Atrophic vaginitis

WikiDoc Resources for Atrophic vaginitis

Articles

Most recent articles on Atrophic vaginitis

Most cited articles on Atrophic vaginitis

Review articles on Atrophic vaginitis

Articles on Atrophic vaginitis in N Eng J Med, Lancet, BMJ

Media

Powerpoint slides on Atrophic vaginitis

Images of Atrophic vaginitis

Photos of Atrophic vaginitis

Podcasts & MP3s on Atrophic vaginitis

Videos on Atrophic vaginitis

Evidence Based Medicine

Cochrane Collaboration on Atrophic vaginitis

Bandolier on Atrophic vaginitis

TRIP on Atrophic vaginitis

Clinical Trials

Ongoing Trials on Atrophic vaginitis at Clinical Trials.gov

Trial results on Atrophic vaginitis

Clinical Trials on Atrophic vaginitis at Google

Guidelines / Policies / Govt

US National Guidelines Clearinghouse on Atrophic vaginitis

NICE Guidance on Atrophic vaginitis

NHS PRODIGY Guidance

FDA on Atrophic vaginitis

CDC on Atrophic vaginitis

Books

Books on Atrophic vaginitis

News

Atrophic vaginitis in the news

Be alerted to news on Atrophic vaginitis

News trends on Atrophic vaginitis

Commentary

Blogs on Atrophic vaginitis

Definitions

Definitions of Atrophic vaginitis

Patient Resources / Community

Patient resources on Atrophic vaginitis

Discussion groups on Atrophic vaginitis

Patient Handouts on Atrophic vaginitis

Directions to Hospitals Treating Atrophic vaginitis

Risk calculators and risk factors for Atrophic vaginitis

Healthcare Provider Resources

Symptoms of Atrophic vaginitis

Causes & Risk Factors for Atrophic vaginitis

Diagnostic studies for Atrophic vaginitis

Treatment of Atrophic vaginitis

Continuing Medical Education (CME)

CME Programs on Atrophic vaginitis

International

Atrophic vaginitis en Espanol

Atrophic vaginitis en Francais

Business

Atrophic vaginitis in the Marketplace

Patents on Atrophic vaginitis

Experimental / Informatics

List of terms related to Atrophic vaginitis

For patient information, click here
To view the Vaginitis main page  Click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dima Nimri, M.D. [2] Aravind Kuchkuntla, M.B.B.S[3]

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

## Overview

[edit | edit source]

Atrophic vaginitis is defined as inflammation of the vaginal epithelium due to atrophy secondary to decreased levels of circulating estrogen. The features of this disease are estimated to be seen in 15% of premenopausal and 50% menopausal women. Patients present with the symptoms of vaginal dryness, itching, irritation, and dyspareunia. Diagnosis of atrophic vaginitis requires subjective assessment of the severity of symptoms to be correlated with the physical examination findings. The prominent physical examination findings include atrophic vaginal or vulvar tissue, pale, smooth and shiny vaginal epithelium with increased friability and inflammation with patchy erythema. The characteristic findings to confirm the diagnosis are: a left shift of the vaginal maturation index on a vaginal smear and a alkaline pH of the vagina. However, other secondary causes such as lichen sclerosus and lichen planus must be ruled before the confirmation of the diagnosis. The therapeutic management is based on the severity of the symptoms: lubricants are the first line of therapy for mild symptoms, in patients unresponsive to lubricants and with moderate to severe symptoms topical or oral estrogen therapy is effective for the management of patients . Majority of the patients have resolution of symptoms but due to the chronic nature of the condition it requires continuous treatment.

