovarian Reserve Testing: Transvaginal Ultrasound, Part 1 Diminished ovarian reserve means that fewer follicles are available for stimulation and recruitment by fertility drugs. By allowing physicians to view the ovaries and assess the number of follicles, transvaginal ultrasound can aid in the assessment of ovarian volume.
Previous investigators have documented that the ovary reduces in size with increasing age, regardless of whether the woman has given birth [56]. Other researchers have found that the lower the ovarian volume, the greater the dose of fertility drugs required to stimulate the ovaries [57]. Ultrasound ovarian volume has also been used to predict the risk for ovarian hyperstimulation syndrome [58]. However, it has been theorized that ultrasound ovarian volume done at the beginning of the treatment cycle is more closely related to the number of follicles found during the pre-treatment period rather than the number of oocytes developed during treatment [59]. It is uncertain that ovarian size or follicular number is a better indicator of ovarian reserve. The more follicles you have, the larger the number of eggs retrieved during the treatment cycle. Is it better to measure prior to any medical therapy or after GnRH-a is administered but prior to gonadotropin injections? Studies to clarify the relative predictive value of follicular number and ovarian size have yet to be done.
Passive Ovarian Reserve Testing: Transvaginal Ultrasound, Part 2 Among patients taking GnRH-a (Lupron) before a treatment cycle, abnormally high E2 levels are often associated with large ovarian cysts (identified by transvaginal ultrasound). Such E2 elevations may be improved by short-term continuation of GnRH-a. Using this approach, the cyst frequently resolves and the treatment cycle can continue. It is important to note that the additional GnRH-a exposure during this brief interval has not been associated with significantly reduced response to fertility drugs, nor has it adversely affected pregnancy rates [62].
Dynamic Ovarian Reserve Testing: Clomiphene Citrate Challenge Test, Part 1 In contrast to the static measurements of ovarian reserve mentioned previously, the clomiphene citrate challenge test (CCCT) is a dynamic approach. Its purpose is to stimulate the ovary to initiate egg production in response to a fertility drug called clomiphene (Clomid or Serophene). In theory, the CCCT was designed to detect low ovarian reserve that would not be discovered by a single FSH and/or E2 measurements.
The CCCT is based on the assumption that adequate ovarian reserve is associated with a healthy group of developing follicles. This healthy group of follicles should be capable of producing enough inhibin and E2 to suppress FSH production and resist the effects of clomiphene.
Clomiphene works by shutting down the estrogen receptors on the hypothalamus and tricking the hypothalamus into thinking the patient doesn’t have enough estrogen. In response, the hypothalamus works harder to induce the pituitary gland to produce more FSH and LH. This, in turn, initiates follicular growth.
Dynamic Ovarian Reserve Testing: Clomiphene Citrate Challenge Test, Part 2 When undergoing CCCT, the first step is to measure day 3 FSH and E2. Then 100mg of clomiphene is administered on cycle days 5 through 9, and FSH and E2 measurements are repeated on cycle day 10 [63]. In general, a high day 10 FSH suggests poor ovarian reserve.
In the original report describing the CCCT, 18 patients out of 51 had abnormal responses. Of those with abnormal responses, only one pregnancy resulted (1 of 18, or 6%). The pregnancy rate among those with normal CCCT response was substantially higher (14 of 33, or 42%) [63]. Several other investigators have confirmed the good predictive value of CCCT before treatment [64-66].
Evaluation of a large number of infertility patients found a 10% prevalence of abnormal CCCT responders [67]. Another report found CCCT to be a better predictor of ovarian reserve than day 3 FSH measurement alone [68].
Dynamic Ovarian Reserve Testing: Gonadotropin-releasing Hormone Agonist Stimulation Test, Part 1 A gonadotropin-releasing hormone agonist (such as Lupron) initially elevates E2, then profoundly suppresses both FSH and LH [69]. This is sometimes called a “flare-effect”. More than a decade ago, it was theorized that low ovarian reserve might be detected by evaluating differences in LH, FSH, and E2 levels following the administration of GnRH-a during IVF [24]. This approach was later formalized as a diagnostic tool known as the GnRH-a stimulation test, or GAST [70].
The purpose of GAST is to evaluate changes in E2 on cycle day 2 and 3 following administration of leuprolide acetate (Lupron). Patients with greater elevations of E2 have correspondingly higher pregnancy rates. Four GAST E2 patterns have emerged:
1) prompt E2 elevation, then decrease by cycle day 4
2) delayed E2 rise with fall by cycle day 6
3) persistent E2 elevation
4) no E2 response after GnRH-a
Clinical pregnancy rates for these groups were strikingly different: 46%, 38%, 16%, and 6% were observed in patterns 1 through 4, respectively [9].
In summary, GAST has been a better predictor of the functional abilities of the ovary than either FSH or age [70]. Because the GnRH-a is costly and involves an injection and repeated blood tests, the GAST is not widely used in clinical practice.
The Value of Medical Records Clinicians can often uncover valuable information about possible ovarian reserve from records describing a patient’s response to earlier ovulation induction attempts. Unlike any of the other assessment tools described, knowing how a patient responded previously shows reproductive performance over the broadest possible range. When available, such records represent the ultimate dynamic test of ovarian status.
Obviously, records would not be available for patients who have no prior ovulation induction attempts. However, the availability of old stimulation records does not mean that repeat assessment of ovarian reserve can be left out. Prior stimulation records can guide both the estimation of ovarian reserve and the selection of the appropriate treatment plan in an upcoming cycle.
Summary Several methods have been developed to estimate the functional or biological age of the ovary. Since ovarian reserve can vary over time, any results suggesting limited ovarian reserve should be confirmed by further testing in subsequent months. It may be that inflammatory, infectious or autoimmune conditions are contributing to the abnormal results. Such potentially reversible causes of low ovarian reserve should be corrected, particularly in younger woman.
When further testing confirms compromised ovarian reserve, it is important to point out that the likelihood of success with infertility treatment is low. Such patients may want to consider other options, such as donor-egg treatment. However, we realize that donor eggs will not be acceptable to everyone with poor ovarian reserve.
