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Vulvar cancer

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Monalisa Dmello, M.B,B.S., M.D. [2] Syed Musadiq Ali M.B.B.S.[3]

Synonyms and keywords: Vulva cancer, cancer of vulva, vulvar carcinoma, vulvar neoplasm, neoplasm of vulva, malignant tumor of vulva, primary vulval cancer, primary vulvar cancer, primary vulva cancer, vulval carcinoma, vulva carcinoma, carcinoma of vulva, vulval cancer, vulval neoplasia.

Overview

Overview


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Syed Musadiq Ali M.B.B.S.[2] Monalisa Dmello, M.B,B.S., M.D. [3]

Overview

Vulvar cancer accounts for about 5% of cancers of the female genital system in the United States. The vulva is the area immediately external to the vagina, including the mons pubis, labia, clitoris, bartholin glands, and perineum. The labia majora are the most common site of vulvar carcinoma involvement and account for about 50% of cases. The labia minora account for 15% to 20% of vulvar carcinoma cases. The clitoris and Bartholin glands are less frequently involved. Lesions are multifocal in about 5% of cases. About 90% of vulvar carcinomas are squamous cell cancers. The vulvar intraepithelial neoplasias (VIN), may be precursors to invasive squamous cell cancers. Common risk factors in the development of vulvar cancer are human papilloma virus, human immunodeficiency virus, vulvar intraepithelial neoplasia, and lichen sclerosus. Vulvar cancer may be classified according to histology into 3 groups: vulvar carcinoma, vulvar sarcoma, and vulvar malignant melanoma. If left untreated, patients with vulvar cancer may progress to develop ulcer on vulva or wart-like patches on vulva, and chronic pruritus of the vulva. Common complications of vulvar cancer include fistula and metastasis. Prognosis is generally good, and the 5 year survival rate of patients with vulvar cancer is approximately 71.2%. Common physical examination findings of vulvar cancer include vulvar ulcers, mass, and inguinal lymphadenopathy. Vulvar biopsy is the confirmatory test for the diagnosis of vulvar cancer or precancerous lesions.The optimal therapy for vulvar cancer depends on the stage at diagnosis.The feasibility of surgery depends on the stage of vulvar cancer at diagnosis.


Classification

Vulvar cancer may be classified according to histology into 3 groups vulvar carcinoma, vulvar sarcoma, and vulvar malignant melanoma.

Pathophysiology

Development of vulvar cancer is the result of multiple genetic mutations.

Causes

Vulvar cancer may be caused by either HPV infection, or vulvar dermatoses.

Differential Diagnosis

Vulvar cancer must be differentiated from other neoplastic vulvar lesions, non neoplastic vulvar lesions, and infectious disease lesions of vulva.

Epidemiology and Demographics

In 2012, the incidence of vulvar cancer was estimated to be 2.4 per 100,000 females in the United States. The incidence of vulvar cancer increases with age, the median age at diagnosis is 68 years. Vulvar cancer is more prevalent in the caucasian race.

Risk factors

Common risk factors in the development of vulvar cancer are human papilloma virus, human immunodeficiency virus, vulvar intraepithelial neoplasia, and lichen sclerosus.

Screening

Screening for vulvar cancer is not recommended.

Natural History, Complications and Prognosis

If left untreated, patients with vulvar cancer may progress to develop ulcer on vulva or wart-like patches on vulva, and chronic pruritus of the vulva. Common complications of vulvar cancer include fistula and metastasis. Prognosis is generally good and the 5 year survival rate of patients with vulvar cancer is approximately 71.2%.

Diagnosis

Staging

According to the FIGO cancer staging system, there are 4 stages of vulvar cancer.

History and Symptoms

Symptoms of vulvar cancer include vulvar ulcers, lumps, discoloration, and chronic pruritis of the vulva.

Physical Examination

Common physical examination findings of vulvar cancer include vulvar ulcers, mass, and inguinal lymphadenopathy.

Chest X-ray

Chest radiography (CXR) may be helpful in the diagnosis of pulmonary metastasis of vulvar cancer. The characteristic findings of pulmonary metastasis are peripheral, rounded nodules of variable size scattered throughout both lungs.

CT scan

A CT scan for vulvar cancer may be helpful in determination of tumor size, tumor shape, and to detect metastasis of vulvar cancer.

MRI

MRI is useful in accurately assessing the size of vulval lesion and assessing groin lymph node metastasis.

Other Diagnostic Studies

Vulvar biopsy is the confirmatory test for the diagnosis of vulvar cancer or precancerous lesions.

Treatment

Medical therapy

The optimal therapy for vulvar cancer depends on the stage at diagnosis.

Surgery

The feasibility of surgery depends on the stage of vulvar cancer at diagnosis.

Primary Prevention

Prevention of vulvar cancer includes a comprehensive approach involving awareness, screening, and preventative vaccinations.

References

Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Musadiq Ali M.B.B.S.[2]

Overview

There is limited information about the historical perspective of vaginal cancer.

Historical Perspective

Discovery

  • There is limited information about the historical perspective of Vaginal cancer.
Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Syed Musadiq Ali M.B.B.S.[2] Monalisa Dmello, M.B,B.S., M.D. [3]

Overview

Vulvar cancer may be classified according to histology:Squamous cell carcinoma, Basal cell carcinoma, vulvar malignant melanoma Vulvar sarcoma, Vulvar Paget disease, Bartholin gland carcinoma.

