Atrophic vaginitis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dima Nimri, M.D. [2]

Synonyms and keywords: Atrophic vulvovaginitis; vaginal atrophy; urogenital atrophy; genitourinary syndrome of menopause

Overview

Atrophic vaginitis is defined as inflammation of the vaginal epithelium due to atrophy, secondary to decreased levels of circulating estrogen levels which manifests in elderly women with the symptoms of vaginal dryness, itching, irritation, and dyspareunia.

Historical Perspective

Classification

Atrophic vaginitis is classified based on the symptom severity into:

  • Mild: Patients with symptoms related to sexual activity.
  • Moderate to severe: Patients with symptoms not related to sexual activity.

Pathophysiology

Pathogenesis

The pathogenesis of atrophic vaginitis is due to decreased estrogen levels. Estrogen is a vasoactive hormone, which increases blood flow and maintain vaginal lubrication through fluid transudation from blood vessels.[1] The following are the manifestations of decreased estrogen levels:[1][2][3]

  • A hypoestrogenic state, such as that seen in menopause causes breakdown of collagen and elastic fibres in the vagina resulting in vaginal epithelium to lose its rugae to become thin and pale or erythematous with fine petechial hemorrhages and a narrow and shortened vagina.
  • Decreased glycogen content within the epithelium due to decreased thickness leads to less glycogen content available for the lactobacilli to utilize and turn it into lactic acid. As a result, the vaginal pH rises with a resultant overgrowth of other bacteria, such as group B streptococci, Staphylococci and diptheroids resulting in recurrent vaginal infections and UTI.

Genetics

There are no genetic factors associated with atrophic vaginitis.

Gross Pathology

Gross pathology findings in atrophic vaginitis include:[4]

  • Vaginal dryness
  • Loss of vaginal rugae
  • Changes in vaginal mucosa: pallor and friability or redness and petechiae of the mucosa

Microscopic Pathology

  • Cytology of the vaginal cells show an increase in the parabasal cells and decreased superficial cells. In situations of low estrogen levels the vaginal epithelium ceases to produce superficial and intermediate squamous cells, leaving only the parabasal and basal cells lining the vaginal wall.

Associated Conditions

Causes

Atrophic vaginitis is caused by any condition that may lead to decreased circulating estrogen levels. A hypoestrogenic state may be due to ovarian failure or other causes:[1]

Ovarian Failure Other causes
Menopause Elevated Prolactin Postpartum
Premature Ovarian Failure

Bilateral oophorectomy

Pituitary Adenoma
Chemotherapy and Radiation Medication with anti-estrogenic effect

Epidemiology and Demographics

  • Atrophic vaginitis is often an underdiagnosed condition and exact prevalence estimation is difficult because of the following reasons:
    • Majority of women are embarrassed to discuss their symptoms with doctors and few others think the symptoms associated with atrophic vaginitis as a process of natural aging.[5]
    • Only 25% of patients with symptoms seek medical care.[6]
    • Inadequate relief of symptoms with treatment.[7]
  • The features of atrophic vaginitis are estimated to be seen in 15% of premenopausal women and 40-54% of post-menopausal women.[8]
  • Based on self-reported symptoms of vaginal dryness, the prevalence of atrophic vaginitis ranged from 4% to 47%, depending on the stage of menopause (early or late menopause).[2]

Risk Factors

The risk factors associated with vaginal atrophy are related to decreased estrogen levels, which can be due to menopause (most common cause) or other causes that may lead to hypoestrogenism or vaginal atrophy. These include:[1]

Screening

There are no screening recommendations for atrophic vaginitis.[9]

Differentiating atrophic vaginitis from other diseases

Atrophic vaginitis must be differentiated from other disease processes that may present with similar symptoms. These can be divided into 4 categories:[2] [1]

The following is a list of differential diagnosis for Atrophic Vaginits: [10][11][12][13][14]