We have found that when ovarian reserve is low, the best course of action for the physician is compassionate honesty. After all, time is precious by the time a couple reaches infertility specialists, so little can be gained by creating false hope or continuing down a fruitless path. Instead, physicians can provide invaluable assistance by helping the couple re-evaluate their parenting needs and determine what, if any, other options they might pursue. In the world of infertility, some doors shut while others open. The door may not reveal what the couple thought they wanted, but for many, it might reveal something that is even better.
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| 34. | Buyalos RP, Daneshmad S, Brzechffa PR. Basal estradiol and follicle stimulating hormone predict fecundity in women of advanced reproductive age undergoing ovulation induction therapy. Fertil Steril 1997;68:272-7. |
| 35. | Smotrich DB, Widra EA, Gindoff PR et al. Prognostic value of day 3 estradiol on in vitro fertilization outcome. Fertil Steril 1995;64:1136-40. |
| 36. | Evers JL, Slaats P, Land JA, Dumoulin JC, Dunselman GA. Elevated levels of basal estradiol 17-ß predict poor response in patients with normal basal levels of follicle stimulating hormone undergoing in vitro fertilization. Fertil Steril 1998;69:1010-14. |
| 37. | Ranieri DM, Quinn F, Makhlouf A et al. Simultaneous evaluation of basal follicle stimulating hormone and 17-ß estradiol response to gonadotropin-releasing hormone analogue stimulation: an improved predictor of ovarian reserve. Fertil Steril 1998;70:227-33. |
| 38. | Thatcher SS 3rd, Naftolin F. The aging and aged ovary. Semin Reprod Endocrinol 1991;9:189-99. |
| 39. | Hofmann GE, Scott RT Jr, Horowitz GM, Thie J, Navot D. Evaluation of the reproductive performance of women with elevated day 10 progesterone levels during ovarian reserve screening. Fertil Steril 1995;63:979-83. |
| 40. | Kingsley DM. The TGF-ß superfamily: new members, new receptors and new genetic tests of function in different organisms. Gene Dev 1994;8:133-46. |
| 41. | McCullagh R. Dual endocrine activity of the testes. Science 1932;76:19-20. |
| 42. | De Jong FH, Sharpe RM. Evidence for inhibin-like activity in bovine follicular fluid. Nature 1976;263:71-2. |
| 43. | Vale W, Rivier C, Hsueh A et al. Chemical and biological characterization of the inhibin family of protein hormones. Recent Prog Res 1988;44:1-30. |
| 44. | Barton DE, Yang-Feng TL, Mason AJ et al. Mapping of genes for inhibin subunits alpha, beta A, beta B on human and mouse chromosomes and studies of jsd mics. Genomics 1989;5:91-9. |
| 45. | Mathews LS. Activin receptors and cellular signaling by the receptor serine kinase family (review). Endocrinol Rev 1994;15:310-25. |
| 46. | Robertson DM, Klein R, de Vos FI et al. The isolation of polypeptides with FSH suppressing activity from bovine follicular fluid which are structurally different to inhibin. Biochem Biophys Res Commun 1987;149:744-9. |
| 47. | Hazout A, Frydman R, Fanchin R, Dumont-Hassan M. Day 3 serum inhibin-B and estradiol are the best predictors factors of success in assisted reproductive technologies [abstract O-023]. Fertil Steril 1999;72(Suppl 1):S9. |
| 48. | Smith D, Carr B, O’Neil J, Ackerman G, Byrd W. Levels of inhibin A and B in GnRH agonist downregulated women prior to gonadotropin stimulation for in vitro fertilization are highly predictive of pregnancy outcome [abstract O-024]. Fertil Steril 1999;72(Suppl 1):S9-10. |
| 49. | Knight PG, Muttakrishna S, Groome NP. Development and application of a two-site enzyme immunoassay for the determination of ‘total’ activin-A concentrations in serum and follicular fluid. J Endocrinol 1996;148:267-79. |
| 50. | McConnell DS, Wang Q, Sluss PM et al. A two-site chemiluminescent assay for actvin-free follistatin reveals that most follistatin circulating in men and normal cycling women is in an activin-bound state. J Clin Endocrinol Metab 1998;83:851-8. |
| 51. | Klein NA, Illingworth PJ, Groome NP, McNeilly AS, Battaglia DE, Soules MR. Decreased inhibin-B secretion is associated with the monotrophic FSH rise in older, ovulatory women: a study of serum and follicular fluid levels of dimeric inhibin A and B in spontaneous menstrual cycles. J Clin Endocrinol Metab 1996;81:2742-5. |
| 52. | Seifer DB, Lambert-Messerlian G, Hogan JW, Gardiner AC, Blazar AS, Berk CA. Day 3 serum inhibin-B is predictive of assisted reproductive technologies outcome. Fertil Steril 1997;67:110-4. |
| 53. | Hofmann GE, Danforth DR, Seifer DB. Inhibin-B: the physiologic basis of the clomiphene citrate challenge test for ovarian reserve screening. Fertil Steril 1998;69:474-7. |
| 54. | Renier MA, Vereecken A, Buytaert P. Inhibins, activins and follistatins: a review of complex regulators of the reproductive system. Eur J Contracept Reprod Health 1998;3:129-35. |
| 55. | Seifer DB, Scott RT Jr., Bergh PA et al. Women with declining ovarian reserve may demonstrate a decrease in day 3 serum inhibin-B before a rise in day 3 follicle-stimulating hormone. Fertil Steril 1999;72:63-5. |
| 56. | Andolf E, Jorgensen C, Svalenius E et al. Ultrasound measurement of the ovarian voulume. Acta Obstet Gynecol Scand 1987;66:387-9. |
| 57. | Lass A, Skull J, McVeigh E, Margara R, Winston RM. Measurement of ovarian volume by transvaginal sonography before ovulation induction with human menopausal gonadotropin for in vitro fertilization can predict poor response. Hum Reprod 1997;12:294-7. |
| 58. | Danninger B, Brunner M, Obruca A, Feichtinger W. Prediction of ovarian hyperstimulation syndrome by ultrasound volumetric assessment [corrected] of baseline ovarian volume prior to stimulation.Hum Reprod 1996;11:1597-9. |
