Menopause and After Breast Cancer Diagnoses Getting Period Again
Mayo Clin Proc. 2011 Mar; 86(three): 229–240.
Challenges in the Gynecologic Intendance of Premenopausal Women With Breast Cancer
Jamie N. Bakkum-Gamez, Dr., Shannon Grand. Laughlin, MD, Jani R. Jensen, Doc, Cloudless O. Akogyeram, PharmD, RPh, and Sandhya Pruthi, MD
Abstruse
Premenopausal women with a new diagnosis of breast cancer are faced with many challenges. Providing health intendance for issues such as gynecologic comorbidities, reproductive health concerns, and vasomotor symptom command can be complicated because of the risks of hormone treatments and the adverse effects of adjuvant therapies. Information technology is paramount that health care professionals understand and exist knowledgeable nearly hormonal and nonhormonal treatments and their pharmacological parameters so they tin offer appropriate intendance to women who have chest cancer, with the goal of improving quality of life. Articles for this review were identified by searching the PubMed database with no date limitations. The following search terms were used: abnormal uterine haemorrhage, physiologic sex activity steroids, endometrial ablation, hysteroscopic sterilization, fertility preservation in endometrial cancer, tranexamic acrid and breast cancer, menorrhagia treatment and breast cancer, abnormal uterine bleeding and premenopausal breast cancer, levonorgestrel IUD and chest cancer, tamoxifen and gynecologic abnormalities, tamoxifen metabolism, hormones and chest cancer risk, contraception and breast cancer, pregnancy and breast cancer, and breast cancer and infertility handling.
Breast cancer is the leading cause of cancer decease in women in the U.s.a. who are anile 20 to 59 years.1 In 2010, an estimated 207,090 new cases of chest cancer were identified in the United States.2 Although breast cancer risk increases with historic period, approximately 35% of breast cancers occur during the reproductive and perimenopausal years.three The 5-year relative survival rate for women of all ages with breast cancer diagnosed between 1999 and 2005 is 89%.3 Of the premenopausal breast cancers diagnosed, approximately 58% are both estrogen receptor (ER) and progesterone receptor (PR) positive, vi% are ER positive but, 17% are PR positive only, and 20% are both ER and PR negative.4
The direction and handling of breast cancer in premenopausal women can affect menses, reproduction, and gynecologic health. Breast cancer treatment tin have a marked bear upon on fertility in women who have delayed childbearing and have fewer remaining reproductive years. Among premenopausal women with chest cancer, more than l% wish to retain their fertility.5 Additionally, other gynecologic problems and atmospheric condition are prevalent in reproductive-age women. In the full general population, more than xxx% of reproductive-age women fulfill criteria for the diagnosis of menorrhagia,6 25% have symptomatic fibroids,seven and most 67% have an underlying uterine disorder with potential to crusade aberrant uterine bleeding (AUB).viii
Among premenopausal women with breast cancer, management of menstrual disorders, contraception, vasomotor symptoms, and fertility presents a challenge. Common and effective hormonal options are less well studied in this population because of significant concern well-nigh recurrence of breast cancer. Herein,nosotros present the challenges and talk over management options for young women with chest cancer who nowadays with various common gynecologic conditions.
Articles for this review were identified past searching the PubMed database with no engagement limitations. The following search terms were used: abnormal uterine haemorrhage, physiologic sexual activity steroids, endometrial ablation, hysteroscopic sterilization, fertility preservation in endometrial cancer, tranexamic acid and chest cancer, menorrhagia treatment and breast cancer, abnormal uterine bleeding and premenopausal breast cancer, levonorgestrel IUD and breast cancer, tamoxifen and gynecologic abnormalities, tamoxifen metabolism, hormones and breast cancer hazard, contraception and chest cancer, pregnancy and chest cancer, and breast cancer and infertility treatment.
PREMENOPAUSAL SEX STEROIDS AND THEIR PHARMACOLOGY
Physiologically, premenopausal women with regular cycles take cyclic variation in levels of estradiol (E2) (xv-350 pg/mL [to catechumen to pmol/Fifty, multiply by iii.671]) and progesterone (0.2-27 ng/mL [to catechumen to nmol/Fifty, multiply past 3.18]). These "free" (unbound) hormones are biologically active and can enter a target cell and actuate its receptor.