## Historical Perspective

[edit | edit source]

* In 1898, Charles B. Penrose described vaginitis in elderly women as senile Vaginitis. The areas of patchy inflammation were treated with 5% silver nitrate solution.[1]
* In 1940, Jacob described the use of vaginal pH in determination of hypoestrogenic state.[2]
* In 1947, Racoff gave a description the efficacy and safety of a synthetic estrogen, dienestrol for the treatment of menopausal syndrome and atrophic vaginitis is described.[3]
* In 1963, topical Dinesterol vaginal cream was used for the treatment of senile vaginitis.[4]
* In 1967, the relationship between the vaginal maturation index and estrogen therapy was described.[5]
* In 2013, vulvovaginal atrophy is renamed as genitourinary syndrome of menopause.[6]

## Classification

[edit | edit source]

Atrophic vaginitis is classified based on the symptom severity into:[7]

* Mild: Patients present with symptoms related to sexual activity.
* Moderate to severe: Patients with persistent symptoms not related to sexual activity.

## Pathophysiology

[edit | edit source]

#### Pathogenesis

[edit | edit source]

The pathogenesis of atrophic vaginitis is due to decreased estrogen levels. Estrogen is a vasoactive hormone, which increases blood flow and maintains vaginal lubrication through fluid transudation from blood vessels.[8] The following are the manifestations of decreased estrogen levels:[8][9][10]

* A hypoestrogenic state causes the 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.
* 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. Vaginal pH rises with a resultant overgrowth of other bacteria, such as group B streptococci, staphylococci and diptheroids leading to recurrent vaginal infections and UTI.

#### Genetics

[edit | edit source]

There are no genetic factors associated with atrophic vaginitis.

#### Gross Pathology

[edit | edit source]

Gross pathology findings in atrophic vaginitis include:[11]

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

#### Microscopic Pathology

[edit | edit source]

* 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.[12]

#### Associated Conditions

[edit | edit source]

* Atrophic vaginitis is characterized with pale dry vaginal epithelium and increased pH. This predisposes the patients to recurrent vaginal infections with common pathogens such as candida, gardnerella vaginalis and trichomonas, therefore it is essential to rule out these infections.
* Scarring and atrophy are features of lichen sclerosis and lichen planus which can co-exist with atrophic vaginitis.[13]

## Causes

[edit | edit source]

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:[8]

Ovarian Failure  | Other causes

|

Menopause | Elevated Prolactin during the Postpartum period
Premature Ovarian Failure

Bilateral oophorectomy

| Pituitary Adenoma
Chemotherapy and Radiation | Medications with anti-estrogenic effect

## Epidemiology and Demographics

[edit | edit source]

* 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.[14]
* Only 25% of patients with symptoms seek medical care.[15]
* Inadequate relief of symptoms with treatment.[16]
* The features of atrophic vaginitis are estimated to be seen in 15% of premenopausal women and 40-54% of post-menopausal women.[17]
* 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).[9]

## Risk Factors

[edit | edit source]

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:[8]

* Menopause (most common cause)
* Bilateral oophorectomy
* Premature ovarian failure
* Decreased ovarian function, due to chemotherapy or radiation
* Medications with an anti-estrogenic side effect:
* Tamoxifen
* Danazol
* Medroxyprogesterone acetate
* GnRH agonsists: leuprolide, nafarelin, goserelin
* GnRH antagonists: ganirelix
* Elevated prolactin levels during lactation
* Sexual abstinence
* Vaginal nulliparity
* Smoking
* Alcohol abuse
* Lack of exercise

## Screening

[edit | edit source]

There are no screening recommendations for atrophic vaginitis.[18]

## Differentiating atrophic vaginitis from other diseases

[edit | edit source]

Atrophic vaginitis must be differentiated from other disease processes that may present with similar symptoms. These can be divided into 4 categories:[9] [8]

* Vaginal infections: Candida vulvovaginitis, bacterial vaginosis and trichomoniasis
* Vulvovaginal dermatoses: Lichen sclerosus, lichen planus and lichen simplex chronicus
* Cancer and precancerous lesions: Vulvar intraepithelial neoplasia, vulvar cancer and extramammary paget disease
* Others: Foreign body, sexual trauma and contact irritants