| 59. | Thomas C, Nuojua-Huttumen S, Martikainen H. Pretreatment transvaginal ultrasound examination predicts ovarian responsiveness to gonadotrophins in in vitro fertilization. Hum Reprod 1997;12:220-3. |
| 60. | Agrawal R, Conway GS, Sladkevicius P et al. Serum endothelial growth factor (VEGF) in the normal menstrual cycle: association with changes in ovarian and uterine Doppler blood flow. Clin Endocrinol (Oxf) 1999;50:101-6. |
| 61. | Van Blerkom J. Epigenetic influences on oocyte developmental competence: perifollicular vascularity and intrafollicular oxygen. J Assist Reprod Genet 1998;15:226-34. |
| 62. | Damario M, Moomjy M, Tortoriello D, Moy F, Davis OK, Rosenwaks Z. Delay of gonadotropin stimulation in patients receiving gonadotropin-releasing hormone agonist (GnRH-a) therapy permits increased clinic efficiency and may enhance in vitro fertilization (IVF) pregnancy rates. Fertil Steril 1997;68:1004-10. |
| 63. | Navot D, Rosenwaks Z, Margalioth EJ. Prognostic assessment of female fecundity. Lancet 1987;2:645-7. |
| 64. | Loumaye E, Billion JM, Mine JM et al. Prediction of individual response to controlled ovarian hyperstimulation by means of a clomiphene citrate challenge test. Fertil Steril 1990;53:295-301. |
| 65. | Tanbo T, Dale PO, Lunde O, Norman N, Abyholm T. Prediction of response to controlled ovarian hyperstimulation: a comparison of basal and clomiphene citrate-stimulated follicle stimulating hormone levels. Fertil Steril 1990;53:295-301. |
| 66. | Tanbo T, Dale PO, Lunde O et al. Prediction of individual response to controlled ovarian hyperstimulation: a comparison of basal and clomiphene citrate-stimulated follicle stimulating hormone levels. Fertil Steril 1992;57:819-24. |
| 67. | Scott RT, Leonardi MR, Hofmann GE, Illions EH, Neal GS, Davot D. A prospective evaluation of clomiphene citrate challenge test screening of the general infertility population. Obstet Gynecol 1993;82:539-44. |
| 68. | Kahraman S, Vicdan K, Isik AZ et al. Clomiphene citrate challenge test in the assessment of ovarian reserve before controlled ovarian hyperstimulation for intracytoplasmic sperm injection. Eur J Obstet Gynecol Reprod Biol 1997;73:177-82. |
| 69. | Garcia JE. Gonadotropin-releasing hormone and its analogues: applications in gynecology. Clin Obstet Gynecol 1993;36:719-26. |
| 70. | Winslow KL, Toner JP, Brzyski RG, Oehninger SC, Acosta AA, Muasher SJ. The gonadotropin-releasing hormone agonist stimulation test: a sensitive predictor of performance in the flare-up in vitro fertilization cycle. Fertil Steril 1991;56:711-7. |
Tubal Ligation by Fimbriectomy
Fimbriectomy is an infrequent type of tubal ligation in the United States. This female sterilization method is performed by removing the fimbrial end of the fallopian tube. At the fimbrial end of the tube, the inner tubal lining faces outward towards the ovary. The tubal lining is rich in cilia that beat in coordinated waves to pull the egg into the tubal opening.Many doctors think that tubal reversal cannot be successful following a fimbriectomy because of the loss of the egg-capturing fimbria. This is a mistaken notion. Cilia are abundant in the ampullary segment of the fallopian tube. The inner lining of the remaining ampullary tubal segment can be folded outward after opening the tube and can function as a new fimbrial end. The tubal reversal procedure for fimbriectomy reversal is called ampullary salpingostomy.
Fimbriectomy Reversal Pregnancy Rates
Chapel Hill Tubal Reversal Center publishes statistics updated annually regarding pregnancy rates and pregnancy outcomes for all of the women who have had tubal reversal procedures performed by Dr. Berger. The data for women who had tubal ligation procedures by fimbriectomy are from our Tubal Reversal Pregnancy Study Report 2007.
The overall pregnancy rate after fimbriectomy tubal reversal is 56% for patients at Chapel Hill Tubal Reversal Center. The following table shows the numbers and pregnancy rates according to womens’ ages at the time of their tubal reversal procedure.
Pregnancy Rates After Fimbriectomy Reversal
|
|
|
|
|
|
<30 |
29 |
20 |
69% |
|
30-34 |
82 |
52 |
63% |
|
35-39 |
131 |
81 |
62% |
|
40+ |
70 |
22 |
31% |
Recommendations for Fimbriectomy Reversal
The success of fimbriectomy reversal depends upon having an adequate length of ampullary segment of the fallopian tube. The length of the remaining ampullary tubal segment can be determined from a hysterosalpingogram (HSG) or from diagnostic laparoscopy.
I recommend having an HSG or choosing the screening laparoscopy option when tubal ligation has been performed by fimbriectomy. An HSG can be ordered by the patient’s local doctor and the x-ray films sent to me for examination prior to scheduling tubal reversal surgery. Alternatively, patients can omit having an HSG and schedule their reversal surgery to start with screening laparoscopy. This will show if ampullary salpingostomy will be effective. If so, the tubal reversal procedure will be performed at the same time while the patient is under anesthesia.
Article Source: Tubal-reversal.net
Recurrent Miscarriage
Miscarriage is defined as the loss of a pregnancy before 20 weeks of gestation. Nearly 20% of pregnancies end in miscarriage, most often within the first 12 weeks. Recurrent miscarriage, or habitual pregnancy loss, is defined as three or more consecutive, spontaneous pregnancy losses.
Often no cause for miscarriages is found but possible causes include genetic defect, abnormally shaped uterus, uterine fibroids, scar tissue, hormonal imbalances and illness such as diabetes. Increased age, habits such as smoking, caffeine and alcohol, and the use of certain medications increase a woman’s risk for miscarriage.