Disease Findings
Atrophic vaginitis
  • Progressive symptoms
  • Presents with yellow and malodorous vaginal discharge, vaginal dryness, postcoital bleeding, and dyspareunia with the signs of vaginal inflammation and elevated vaginal pH (>5)
  • Diagnosis is critical and laboratory tests help to confirm hypoestrogenic state
Trichomoniasis
  • Presents with purulent, malodorous, thin discharge associated with burning, pruritus, and dysuria, with the signs of vaginal inflammation and elevated vaginal pH (>4.5)
  • Motile trichomonads on wet mount are demonstrated
  • Positive culture (Gold standard)
  • Positive nucleic acid amplification test (NAAT)
Bacterial Vaginosis
  • Presents with dysuria, vaginal discharge
  • Fishy odor (positive whiff test)
  • Normal vaginal PH (<4.5)
  • On speculum examination signs of vaginal inflammation are demonstrated
Candida Vulvovaginitis
  • Presents with vulvar pruritus and cottage cheese-like vaginal discharge with no or minimal odor with normal vaginal pH (4-4.5)
  • presence of Candida on wet mount (adding 10% KOH destroys the cellular elements and facilitates recognition of budding yeast, pseudohyphae, and hyphae)
Lichen Sclerosus
  • Affects pre-pubertal and post-menopausal women, reflecting its nature of occurrence in low estrogen states[15]
  • Pruritus is the predominant symptom, burning with urination and dyspareunia can also be seen
  • On examination characteristically the lesions follow a figure of eight pattern affecting the areas around the vagina and anus
  • Signs of active disease include white atrophic plaques with cigarette-paper wrinkling, petechiae, fissures and erosions can be demonstrated
  • Examination findings of chronic disease include clitoral hood phimosis and labia minora resorption
  • Diagnosis confirmed with skin punch biopsy
Lichen Planus
  • Affects pre-menopausal and post menopausal women[16]
  • T-cell mediated inflammatory disease affecting mucosal membranes.
  • In erosive form patients present with vulvar pain, dyspareunia and dysuria.
  • Non-erosive form presents with pruritus
  • On examination appears lesions appear as red plaques or erosions, with overlying white violaceous or reticular plaques( Wickham Striae)
  • Diagnosis confirmed by shave or punch biopsy
Lichen simplex chronicus
  • On examination leasion appear as thick, erythematous lichenified skin (epidermal thickening and accentuation of skin markings)
  • Due to long-term rubbing or scratching secondary to conditions such as recurrent yeast infections, contact dermatitis, psychiatric illness[17]
Contact dermatitis
  • It could be allergic or irritant contact dermatitis
  • Presents with redness, swelling, and pruritus[18]
  • Ocassionally blistering and painful bright red swelling can be seen
Vulvar intraepithelial neoplasm
  • Bimodal peak is observed - between 40-44years and above 55years[19]
  • Red, white, or dark raised or eroded multifocal lesions [20][21]
Vulvar Cancer
  • Presents as a solitary ulcer with raised or indurated edge
  • Histologically it can be a melanoma, squamous cell carcinoma, basal cell carcinoma or neuroendocrine cancer[22]
Extramammary Paget disease
  • Seen in postmenopausal women
  • On examination it appears as a erythematous plaque with typical white scaling known as “cake-icing scaling”[23]
  • Biopsy is characterized by the presence of intraepithelial mucin-producing neoplastic cells known as Paget cells[24]

Natural History, Complications and Prognosis

Natural History

Atrophic vaginitis is a chronic progressive medical problem affecting postmenopausal women and in younger women with low estrogen levels. Women present with vaginal dryness, pruritus, urinary disturbances and dyspareunia.[25]

Prognosis

Atrophic vagnitis is a chronic disease and requires continuous treatment with estrogen or other alternatives. Majority of the patients have significant resolution of the symptoms with treatment, however the symptoms recur once the treatment is stopped.[26]

Complications

Complications of atrophic vaginitis include:[1][27][8]

Diagnosis

History and Symptoms

Symptoms of atrophic vaginitis can be divided into three categories:[1][2][3]

  • External genital symptoms:
    • Vaginal dryness
    • Vaginal irritation
    • Vaginal itching
    • Yellowish or brown vaginal discharge
  • Sexual symptoms:
    • Painful sexual intercourse (dyspareunia)
    • Postcoital bleeding
    • Loss of bleeding
    • Loss of arousal
    • Pelvic pain
  • Urological symptoms:

Physical Examination

Physical examination in women with atrophic vaginitis includes a general inspection of the external genitalia, as well as a speculum examination of the internal genitalia.[3][12]

  • Physical examination in women with atrophic vaginitis begins with inspection of the external genitalia. Findings include decreased elasticity of the skin, sparsity of pubic hair, dryness of the labia and/or fusion of the labia minora.
  • Gynecologic examination is carried using a small speculum to avoid damage to the atrophic vaginal or vulvar tissue. Vaginal epithelium may be atrophic and appear pale, smooth and shiny. Other findings include increased friability, inflamed epithelium with patchy erythema and petechiae.
  • Other findings may include: pelvic organ prolapse, such as cystocele and/or rectocele, urethral polyps or eversion of the urethral mucosa.

Laboratory Findings

Assessment of Vaginal Atrophy

  • Vaginal Cytology: It demonstrates a decrease in the superficial squamous cells and an increased parabasal cells.[28]
  • Vaginal Maturation Index(VMI): It represents the percentage of the parabasal, intermediate and superficial squamous cells. It is for example represented and read from left to right as follows ; 0/35/65-it represents 0% parabasal cells, 35% intermediate cells and 65% superficial cells. A shift to the left indicates vaginal atrophy.[29]
  • Vaginal Maturation Value (VMV): It is calcualted using a formula: 0 * %parabasal cells + 0.5 * %intermediate cells + 1.0 * superficial cells divided by 2. A lower VMV indicates a low number of superficial cells indicating hypoestrogenic state.[30]
  • Vaginal pH : Normal vaginal pH is acidic and is maintained by the lactobacillus flora by the breakdown of glucose (from the vaginal epithelial cell glycogen-the level of which is based on the estrogen) to lactic acid.
    • In lower estrogen states the vaginal pH is typically greater then 5; higher than normal due to lower levels of glycogen in the epithelial cells. It is a useful and inexpensive test in the absence of bacterial vaginosis to indicate vaginal atrophy.[31]
  • Wet mount of vaginal smear : Demonstrates the paucity of Lactobacillus.

Ultrasound

An ultrasound of the uterus may demonstrate thinning of the endometrium lining to 4-5mm.

Treatment

Medical Therapy

Atrophic vaginitis is a chronic condition which mandates continuous treatment. The choice of therapy is based on the severity of the symptoms and associated factors such as history of hormone dependent cancer. [32][33]

  • In patients with mild symptoms lubricants are the first line therapeutic choice to relieve symptoms.[34]
  • In patients with moderate to severe symptoms unresponsive to lubricants topical estrogen or oral estrogen therapy is preferred. In patients with menopause topical agents are preferred over systemic.
  • In patients with history of hormone dependent cancer, discuss the risks and benefits with the patient and the oncologist before initiation of therapy.
  • Progesterone is not indicated in patients with topical low dose estrogen therapy, however endometrial safety studies are lacking in this group who receive treatment greater than a year.
  • Patients at a higher risk of developing endometrial cancer secondary to estrogen therapy, annual transvaginal ultrasound is recommended .
  • All the patients with post-menopausal bleeding with a uterus, should be evaluated with transvaginal ultrasound and endometrial biopsy.
  • The following table is the description of available options for the treatment of Atrophic vaginitis[35]:
Treatment Modality Improvement in symptoms Advantages Limitations
Topical Estrogen[36][2][37]

(Creams and Estradiol releasing vaginal rings)

  • Restores vaginal epithelium and associated vaginal vasculature[38]
  • Improves vaginal secretions
  • Lowers vaginal pH and restores healthy vaginal flora
  • Relieves urinary symptoms
  • Effective resolution of dyspareunia, vaginal itching, and dryness[39]
  • No systemic absorption
  • 80 to 90% patients have symptomatic improvement[40]
  • Creams can be messy to use
  • Rings are expelled in patients with cystocele and rectocele
  • Side effects include vaginal secretion, vaginal spotting, and genital pruritus
Oral Estrogen Therapy

