How Long Does It Take for Tissues to Become Thin Again After Using an Estring
Diagnosis and Treatment of Atrophic Vaginitis
Am Fam Physician. 2000 May 15;61(10):3090-3096.
Upwards to 40 percent of postmenopausal women have symptoms of atrophic vaginitis. Because the condition is attributable to estrogen deficiency, it may occur in pre-menopausal women who take antiestrogenic medications or who have medical or surgical conditions that upshot in decreased levels of estrogen. The thinned endometrium and increased vaginal pH level induced past estrogen deficiency predispose the vagina and urinary tract to infection and mechanical weakness. The primeval symptoms are decreased vaginal lubrication, followed by other vaginal and urinary symptoms that may be exacerbated past superimposed infection. Once other causes of symptoms take been eliminated, treatment commonly depends on estrogen replacement. Estrogen replacement therapy may be provided systemically or locally, only the dosage and delivery method must be individualized. Vaginal moisturizers and lubricants, and participation in coitus may too exist beneficial in the handling of women with atrophic vaginitis.
Considering of declining estrogen levels, women who are in mid-life or beyond often present with symptoms of atrophic vaginitis. An estimated ten to 40 percent of postmenopausal women have symptoms of atrophic vaginitis, also referred to as urogenital atrophy.i Despite the prevalence of symptoms, only twenty to 25 percent of symptomatic women seek medical attention.2,3 Therefore, physicians have an opportunity to improve the urogenital health and quality of life of a large patient population through identification of and intervention in this often overlooked and underdiagnosed condition.
Throughout a adult female'southward life cycle, the vaginal epithelium undergoes changes in response to the level of circulating estrogen. Stimulated by maternal estrogen, the vaginal epithelium is rugated and rich in glycogen in the newborn. During childhood, the epithelium remains thin until puberty, when it once again thickens as a result of estrogen stimulation. Estrogen stimulation produces copious amounts of glycogen. Döderlein's lactobacilli depend on glycogen from sloughed vaginal cells.3 Lactic acid produced by these leaner lowers vaginal pH levels to 3.5 to 4.5; this is essential for the trunk's natural defense against vaginal and urinary tract infections.iv Increased vaginal pH levels predispose the vagina to infection by streptococci, staphylococci, coliforms and diphtheroid.iii Later menopause, circulating estrogen levels (mainly estradiol), are dramatically reduced from greater than 120 pg per mL to effectually 18 pg per mL.3 Numerous cytologic transformations follow estrogen reduction, including proliferation of connective tissue, fragmentation of elastin and hyalinization of collagen. These changes may event in granulation, fissures, ecchymoses, telangiectases and ulcerations.5 Postmenopausal changes in tissue limerick are not limited to the genital tract but also include the urinary tract considering of the shared common embryologic origin. Vaginal and urethral epithelia are estrogen dependent and adversely modify in an estrogen-deprived environment.
Predisposing Factors
Menopause is the leading cause of decreased levels of circulating estrogen; therefore, it is the etiology in almost all cases of atrophic vaginitis. In nonmenopausal women, product of ovarian estrogen can be interrupted by radiations therapy, chemotherapy, immunologic disorders and oophorectomy. The postpartum decline in estrogen levels accompanies the loss of placental estrogen and the combative action of prolactin on estrogen production during lactation. Side effects of antiestrogen medications, including medroxyprogesterone (Provera), tamoxifen (Nolvadex), danazol (Danocrine), leuprolide (Lupron) and nafarelin (Synarel), are also implicated as causes of atrophic vaginitis.6 An increment in the severity of symptoms occurs in women who are naturally premenopausally estrogen deficient, smoke cigarettes, have not given nascency vaginally or exhibit nonfluctuating levels of estrogen.3,seven,8 Milder cloudburst occurs in postmenopausal women who participate in coitus, have higher androgen levels and accept non undergone vaginal surgery (Table 1).3,6–9
TABLE 1
Factors That Increase the Risk of Developing Atrophic Vaginitis
| Menopause | |
| Decreased ovarian functioning | |
| Radiation therapy | |
| Chemotherapy | |
| Immune disorder | |
| Oophorectomy | |
| Postpartum loss of placental estrogen | |
| Elevated prolactin level during lactation | |
| Medications containing antiestrogen properties6 | |
| Tamoxifen (Nolvadex) | |
| Danazol (Danocrine) | |
| Medroxyprogesterone (Provera) | |
| Leuprolide (Lupron) | |
| Nafarelin (Synarel) | |
| Natural estrogen deficiency before menopause3 | |
| Cigarette smoking7 | |
| Vaginal nulliparity | |
| Nonfluctuating estrogen levels8 | |
| Cessation of coital activity9 | |
Presenting Signs and Symptoms
A long-term decrease in estrogen stimulation is mostly required before symptoms of atrophic vaginitis ascend. A subtract in vaginal lubrication is an early hallmark of hormone insufficiency.10 Genital symptoms include dryness, burning, dyspareunia, loss of vaginal secretions, leukorrhea, vulvar pruritus, feeling of pressure, itching and yellowish malodorous discharge.iii,6,11 Urinary symptoms of urethral discomfort, frequency, hematuria, urinary tract infection, dysuria and stress incontinence may be later symptoms of vaginal atrophy (Table two).3,six,x,xi All atrophic vaginitis symptoms can exist exacerbated by a simultaneous infection of candidiasis, trichomoniasis or bacterial vaginosis. Over time, the lack of vaginal lubrication ofttimes results in sexual dysfunction and associated emotional distress.