There are a number of tests that your physician may run, in addition to reviewing your medical history and conducting a pelvic exam, to diagnose the possible cause of your recurring miscarriages. These tests may include a mapping of your chromosomes to detect genetic defects, a hysterosalpingogram, blood tests to detect immune system abnormalities and measure hormone levels, a vaginal ultrasound and an endometrial biopsy. Once the cause has been determined, your physician will work with you to map out a treatment plan, which may include surgery to correct problems with the shape of the uterus or medication to correct immune problems and hormone imbalances.
Treatment increases your chances of becoming pregnant and carrying a pregnancy to term. However, even if no cause is found and no treatment is given your chances of eventually delivering a baby after recurring miscarriages is about 60%.
Recurrent Pregnancy Loss
Thrombophilia
For Those Who’ve Miscarried
Recurrent Miscarriage Overview
Why Did I have a Miscarriage
Immunotherapy for Recurrent Miscarriage
Fibroids
Hygeia Foundation, Inc.
Article Source: IVF.com
Sonohysterogram – Hysterosonogram
Sonohysterogram or Hysterosonogram
What is a sonohysterogram?
A hysterosonogram or HSN is also known by the names sonohysterogram, saline ultrasound, saline sonogram, or saline infusion sonogram. A hysterosonogram is an office based ultrasound procedure that can determine if there are abnormalities inside the uterus that might interfere with pregnancy. It is important to have an evalaution of the uterine cavity with a sonohysterogram or other method before proceeding with an IVF cycle. This test involves no radiation, and there are very few risks from the procedure. Compared to a regular ultrasound, a sonohysterogram is better at detecting abnormalities on the inside walls of the uterus because it involves infusing sterile fluid inside the uterus. This way, the walls of uterus separate from each other and any abnormalities that might have been hiding right along the sides of the walls will be easily identified.
Here is an example to help understand why we do a hysterosonogram. Think of your uterus like a collapsed balloon. If there was a small growth or bump on the inside wall of the collapsed balloon, it might be hard to see since the top and bottom walls are touching each other. However, if we inflated the balloon, the small growth will be easier to see since it will likely be able to hang away from the wall.
Traditionally, the “best” way to look for abnormalities inside the uterus was a test called a hysteroscopy, which involves an out-patient surgery using a type of telescope to look inside the uterus. However, in recent years, the techniques for a sonohysterogram have become so advanced that it has usually replaced hysteroscopy as the first procedure to look for abnormalities in the uterus. Compared to a hysteroscopy, a sonohysterogram is less invasive, less expensive and nearly as effective at detecting abnormalities.
What kind of problems can a hysterosonogram diagnosis?
A hysterosonogram is often recommended for women who are having difficulty conceiving a pregnancy or for women who are having recurrent miscarriages. In some cases, a hysterosonogram may be used for a woman who is having abnormal vaginal bleeding. Since a sonohysterogram gives such a detailed view of the inside walls of the uterus, it can identify many types of abnormalities that might prevent a normal pregnancy from developing. Studies have shown that it can detect over 90% of abnormalities inside the uterus. Some of these abnormalities include:
- Polyps
- Fibroids
- Scar tissue
- Uterine septum
- Bicornuate Uterus
How is a sonohysterogram performed?
The procedure for performing a sonohysterogram is very simple and usually takes about 5 minutes. In order to schedule a sonohysterogram, you will need to call with the first day of your period. You will be given an appointment for some time point after the bleeding from the period has ended but before it is thought that ovulation might occur. This ensures that the uterine lining is as thin as possible. This is important since it will assist the doctor in visualization of the cavity. The hysterosonogram is performed in the office. Using a speculum, a very then, soft, flexible plastic catheter will be inserted through the vagina and cervix into the lower part of the uterine cavity. The speculum is then carefully removed so as not to disturb the catheter. A vaginal ultrasound probe is then placed into the vagina. Through the catheter, a small amount of saline (sterile salt water) is injected into the uterine cavity to separate the walls.
During a sonohysterogram, the ultrasound probe can be rotated to show the long axis of the uterus or a transverse axis. In the long axis, the uterine cavity appears long and ovoid.
In the transverse view, the uterine cavity looks triangular.
The saline appears dark black on the ultrasound. Abnormal growths in the uterine cavity will appear as ovoid, grey to white growths that protrude into the cavity. A cavity that is split will show the black appearing saline separated into two areas.
Sometimes after the procedure, a small amount of the saline fluid may leak out of the vagina. It is also possible that the patient may experience some bleeding or spotting. It is recommended that the patient wear a light pad or tampon for the rest of the day.
What do you need to do before a hysterosonogram?
Occasionally, a woman might experience some cramping during or after a hysterosonogram. If she desires, she may take 1-2 tablets of ibuprofen (Motrin or Advil) 1-2 hours before the procedure to decrease cramping. This may be repeated 3-4 hours later in the unlikely event that cramping persists.
What do you need to do after a sonohysterogram?
You will be able to watch the sonohysterogram on a monitor while it is being performed. Afterwards, the doctor will review the findings with you and answer any questions about those findings. If there are any abnormalities that are found on the inside of your uterus, don’t worry! Nearly all of these conditions are easily corrected with minimally invasive, outpatient surgery (usually with hysteroscopy).
Last Updated ( Monday, 17 March 2008 )
All Contents © IVF 1
Article Source: IVF1.com
Varicocele pain
Varicocele is a term used to describe abnormally dilated veins of the testis located in the scrotum. The term varicosity is familiar to those who have seen varicose veins of the leg. Veins are vascular structures that carry blood away from an organ such as a foot and arteries are the vessels that supply oxygen rich blood to organs. Veins normally have one-way valves present within their lumen to prevent the back flow of blood. This is useful for instance to prevent pooling of blood in the feet whilst a person is standing. This is the mechanism of varicose veins in the legs. Enlarged veins may be visible within the scrotal skin giving the appearance of a “bag of worms”. More often than not, the varicocele is only detectable by an examination by a physician. However, even small varicoceles may have an effect upon fertility. Varicoceles are first develop during puberty and are present in approximately 15% of all men undergoing military induction. Although the majority of men with varicoceles are fertile and without symptoms, varicoceles remain the most common identifiable cause of male infertility, found in approximately 30 % of infertile men.