The conditions which may need to be differentiated from the atrophic vagintis and presents as vulvar or vaginal pruritus, dryness, discharge and dyspareunia include the following: [19][20][21][22][23]

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 on 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[24]
* 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[25]
* 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, 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, the lesion 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[26]

Contact dermatitis |

* It could be allergic or irritant contact dermatitis
* Presents with redness, swelling, and pruritus[27]
* Ocassionally blistering and painful bright red swelling can be seen

Vulvar intraepithelial neoplasm |

* Bimodal peak is observed between 40-44 years and above 55 years[28]
* Red, white, or dark raised or eroded multifocal lesions [29][30]

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[31]

Extramammary Paget disease |

* Seen in postmenopausal women
* On examination it appears as a erythematous plaque with typical white scaling known as “cake-icing scaling”[32]
* Biopsy is characterized by the presence of intraepithelial mucin-producing neoplastic cells known as Paget cells[33]

## Natural History, Complications and Prognosis

[edit | edit source]

### Natural History

[edit | edit source]

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.[34]

### Prognosis

[edit | edit source]

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.[35]

### Complications

[edit | edit source]

Complications of atrophic vaginitis include:[8][36][17]

* If left untreated, the greatest impact is the lack of sexual enjoyment and other effects such as sleep disturbances.[37]
* Stress urinary incontinence
* Urge incontinence
* Pelvic organ prolapse
* Recurrent urinary tract infections

## Diagnosis

[edit | edit source]

### History and Symptoms

[edit | edit source]

Symptoms of atrophic vaginitis can be divided into three categories:[8][9][10]

* External genital symptoms:
* Vaginal dryness
* Vaginal irritation
* Vaginal pruritus
* Yellowish or brown vaginal discharge
* Sexual symptoms:
* Painful sexual intercourse (dyspareunia)
* Postcoital bleeding
* Lack of arousal
* Pelvic pain
* Urological symptoms:
* Burning on urination (dysuria)
* Increased Urinary frequency
* Increased Urinary urgency
* Nocturia
* Urinary incontinence
* Recurrent urinary tract infections (UTI)

### Physical Examination

[edit | edit source]

Physical examination in women with atrophic vaginitis includes a general inspection of the external genitalia, a speculum examination.[10][21]

* Physical examination in women with atrophic vaginitis begins with inspection of the external genitalia. Findings include 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

[edit | edit source]

#### Assessment of Vaginal Atrophy

[edit | edit source]

* Vaginal Cytology: It demonstrates a decrease in the superficial squamous cells and an increased parabasal cells.[12]
* Vaginal Maturation Index(VMI): It represents the percentage of the parabasal, intermediate and superficial squamous cells. It read from left to right as follows, for example if its represented as 0/35/65-it means the smear has 0% parabasal cells, 35% intermediate cells and 65% superficial cells. A shift to the left indicates vaginal atrophy.[38]
* Vaginal Maturation Value (VMV): It is calculated 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.[39]
* 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.[40]
* Wet mount of vaginal smear : Demonstrates the paucity of lactobacillus.
* FSH Level: Estimation of FSH is not neccessary for the diagnosis of hypoestrogenic state as alkaline pH of vaginal secretions is equally sensitive.[41]

### Ultrasound

[edit | edit source]

An ultrasound of the uterus may demonstrate thinning of the endometrium lining to 4-5mm.[8]

## Treatment

[edit | edit source]

### Medical Therapy

[edit | edit source]

Atrophic vaginitis is a chronic condition requiring continuous treatment. The choice of therapy is based on the severity of the symptoms and associated factors such as history of hormone dependent cancer. [42][43]

* In patients with mild symptoms, the vaginal lubricants are the first line therapeutic choice to relieve symptoms.[44]
* In patients with moderate to severe symptoms unresponsive to lubricants, the topical estrogen or oral estrogen therapy is preferred. In patients with menopause, the topical agents are preferred over systemic therapy.
* In patients with the history of harmone 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[45]:

Treatment Modality  | Improvement in symptoms  | Advantages  | Limitations

|
|
|

Topical Estrogen[46][9][47]

(Creams and Estradiol releasing vaginal rings)

* Restores vaginal epithelium and associated vaginal vasculature[48]
* Improves vaginal secretions
* Lowers vaginal pH and restores healthy vaginal flora
* Relieves urinary symptoms
* Effective resolution of dyspareunia, vaginal itching, and dryness[49]

* No systemic absorption
* 80 to 90% patients have symptomatic improvement[50]

* 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 with or without enlargement, vaginal bleeding or spotting, nausea, and weight gain
* Contraindications to estrogen inlcude: 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, coronary heart disease, pregnancy, smoking in those age >35 years, migraines with neurologic symptoms, and acute cholecystitis/cholangitis.

Selective estrogen receptor modulator

Ospemifene[51]

* Safe in treating vulvovaginal atrophy
* Treats dyspareunia by improving vaginal structure and pH

* Less than 1% risk of developing endometrial hyperplasia after treatment for 52 weeks[52]

* Increased risk of venous thromboembolism

Laser Therapy  |

* Fractional microablative carbondioxide laser improves vascularity, glycogen storage, extracellular matrix production cellular proliferation[53]
* Improvement of vaginal epithelial thickness and viability[54]

* Improvement of symptoms sustained at 12 weeks after therapy
* Improved sexual activity[55]

| Lack of long term evidence on efficacy and safety[56]

* Common adverse effect is hot flashes
* Contraindicated in patients with DVT

Tibolone

Synthetic steriod

* Improves VMI, sexual desire with the androgenic activity[57]
* Improvement in urinary symptoms

* Improvement of urinary symptoms
* No endometrial hyperplasia [58]

* Lack of long term evidence on efficacy
* Increases recurrence risk of breast cancer in patients with history of breast cancer
* Vaginal spotting and bleeding[59]

Oxytocin |

* Oxytocin gel improves vaginal secretions and epithelial thickness and pH[60][61]

* No endometrial hyperplasia

* No long term evidence[62]

Intravaginal dehydroepiandrosterone |

* Improves vaginal epithelium thickness and secretions[63][64]

* None

* Lacks long term studies

Moisturizers and lubricants[65] |

* Polymers adhere to the epithelial and mucin improving vaginal lubrication

* Temporary relief for patients with mild symptoms

* No effect on reversal of atrophic changes

### Assessment of Response to treatment

[edit | edit source]

* Atrophic vaginitis being a chronic disease, continuous therapy is recommended. Response to treatment is assessed by the following:[8]
* Vaginal Maturation Index(VMI) assessment
* Vaginal pH assessment

## Prevention

[edit | edit source]

### Primary Prevention

[edit | edit source]

There are no primary preventive measures for atrophic vaginitis.

### Secondary Prevention

[edit | edit source]

The following behavioral changes are advised to slow down the progression of atrophic vaginitis, and also help in maintenance of normal vaginal tissue:[66]

* Encouraging sexual activity helps in the maintenance of vaginal elasticity and lubrication in response to sexual stimulation.
* Stress reduction therapy is helpful in patients with non-organic causes of vaginal dryness.
* Cessation of smoking
* Encourage the use of looser undergarments; it increases the vascularity and prevents infections.