Classification

Histologic subtypes of vulvar cancer include:[1]

Squamous cell carcinoma

  • Seventy-five percent or more of vulvar malignancies are squamous cell carcinomas[2]. There are two subtypes, both of which usually occur on the labia or vestibule:[3]
  • The keratinizing, differentiated, or simplex type is more common. This occurs in older women and is not related to human papillomavirus (HPV) infection, but is associated with vulvar dystrophies such as lichen sclerosus and, in developing countries, chronic venereal granulomatous disease.
  • The classic, warty, or Bowenoid type is predominantly associated with HPV 16, 18, and 33, and found in younger women[4].These women tend to present with early-stage disease.[5]
  • There is evidence that some high-grade vulvar and vaginal intraepithelial neoplasias are monoclonal lesions derived from high-grade or malignant cervical disease[6].
  • Presence of the cervix does not appear to be necessary for oncogenic HPV to infect the genital tract.

Verrucous carcinoma

  • Verrucous vulvar carcinoma is a variant of squamous cell carcinoma that has distinctive features.
  • Although cauliflower-like in appearance, it is differentiated from squamous cell carcinoma with a verrucous configuration.
  • Biopsy shows papillary fronds without the central connective tissue core typical of condylomata acuminata.
  • The lesion grows slowly and rarely metastasizes to lymph nodes, but it may be locally destructive.

Basal cell carcinoma

  • Basal cell carcinoma is a squamous histology, but is distinct from squamous cell vulvar carcinoma.
  • Approximately 2 to 8 percent of vulvar cancers are basal cell cancers, and 2 percent of basal cell cancers occur on the vulva[7].
  • Basal cell vulvar carcinoma usually affects postmenopausal white women and may be locally invasive, although it is usually non-metastasizing [8].
  • The typical appearance is that of a “rodent” ulcer with rolled edges and central ulceration.
  • It is often asymptomatic, but pruritus, bleeding, or pain may occur.
  • Basal cell carcinomas are associated with a high incidence of antecedent or concomitant malignancy elsewhere in the body[8].

Melanoma

  • Melanoma is the second most common vulvar cancer histology, accounting for approximately 2 to 10 percent of primary vulvar neoplasms[9].
  • Melanoma of the vulva occurs predominantly in postmenopausal, white, non-Hispanic women, at a median age of 68 years[10]. By contrast, cutaneous melanomas presenting at other sites often develop before age 45.
  • Vulvar melanoma is usually a pigmented lesion, but amelanotic lesions also occur.
  • Most arise de novo on the clitoris or labia minora, but can also develop within preexisting junctional or compound nevi.

Sarcoma

  • Soft tissue sarcomas (including leiomyosarcomas, rhabdomyosarcomas, liposarcomas, angiosarcomas, neurofibrosarcomas, epithelioid sarcomas, and undifferentiated/unclassified soft tissue sarcomas) constitute 1 to 2 percent of vulvar malignancies. The prognosis is generally poor[11].
  • As with soft tissue sarcomas located elsewhere on the extremities and trunk, high-grade lesions that are larger than 5 cm in diameter, with infiltrating margins and a high mitotic rate, are those most likely to recur.

Paget disease of the vulva

  • Extramammary Paget disease, an intraepithelial adenocarcinoma, accounts for less than 1 percent of all vulvar malignancies[12]. Most patients are in their 60s and 70s and white.
  • Pruritus is the most common symptom, present in 70 percent of patients. Vulvar Paget disease is similar in appearance to Paget disease of the breast. The lesion has an eczematoid appearance; it is well-demarcated and has slightly raised edges and a red background, often dotted with small, pale islands. It is usually multifocal and may occur anywhere on the vulva, mons, perineum/perianal area, or inner thigh.
  • Diagnosis is based upon characteristic histopathology. Vulvar biopsy should be performed in patients with suspicious lesions, including those with persistent pruritic eczematous lesions that fail to resolve within six weeks of appropriate anti-eczema therapy.
  • Invasive adenocarcinomas may be present within or beneath the surface lesion[13].
  • Women with Paget disease of the vulva should also be evaluated for the possibility of synchronous neoplasms, as approximately 20 to 30 percent of these patients have a noncontiguous carcinoma[14].

Bartholin gland carcinoma

  • Bartholin gland carcinoma comprises approximately 0.1 to 5 percent of all vulvar carcinomas and 0.001 percent of all female malignancies[15].
  • The incidence of Bartholin gland carcinoma in one series was 0.023 per 100,000 woman-years in premenopausal women[16].
  • The incidence of Bartholin gland carcinoma is highest among women in their 60s.
  • Most affected women do not have a past history of benign Bartholin gland disorders.
  • Cancers arising in the Bartholin gland are most often adenocarcinomas or squamous cell carcinomas, but transitional cell carcinomas, adenosquamous, and adenoid cystic carcinomas may also develop. Most primary adenocarcinomas of the vulva occur in the Bartholin gland.[17]
  • Only the squamous cell carcinomas of the Bartholin gland are related to HPV infection[17].
  • Metastatic disease is common in cancers of the Bartholin gland because of the rich vascular and lymphatic network in this area. In one series of 11 women with Bartholin gland cancer, 55 percent developed recurrent disease, and 67 percent were alive at five years[18].