The exact cause of varicoceles and the method by which they damage the testis remains unknown despite the fact that physicians and scientists have observed this phenomenon since the time of Celsus in 100 AD. The most popular theories held amongst fertility specialists today is that varicoceles are induced by absent or abnormal valves within the veins that normally drain the testis. The reduced drainage of blood from the scrotum along with the reflux of blood from the abdominal cavity increases scrotal temperature by two to three degrees. The testis, unlike the ovary, functions best at temperatures lower than intrabdominal temperatures, which explains its more vulnerable location in the scrotum. The minor elevation of scrotal temperature associated with a varicocele is believed to induce testicular damage over time especially when other gonadal toxins are present.
There are three clinical scenarios related to varicoceles:
- The most common, is finding a completely asymptomatic varicocele in a man being evaluated for infertility,
- Young asymptomatic men who find a mass in the scrotum either on their own or during routine exam and are concerned about future fertility and
- A man with pain in the scrotum.
Varicocele is a potential cause of scrotal pain that is either dull like in quality or extreme. The typical varicocele is asymptomatic, however occasional patients note an aching feeling in the scrotum associated with prolonged standing or activity and the aching pain is relieved by lying down supine with the feet raised. Varicoceles may cause more severe pain if the veins develop thrombophlebitis. The evaluation of patients with scrotal pain should include scrotal ultrasonography to rule out other pathology and cultures to rule out infection. Repair of the varicocele may be considered when there is no other identifiable cause of the pain and the pain qualities are consistent with a varicocele, however there can be no guarantee that varicocele repair will eradicate the pain.
Management of the young man with an incidental finding of an asymptomatic varicocele is somewhat more controversial. There is strong evidence to suggest that repairing a varicocele improves testicular function and may prevent any further testicular damage over time. Thus, the first step in the evaluation of this patient is to assess testicular function directly by semen analysis or indirectly by measuring testis volume. Repair of the varicocele is indicated if there is any evidence of testicular damage. The controversial aspect in the management of these patients is if current testicular function appears normal. The issues related to this controversy include the fact that since the patient is not currently trying to conceive we cannot assure him that his fertility is actually intact just because he has a normal semen parameters or testis volume. There is some evidence to suggest that varicoceles exert a progressive deleterious effect over time that would imply that all varicoceles should be repaired if future fertility is being considered. However, there is equal evidence against a progressive effect of varicoceles upon the testis and the fact remains that the vast majority of men with varicoceles (80%) are able to conceive on their own without utilizing fertility services. Thus, the controversy is whether to repair all varicoceles, repair only those varicoceles associated with signs of testicular damage or to observe patients with varicoceles over time with serial semen analyses.
Varicoceles are found on physical examination of roughly one third of men being evaluated for failure to conceive. They are categorized by size (large, medium and small) and by their presence on one or both sides of the scrotum. It is important to know that varicoceles of all sizes may affect fertility and the chance of improvement is equivalent after repair. In addition, a varicocele on side of the scrotum has an effect upon both testes in regards to function and temperature. Varicoceles that cannot be felt by the physician but are diagnosed by imaging studies, such as ultrasonography, are not clinically significant.
Repair of a varicocele in the male partner of an infertile couple is indicated when:
- There is objective evidence of a male factor (i.e. abnormal semen analysis),
- the wife’s fertility status is intact and
- there are no other obvious causes for male infertility (i.e. obstruction or genetic abnormality).
Varicocele repair can be performed surgically or non-surgically. There is no ideal method or absolutes in making this decision. The non-surgical repair is a minimally invasive technique performed by an interventional radiologist on an outpatient basis. The success rate varies significantly dependent upon the experience of the radiologist, the anatomy of the patient and the presence of varicoceles on both sides. Surgical repair may be performed through a small incision in the groin or laparoscopically. Both are equally effective and have minimal side effects, however, the open microsurgical approach can be performed under local anesthesia. Most varicocele repairs are performed using the microscope through a small incision, approximately 2 inches, just in the crease of the upper scrotum. This procedure has the greatest chance of repair with the least morbidity and lowest cost. Non-surgical approach is utilized primarily in patients with a previously failed surgical repair, pain as the main indication and body features that increase the risk of surgery such as morbid obesity. Potential complications from varicocele repair include persistent/recurrent varicocele, bruising, infection and testicular tenderness. A hydrocele, collection of water around the testis, occurs in an extremely small number of men. For those patients undergoing the non-surgical repair, there is the added risk of reaction to the contrast agent used in the procedure. Finally, there is an extremely low risk of loss of the testicle.
Article Source: Urology.jhu.edu
Methotrexate for ectopic pregnancy
Examples
| Generic Name | Brand Name |
|---|---|
| methotrexate | Abitrexate, Folex PFS, Mexate-AQ |
Methotrexate is typically given by injection. Two injection sites are sometimes used to administer one dose-this increases absorption of all of the medicine.
Methotrexate can be given by mouth. But ectopic pregnancy treatment success rates are lower with oral use than with injections.1
How It Works
Methotrexate stops the growth of rapidly dividing cells, such as embryonic, fetal, and early placenta cells.
During the week that you have methotrexate injections, your pregnancy hormone levels (human chorionic gonadotropin, or hCG) are tested several times. Your health professional will look for a drop in hCG levels, which is a sign that the pregnancy is ending (hCG levels sometimes rise during the first few days of treatment, then drop).
- If your hCG levels have dropped enough after 1 week, you are then tested on a weekly basis until they are low enough to suggest that the pregnancy has safely ended. This usually takes about a month but can take more than 3 months.
- If your hCG levels aren’t dropping enough after 1 week, you will be given another dose of methotrexate. Your hCG levels will be monitored as above.
- If your hCG levels continue at higher levels, or if your health professional becomes concerned about tubal rupture, surgery will be needed to remove the ectopic growth.
Why It Is Used
- End an early ectopic pregnancy.
- Prevent the growth of any embryonic or fetal cells that are left behind after surgery to end an ectopic pregnancy.
It is also used to treat certain types of cancer, rheumatoid arthritis, and as part of an induced abortion.