Free E2 and progesterone levels are affected by serum carrier protein levels, with less than 2% of unconjugated steroids circulating unbound in the blood.nine The carrier proteins for sex steroid hormones are mainly sex hormone–bounden globulin (SHBG) and, to a lesser degree, serum albumin.10 The bioavailability and dynamic equilibrium of sexual practice hormones are influenced by the level of serum SHBG and other carrier proteins.xi In premenopausal women, serum SHBG, also as E2 and progesterone levels, can exist increased with tamoxifen and other selective ER modulators.12,13 Uses of estrogen and progestin preparations in the gynecologic care of premenopausal women and the effects of exogenous hormones on serum E2, progesterone, and SHBG levels are discussed subsequently.
MANAGEMENT OF AUB
Abnormal uterine bleeding includes menorrhagia (abnormally heavy or extended menstrual menstruum), metrorrhagia (light bleeding at irregular intervals), and intermenstrual bleeding; AUB affects nearly one-third of all reproductive-historic period women.6 Abnormal uterine bleeding has various anatomic and physiologic causes (Table 1). Bleeding owing to systemic weather condition, pregnancy, and medications can most oftentimes exist treated by managing the underlying cause. For women with a history of breast cancer and AUB with a gynecologic cause, treatment options are express because of the risks and fears associated with hormonal therapies and because many treatments lack evidence regarding rubber and adventure of chest cancer recurrence.8 Management options for AUB in premenopausal women with breast cancer are summarized in Table 2.
TABLE ane.
Causes of Abnormal Uterine Bleeding in Premenopausal Women
Table 2.
Management of Abnormal Uterine Bleeding in Premenopausal Women With Breast Cancera,b
AUB Acquired by Anatomic Abnormalities
For the most part, AUB caused by uterine or cervical abnormalities, independent of a history of breast cancer, can be treated surgically.14,15 Benign endocervical polyps can be removed surgically, and treatment of cervical dysplasia and invasive cervical cancer is non influenced past a prior diagnosis of breast cancer. Benign endometrial polyps may exist resected hysteroscopically or past dilation and curettage; hysterectomy is not necessitary. Withal, if endometrial cancer (EC) or circuitous atypical hyperplasia is detected, the standard treatment is hysterectomy.
Endometrial hyperplasia without atypia and select cases of circuitous atypical hyperplasia and form 1 EC can be managed with progestin therapy if patients desire fertility preservation.16-nineteen The safety of systemic progestins is unknown in women with a history of breast cancer. Synthetic progestins appear to increase the risk of breast cancer development,twenty but data regarding the use of medroxyprogesterone acetate in breast cancer survivors are lacking. Thus, more localized progestin therapy (eg, the levonorgestrel intrauterine device [LNG-IUD]) is a new, effective, and popular pick, but patients crave counseling about unknown risks of breast cancer recurrence.18
Some other cause of AUB is uterine fibroids, which are clinically apparent in up to 25% of women.7 Many treatment options are bachelor for symptomatic fibroids. Submucosal fibroids can be resected hysteroscopically, depending on the size and amount of fibroid in the cavity. Larger intramural fibroids tin exist treated through myomectomy for women who want fertility; focused ultrasonographic therapy is also an choice if patients are counseled about the limited merely promising fertility information.21-23 Uterine artery embolization and hysterectomy are effective treatments that are recommended for women who have completed childbearing.24,25
AUB Associated With Anovulatory Cycles
Anovulatory cycles are caused by a disturbance of the normal hypothalamic-pituitary-ovarian axis, resulting in an absent-minded luteal stage and failure of the ovary to produce the increased progesterone levels needed for endometrial stabilization. The E2 serum levels in anovulation remain consistent with E2 levels normally associated with proliferative-phase endometrium.26 As the endometrium proliferates without a secretory phase, irregular haemorrhage ensues, and untreated proliferation can lead to endometrial hyperplasia or EC. An endometrial biopsy is necessary to exclude malignancy. Standard handling for anovulatory haemorrhage is systemic hormones—oral, transdermal, or vaginal combined estrogen and progestin preparations.27 Among women with a history of breast cancer, systemic hormones are of concern because they may increment the risk of breast cancer recurrence.28 Management options include (i) ascertainment with periodic endometrial biopsies, (two) LNG-IUD in select women who wish to preserve fertility, or (3) hysterectomy.