References

  1. ↑ Hoffman, Barbara (2012). Williams gynecology. New York: McGraw-Hill Medical. ISBN 9780071716727.
  2. ↑ Schuurman MS, van den Einden LC, Massuger LF, Kiemeney LA, van der Aa MA, de Hullu JA (December 2013). “Trends in incidence and survival of Dutch women with vulvar squamous cell carcinoma”. Eur. J. Cancer. 49 (18): 3872–80. doi:10.1016/j.ejca.2013.08.003. PMID 24011936.
  3. ↑ Saraiya M, Watson M, Wu X, King JB, Chen VW, Smith JS, Giuliano AR (November 2008). “Incidence of in situ and invasive vulvar cancer in the US, 1998-2003”. Cancer. 113 (10 Suppl): 2865–72. doi:10.1002/cncr.23759. PMID 18980209.
  4. ↑ Hildesheim A, Han CL, Brinton LA, Kurman RJ, Schiller JT (November 1997). “Human papillomavirus type 16 and risk of preinvasive and invasive vulvar cancer: results from a seroepidemiological case-control study”. Obstet Gynecol. 90 (5): 748–54. doi:10.1016/S0029-7844(97)00467-5. PMID 9351758.
  5. ↑ Al-Ghamdi A, Freedman D, Miller D, Poh C, Rosin M, Zhang L, Gilks CB (January 2002). “Vulvar squamous cell carcinoma in young women: a clinicopathologic study of 21 cases”. Gynecol. Oncol. 84 (1): 94–101. doi:10.1006/gyno.2001.6466. PMID 11748983.
  6. ↑ Vinokurova S, Wentzensen N, Einenkel J, Klaes R, Ziegert C, Melsheimer P, Sartor H, Horn LC, Höckel M, von Knebel Doeberitz M (December 2005). “Clonal history of papillomavirus-induced dysplasia in the female lower genital tract”. J. Natl. Cancer Inst. 97 (24): 1816–21. doi:10.1093/jnci/dji428. PMID 16368943.
  7. ↑ de Giorgi V, Salvini C, Massi D, Raspollini MR, Carli P (April 2005). “Vulvar basal cell carcinoma: retrospective study and review of literature”. Gynecol. Oncol. 97 (1): 192–4. doi:10.1016/j.ygyno.2004.12.008. PMID 15790457.
  8. ↑ 8.0 8.1 Benedet JL, Miller DM, Ehlen TG, Bertrand MA (November 1997). “Basal cell carcinoma of the vulva: clinical features and treatment results in 28 patients”. Obstet Gynecol. 90 (5): 765–8. doi:10.1016/S0029-7844(97)00416-X. PMID 9351761.
  9. ↑ Stang A, Streller B, Eisinger B, Jöckel KH (January 2005). “Population-based incidence rates of malignant melanoma of the vulva in Germany”. Gynecol. Oncol. 96 (1): 216–21. doi:10.1016/j.ygyno.2004.09.052. PMID 15589604.
  10. ↑ Sugiyama VE, Chan JK, Shin JY, Berek JS, Osann K, Kapp DS (August 2007). “Vulvar melanoma: a multivariable analysis of 644 patients”. Obstet Gynecol. 110 (2 Pt 1): 296–301. doi:10.1097/01.AOG.0000271209.67461.91. PMID 17666603.
  11. ↑ Nasioudis D, Alevizakos M, Chapman-Davis E, Witkin SS, Holcomb K (August 2017). “Rhabdomyosarcoma of the lower female genital tract: an analysis of 144 cases”. Arch. Gynecol. Obstet. 296 (2): 327–334. doi:10.1007/s00404-017-4438-1. PMID 28634755.
  12. ↑ Parker LP, Parker JR, Bodurka-Bevers D, Deavers M, Bevers MW, Shen-Gunther J, Gershenson DM (April 2000). “Paget’s disease of the vulva: pathology, pattern of involvement, and prognosis”. Gynecol. Oncol. 77 (1): 183–9. doi:10.1006/gyno.2000.5741. PMID 10739709.
  13. ↑ Fanning J, Lambert HC, Hale TM, Morris PC, Schuerch C (January 1999). “Paget’s disease of the vulva: prevalence of associated vulvar adenocarcinoma, invasive Paget’s disease, and recurrence after surgical excision”. Am. J. Obstet. Gynecol. 180 (1 Pt 1): 24–7. PMID 9914572.
  14. ↑ Feuer GA, Shevchuk M, Calanog A (July 1990). “Vulvar Paget’s disease: the need to exclude an invasive lesion”. Gynecol. Oncol. 38 (1): 81–9. PMID 2162317.
  15. ↑ DePasquale SE, McGuinness TB, Mangan CE, Husson M, Woodland MB (April 1996). “Adenoid cystic carcinoma of Bartholin’s gland: a review of the literature and report of a patient”. Gynecol. Oncol. 61 (1): 122–5. doi:10.1006/gyno.1996.0109. PMID 8626099.
  16. ↑ Visco AG, Del Priore G (February 1996). “Postmenopausal bartholin gland enlargement: a hospital-based cancer risk assessment”. Obstet Gynecol. 87 (2): 286–90. PMID 8559540.
  17. ↑ 17.0 17.1 Felix JC, Cote RJ, Kramer EE, Saigo P, Goldman GH (March 1993). “Carcinomas of Bartholin’s gland. Histogenesis and the etiological role of human papillomavirus”. Am. J. Pathol. 142 (3): 925–33. PMC 1886794. PMID 8384409.
  18. ↑ Cardosi RJ, Speights A, Fiorica JV, Grendys EC, Hakam A, Hoffman MS (August 2001). “Bartholin’s gland carcinoma: a 15-year experience”. Gynecol. Oncol. 82 (2): 247–51. doi:10.1006/gyno.2001.6304. PMID 11531274.
Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Monalisa Dmello, M.B,B.S., M.D. [2] Syed Musadiq Ali M.B.B.S.[3]

Overview

Development of vulvar cancer is the result of multiple genetic mutations.