How Well It Works
Methotrexate treatment is most likely to be successful:
- When your pregnancy hormone (hCG) levels are low (less than 5,000).
- During the first 6 weeks of pregnancy.
- When the embryo has no heart activity.
Methotrexate treatment can be given as a single shot or as several injections. If an ectopic pregnancy continues after 2 or 3 doses of methotrexate, surgical treatment is needed to remove the ectopic pregnancy.
Methotrexate series. Although it is an uncommon practice, methotrexate can be given every other day until pregnancy hormone (hCG) blood tests confirm that the pregnancy has ended. On alternate days, a medicine called leucovorin (folinic acid) is given by injection to decrease methotrexate side effects. Treatment time for a methotrexate series varies from case to case but can take a month or longer.
Side Effects
Severe side effects from methotrexate treatment are usually related to longer-term use, such as for cancer treatment. Using alcohol or certain medicines during treatment can also lead to severe methotrexate side effects.
You will be advised to completely avoid the following until your treatment has finished:
- Vitamins containing folic acid, including prenatal vitamins
- Alcohol
- Penicillin
During treatment with methotrexate, only use a nonsteroidal anti-inflammatory drug (NSAID) for pain with your doctor’s approval. NSAIDs can affect the level of methotrexate in the body. If you have nausea, do not use NSAIDs, which may make your nausea worse.
Common side effects of methotrexate treatment for ectopic pregnancy include:2
- Abdominal pain. Cramping abdominal pain is the most common side effect, and it usually occurs during the first 2 to 3 days of treatment. Because abdominal pain is also a sign of a ruptured ectopic pregnancy, report any abdominal pain to your health professional.
- Vaginal bleeding or spotting.
- Nausea, vomiting, and indigestion.
- Fatigue, lightheadedness, or dizziness.
Rare side effects from methotrexate treatment for ectopic pregnancy include:
- Skin sensitivity to sunlight.
- Inflammation of the membrane covering the eye.
- Sore mouth and throat.
- Temporary hair loss.
- Severe low blood counts (bone marrow suppression).
- Inflammation of the lung (pneumonitis).
Because of the risk of side effects, methotrexate treatment requires close medical supervision by a health professional who is experienced with this medicine. During methotrexate treatment, keep your health professional informed of any symptoms that you have.
See Drug Reference for a full list of side effects. (Drug Reference is not available in all systems.)
What To Think About
Methotrexate is sometimes used just after surgical treatment to stop the growth of any remaining fetal cells.
Methotrexate versus surgery
If your ectopic pregnancy is not too far advanced and has not ruptured, methotrexate may be a treatment option for you. Methotrexate treatment avoids the risks of surgery, may be less likely to damage the fallopian tube than surgery, and may offer a better chance of maintaining your fertility after treatment.
If you are not concerned with preserving fertility, surgery for an ectopic pregnancy is faster than methotrexate treatment and causes less bleeding.
Some women who receive a methotrexate series for ectopic pregnancy report more side effects and less overall comfort than women who have laparoscopy. On the other hand, women who have laparoscopy may experience side effects related to general anesthesia and surgery, such as fatigue, abdominal bloating, and shoulder pain.
Successful methotrexate treatment is less expensive than laparoscopic surgery for ectopic pregnancy.3
Methotrexate instead of surgery
Methotrexate can be used instead of surgery in the following cases:
- Pregnancy hormone (hCG) levels are low. Methotrexate treatment is not likely to be successful when hCG levels are high.
- No fetal heart movement is noted on ultrasound (methotrexate treatment is not as likely to be successful when the embryo is more developed and growing and has heart activity).
- The ectopic pregnancy is smaller than 4cm.
- There is no bleeding into the abdomen.
- The fallopian tube has not ruptured.
- The use of anesthesia during surgery would pose a significant risk (for example, if you have a respiratory infection).
- You want to maximize your chances of becoming pregnant in the future.
When methotrexate cannot be used
Methotrexate cannot be used if you:
- Are breast-feeding.
- Have liver or kidney disease.
- Have a low red blood cell count (anemia).
- Have an impaired immune system.
- Have a ruptured fallopian tube.
If you are treated with methotrexate
You may be advised to avoid:
- Gas-producing foods, such as beans and cabbage, because abdominal discomfort is common with methotrexate.
- Exposure to the sun, because methotrexate can cause skin sensitivity to sunlight.
- Use of alcohol and other medicines.
Complete the new medication information form (PDF)
(What is a PDF document?) to help you understand this medication.
Citations
- Lipscomb GH, et al. (2002). Oral methotrexate for treatment of ectopic pregnancy. American Journal of Obstetrics and Gynecology, 186(6): 1192–1195.
- American College of Obstetricians and Gynecologists (1998). Medical management of tubal pregnancy. ACOG Practice Bulletin No. 3. Obstetrics and Gynecology, 92(6): 1–7.
- American Society of Reproductive Medicine (2006). Technical bulletin: Medical treatment of ectopic pregnancy. Fertility and Sterility, 86(4): S96–S102.
WebMD Medical Reference from Healthwise
Article Source: WebMD
Alternative Medicine and Therapies – Female
| Naturopathy
A healthy, balanced diet; regular, moderate exercise; and a positive attitude are essential for general health and fertility. A naturopathic practitioner may advise you to avoid caffeine, which is suspected of interfering with ovulation, to maintain a normal weight, and to eat only organic fruits and vegetables, grown without the use of potentially toxic chemical pesticides.
You will also be advised to restrict alcohol, since excessive amounts increase the hormone prolactin, which may disturb the menstrual cycle. Smoking is also seen as harmful, reducing blood flow to the cervix and inhibiting the action of cilia, the tiny hairs in the fallopian tubes that guide the egg toward the uterus. Splashing hot and cold water alternately on the genital area helps to stimulate local circulation. (See Hydrotherapy) Do not take a hot bath before sexual intercourse, as sperm need cool temperatures to survive.