Management of Menorrhagia. Women with menorrhagia should undergo an endometrial biopsy to exclude malignancy. If no disease is evident, management of menorrhagia may include the following: (1) ascertainment, (2) nonsteroidal anti-inflammatory drugs (NSAIDs), (iii) antifibrinolytics, (4) endometrial ablation (EA), (five) LNG-IUD, and (6) hysterectomy.
NSAIDs such equally ibuprofen, naproxen, and mefenamic acid meliorate menorrhagia by blocking cyclooxygenase, which converts arachidonic acid to prostaglandins.29 Prostaglandin F2α is elevated in the endometrium of women with menorrhagia compared with those without menorrhagia.30 Additionally, NSAIDs increase uterine vasoconstriction and platelet aggregation. In a Cochrane Review,31 NSAID use significantly improved haemorrhage compared with placebo but was not equally effective as LNG-IUDs or tranexamic acid. NSAID treatment is initiated just earlier the onset of menstruation and connected for approximately five days; adverse effects such as intestinal hurting, nausea, gastric bleeding, and ulcer development29 are reduced considering the medications are taken cyclically; nevertheless, precautions should be taken. Additional benefits of NSAID utilize include comeback of menstrual cramps and pain.
Tranexamic acid, a fibrinolytic inhibitor, has been used extensively in Europe for treatment of menorrhagia merely was canonical only recently past the Us Food and Drug Administration (FDA). The mechanism of action is inhibition of the conversion of plasminogen to plasmin; this blocks fibrinoly sis in the endometrium. Multiple studies have demonstrated a 40% to 54% decrease in haemorrhage,29,32 just tranexamic acrid does not manage menstrual cramps as finer as NSAIDs. Potential concerns about an increased thrombosis risk have been evaluated, and the rate of thrombosis associated with tranexamic acrid employ appears similar to that of the general population.32,33 Tranexamic acid reduces wound complications during breast cancer surgery when it is used at doses similar to those for menorrhagia34; nonetheless, no information have been published on long-term employ in women with chest cancer.
As an constructive, minimally invasive, localized treatment for menorrhagia, EA can be performed using electrocautery, light amplification by stimulated emission of radiation, cryotherapy, thermal balloon, heated saline, microwave, or radiofrequency techniques. Both thermal balloon ablation and radiofrequency ablation subtract menstrual claret loss by approximately 90% in the first three years after treatment, and the rate of amenorrhea after radiofrequency ablation is more 30%.35 Women older than 45 years, with a small-scale uterus and thin lining, have the highest take chances of amenorrhea.36 Failure of EA is associated with preoperative dysmenorrhea or tubal ligation.36 Although EA does not appear to increase the hazard of EC,37,38 EC tin can occur after ablation. Endometrial cancer is associated with type II diabetes mellitus, obesity, hypertension, colon cancer, anovulatory syndromes such every bit polycystic ovarian syndrome, history of endometrial hyperplasia, and failure of progestin handling of whatsoever cause of AUB.38,39 Patients because EA should exist counseled appropriately, and EA should be avoided in patients with loftier risk of EC. Patients must be counseled about the lower likelihood of successful endometrial biopsy, if it is indicated after EA.forty
In 2009, the LNG-IUD was FDA canonical for the treatment of menorrhagia.41 The device is a T-shaped polyethylene frame with a reservoir containing 52 mg of the progestin LNG. The initial dose, released daily into the uterine cavity, is twenty μg. This dose gradually decreases; by 5 years, the daily dose is approximately 10 μg. The effect of the LNG-IUD is primarily within the uterus. Information technology causes stromal pseudodecidualization, glandular atrophy, decreased glandular and stromal mitoses, and leukocytic infiltration.42 The LNG-IUD appears to have minimal effects on ovulation and breast milk product and does non markedly affect serum levels of E2, progesterone, or luteinizing hormone.42,43 However, LNG is one of the most potent progestins and has high binding analogousness for PRs.44 In add-on, LNG strongly binds SHBG and lowers serum SHBG levels.43 Utilize of the LNG-IUD has been associated with increased incidence of gallbladder affliction (relative take chances, 1.5), hypertension (relative run a risk, i.8), headache, malaise, weight alter, anxiety, depression, arthropathies, upper-limb neuropathies, and minor visual disturbances.45 Thus, although some reproductive functions announced to exist unaffected, LNG administered via an IUD does seem to take systemic effects.