Pathogenesis

  • Human papillomaviruses subtypes 16 and 18 (High risk) play an essential role in the pathogenesis of vulvar cancer. Once HPV enters an epithelial cell, the virus begins to make the proteins it encodes.
  • Two of the proteins made by high-risk HPVs (E6 and E7) interfere with cell functions that normally prevent excessive growth, helping the cell to grow in an uncontrolled manner and to avoid cell death.
  • Many times these infected cells are recognized by the immune system and eliminated. Sometimes, however, these infected cells are not destroyed, and a persistent infection results.
  • Persistently infected cells continue to grow, they may develop mutations in cellular genes that promote even more abnormal cell growth.
  • HPV- related vulvar carcinoma is most commonly seen in younger women. Vulvar intraepithelial neoplasia (VIN), related to HPV infection, subsequently leads to invasive vulvar cancer.[1]
  • The development of both vulvar low-grade squamous intraepithelial lesions (LSIL) and vulvar high-grade squamous intraepithelial lesions (HSIL; formerly VIN usual type) is associated with human papillomavirus (HPV) infection, as is the corresponding vulvar cancer of the warty and basaloid subtypes.
  • Multifocal vulvar HSIL and multicentric vulvar HSIL are most often associated with high-oncogenic-risk HPV subtypes 16, 18, and 31 and should be considered premalignant lesions[2]. By contrast, vulvar condylomata acuminata are usually associated with low-oncogenic-risk HPV subtypes 6 and 11[3].
  • The anogenital epithelium is derived from the embryonic cloaca and includes the cervix, vagina, vulva, anus, and lower three centimeters of rectal mucosa up to the dentate line.
  • Since the entire region shares the same embryological origin and is susceptible to similar exogenous agents (eg, HPV infection), squamous intraepithelial lesions in this area are often both multifocal (multiple foci of disease within the same organ) and multicentric (foci of disease involving more than one organ).
  • Women with VIN may have synchronous or metachronous squamous neoplasia of other lower genital tract sites (cervix, vagina, anus). There is evidence that some cases of high-grade VIN and vaginal intraepithelial neoplasia represent a monoclonal lesion derived from high-grade or malignant cervical neoplasia.[4]
  • The pathogenesis of differentiated VIN is less well understood than vulvar LSIL or HSIL.
  • It is typically associated with lichen sclerosus. The risk of vulvar squamous cell carcinoma in women with lichen sclerosus is approximately 5 percent[5].
  • Differentiated VIN is found adjacent to 80 percent of vulvar squamous cell carcinomas. The diagnosis of solitary differentiated VIN is very challenging and appears to be associated with rapid progression to squamous cell carcinoma.
  • Patients with lichen sclerosus with dyskeratosis and parakeratosis, hyperplasia, and/or basal cellular atypia tend to have the highest risk of progression to squamous cell carcinoma. There are no known biomarkers to reliably identify the patients at highest risk[6].

Gross Patholgy

Vulvar Carcinomas Subtype Features on Gross Pathology
Squamous cell carcinoma of vulva
Basal cell carcinoma of vulva
  • Pearly nodule with telangiectasias
Vulvar melanoma
  • Superficial spreading is the most common type
  • Brown/black color, but may include reddish brown or white
  • Hyperkeratotic, diffused borders with no distinct demarcation
  • Irregular and elevated

Microscopic Pathology

Histologic subtypes of vulvar cancer include:[7][8][9][10]

  • Vulvar carcinomas
Vulvar Carcinomas Subtype Features on Histopathological Microscopic Analysis Image
Squamous cell carcinoma of vulva
  • Eosinophilia
  • Extra large nuclei/bizarre nuclei
  • Inflammation (lymphocytes, plasma cells)
  • Long rete ridges
  • Numerous beeds/blobs of epithelial cells that seem unlikely to be rete ridges
Basal cell carcinoma of vulva
  • Basaloid cells – similar in appearance to basal cells
  • Moderate blue/grey cytoplasm
  • Dark ovoid/ellipsoid nucleus with uniform chromatin
  • Palisading of cells at the edge of the cell nests
  • Artefactual separation of cells (forming the nests) from the underlying stroma – key feature
  • Surrounded by blue (myxoid) stroma – key feature
Vulvar melanoma

References

  1. ↑ The Histopathology of Vulvar Neoplasia. Glown. http://www.glowm.com/section_view/heading/The%2520Histopathology%2520of%2520Vulvar%2520Neoplasia/item/256#13421 URL Accessed on September 30, 2015
  2. ↑ Ogunbiyi OA, Scholefield JH, Robertson G, Smith JH, Sharp F, Rogers K (February 1994). “Anal human papillomavirus infection and squamous neoplasia in patients with invasive vulvar cancer”. Obstet Gynecol. 83 (2): 212–6. PMID 8290182.
  3. ↑ Hørding U, Junge J, Poulsen H, Lundvall F (February 1995). “Vulvar intraepithelial neoplasia III: a viral disease of undetermined progressive potential”. Gynecol. Oncol. 56 (2): 276–9. doi:10.1006/gyno.1995.1046. PMID 7896198.
  4. ↑ Vinokurova S, Wentzensen N, Einenkel J, Klaes R, Ziegert C, Melsheimer P, Sartor H, Horn LC, Höckel M, von Knebel Doeberitz M (December 2005). “Clonal history of papillomavirus-induced dysplasia in the female lower genital tract”. J. Natl. Cancer Inst. 97 (24): 1816–21. doi:10.1093/jnci/dji428. PMID 16368943.
  5. ↑ Neill SM, Lewis FM, Tatnall FM, Cox NH (October 2010). “British Association of Dermatologists’ guidelines for the management of lichen sclerosus 2010”. Br. J. Dermatol. 163 (4): 672–82. doi:10.1111/j.1365-2133.2010.09997.x. PMID 20854400.
  6. ↑ van de Nieuwenhof HP, Bulten J, Hollema H, Dommerholt RG, Massuger LF, van der Zee AG, de Hullu JA, van Kempen LC (February 2011). “Differentiated vulvar intraepithelial neoplasia is often found in lesions, previously diagnosed as lichen sclerosus, which have progressed to vulvar squamous cell carcinoma”. Mod. Pathol. 24 (2): 297–305. doi:10.1038/modpathol.2010.192. PMID 21057461.
  7. ↑ Hoffman, Barbara (2012). Williams gynecology. New York: McGraw-Hill Medical. ISBN 9780071716727.
  8. ↑ Malignant melanoma. Libre pathology. http://librepathology.org/wiki/index.php/Malignant_melanoma. URL Accessed on September 30, 2015
  9. ↑ Basal cell carcinoma . Libre pathology. http://librepathology.org/wiki/index.php/Basal_cell_carcinoma. URL Accessed on September 30, 2015
  10. ↑ Squamous cell carcinoma. Libre pathology. http://librepathology.org/wiki/index.php/Squamous_cell_carcinoma. URL Accessed on September 30, 2015
Causes