Table 2
Presenting Symptoms of Atrophic Vaginitis
| Genital | |
| Dryness | |
| Itching | |
| Burning | |
| Dyspareunia | |
| Burning leucorrhea | |
| Vulvar pruritus | |
| Feeling of pressure | |
| Yellow malodorous discharge | |
| Urinary | |
| Dysuria | |
| Hematuria | |
| Urinary frequency | |
| Urinary tract infection | |
| Stress incontinence | |
Diagnosis
Concrete EXAMINATION
It is important not to assume a diagnosis of atrophic vaginitis (or solely a diagnosis of atrophic vaginitis) in the postmenopausal patient who presents with urogenital complaints. A patient history should include attention to exogenous agents that may crusade or further aggravate symptoms. Perfumes, powders, soaps, deodorants, panty liners, spermicides and lubricants frequently contain irritant compounds.6 In add-on, tight-fitting clothing and long-term use of perineal pads or synthetic materials tin worsen atrophic symptoms12 (Tabular array 3).vi,12
Tabular array three
Differential Diagnosis of Atrophic Vaginitis
| Candidiasis | |
| Bacterial vaginosis | |
| Trichomoniasis | |
| Contact irritation or reaction to: | |
| Perfumes | |
| Powders | |
| Deodorants | |
| Panty liners | |
| Perineal pads | |
| Soaps | |
| Spermicides | |
| Lubricants | |
| Tight-plumbing equipment or synthetic wearable | |
On examination, several signs of vaginal atrophy volition exist axiomatic. Atrophic epithelium appears pale, smoothen and shiny. Often, inflammation with patchy erythema, petechiae and increased friability may exist present. External genitalia should exist examined for macerated elasticity, turgor of peel, sparsity of pubic hair, dryness of labia, vulvar dermatoses, vulvar lesions and fusion of the labia minora3,vi (Figure 1). Introital stenosis to a width less then two fingers and decreased vaginal depth will exist credible; if these conditions are non diagnosed before insertion of the speculum, the pelvic exam volition cause considerable pain. Friable and poorly rugated vaginal epithelium is more prone to traumatic damage. Ecchymoses and minor lacerations at periintroital and posterior fourchette may also recur after coitus or during a speculum exam. Vaginal examination or sexual activity can result in vaginal bleeding or spotting. Vulvar signs of irritation caused past urinary incontinence may besides exist identified on pelvic examination. Cystocele, urethral polyps, urethral caruncle, eversion of urethral mucosa, pelvic organ prolapse and rectocele often back-trail atrophic vaginitis3 (Tabular array 4).3,6
Figure 1.
External ballocks of a 67-year-old woman who is naturally menopausal for ii years and is non on estrogen replacement therapy. Note loss of labial and vulvar fullness, pallor of urethral and vaginal epithelium, and decreased vaginal moisture.