Population-based studies of premenopausal women have shown that the LNG-IUD, used either for AUB or contraception, does non increase the chance of breast cancer.46,47 In add-on, when used by premenopausal women after initiation of breast cancer treatment, the LNG-IUD does not appear to increment the take chances of breast cancer recurrence.48 Thus, for premenopausal women who wish to retain fertility simply have menstrual disturbances, the LNG-IUD seems to be a reasonable, short-term treatment. In postmenopausal women, the LNG-IUD should exist removed. One example-control written report of women aged l to 62 years showed that the gamble of a new breast cancer diagnosis was one.5 times higher in women using the LNG-IUD alone and was 2 times the baseline risk when combined with either transdermal or oral estrogen replacement.49
TAMOXIFEN Use AND AUB
Tamoxifen is an FDA-approved, nonsteroidal, selective ER modulator that is indicated for v years of therapy for chemo-prevention among women with increased risk of breast cancer and adjuvant treatment in premenopausal and postmenopausal women with hormone-sensitive breast cancer.fifty Tamoxifen is a competitive inhibitor of estrogen; it binds to ERs51 in the chest and blocks tumor proliferation.51,52 In postmenopausal women, tamoxifen has an estrogen-agonist holding and can stimulate endometrial proliferation, resulting in singular hyperplasia and EC. Tamoxifen utilise increases symptomatic endometrial affliction past virtually 27% within 2 years of initiation of treatment53; for these patients, the relative risk of EC is two.2 to iv compared with population-based rates of EC.54,55 However, tamoxifen has an antiestrogenic effect on the premenopausal endometrium,56-58 and asymptomatic premenopausal women who take tamoxifen do not appear to have increased take a chance of polyps, hyperplasia, or EC.58,59
Abnormal uterine haemorrhage occurs in more than than 50% of premenopausal women taking tamoxifen,58,60 and in this group of women, up to 23% volition have an underlying endometrial abnormality such as polyps, hyperplasia, or EC. Nonetheless, the incidence of endometrial disease is not markedly different compared with that in premenopausal women with breast cancer and AUB who are not taking tamoxifen.60,61 This supports the notion that tamoxifen does not increase the hazard of EC and its precursors in premenopausal women. Additionally, nigh half of all premenopausal women treated with tamoxifen will have intermittent or long-term amenorrhea or oligomenorrhea57,58,60; therefore, menstrual history in this group of women is an unreliable indicator of menopausal status.58 Circumspection must be exercised in premenopausal women who become amenorrheic while taking tamoxifen, and clinical menopause should be confirmed with serum hormone levels. Both E2 and follicle-stimulating hormone levels remain reliable endocrinologic markers in the setting of tamoxifen use.58 Amenorrheic women with low serum E2 levels may have entered menopause and are at an increased risk of EC development.62
Given the higher charge per unit of endometrial disease in premenopausal women taking tamoxifen who take evolution of AUB, further evaluation is warranted via endometrial sampling with an function biopsy or with operative curettage (with or without hysteroscopy).61 Although dilation and curettage is the criterion standard, an office biopsy with an endometrial suction curette is comparable to dilation and curettage, with up to 88% sensitivity, 100% specificity, 100% positive predictive value, and 98% negative predictive value.63 Furthermore, information technology is 95% accurate in detecting endometrial abnormalities in symptomatic premenopausal women taking tamoxifen.64 If endometrial sampling shows benign pathologic findings, recurrent AUB can be observed and followed up with periodic endometrial sampling to exclude endometrial disease.
For women with AUB, the LNG-IUD appears to exist safe to utilize in conjunction with tamoxifen48; withal, for irregular or intermittent bleeding in the setting of amenorrhea, premenopausal status should be confirmed earlier placement. The LNG-IUD does not protect against circuitous singular hyperplasia or EC associated with postmenopausal tamoxifen utilize,65-67 and information technology should exist removed when a woman reaches menopause.