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Monalisa Dmello, M.B,B.S., M.D. [2] Syed Musadiq Ali M.B.B.S.[3]

Overview

There are no established causes for vulvar cancer. To review risk factors for the development of vulvar cancer click here.

Causes

Unfortunately, researchers do not yet know the exact causes of vulvar cancer. They have, however, identified several risk factors for developing vulvar cancer. To review risk factors for the development of vulvar cancer click here.

Differentiating Vulvar cancer from other Diseases

Differentiating Vulvar cancer from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Monalisa Dmello, M.B,B.S., M.D. [2]

Overview

Vulvar cancer must be differentiated from other neoplastic vulvar lesions, non neoplastic vulvar lesions, and infectious disease lesions of vulva.

Differentiating vulvar cancer from other Diseases

  • Vulvar cancer must be differentiated from other neoplastic vulvar lesions such as:
  • Vulvar cancer must be differentiated from other non neoplastic vulvar lesions such as:
  • Vulvar cancer must be differentiated from infectious disease lesions of vulva such as:

Other differential considerations include:

Diseases Clinical manifestations Para-clinical findings Gold standard
Symptoms Physical exam Lab Findings Imaging Histopathology
Abnormal

vaginal bleeding

Abnormal vaginal dyscharge Pelvic

pain

Itching or

burning of the vulva

Other Genitourinary/ Gastrointestinal symptoms B symptoms Abdominal pain Gynecological examinations Abdominal

mass

HPV Pap smear STI Panel Ultrasound MRI CT Scan
Vulvar cancer

+

+ +/- +/- + − − − Ultrasound: MRI:
  • Isointense on T1-weighted images
  • Soft-tissue mass with intermediate-to-high signal intensity on T2-weighted images
 Biopsy findings:
Vaginal cancer[1][2][3][4]

+

+ +/- +/- + − − − Ultrasound: MRI:
  • Isointense on T1-weighted images
  • Soft-tissue mass with intermediate-to-high signal intensity on T2-weighted images
 Biopsy findings:
Cervical cancer[5][6][7][8][9][10][11][12] + + + +

+

+ ± ±Chlamydia T2-weighted MRI :
  • Ovoid, heterogeneous tumor distending the cervical canal with stromal involvement.
 PET/CT scan:
Cervical polyp[13][14][15] + − − − − − − − − − May reveal presence of tumor CT contrast may show presence of a well defined mass
Cervical leiomyoma[16][17][18][19][20][21][22][23] + + − − + ±
    		− − −
    • Well circumscribed hyperechoic mass
    		 T2-weighted MRI:
    • Hypointense masses
    • Homogeneous

    enhancement

    • Red degeneration
    		 N/A
    Cervical lymphoma[24][25][26] − + − + +
    • Irregularity
    		 + − − −
    • Well-defined, solid, concentric, hypoechoic mass
    		 MRI: Diffuse heterogeneous uterine/cervical mass & hypoechoic enlarged iliac lymph nodes
    Cervical sarcoma[27][28][29][30] ± + − ± + + − − − MRI: N/A
    Cervical erosion(Ectropion)[31][32][33][34][35] + + ± − + − − − − – N/A N/A N/A
    Cervicitis[36][37][38][39] + + +/- − − − To detect complications like PID N/A N/A N/A
    IUD use[40][41][42] ± + − +/- − − − ± To detect IUD location and pregnancy N/A N/A N/A Physical exam and ultrasound
    Pelvic inflammatory diseases[43][44] + +
    • Fever
    		 ±Abdominal

    pain

    		− − − Thickened fluid filled fallopian tubes N/A May show endometritis
    Endometriosis[45][46][47][48][49][50] ± − − + + − − −
    • Unilocular/multilocular cysts contating thin/thick septations
    • Increased vascularity showing increased doppler flow
    • Hyperintensity on T1 weighted images
    • Hypointensity on T2 weighted images
    		 Presence of endometrial tissue outside the uterus
    Adenomyosis[51][52][53][54][55] − + − − +/- +/- − − − MRI:
    • Thickened junctional zone
    Cervical ectopic pregnancy[56][57] − − − − + − − T2-weighted MRI:
    • Hypointense large mass

    T1-weighted MRI:

    • Partially hyperintense mass
    		 N/A
    DES exposure (Clear cell adenocarcinoma)[58][59][60] + +/- +/- +/- + – − − − To determine uterine extent To detect metastases
    Paget’s disease of vulva to cervix[61][62][63] ± − − −
      		− − − − − N/A MRI:
      • Hyperintense on diffusion weighted images
      Nabothian cyst[64][65][66][67] + − − − – − − − −
      • Intermediate or slightly high signal intensity on T1-weighted
      • High signal intensity on T2-weighted images
      • Small cysts not visible on CT
      • Large cysts seen as focal low attenuation region
      Rectal cancer[68][69][70][71][72] – – + – Weight loss + LLQ + NL + – – +/- Endoscopic/transrectal US detects tumor extent Determine tumor stage Determine tumor stage Colonoscopy with biopsy
      Submucous uterine leiomyoma[73][74][75] Menorrhagia – + – – + Enlarged, irregular, firm, nontender uterus + – – – Provides information on no: of fibroids, size, vascularization, relationship with endometrial cavity & serosal surface Not required Not required Physical examination with Ultrasound
      Uterine cancer[76][77][78][79] + + – + + – – – Thickened endometrial lining >4cm Not required Histologic diagnosis
      Vaginal lymphoma[80][81][82] + + + + Abdominal/pelvic pain – + Palpable mass between rectum & vagina +/- – – – Diffuse mass in external cervical orifice & invading the vagina Diffuse mass in external cervical orifice & invading the vagina Not required CD20 & CD79a positive Immunohistochemistry & biopsy
      Vaginal polyp[83][84][85][86] Postmenopausal bleeding + + + – + Mass protruding from vagina +/- – – – To exclude uterine hyperplasia/carcinoma To determine the extent N/A Benign tissue/premalignant cells Excisional biopsy
      Vaginal adenosis[87][88] +/- +/- +/- – – – Palpable cysts,nodularity or ulcers – – – – N/A N/A N/A Columnar cells in the ectocervix Biopsy with histopathological examination