In addition to the changes with topical estrogen other actions include:

  • Relief from hot flashes and protection from osteoporosis
 Treats menopausal symptoms like hot flashes
  • Adverse effects include :breast tenderness and/or enlargement, vaginal bleeding or spotting, nausea, and weight gain
  • Contraindications include: known or suspected cases of breast cancer, estrogen-dependent cancers, undiagnosed vaginal bleeding, history of thromboembolism, endometrial hyperplasia or cancer, hypertension, hyperlipidemia, liver disease,history of stroke, venothrombotic events, coronary heart disease, pregnancy, smoking in those age >35 years, migraines with neurologic symptoms, and acute cholecystitis/cholangitis.
Selective estrogen receptor modulator

Ospemifene[41]

  • Safe in treating vulvovaginal atrophy
  • Treats dyspareunia by improving vaginal structure and pH
 Less than 1% risk of developing endometrial hyperplasia after treatment for 52weeks[42] Increased risk of venous thromboembolism
Laser Therapy
  • Fractional microablative carbon-dioxide lazer improves vascularity, glycogen storage, extracellular matrix production cellular proliferation[43]
  • Impreovement of vaginal epithelial thickness and viability[44]
  • Improvement of symptoms sustained at 12 weeks after therapy
  • Improved sexual activity[45]
 Lack of longterm evidence on efficacy and safety[46]
  • Common adverse effect is hot flashes
  • Contraindicated in patients with DVT
Tibolone

Synthetic steriod

  • Improves VMI, sexual desire with the androgenic activity[47]
  • Improvement in urinary symptoms
  • Improvement of urinary symptoms
  • No endometrial hyperplasia [48]
 Lack of longterm evidence on efficacy

Increases recurrence risk of breast cancer in patients with history of breast cancer

Vaginal spotting and bleeding[49]

Oxytocin Oxytocin gel improves vaginal secretions and epithelial thickness and pH[50][51] No endometrial hyperplasia No longterm evidence[52]
Intravaginal dehydroepiandrosterone Improves vaginal epithelium thickness and secretions[53][54] None Lacks longterm studies
Moisturizers and lubricants[55] Polymers adhere to the epithelial and mucin improving vaginal lubrication Temporary relief for patients with mild symptoms Doesnt reverse atrophic changes

Assessment of Response to treatment

  • Atrophic vaginitis being a chronic disease continuous therapy is recommended. Response to treatment is assessed by the following:
    • Vaginal Maturation Index(VMI) assessment
    • Vaginal pH assessment