A balanced diet is essential for the body to function property. Supplements help improve fertility. Lack of protein and calories from malnourishment is a cause of infertility, so adequate nutrition should be the basis for treatment of any illness, including infertility. Eat pumpkin seeds for zinc, which is important for the health of reproductive organs. Bee pollen and royal jelly are extremely nutrient-rich bee products that help stimulate fertility. Avoid coffee, tea and colas; caffeine promotes infertility. Dietary and Lifestyle Recommendations
A nutritional therapist may recommend life style changes including diet:
Nutritionists say that slight vitamin and mineral deficiencies, and exposure to chemical toxins, interfere with sperm and egg production and can encourage miscarriage. A practitioner may recommend alkaline foods, such as bean sprouts, peas, and milk, to offset acidity in the cervical mucus, which can inhibit sperm. Avoid acidic foods, such as red meat and tea. Foods rich in vitamin E, like vegetable oils, nuts, and eggs, protect fatty tissues (thought to be important for fertility). Foods containing essential fatty acids, such as seeds, legumes, and oily fish, are also good. Supplements such as evening primrose oil, starflower oil, linseed oil, borage seed oil, and blackcurrant oil are also valuable. Folic acid and vitamin B supplements may be suggested, since deficiencies can lead to anemia that is associated with infertility. Some practitioners also claim that supplements of vitamin B6 may raise levels of progesterone in women with irregular or absent periods. Here is a summary of the action of the most important vitamins/minerals/amino acids that play a role in conception. More detailed information on these vitamins can be obtained by visiting holisticonline.com nutrition infocenter. Vitamin E Diet Vitamin E is the fertility vitamin. Vitamin E helps to normalize hormone production by rejuvenating the endocrine system. It is also essential in cellular respiration and the absorption of fat-soluble vitamins. Choose a product containing mixed tocopherols and begin by taking 200 international units daily, then gradually increase the dosage until you are taking 400 international units twice daily. Natural sources of vitamin E include green, leafy vegetables, and watercress. Drink one tablespoon of watercress juice daily or add a few fresh sprigs to a salad. Wheat germ is an excellent source of vitamin E. In certain cases miscarriage can be prevented if the pregnant woman eats wheat germ on a regular basis. Foods rich in vitamin E, such as liver, sunflower oil, and pumpkin seeds, may counter infertility. Note: If you have high blood pressure, limit your intake of supplemental vitamin E to a total of 400 international units daily. If you are taking an anticoagulant (blood thinner), consult your physician before taking supplemental vitamin E. Vitamin B The B vitamins are required for a healthy nervous system and help maintain muscle tone in the intestinal tract. Take a good B-complex supplement that supplies 25 to 50 milligrams of each of the major B vitamins daily. Vitamin B6 given for six months or more can make a marked difference in some women having problems conceiving, as this vitamin helps balance progesterone levels. The other B vitamins are best taken together to prevent imbalances from occurring. Supplemental Digestive Enzymes Taking supplemental digestive enzymes ensures full utilization of all nutrients. Take a full-spectrum digestive- enzyme supplement providing 5,000 international units of lipase, 2,500 international units of amylase, and 300 international units of protease, plus 500 to 1,000 milligrams of pancreatin, immediately before each meal. Note: Long-term supplementation with pancreatin is not advised, as it can cause your pancreas to reduce its own production of this important enzyme. Overuse also has the potential to cause nausea or diarrhea. After two months on pancreatin, discontinue use and monitor your reaction. If you find that your digestive problems recur, discuss pancreatin supplementation with your health-care provider. Essential Fatty Acids Essential fatty acids, found in black currant seed oil, borage oil, evening primrose oil, and flaxseed oil, are required for normal glandular activity. This supplement is especially important for women who are highly athletic and/or very strict about eating a low-fat diet. Take 500 to 1,000 milligrams of any of these oils two or three times daily. Folic Acid Folic acid is necessary for successful conception and pregnancy. Moreover, low levels of folic acid early in pregnancy have been linked with an increased risk in so- called neural tube defects, such as spina bifida, in the developing fetus. A woman who wishes to become pregnant should take 400 milligrams of supplemental folic acid twice a day. Royal Jelly Royal jelly is rich in hormonal factors that help optimize hormone balance in both sexes. Many believe it enhances sexual performance. Take 20 milligrams of royal jelly daily. Selenium Selenium is an antioxidant that prevents free-radical damage, works synergistically with vitamin E, and preserves tissue elasticity. Take 200 micrograms of selenium daily. Vitamin/Mineral Supplement for Absence of Ovulation
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Nutrition Recommendations for General Infertility |
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| Supplement | Suggested Dosage | Comments |
| Selenium | 200-400 mcg daily | Deficiency has been linked to infertility in women. |
| Vitamin C | 2,000-6,000 daily, in divided doses. | See Description |
| Vitamin E | Start with 200 IU daily and increase gradually to 400-1,000 IU daily. | Needed for balanced hormone production. Has been known as the ‘sex vitamin” that carries oxygen to the sex organs. |
| Zinc | 80 mg daily. Do not exceed a total of 100 mg daily from all supplements. | Important for the functioning of the reproductive organs. Use zinc gluconate lozenges for best absorption. |
| For women, an overgrowth of unfriendly or pathogenic bacteria, candida, fungi or parasites may lead to bloating, gas, alternating diarrhea with constipation, and bad breath. Most gynecological infections with resulting infertility stem from microbes that have crept into the vagina or uterus from the anus. Stool cultures for these potential problems may help make the diagnosis. Treatment will be aimed at balancing the large bowel flora with supplements like Lactobacillus acidophilus.
See Also: Nutrition for Stress Management
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Next Topic: Alternative Therapies – Female (Contd)
Copyright © 2000 – 2002, ICBS, Inc.
Article Source: HolisticOnline.com
Amenorrhea
Many women still believe that osteoporosis is a condition that only affects bone density later in life, regardless of recent efforts of medical experts to establish otherwise. In the most recent issue of Women’s Health Orthopedic Edition, Rebecca J. Locke and Michelle P. Warren, MD from Columbia Presbyterian Medical Center in New York discuss the relationship between nutrition, hypothalamic amenorrhea (HA), osteopenia and osteoporosis, a link which clearly puts many young women at increased risk of low bone density. Recognizing that bone loss can occur early in a woman’s life is a crucial step in the prevention of this process.