      References

      1. ↑ Tarney CM, Han J (2014). “Postcoital bleeding: a review on etiology, diagnosis, and management”. Obstet Gynecol Int. 2014: 192087. doi:10.1155/2014/192087. PMC 4086375. PMID 25045355.
      2. ↑ Miccò, Maura; Sala, Evis; Lakhman, Yulia; Hricak, Hedvig; Vargas, Hebert Alberto (2015). “Imaging Features of Uncommon Gynecologic Cancers”. American Journal of Roentgenology. 205 (6): 1346–1359. doi:10.2214/AJR.14.12695. ISSN 0361-803X.
      3. ↑ Kim, Hwi-Gon; Song, Yong Jung; Na, Yong Jin; Choi, Ook-Hwan (2013). “A Case of Vaginal Cancer with Uterine Prolapse”. Journal of Menopausal Medicine. 19 (3): 139. doi:10.6118/jmm.2013.19.3.139. ISSN 2288-6478.
      4. ↑ Karateke A, Tugrul S, Yakut Y, Gürbüz A, Cam C (2006). “Management of a case of primary vaginal cancer with irreducible massive uterine prolapse–a case report”. Eur. J. Gynaecol. Oncol. 27 (5): 528–30. PMID 17139994.
      5. ↑ Hippisley-Cox J, Coupland C (January 2013). “Symptoms and risk factors to identify women with suspected cancer in primary care: derivation and validation of an algorithm”. Br J Gen Pract. 63 (606): e11–21. doi:10.3399/bjgp13X660733. PMC 3529288. PMID 23336450.
      6. ↑ Dunyo, Priscilla; Effah, Kofi; Udofia, Emilia Asuquo (2018). “Factors associated with late presentation of cervical cancer cases at a district hospital: a retrospective study”. BMC Public Health. 18 (1). doi:10.1186/s12889-018-6065-6. ISSN 1471-2458.
      7. ↑ Khalife D, El Housheimi A, Khalil A, Saba C S, Seoud M, Rammal R, Abdallah IE, Abdallah R (February 2019). “Treatment of cervical cancer metastatic to the abdominal wall with reconstruction using a composite myocutaneous flap: A case report”. Gynecol Oncol Rep. 27: 38–41. doi:10.1016/j.gore.2018.12.006. PMC 6302027. PMID 30603660. Vancouver style error: name (help)
      8. ↑ . doi:10.1097/PAS.0000000000000498. Check |doi= value (help). Missing or empty |title= (help)
      9. ↑ Brenner PF (September 1996). “Differential diagnosis of abnormal uterine bleeding”. Am. J. Obstet. Gynecol. 175 (3 Pt 2): 766–9. PMID 8828559.
      10. ↑ Alcázar, Juan Luis; Arribas, Sara; Mínguez, José Angel; Jurado, Matías (2014). “The Role of Ultrasound in the Assessment of Uterine Cervical Cancer”. The Journal of Obstetrics and Gynecology of India. 64 (5): 311–316. doi:10.1007/s13224-014-0622-4. ISSN 0971-9202.
      11. ↑ Qing L, Xiang T, Guofu Z, Weiwei F (September 2014). “Leukemoid reaction in cervical cancer: a case report and review of the literature”. BMC Cancer. 14: 670. doi:10.1186/1471-2407-14-670. PMC 4174654. PMID 25223869.
      12. ↑ Qing L, Xiang T, Guofu Z, Weiwei F (September 2014). “Leukemoid reaction in cervical cancer: a case report and review of the literature”. BMC Cancer. 14: 670. doi:10.1186/1471-2407-14-670. PMC 4174654. PMID 25223869.
      13. ↑ Mitchell H (May 2004). “Vaginal discharge–causes, diagnosis, and treatment”. BMJ. 328 (7451): 1306–8. doi:10.1136/bmj.328.7451.1306. PMC 420177. PMID 15166070.
      14. ↑ Irene Pecorella, Marco Monti, Maria Luisa Framarino Dei Malatesta & Gaia Ciardi (2018). “Polyp of the uterine cervix with heterologous fatty tissue”. Indian journal of pathology & microbiology. 61 (4): 593–595. doi:10.4103/IJPM.IJPM_105_17. PMID 30303160. Unknown parameter |month= ignored (help)
      15. ↑ Seema Anushka Tirlapur, Adewale Adeyemo, Neil O’Gorman & Dan Selo-Ojeme (2010). “Clinico-pathological study of cervical polyps”. Archives of gynecology and obstetrics. 282 (5): 535–538. doi:10.1007/s00404-010-1364-x. PMID 20091045. Unknown parameter |month= ignored (help)
      16. ↑ Al-Habib A, Elgamal EA, Aldhahri S, Alokaili R, AlShamrani R, Abobotain A, AlRaddadi K, Alkhalidi H (November 2016). “Large primary leiomyoma causing progressive cervical deformity”. J Surg Case Rep. 2016 (11). doi:10.1093/jscr/rjw190. PMC 5159177. PMID 27887011.
      17. ↑ Adaikkalam J (April 2016). “Lipoleiomyoma of Cervix”. J Clin Diagn Res. 10 (4): EJ01–2. doi:10.7860/JCDR/2016/16505.7531. PMID 27190823.
      18. ↑ Houser, L. Murray; Carrasco, C. H.; Sheehan, C. R. (1979). “Lipomatous tumour of the uterus: radiographic and ultrasonic appearance”. The British Journal of Radiology. 52 (624): 992–993. doi:10.1259/0007-1285-52-624-992. ISSN 0007-1285.
      19. ↑ Keriakos, Remon; Maher, Mark (2013). “Management of Cervical Fibroid during the Reproductive Period”. Case Reports in Obstetrics and Gynecology. 2013: 1–3. doi:10.1155/2013/984030. ISSN 2090-6684.
      20. ↑ Coronado GD, Marshall LM, Schwartz SM (May 2000). “Complications in pregnancy, labor, and delivery with uterine leiomyomas: a population-based study”. Obstet Gynecol. 95 (5): 764–9. PMID 10775744.
      21. ↑ Kamra, Hemlata T (2013). “Myxoid Leiomyoma of Cervix”. JOURNAL OF CLINICAL AND DIAGNOSTIC RESEARCH. doi:10.7860/JCDR/2013/6171.3805. ISSN 2249-782X.
      22. ↑ El-agwany, Ahmed Samy (2015). “Lipoleiomyoma of the uterine cervix: An unusual variant of uterine leiomyoma”. The Egyptian Journal of Radiology and Nuclear Medicine. 46 (1): 211–213. doi:10.1016/j.ejrnm.2014.10.001. ISSN 0378-603X.
      23. ↑ Chaparala RP, Fawole AS, Ambrose NS, Chapman AH (March 2004). “Large bowel obstruction due to a benign uterine leiomyoma”. Gut. 53 (3): 386, 430. PMC 1773948. PMID 14960521.
      24. ↑ Grace A, O’Connell N, Byrne P, Prendiville W, O’Donnell R, Royston D, Walsh CB, Leader M, Kay E (1999). “Malignant lymphoma of the cervix. An unusual presentation and a rare disease”. Eur. J. Gynaecol. Oncol. 20 (1): 26–8. PMID 10422676.