Women taking tamoxifen should be counseled carefully when considering EA. Residue endometrium is present later EA, and a post-EA uterine cavity assessment with an part biopsy or sonohysterography is unsuccessful in one-quarter of women.twoscore In addition, although EA does non appear to increase the risk of EC,37,38 EA in the context of tamoxifen employ has not been well studied. Definitive management via hysterectomy can exist considered for women who take uncontrolled AUB associated with tamoxifen utilize and accept completed their childbearing. Management of tamoxifen and other treatment-related sequelae is summarized in Table 3.
Table 3.
Chest Cancer Treatment–Associated Gynecologic Sequelae and Direction Options
Endometrial thickness (assessed by transvaginal ultrasonography) has been well studied in postmenopausal women, and the likelihood of EC increases with endometrial thickness greater than v mm.68,69 However, endometrial thickness has not been well studied in premenopausal women. In premenopausal women taking tamoxifen, endometrial thickening has been defined in the literature as greater than 8 mm to greater than 12 mm,58,64 but neither occult hyperplasia nor EC has been reported in screened, asymptomatic premenopausal women (premenopausal status was endocrinologically proven) who had a thickened endometrium while taking tamoxifen.58 Thus, screening with transvaginal ultrasonography appears to have low yield in this low-take chances population of women.
CONTRACEPTION DURING AND Afterward Chest CANCER Handling
Pregnancy is not recommended during systemic cytotoxic chemotherapy, during tamoxifen therapy, or for 2 months later on completion of tamoxifen therapy.70 Although premenopausal women treated with chemotherapy take an increased gamble of premature ovarian failure, an alternative method of contraception is nevertheless required until menopause is confirmed.71,72
Those who have completed their childbearing should be counseled almost permanent contraceptive options. Failure rates of permanent contraceptive methods, natural family planning, and bulwark methods are listed in Tables 4 and 5. The more than constructive nonhormonal or hormonal methods with limited systemic effects may be more attractive to some women. Contraceptive options for women with a history of breast cancer are shown in the Figure.
TABLE four.
One-Yr Failure Rates for Permanent Contraceptive Methods
Table 5.
One-Year Failure Rates for Barrier Contraceptive Methods
Contraception algorithm for premenopausal women with breast cancer. BSO = bilateral salpingo-oophorectomy; IUD = intrauterine device.
Although systemic hormones are the most mutual reversible contraceptive methods, they are not recommended for women with a history of breast cancer. Intrauterine devices are highly effective, with rates of pregnancy after 1 year of typical use at 0.8% for copper IUDs and 0.two% for LNG-IUDs.77 The electric current FDA-approved copper IUD (ParaGard, Duramed Pharmaceuticals, Inc, Pomona, NY) remains in identify for 10 years. It is associated with high patient satisfaction, similar to that with the LNG-IUD,78 which was FDA-approved for contraception in 2000 and tin can remain in identify for 5 years. The copper IUD may be associated with a higher charge per unit of abnormal bleeding.79 In women with a history of AUB or run a risk factors for AUB, the LNG-IUD may exist preferred.
Permanent sterilization can exist performed laparoscopically, hysteroscopically, transvaginally, or concurrently with whatever abdominal surgery. The hysteroscopic methods Essure (Conceptus Inc, Mountain View, CA) and Adiana (Hologic, Inc, Bedford, MA) are performed equally outpatient surgical procedures, and patients usually are able to render to work the next day. The Essure procedure uses 4-cm long nickel-titanium coils that are placed into the fallopian tubes.80 In the Adiana procedure, a radiofrequency ablation creates a lesion at the isthmus of the fallopian tube, and a silicone matrix is so injected at the site. For both methods, tissue in-growth occludes the tubes in a 3-calendar month period. Patients volition need a redundancy method of contraception during that menstruum.81 A hysterosalpingogram is obtained after 3 months to confirm bilateral tubal apoplexy.
Laparoscopic methods of tubal ligation include Filshie clips (Cooper Surgical, Trumbull, CT), cauterization, suture ligation, or removal of a portion or all of the fallopian tubes bilaterally. These outpatient procedures require 2 to 4 small incisions in the belly and have a postoperative recovery fourth dimension of virtually 1 week. Bilateral salpingectomy tin can as well be performed via a vaginal culdotomy.82 These methods are immediately effective and do non require back-up contraception or a hysterosalpingogram. For women with a BRCA mutation, bilateral salpingo-oophorectomy provides permanent sterilization and reduces the take a chance of ovarian cancer.83
FERTILITY AFTER Breast CANCER
Reproductive-historic period women with cancer diagnoses are highly concerned about future fertility; approximately three-quarters of women younger than 35 years who are childless at cancer diagnosis want to preserve their fertility.84 Although potentially life-saving, cancer therapy can result in subfertility or even sterility because of permanent germ cell damage. In 2006, the American Society of Clinical Oncology recommended that oncologists discuss the possibility of infertility with reproductive-age cancer patients and offering referral for fertility preservation consultation and therapy.85 Rapid referral is essential because some strategies require 2 to 3 weeks to complete; ideally, fertility-preserving procedures tin can be performed betwixt surgery and the start of adjuvant therapy.