TABLE 4
Concrete Signs of Atrophic Vaginitis
| Genital | |
| Pale, smoothen or shiny vaginal epithelium | |
| Loss of elasticity or turgor of skin | |
| Sparsity of pubic hair | |
| Dryness of labia | |
| Fusion of labia minora | |
| Introital stenosis | |
| Friable, unrugated epithelium | |
| Pelvic organ prolapse | |
| Rectocele | |
| Vulvar dermatoses | |
| Vulvar lesions | |
| Vulvar patch erythema | |
| Petechiae of epithelium | |
| Urethral | |
| Urethral caruncle | |
| Eversion of urethral mucosa | |
| Cystocele | |
| Urethral polyps | |
| Ecchymoses | |
| Minor lacerations at peri-introital and posterior fourchette | |
LABORATORY FINDINGS
Laboratory diagnostic testing, including serum hormone levels and Papanicolaou smear, can confirm the presence of urogenital cloudburst (Figures 2 and 3; Table 5).3,13 Cytologic test of smears from the upper one third of the vagina bear witness an increased proportion of parabasal cells and a decreased percentage of superficial cells. An elevated pH level (postmenopausal pH levels exceeding 5),3 monitored by a pH strip in the vaginal vault, may too be a sign of vaginal atrophy. In addition, a vaginal ultrasonogram of the uterine lining that demonstrates a sparse endometrium measuring between 4 and 5 mm signifies loss of adequate estrogenic stimulation.13 On microscopic evaluation, loss of superficial cells is obvious with cloudburst, but there may too be evidence of infection with Trichomonas, candida or bacterial vaginitis.
Figure 2.
Normal cervical Papanicolaou smear demonstrating squamous cells from the superficial and intermediate layers of the epithelium. The cells have abundant cytoplasm and a low nuclear-cytoplasmic ratio. As the cells mature toward the surface, the cytoplasm becomes keratinized, acquiring a pink color, and the nucleus turns small and condensed, reflecting pyknosis.
Figure 3.
Papanicolaou smear demonstrating atrophic vaginitis with immature (parabasal) squamous epithelial cells with enlarged nuclei in a background of basophilic granular debris and inflammatory exudate. Feature circular-shaped, baggy basophilic structures ("blue blobs") are present.
Tabular array 5
Laboratory Diagnosis of Atrophic Vaginitis
| Laboratory examination | Positive indication |
|---|---|
| Wet preparation/cytologic smear of cells from upper one third of vagina | Atrophic cytologic changes including increase in proportion of parabasal cells |
| Ultrasonograhy of uterine lining | Uterine lining demonstrating endometrial thinness between 4 and v mm13 |
| Serum hormone concentration | Depression level of circulating estrogen ≤ iv.5 |
| Vaginal pH | pH elevation above normal postmenopausal levels (pH exceeding 5)iii |
| Microscopy | Emptying of diagnosis of trichomoniasis, candidiasis and bacterial vaginosis |
Handling
ESTROGEN REPLACEMENT
Considering the lack of circulating, natural estrogens is the primary cause of atrophic vaginitis, hormone replacement therapy is the almost logical option of treatment and has proved to be effective in the restoration of anatomy and the resolution of symptoms. Estrogen replacement restores normal pH levels and thickens and revascularizes the epithelium. Adequate estrogen replacement therapy increases the number of superficial cells.3 Estrogen therapy may alleviate existing symptoms or fifty-fifty prevent evolution of urogenital symptoms if initiated at the time of menopause. Contraindications to estrogen therapy include estrogen-sensitive tumors, end-stage liver failure and a past history of estrogen-related thromboembolization. Adverse effects of estrogen therapy include breast tenderness, vaginal bleeding and a slight increase in the run a risk of an estrogen-dependent neoplasm.14 An increased take a chance of developing endometrial carcinoma and hyperplasia is conclusively related to unopposed, exogenous estrogen intake.15 Factors that make up one's mind the degree of increased risk include duration, dosage and method of estrogen delivery. Routes of assistants include oral, transdermal and intravaginal. Dose frequency may be continuous, cyclic or symptomatic. The amount of estrogen and the duration of time required to eliminate symptoms depend profoundly on the degree of vaginal atrophy and vary among patients.