## References

[edit | edit source]

1. ↑ "A Text-book of Diseases of Women - Charles Bingham Penrose - Google Books".
2. ↑ Beilly, Jacob S. (1940). "DETERMINATION OF PH OF VAGINAL SECRETION AS AN INDEX OF OVARIAN ACTIVITY IN HYPOOVARIAN STATES". Endocrinology. 26 (6): 959–964. doi:10.1210/endo-26-6-959. ISSN 0013-7227.
3. ↑ Rakoff, A. E.; Paschkis, K. E.; Cantarow, A. (1947). "A CLINICAL EVALUATION OF DIENESTROL, A SYNTHETIC ESTROGEN1". The Journal of Clinical Endocrinology & Metabolism. 7 (10): 688–700. doi:10.1210/jcem-7-10-688. ISSN 0021-972X.
4. ↑ Falk, Henry C.; Hassid, Roger (1963). "ATROPHIC OR SENILE VAGINITIS: TREATMENT WITH DIENESTROL CREAM". Journal of the American Geriatrics Society. 11 (12): 1152–1157. doi:10.1111/j.1532-5415.1963.tb02686.x. ISSN 0002-8614.
5. ↑ "Limited Relationship of Maturation Index to Estrogen Therapy... : Obstetrics & Gynecology".
6. ↑ Portman DJ, Gass ML, Vulvovaginal Atrophy Terminology Consensus Conference Panel (2014). "Genitourinary syndrome of menopause: new terminology for vulvovaginal atrophy from the International Society for the Study of Women's Sexual Health and the North American Menopause Society". Maturitas. 79 (3): 349–54. doi:10.1016/j.maturitas.2014.07.013. PMID 25179577.CS1 maint: Multiple names: authors list (link)
7. ↑ Domoney, Claudine (2014). "Treatment of vaginal atrophy". Women's Health. 10 (2): 191–200. doi:10.2217/whe.14.9. ISSN 1745-5057.
8. ↑ 8.0 8.1 8.2 8.3 8.4 8.5 8.6 8.7 8.8 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.
9. ↑ 9.0 9.1 9.2 9.3 9.4 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.
10. ↑ 10.0 10.1 10.2 Pandit L, Ouslander JG (1997). "Postmenopausal vaginal atrophy and atrophic vaginitis". Am. J. Med. Sci. 314 (4): 228–31. PMID 9332260.
11. ↑ 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.
12. ↑ 12.0 12.1 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.CS1 maint: Multiple names: authors list (link)
13. ↑ Lewis, F. M. (2015). "Vulval symptoms after the menopause - Not all atrophy!". Post Reproductive Health. 21 (4): 146–150. doi:10.1177/2053369115608019. ISSN 2053-3691.
14. ↑ Palacios, Santiago (2009). "Managing urogenital atrophy". Maturitas. 63 (4): 315–318. doi:10.1016/j.maturitas.2009.04.009. ISSN 0378-5122.
15. ↑ 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.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
16. ↑ 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.CS1 maint: Multiple names: authors list (link)
17. ↑ 17.0 17.1 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.
18. ↑ U.S. Preventive Services Task Force https://www.uspreventiveservicestaskforce.org/BrowseRec/Search?s=atrophic+vaginitis. Accessed on Oct. 24, 2016
19. ↑ Guerrero A, Venkatesan A (2015). "Inflammatory Vulvar Dermatoses". Clin Obstet Gynecol. 58 (3): 464–75. doi:10.1097/GRF.0000000000000125. PMID 26125955.
20. ↑ 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
21. ↑ 21.0 21.1 Bachmann GA, Nevadunsky NS (2000). "Diagnosis and treatment of atrophic vaginitis". Am Fam Physician. 61 (10): 3090–6. PMID 10839558.
22. ↑ 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.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
23. ↑ 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.CS1 maint: Multiple names: authors list (link)
24. ↑ 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.
25. ↑ 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.
26. ↑ 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.
27. ↑ 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.
28. ↑ 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.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
29. ↑ 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.CS1 maint: Multiple names: authors list (link)
30. ↑ 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.
31. ↑ Chokoeva AA, Tchernev G, Castelli E, Orlando E, Verma SB, Grebe M; et al. (2015). "Vulvar cancer: a review for dermatologists". Wien Med Wochenschr. 165 (7–8): 164–77. doi:10.1007/s10354-015-0354-9. PMID 25930015.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
32. ↑ van der Linden, M.; Meeuwis, K.A.P.; Bulten, J.; Bosse, T.; van Poelgeest, M.I.E.; de Hullu, J.A. (2016). "Paget disease of the vulva". Critical Reviews in Oncology/Hematology. 101: 60–74. doi:10.1016/j.critrevonc.2016.03.008. ISSN 1040-8428.