Fertility preservation options (Tabular array 3) vary by historic period, blazon of malignancy, and anticipated cancer treatment. For example, alkylating agents, which are not–prison cell-bike-specific, are associated with the highest chance of ovarian failure. The odds ratio for inducing complete ovarian failure with the alkylating agent cyclophosphamide is three.98 compared with unexposed women.72 Historic period is also a critical factor; in ane report, the incidence of amenorrhea after chemotherapy in women who received cyclophosphamide, methotrexate, and 5-fluorouracil was 61% for women younger than 40 years and 95% for those older than 40 years.71 Rates of amenorrhea after common adjuvant chemotherapy regimens for breast cancer are outlined in Table 6.71,86-89
TABLE six.
Amenorrhea Associated With Chest Cancer Adjuvant Chemotherapy Regimens Usually Used in the United States
At the initial consultation, the patient'due south adventure of fertility damage should be discussed, taking into account the patient's current ovarian part, family unit-building goals, and planned cancer therapy. Current fertility preservation options include established and experimental strategies. Established therapies include standard assisted-reproductive technologies such as in vitro fertilization. For patients undergoing in vitro fertilization, exogenous gonadotropins are given to induce a cohort of immature oocytes to synchronously develop, a procedure typically requiring ten to 12 days. Endogenous estrogen levels become supraphysiologic during ovarian stimulation, raising concerns nigh excess hormone exposure in women who may already have a hormone-sensitive malignancy. Yet, the elevation in estrogen levels is brief (<3 weeks), and levels rapidly return to baseline. Special stimulation protocols using aromatase inhibitors also have been developed to limit estrogen exposure.90 Chest cancer patients who undergo ovarian stimulation and embryo cryopreservation do not appear to have an increased risk of illness recurrence or death.91
After ovarian stimulation, mature oocytes are harvested and can exist cryopreserved immediately in an unfertilized state or they can exist fertilized to create embryos that are after frozen. Cryopreserved embryos and oocytes can exist used years or even decades after the initial freezing. Frozen embryos have more uniform cellularity than unfertilized oocytes and thus survive the freeze-thaw process better than oocytes. Although laboratory-specific rates vary, greater than ninety% of embryos can survive the thawing process compared with approximately 50% to 60% of cryopreserved oocytes. Pregnancy rates too vary by the type of procedure performed and past oocyte age. For women younger than 35 years, pregnancy rates subsequently the transfer of thawed embryos arroyo 50%, whereas those from frozen oocytes are considerably lower (10%-xx% at best). Thus, some centers consider oocyte cryopreservation to be an experimental therapy. When feasible, well-nigh women considering oocyte or embryo cryopreservation are counseled toward embryo creation, even if it requires donor sperm purchased from a commercial sperm depository financial institution.
For women without sufficient time or resource or who are unwilling to undergo embryo or oocyte cryopreservation, other fertility preservation options include medical ovarian suppression and cryopreservation of ovarian tissue. Ovarian suppression is primarily achieved by administering gonadotropin-releasing hormone (GnRH) agonists to temporarily suppress the hypothalamic-pituitary-ovarian axis. Agin effects of GnRH agonists include hot flashes and vaginal dryness. Os density may decrease if GnRH agonists are given for an extended period (>6 months). A contempo, prospective, randomized study of concurrent GnRH agonist use during chemotherapy in premenopausal women with breast cancer92 showed that nearly 90% of women treated with GnRH agonists resumed menses and 69% resumed spontaneous ovulation subsequently treatment. In dissimilarity, of women who received chemotherapy but, 33.3% resumed menstruum, and 25.six% resumed spontaneous ovulation.