Systemic administration of estrogen has been shown to have a therapeutic effect on symptoms of atrophic vaginitis. Additional advantages of systemic administration include a decrease in postmenopausal bone loss and consolation of vasomotor dysfunction (hot flushes). Standard dosages of systemic estrogen, however, may not eliminate the symptoms of atrophic vaginitis in 10 to 25 percent of patients.16 Systemic estrogen in higher dosages may be necessary to convalesce symptoms. Some women require coadministration of a vaginal estrogen product that is applied locally. Up to 24 months of therapy may be necessary to totally eradicate dryness; notwithstanding, some patients do not fully respond even to this treatment regimen.10
Other treatment options include transvaginal delivery of estrogen in the form of creams, pessaries or a hormone-releasing ring (Estring). Treatment with a low-dose transvaginal estrogen has proved effective in relieving symptoms without causing significant proliferation of the vaginal epithelium.2,12,14,17 The genitourinary pH level is likewise lowered, leading to a decreased incidence of urinary tract infections. Absorption rates increase with treatment duration because of the enhanced vascularity of the treated epithelium. The advantage of transvaginal treatment may be a decreased risk of endometrial carcinoma because a lower hormone amount is required to eliminate urogenital symptoms. Negative effects of transvaginal treatment include patient dislike of vaginal manipulation, less prevention of postmenopausal bone loss and vasomotor dysfunction, decreased control of assimilation with vaginal creams compared to oral and transdermal commitment, and irregular handling intervals that may cause patients to forget to administer the treatment.six
Transvaginal rings offer convenience, constancy of hormonal concentration in the claret stream and a therapeutic value equivalent to creams without the need for frequent application. Control of hormone dosage is manipulated by irresolute the surface area of the ring. Atrophic vaginitis symptoms are relieved (with a dosage of 5 to 10 μg per 24 hours) without stimulation of endometrial proliferation, thereby eliminating the demand to add together opposing progestogen to the regimen.eighteen Rings may exist removed and reinserted by nearly patients with little difficulty and can be worn during coitus.
MOISTURIZERS AND LUBRICANTS
Moisturizers and lubricants may be used in conjunction with estrogen replacement therapy or equally culling treatments.17 Some patients choose non to have hormone replacement, or they may have medical contraindications or experience hormonal side effects. Patients who wish to avoid using estrogen should not use moisturizers that comprise ginseng considering they may accept estrogenic properties.19 Moisturizers help maintain natural secretions and coital condolement. The length of effectiveness is by and large less than 24 hours.
Sexual practice
Sexual activity is a healthful prescription for postmenopausal women who accept a substantially estrogenized vaginal epithelium. It has been shown to encourage vaginal elasticity and pliability, and the lubricative response to sexual stimulation. Women who participate in sexual activity report fewer symptoms of atrophic vaginitis and, on vaginal examination, have less show of stenosis and shrinkage in comparison with sexually inactive women. A negative relationship exists betwixt coital activity, including masturbation, and symptoms of vaginal atrophy.9
Because no positive human relationship has been shown to exist between estrogen levels and sex, coitus is not hypothesized to restore or maintain estrogen in postmenopausal women. The existence of a positive relationship between coital activities and both gonadotropins and androgens indicates the importance of these compounds to healthy vaginal epithelium when estrogen levels are decreased.9 All sexually active women should take appropriate precautions against sexually transmitted diseases, including the human immunodeficiency virus.
Final Annotate
Vaginal atrophy need not be an inevitable effect of menopause or other events that upshot in long-term estrogen loss. Active diagnosis and intervention may prevent development of atrophic vaginitis or eliminate existing symptoms. Awareness of the many choices for commitment of estrogen replacement, too as alternative therapies, profoundly increases a physician's power to prescribe treatment that is compatible with a patient's physical needs and lifestyle. In the appropriate circumstances, encouragement of sex is also an important source of nonpharmacologic treatment nigh which many patients may not exist informed. Ironically, continued coital relations may heighten a woman'south ability to bask a healthy sexual activity life later menopause past encouraging maintenance of a physiologic surround defensive to atrophic changes.
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Figures ii and 3 provided by Renee Artymyshyn, M.D., associate professor, Department of Pathology, and Salim Haddad, M.D., senior resident, Department of Pathology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, New Brunswick.
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6. Bristles MK. Atrophic vaginitis. Tin it exist prevented too every bit treated? Postgrad Med. 1992;91:257–60.
7. Kalogeraki A, Tamiolakis D, Relakis K, Karvelas 1000, Froudarakis One thousand, Hassan E, et al. Cigarette smoking and vaginal atrophy in postmenopausal women. In Vivo. 1996;10:597–600.
8. Dupont A, Dupont P, Cusan L, Tremblay One thousand, Rioux J, Cloutier D, et al. Comparative endocrinological and clinical effects of percutaneous estradiol and oral conjugated estrogens as replacement therapy in menopausal women. Maturitas. 1991;13:297–311.
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16. Smith RN, Studd JW. Recent advances in hormone replacement therapy. Br J Hosp Med. 1993;49:799–808.
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