33. ↑ 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.CS1 maint: Multiple names: authors list (link)
34. ↑ "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.
35. ↑ "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.
36. ↑ 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.
37. ↑ Simon, James A.; Kokot-Kierepa, Marta; Goldstein, Jeffrey; Nappi, Rossella E. (2013). "Vaginal health in the United States". Menopause. 20 (10): 1043–1048. doi:10.1097/GME.0b013e318287342d. ISSN 1072-3714.
38. ↑ McEndree B (1999). "Clinical application of the vaginal maturation index". Nurse Pract. 24 (9): 48, 51–2, 55–6. PMID 10507070.
39. ↑ Weber, M. A.; Limpens, J.; Roovers, J. P. W. R. (2014). "Assessment of vaginal atrophy: a review". International Urogynecology Journal. 26 (1): 15–28. doi:10.1007/s00192-014-2464-0. ISSN 0937-3462.
40. ↑ Caillouette JC, Sharp CF, Zimmerman GJ, Roy S (1997). "Vaginal pH as a marker for bacterial pathogens and menopausal status". Am J Obstet Gynecol. 176 (6): 1270–5, discussion 1275-7. PMID 9215184.CS1 maint: Multiple names: authors list (link)
41. ↑ Roy S, Caillouette JC, Roy T, Faden JS (2004). "Vaginal pH is similar to follicle-stimulating hormone for [[menopause]] diagnosis". Am J Obstet Gynecol. 190 (5): 1272–7. doi:10.1016/j.ajog.2003.12.015. PMID 15167829. URL–wikilink conflict (help)CS1 maint: Multiple names: authors list (link)
42. ↑ "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.
43. ↑ 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.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
44. ↑ Lethaby A, Ayeleke RO, Roberts H (2016). "Local oestrogen for vaginal atrophy in postmenopausal women". Cochrane Database Syst Rev (8): CD001500. doi:10.1002/14651858.CD001500.pub3. PMID 27577677.CS1 maint: Multiple names: authors list (link)
45. ↑ Domoney C (2014). "Treatment of vaginal atrophy". Womens Health (Lond). 10 (2): 191–200. doi:10.2217/whe.14.9. PMID 24601810.
46. ↑ North American Menopause Society (2007). "The role of local vaginal estrogen for treatment of vaginal atrophy in postmenopausal women: 2007 position statement of The North American Menopause Society". Menopause. 14 (3 Pt 1): 355–69, quiz 370-1. doi:10.1097/gme.0b013e31805170eb. PMID 17438512.
47. ↑ 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.
48. ↑ 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.
49. ↑ 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.CS1 maint: Multiple names: authors list (link)
50. ↑ 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.
51. ↑ 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.CS1 maint: Multiple names: authors list (link)
52. ↑ 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.CS1 maint: Multiple names: authors list (link)
53. ↑ 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.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
54. ↑ 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.CS1 maint: Multiple names: authors list (link)
55. ↑ 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.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
56. ↑ 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.
57. ↑ 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.CS1 maint: Multiple names: authors list (link)
58. ↑ 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.CS1 maint: Multiple names: authors list (link)
59. ↑ 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.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
60. ↑ 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.
61. ↑ 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.CS1 maint: Multiple names: authors list (link)
62. ↑ 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.CS1 maint: Multiple names: authors list (link)
63. ↑ 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.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
64. ↑ 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.
65. ↑ 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.
66. ↑ "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.

Template:Diseases of the pelvis, genitals and breasts

Template:WH Template:WS