Prevention

Primary Prevention

Secondary Prevention

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Gandhi J, Chen A, Dagur G, Suh Y, Smith N, Cali B, Khan SA (2016). "Genitourinary syndrome of menopause: an overview of clinical manifestations, pathophysiology, etiology, evaluation, and management". Am. J. Obstet. Gynecol. doi:10.1016/j.ajog.2016.07.045. PMID 27472999.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 Mac Bride MB, Rhodes DJ, Shuster LT (2010). "Vulvovaginal atrophy". Mayo Clin. Proc. 85 (1): 87–94. doi:10.4065/mcp.2009.0413. PMC 2800285. PMID 20042564.
  3. ↑ 3.0 3.1 3.2 Pandit L, Ouslander JG (1997). "Postmenopausal vaginal atrophy and atrophic vaginitis". Am. J. Med. Sci. 314 (4): 228–31. PMID 9332260.
  4. ↑ Wysocki S, Kingsberg S, Krychman M (2014). "Management of Vaginal Atrophy: Implications from the REVIVE Survey". Clin Med Insights Reprod Health. 8: 23–30. doi:10.4137/CMRH.S14498. PMC 4071759. PMID 24987271.
  5. ↑ Palacios, Santiago (2009). "Managing urogenital atrophy". Maturitas. 63 (4): 315–318. doi:10.1016/j.maturitas.2009.04.009. ISSN 0378-5122.
  6. ↑ Johnston SL, Farrell SA, Bouchard C, Farrell SA, Beckerson LA, Comeau M; et al. (2004). "The detection and management of vaginal atrophy". J Obstet Gynaecol Can. 26 (5): 503–15. PMID 15151738.
  7. ↑ Kingsberg SA, Wysocki S, Magnus L, Krychman ML (2013). "Vulvar and vaginal atrophy in postmenopausal women: findings from the REVIVE (REal Women's VIews of Treatment Options for Menopausal Vaginal ChangEs) survey". J Sex Med. 10 (7): 1790–9. doi:10.1111/jsm.12190. PMID 23679050.
  8. ↑ 8.0 8.1 DiBonaventura, Marco; Luo, Xuemei; Moffatt, Margaret; Bushmakin, Andrew G.; Kumar, Maya; Bobula, Joel (2015). "The Association Between Vulvovaginal Atrophy Symptoms and Quality of Life Among Postmenopausal Women in the United States and Western Europe". Journal of Women'sHealth. 24 (9): 713–722. doi:10.1089/jwh.2014.5177. ISSN 1540-9996.
  9. ↑ U.S. Preventive Services Task Force https://www.uspreventiveservicestaskforce.org/BrowseRec/Search?s=atrophic+vaginitis. Accessed on Oct. 24, 2016
  10. ↑ Guerrero A, Venkatesan A (2015). "Inflammatory Vulvar Dermatoses". Clin Obstet Gynecol. 58 (3): 464–75. doi:10.1097/GRF.0000000000000125. PMID 26125955.
  11. ↑ Centers for Disease Control and Prevention. 2015 Sexually Transmitted Diseases Treatment Guidelines. Bacterial Vaginosis. http://www.cdc.gov/std/tg2015/bv.htm Accessed on October 13, 2016
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  13. ↑ Krieger JN, Tam MR, Stevens CE, Nielsen IO, Hale J, Kiviat NB; et al. (1988). "Diagnosis of trichomoniasis. Comparison of conventional wet-mount examination with cytologic studies, cultures, and monoclonal antibody staining of direct specimens". JAMA. 259 (8): 1223–7. PMID 2448502.
  14. ↑ Eckert LO, Hawes SE, Stevens CE, Koutsky LA, Eschenbach DA, Holmes KK (1998). "Vulvovaginal candidiasis: clinical manifestations, risk factors, management algorithm". Obstet Gynecol. 92 (5): 757–65. PMID 9794664.
  15. ↑ Zendell K, Edwards L (2013). "Lichen sclerosus with vaginal involvement: report of 2 cases and review of the literature". JAMA Dermatol. 149 (10): 1199–202. doi:10.1001/jamadermatol.2013.4885. PMID 23925660.
  16. ↑ McPherson T, Cooper S (2010). "Vulval lichen sclerosus and lichen planus". Dermatol Ther. 23 (5): 523–32. doi:10.1111/j.1529-8019.2010.01355.x. PMID 20868406.
  17. ↑ Thorstensen KA, Birenbaum DL (2012). "Recognition and management of vulvar dermatologic conditions: lichen sclerosus, lichen planus, and lichen simplex chronicus". J Midwifery Womens Health. 57 (3): 260–75. doi:10.1111/j.1542-2011.2012.00175.x. PMID 22594865.