Hypothalamic amenorrhea (HA), or secondary amenorrhea, is the absence of menstruation in women who previously had regular periods. The term hypothalamic refers to the hypothalamus, an area at the base of the brain that acts as a hormone control center for the body, regulating, among other things, a woman’s menstrual cycle. In certain situations, such as anorexia, excessive exercise and stress, the flow of hormones is interrupted. This results in the failure of the body to produce enough estrogen and progesterone, the suppression of ovulation, and ultimately, the loss of menses. (Mayo Clinic. Amenorrhea: When Menstruation Goes Away.)
Hypothalamic amenorrhea (HA) due to anorexia, excessive exercise and stress can be extremely damaging to the body in many ways. Low body weight, inadequate body fat and energy deficiency contribute to the suppression of hormones in cases of anorexia and excessive exercise, including gonadotropin-releasing hormone (GnRH), luteinizing hormone (LH) and follicle stimulating hormone (FSH) that eventually leads to the loss of menses. Stress-related amenorrhea, also known as psychogenic HA, can affect normal weight, nonathletic women due to high levels of cortisol (a stress-related hormone) and accompanying endocrine and metabolic changes in the body.
Because hypothalamic amenorrhea is the body’s hormonal reaction to a number of different issues, it is usually seen as a red flag that whatever has lead to the loss of menstruation needs to be addressed. Furthermore, long-term amenorrhea has significant complications of its own, such as a significantly increased risk of osteopenia and osteoporosis. Osteopenia is literally defined as “poverty of bone”, and refers to any decrease in bone mass below the normal. The more commonly used term, osteoporosis, is an advanced version of osteopenia, meaning that the loss of bone mass is more significant. (Johns Hopkins. Osteoporosis. www.intelihealth.com)
Because the loss of estrogen at menopause has been implicated in the acceleration of bone loss, some have concluded that targeting the lack of estrogen production associated with amenorrhea is the most effective route to recovery in the pre-menopausal population. However, Locke and Warren point to recent evidence that highlights nutritional deficiency as a common precursor to the loss of estrogen in all types of HA. Women with eating disorders suffer from nutritional insult, low body weight and inadequate body fat, all of which clearly play a role in the loss of estrogen, the development of HA and the subsequent increased risk of osteoporosis. Athletes and excessive exercisers often expend enormous amounts of energy without adding to their diet to make up for this deficit, leading to a form of malnutrition which can trigger the hormonal suppression that leads to amenorrhea.
Finally, in key studies, restrictive eating patterns and subclinical eating and exercise disorders, such as very low fat intake, high fiber intake and more calories expended in aerobic activity daily, were found in normal weight, non-athletic women with amenorrhea, even though overall caloric intake was not significantly altered. Thus, even in the absence of blatant dietary restrictions or excessive exercise, nutritional deficiencies still played a role in their development of amenorrhea. From this evidence, which identifies nutritional deficiency as a common underlying cause of estrogen loss leading to amenorrhea in young women, it seems that targeting nutrition may be a more effective route to recovery than trying to replace estrogen without addressing the cause for loss. (Journal of Clinical Endocrinology & Metabolism, March 1999, p. 873-877).
Other evidence supporting nutrition as a common denominator for HA has been substantiated by the role of the hormone leptin, which is normally secreted by adipose tissues. Studies have shown that levels of leptin fall rapidly with severe nutritional restriction, regardless of body weight, fat, or body mass index. Low levels of leptin are a signal to the brain to shut down other “unnecessary” hormonal pathways, such as ovulation and reproduction, and to slow down cellular metabolism to protect the body’s fat stores. Furthermore, it has been shown that menstruation cannot occur beneath a certain level of leptin in the body. Thus, because lower leptin levels have been found in both normal and underweight women with HA, it can be concluded that nutritional deficiencies, regardless of overall caloric intake or body fat percentage, play a major role in the development of amenorrhea.
By identifying nutritional deficiency as a common, underlying cause for all three types of HA, it is possible to develop preventive measures to minimize bone density loss due to amenorrhea, such as screening for restrictive eating patterns regardless of weight. Patient education efforts must also be increased to ensure that young women realize that the detrimental effects of amenorrhea, such as osteoporosis, extend past the point of the recovery of menses. Peak bone mass can and must be reached through nutrition and exercise into a woman’s late 20′s and possibly early 30′s. After age 40, regardless of what level of density was reached, bone mass begins to decline. Thus, by reaching peak bone mass in the first place a young woman can minimize the amount of bone density decline due to the aging process.
Once a woman has developed hypothalamic amenorrhea, treatment must be pursued as soon as possible. The overall goal of treatment is to restore menses as soon as possible to minimize the loss of bone mass. According to Locke and Warren, this is most effectively accomplished by treating the cause for hormonal suppression (nutrition) instead of merely replacing the lost estrogen. Treatment options also include behavioral and psychiatric counseling to address individual reasons for excessive stress, exercise and eating disorders. As a last resort, oral contraceptives can be used to minimize the loss of bone density caused by a prolonged lack of estrogen, but unless the causes for hormonal loss are addressed, estrogen replacement has not been shown to be very effective.
Women need to be made aware of the role that nutrition plays in the loss of estrogen, the development of amenorrhea, and the subsequent increased risk of osteopenia and osteoporosis. By understanding what initiates the cycle that leads to osteoporosis, it is possible that women at risk can minimize or even avoid substantial bone loss.
Resources:
Locke, Rebecca J. and Warren, Michelle P. How to Prevent Bone Loss in Women with Hypothalamic Amenorrhea. Women’s Health Orthopedic Edition. 2000; 3: 82-88.
Warren MP, Voussoughian F, Geer EB, et al. Functional Hypothalamic Amenorrhea: Hypoleptinemia and Disordered Eating. Journal of Clinical Endocrinology and Metabolism. 1999; 84: 873-877.
Mayo Clinic. Amenorrhea. www.mayohealth.org
Johns Hopkins. Osteoporosis www.intelihealth.com
Links:
www.mayohealth.org
www.intelihealth.com
Article Source: Melpomene.org