Ovarian tissue cryopreservation requires surgery to remove ane or both ovaries. Ideally, oophorectomy is performed as an outpatient surgical procedure before chemotherapy or radiotherapy; in some cases, information technology may exist performed in conjunction with breast cancer surgery. The ovarian cortex is dissected into thin strips and frozen. Thawed oocytes potentially could be fertilized to create embryos that are transferred into the uterus of the patient or a gestational carrier. In experimental atmospheric condition, ovarian tissue strips have been transplanted dorsum into orthotopic or heterotopic sites with rare reports of subsequent pregnancies. Of note, nonetheless, fewer than ten births worldwide accept been reported to date from cryopreserved ovarian tissue.93
EFFECT OF PREGNANCY
Historically, the protective result of pregnancy against breast cancer has been attributed to the full epithelial differentiation inside the chest because of lactation. Notwithstanding, newer bear witness suggests that the protective effect may be brusk-term tissue exposure to pregnancy-level estrogen.94 Physiologically, endogenous hormones contribute to development of the terminal ductal lobular unit in the breast—the site of origin for both benign and malignant chest tumors that result from cellular proliferation.95 Pregnancy accelerates the development and maturity of concluding ductal lobular units.95 Although parity is protective, epidemiologic studies have shown a transient increase in the risk of a new breast cancer diagnosis in the 10 years after a adult female's final pregnancy.96,97
The gamble of breast cancer recurrence does not appear to increase with pregnancy afterward breast cancer treatment.98-101 A large Danish report of 371 women who were pregnant later on breast cancer showed no increase in the risk of cancer recurrence or worsening of prognosis with pregnancy.102 In fact, women with full-term pregnancies had a reduced chance of decease. Additionally, the hazard of recurrence did not appear to increment,98-101 and the five-year survival rate was 100% when the pregnancy occurred ane to 2 years after handling.103,104 However, caution must be used when interpreting the results because a "good for you mother outcome" may exist—that is, only the healthier breast cancer survivors may attempt to excogitate.
LOW LIBIDO AND SEXUAL DYSFUNCTION
Multiple studies accept shown that breast cancer tin negatively impact sexual office. Sexual dysfunction occurs in approximately one-quarter to two-thirds of chest cancer survivors.105 Women who receive chemotherapy appear to exist more than negatively afflicted than those who do not.105 Other factors that affect sexual part include vaginal dryness and lower perceived sexual attractiveness.106 Sexual problems appear to be markedly more astringent in the immediate postsurgical flow; although they diminish with time, they are still more severe 1 year after handling than before diagnosis.106 Treatment of low libido (Tabular array iii) is complex, and few medical options currently exist. Working with a qualified sex therapist to accost self-prototype and relationship issues is a disquisitional component in the treatment of sexual dysfunction.
Studies that have examined the use of testosterone for low libido in women who enter menopause naturally or surgically have shown modest increases in sexual want or activity (or both). Many of these studies were performed in women who received concomitant estrogen therapy.107-111 Safety data are limited; long-term furnishings of testosterone, including effects on the breast, are unknown. Thus, applicability of testosterone is limited in women who take a history of breast cancer and in women who are unable to receive estrogen therapy.