  18. ↑ Harper J, Zirwas M (2015). "Allergic contact dermatitis of the vagina and perineum: causes, incidence of, and differentiating factors". Clin Obstet Gynecol. 58 (1): 153–7. doi:10.1097/GRF.0000000000000094. PMID 25608257.
  19. ↑ Preti M, Igidbashian S, Costa S, Cristoforoni P, Mariani L, Origoni M; et al. (2015). "VIN usual type-from the past to the future". Ecancermedicalscience. 9: 531. doi:10.3332/ecancer.2015.531. PMC 4431399. PMID 25987900.
  20. ↑ Nelson EL, Bogliatto F, Stockdale CK (2015). "Vulvar Intraepithelial Neoplasia (VIN) and Condylomata". Clin Obstet Gynecol. 58 (3): 512–25. doi:10.1097/GRF.0000000000000132. PMID 26133495.
  21. ↑ Reyes MC, Cooper K (2014). "An update on vulvar intraepithelial neoplasia: terminology and a practical approach to diagnosis". J Clin Pathol. 67 (4): 290–4. doi:10.1136/jclinpath-2013-202117. PMID 24399036.
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  24. ↑ Lopes Filho LL, Lopes IM, Lopes LR, Enokihara MM, Michalany AO, Matsunaga N (2015). "Mammary and extramammary Paget's disease". An Bras Dermatol. 90 (2): 225–31. doi:10.1590/abd1806-4841.20153189. PMC 4371672. PMID 25830993.
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  26. ↑ "Management of symptomatic vulvovaginal atrophy". Menopause: The Journal of The North American Menopause Society. 20 (9): 888–902. 2013. doi:10.1097/GME.0b013e3182a122c2. ISSN 1072-3714.
  27. ↑ Woods NF, Mitchell ES (2005). "Symptoms during the perimenopause: prevalence, severity, trajectory, and significance in women's lives". Am. J. Med. 118 Suppl 12B: 14–24. doi:10.1016/j.amjmed.2005.09.031. PMID 16414323.
  28. ↑ van der Laak JA, Schijf CP, Kerstens HM, Heijnen-Wijnen TH, de Wilde PC, Hanselaar GJ (1999). "Development and validation of a computerized cytomorphometric method to assess the maturation of vaginal epithelial cells". Cytometry. 35 (3): 196–202. PMID 10082300.
  29. ↑ McEndree B (1999). "Clinical application of the vaginal maturation index". Nurse Pract. 24 (9): 48, 51–2, 55–6. PMID 10507070.
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  32. ↑ "Management of symptomatic vulvovaginal atrophy". Menopause: The Journal of The North American Menopause Society. 20 (9): 888–902. 2013. doi:10.1097/GME.0b013e3182a122c2. ISSN 1072-3714.
  33. ↑ Stuenkel CA, Davis SR, Gompel A, Lumsden MA, Murad MH, Pinkerton JV; et al. (2015). "Treatment of Symptoms of the Menopause: An Endocrine Society Clinical Practice Guideline". J Clin Endocrinol Metab. 100 (11): 3975–4011. doi:10.1210/jc.2015-2236. PMID 26444994.
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  37. ↑ Holmgren PA, Lindskog M, von Schoultz B (1989). "Vaginal rings for continuous low-dose release of oestradiol in the treatment of urogenital atrophy". Maturitas. 11 (1): 55–63. PMID 2498619.
  38. ↑ Palacios, Santiago; CasteloBranco, Camil; Currie, Heather; Mijatovic, Velja; Nappi, Rossella E.; Simon, James; Rees, Margaret (2015). "Update on management of genitourinary syndrome of menopause: A practical guide". Maturitas. 82 (3): 308–313. doi:10.1016/j.maturitas.2015.07.020. ISSN 0378-5122.
  39. ↑ Suckling J, Lethaby A, Kennedy R (2006). "Local oestrogen for vaginal atrophy in postmenopausal women". Cochrane Database Syst Rev (4): CD001500. doi:10.1002/14651858.CD001500.pub2. PMID 17054136.
  40. ↑ Willhite, Laurie A.; O'Connell, Mary Beth (2001). "Urogenital Atrophy: Prevention and Treatment". Pharmacotherapy: Official Journal of the American College of Clinical Pharmacy. 21 (4): 464–480. doi:10.1592/phco.21.5.464.34486. ISSN 0277-0008.
  41. ↑ McLendon AN, Clinard VB, Woodis CB (2014). "Ospemifene for the treatment of vulvovaginal atrophy and dyspareunia in postmenopausal women". Pharmacotherapy. 34 (10): 1050–60. doi:10.1002/phar.1465. PMID 25052122.
  42. ↑ Wurz GT, Kao CJ, DeGregorio MW (2014). "Safety and efficacy of ospemifene for the treatment of dyspareunia associated with vulvar and vaginal atrophy due to menopause". Clin Interv Aging. 9: 1939–50. doi:10.2147/CIA.S73753. PMC 4235480. PMID 25419123.
  43. ↑ Athanasiou S, Pitsouni E, Antonopoulou S, Zacharakis D, Salvatore S, Falagas ME; et al. (2016). "The effect of microablative fractional CO2 laser on vaginal flora of postmenopausal women". Climacteric. 19 (5): 512–8. doi:10.1080/13697137.2016.1212006. PMID 27558459.
  44. ↑ Pitsouni E, Grigoriadis T, Tsiveleka A, Zacharakis D, Salvatore S, Athanasiou S (2016). "Microablative fractional CO2-laser therapy and the genitourinary syndrome of menopause: An observational study". Maturitas. 94: 131–136. doi:10.1016/j.maturitas.2016.09.012. PMID 27823733.
  45. ↑ Salvatore S, Nappi RE, Parma M, Chionna R, Lagona F, Zerbinati N; et al. (2015). "Sexual function after fractional microablative CO₂ laser in women with vulvovaginal atrophy". Climacteric. 18 (2): 219–25. doi:10.3109/13697137.2014.975197. PMID 25333211.
  46. ↑ Hutchinson-Colas J, Segal S (2015). "Genitourinary syndrome of menopause and the use of laser therapy". Maturitas. 82 (4): 342–5. doi:10.1016/j.maturitas.2015.08.001. PMID 26323234.
  47. ↑ Botsis D, Kassanos D, Kalogirou D, Antoniou G, Vitoratos N, Karakitsos P (1997). "Vaginal ultrasound of the endometrium in postmenopausal women with symptoms of urogenital atrophy on low-dose estrogen or tibolone treatment: a comparison". Maturitas. 26 (1): 57–62. PMID 9032748.
  48. ↑ Szlendak-Sauer K, Wierzba W, Radowicki S (2008). "[The influence of a tibolone therapy on endometrium in postmenopausal women]". Ginekol Pol. 79 (11): 758–61. PMID 19140498.
  49. ↑ Formoso G, Perrone E, Maltoni S, Balduzzi S, Wilkinson J, Basevi V; et al. (2016). "Short-term and long-term effects of tibolone in postmenopausal women". Cochrane Database Syst Rev. 10: CD008536. doi:10.1002/14651858.CD008536.pub3. PMID 27733017.
  50. ↑ Al-Saqi, S. H.; Uvnas-Moberg, K.; Jonasson, A. F. (2015). "Intravaginally applied oxytocin improves post-menopausal vaginal atrophy". Post Reproductive Health. 21 (3): 88–97. doi:10.1177/2053369115577328. ISSN 2053-3691.
  51. ↑ Al-Saqi SH, Jonasson AF, Naessén T, Uvnäs-Moberg K (2016). "Oxytocin improves cytological and histological profiles of vaginal atrophy in postmenopausal women". Post Reprod Health. 22 (1): 25–33. doi:10.1177/2053369116629042. PMID 26883689.
  52. ↑ Jonasson AF, Edwall L, Uvnäs-Moberg K (2011). "Topical oxytocin reverses vaginal atrophy in postmenopausal women: a double-blind randomized pilot study". Menopause Int. 17 (4): 120–5. doi:10.1258/mi.2011.011030. PMID 22120944.
  53. ↑ Labrie F, Archer DF, Koltun W, Vachon A, Young D, Frenette L; et al. (2016). "Efficacy of intravaginal dehydroepiandrosterone (DHEA) on moderate to severe dyspareunia and vaginal dryness, symptoms of vulvovaginal atrophy, and of the genitourinary syndrome of menopause". Menopause. 23 (3): 243–56. doi:10.1097/GME.0000000000000571. PMID 26731686.
  54. ↑ Archer DF (2015). "Dehydroepiandrosterone intra vaginal administration for the management of postmenopausal vulvovaginal atrophy". J Steroid Biochem Mol Biol. 145: 139–43. doi:10.1016/j.jsbmb.2014.09.003. PMID 25201455.
  55. ↑ Edwards D, Panay N (2016). "Treating vulvovaginal atrophy/genitourinary syndrome of menopause: how important is vaginal lubricant and moisturizer composition?". Climacteric. 19 (2): 151–61. doi:10.3109/13697137.2015.1124259. PMC 4819835. PMID 26707589.


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