Management OF VULVOVAGINAL ADVERSE EFFECTS Attributable TO ANTIESTROGEN THERAPY
Tamoxifen and other selective ER modulators take antiestrogenic effects on the premenopausal vagina (like to their effect on the endometrium); these may crusade vaginal cloudburst and dryness, dyspareunia, and urinary urgency and frequency.112,113 Management options are listed in Tabular array 3. Nonestrogenic treatments such as nonhormonal lubricants and vaginal moisturizers should be first-line therapy for women with a history of breast cancer because they take been shown to meliorate blood menstruation to vulvovaginal tissue and improve dryness.114,115
In one case-daily handling with vaginal estrogen preparations (Vagifem E2 tablet, Novo Nordisk, Princeton, NJ) and Premarin conjugated estrogen cream (Pfizer, Inc, New York, NY) has been studied in postmenopausal women. Women applied either a 25 μg E2 tablet or 1 g of conjugated estrogen cream (containing 0.625 mg estrogen) daily to the vagina for 1 week. Among women receiving vaginal E2, a 6.4-fold increase in serum E2 levels was observed (pretreatment mean [SD], iii.12 [0.83] pg/mL; posttreatment, 19.83 [6.07] pg/mL). Among women using conjugated estrogen foam, a 4.2-fold increase in E2 was observed (pretreatment, 2.79 [0.31] pg/mL; posttreatment, 11.63 [0.95] pg/mL),116-119 confirming systemic absorption. These findings have raised concerns about the safety of vaginal estrogen in breast cancer survivors. Still, serum E2 levels in postmenopausal women receiving vaginal estrogen preparations are like to the lowest serum E2 levels in premenopausal women with regular cycles. Vaginal estrogen has non been shown to increase the take a chance of breast cancer recurrence in postmenopausal women, but long-term, large-calibration studies showing safety are defective.117
A more than adequate and desirable pick would exist use of lower-dose vaginal estrogen tablets with less frequency (once per week rather than twice per week) along with the regular employ of nonhormonal lubricants.120 Newer agents such as the E2 x-μg vaginal tablet (Vagifem) and the silastic 17-β-estradiol impregnated slow-release vaginal ring (Estring, Pfizer, Inc, New York, NY) are also FDA approved for vaginal atrophy and are associated with significantly lower systemic E2 concentrations.121,122 Until farther studies that assess long-term rubber are available, localized estrogen for management of vulvovaginal cloudburst remains controversial. The decision to use estrogen therapy for a woman with a history of breast cancer requires consultation with the patient'south oncologist and consideration of the patient's personal values and desire to residual risks against quality of life.
Management OF VASOMOTOR SYMPTOMS
Various nonpharmacological, alternative, nonhormonal, and hormonal therapies are used for management of vasomotor symptoms (Table 3). Systemic hormone replacement is relatively contraindicated in women with breast cancer considering of the increased take a chance of cancer recurrence.28 Although no placebo-controlled, randomized clinical trials of non-pharmacological or culling approaches take been performed, nonpharmacological approaches such as avoiding hot flash triggers (eg, alcohol, hot drinks, and smoking), wearing loose-fitting vesture, and exercising are effective for many women. Additionally, behavioral modifications such equally a salubrious nutrition, paced respiration, meditation, biofeedback, and applied relaxation can exist helpful.123
Alternative methods include acupuncture and herbal remedies. Prospective randomized trials have shown footling or no comeback in hot flashes afterward use of soy preparations, ruddy clover, dong quai, ginseng, primrose oil, and black cohosh compared with placebo treatment.124,125 In addition, the FDA does not regulate most alternative medicine remedies—doses and ingredients may vary widely. Derivatives of soy and cherry-red clover include phytoestrogens and their effect on breast cancer survivors with ER-positive tumors remains inconclusive.126-128
Nonhormonal pharmacological approaches include selective serotonin reuptake inhibitors and selective noradrenergic reuptake inhibitors. Compared with placebo, medications such as paroxetine, fluoxetine, sertraline, and venlafaxine were associated with significant comeback in hot flashes.129,130 The well-nigh constructive oral doses appear to be as follows: paroxetine, 10 to 25 mg/d; fluoxetine, 20 mg/d; sertraline, 100 mg/d; and venlafaxine, 75 mg/d.131,132 Gabapentin, at oral doses ranging from 900 to 2400 mg/d, as well significantly reduced hot flashes compared with placebo.123,130,131
Women who take tamoxifen should avoid medications that inhibit the CYP2D6 enzyme, which is responsible for the metabolism of tamoxifen to its active metabolite, endoxifen. Specifically, tamoxifen, sertraline, paroxetine, and fluoxetine all inhibit the activity of the cytochrome P450 (CYP) 2D6 enzyme. This interaction is not observed with venlafaxine.132 The interactions between tamoxifen and medications that interfere with CYP2D6 enzyme activeness may result in treatment failure and subsequently may increment adventure of breast cancer recurrence.133
CONCLUSION
Many young survivors of breast cancer are seeking options for management of menstrual abnormalities, fertility, family planning, and vasomotor symptoms; such patients may benefit from appropriate counseling and referral to gynecologic and chest health specialists. The clinical dilemma of balancing the adventure of chest cancer recurrence with symptoms and quality of life can be challenging for health care professionals and patients. Wellness care professionals can benefit from understanding available new technologies and their potential to markedly affect and improve the quality of life of premenopausal women who survive breast cancer.
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