      25. ↑ Kanaan, Daniel; Parente, Daniella Braz; Constantino, Carolina Pesce Lamas; Souza, Rodrigo Canellas de (2012). “Linfoma de colo de útero: achados na ressonância magnética”. Radiologia Brasileira. 45 (3): 167–169. doi:10.1590/S0100-39842012000300009. ISSN 0100-3984.
      26. ↑ Frey NV, Svoboda J, Andreadis C, Tsai DE, Schuster SJ, Elstrom R, Rubin SC, Nasta SD (September 2006). “Primary lymphomas of the cervix and uterus: the University of Pennsylvania’s experience and a review of the literature”. Leuk. Lymphoma. 47 (9): 1894–901. doi:10.1080/10428190600687653. PMID 17065003.
      27. ↑ Wright JD, Rosenblum K, Huettner PC, Mutch DG, Rader JS, Powell MA, Gibb RK (November 2005). “Cervical sarcomas: an analysis of incidence and outcome”. Gynecol. Oncol. 99 (2): 348–51. doi:10.1016/j.ygyno.2005.06.021. PMID 16051326.
      28. ↑ Khosla, Divya; Gupta, Ruchi; Srinivasan, Radhika; Patel, Firuza D.; Rajwanshi, Arvind (2012). “Sarcomas of Uterine Cervix”. International Journal of Gynecological Cancer. 22 (6): 1026–1030. doi:10.1097/IGC.0b013e31825a97f6. ISSN 1048-891X.
      29. ↑ Miccò M, Sala E, Lakhman Y, Hricak H, Vargas HA (December 2015). “Imaging Features of Uncommon Gynecologic Cancers”. AJR Am J Roentgenol. 205 (6): 1346–59. doi:10.2214/AJR.14.12695. PMC 5502476. PMID 26587944.
      30. ↑ . doi:10.1097/IGC.0b013e31825a97f6. Check |doi= value (help). Missing or empty |title= (help)
      31. ↑ Mitchell L, King M, Brillhart H, Goldstein A (September 2017). “Cervical Ectropion May Be a Cause of Desquamative Inflammatory Vaginitis”. Sex Med. 5 (3): e212–e214. doi:10.1016/j.esxm.2017.03.001. PMC 5562466. PMID 28460993.
      32. ↑ Mitchell H (May 2004). “Vaginal discharge–causes, diagnosis, and treatment”. BMJ. 328 (7451): 1306–8. doi:10.1136/bmj.328.7451.1306. PMC 420177. PMID 15166070.
      33. ↑ Sharma, Abhishek; Ojha, Ranapratap; Sengupta, Parama; Chattopadhyay, Sarbani; Mondal, Soumit (2013). “Cervical intramural pregnancy: Report of a rare case”. Nigerian Medical Journal. 54 (4): 271. doi:10.4103/0300-1652.119670. ISSN 0300-1652.
      34. ↑ . doi:10.12865/CHSJ.42.02.11. Missing or empty |title= (help)
      35. ↑ Casey PM, Long ME, Marnach ML (February 2011). “Abnormal cervical appearance: what to do, when to worry?”. Mayo Clin. Proc. 86 (2): 147–50, quiz 151. doi:10.4065/mcp.2010.0512. PMC 3031439. PMID 21270291.
      36. ↑ Mattson SK, Polk JP, Nyirjesy P (July 2016). “Chronic Cervicitis: Presenting Features and Response to Therapy”. J Low Genit Tract Dis. 20 (3): e30–3. doi:10.1097/LGT.0000000000000225. PMID 27243142.
      37. ↑ Rosenfeld WD, Clark J (June 1989). “Vulvovaginitis and cervicitis”. Pediatr. Clin. North Am. 36 (3): 489–511. PMID 2660084.
      38. ↑ Meyer T (August 2016). “Diagnostic Procedures to Detect Chlamydia trachomatis Infections”. Microorganisms. 4 (3). doi:10.3390/microorganisms4030025. PMID 27681919.
      39. ↑ Woods, Jennifer L.; Bailey, Sarabeth L.; Hensel, Devon J.; Scurlock, Amy M. (2011). “Cervicitis in Adolescents: Do Clinicians Understand Diagnosis and Treatment?”. Journal of Pediatric and Adolescent Gynecology. 24 (6): 359–364. doi:10.1016/j.jpag.2011.06.006. ISSN 1083-3188.
      40. ↑ Trobough GE (March 1978). “Pelvic pain and the IUD”. J Reprod Med. 20 (3): 167–74. PMID 347074.
      41. ↑ D. Reinprayoon, S. Taneepanichskul, S. Niruthisard & S. Suwajanakon (1999). “Uterine histopathologic changes after Cu-Fix intrauterine device insertion”. Contraception. 59 (1): 63–65. PMID 10342087. Unknown parameter |month= ignored (help)
      42. ↑ Seyma Fadiloglu, B. Dilbaz, E. Fadiloglu & S. Dilbaz (2018). “Relationship between copper IUD complications and ultrasonographic findings”. Archives of gynecology and obstetrics. 297 (4): 989–996. doi:10.1007/s00404-018-4711-y. PMID 29428979. Unknown parameter |month= ignored (help)
      43. ↑ Hoenderboom BM, van Benthem B, van Bergen J, Dukers-Muijrers N, Götz HM, Hoebe C, Hogewoning AA, Land JA, van der Sande M, Morré SA, van den Broek I (January 2019). “Relation between Chlamydia trachomatis infection and pelvic inflammatory disease, ectopic pregnancy and tubal factor infertility in a Dutch cohort of women previously tested for chlamydia in a chlamydia screening trial”. Sex Transm Infect. doi:10.1136/sextrans-2018-053778. PMID 30606817. Vancouver style error: initials (help)
      44. ↑ Jaiyeoba O, Soper DE (2011). “A practical approach to the diagnosis of pelvic inflammatory disease”. Infect Dis Obstet Gynecol. 2011: 753037. doi:10.1155/2011/753037. PMC 3148590. PMID 21822367.
      45. ↑ Hsu AL, Khachikyan I, Stratton P (June 2010). “Invasive and noninvasive methods for the diagnosis of endometriosis”. Clin Obstet Gynecol. 53 (2): 413–9. doi:10.1097/GRF.0b013e3181db7ce8. PMC 2880548. PMID 20436318.
      46. ↑ Chamié, Luciana Pardini; Blasbalg, Roberto; Pereira, Ricardo Mendes Alves; Warmbrand, Gisele; Serafini, Paulo Cesar (2011). “Findings of Pelvic Endometriosis at Transvaginal US, MR Imaging, and Laparoscopy”. RadioGraphics. 31 (4): E77–E100. doi:10.1148/rg.314105193. ISSN 0271-5333.
      47. ↑ Datta S, Kunde K (July 2008). “From vaginal discharge to endometriosis: an unusual case of endometriosis in pregnancy”. J Obstet Gynaecol. 28 (5): 552–3. doi:10.1080/01443610802247352. PMID 18850447.
      48. ↑ Chamié, Luciana Pardini; Blasbalg, Roberto; Pereira, Ricardo Mendes Alves; Warmbrand, Gisele; Serafini, Paulo Cesar (2011). “Findings of Pelvic Endometriosis at Transvaginal US, MR Imaging, and Laparoscopy”. RadioGraphics. 31 (4): E77–E100. doi:10.1148/rg.314105193. ISSN 0271-5333.
      49. ↑ Bedaiwy MA, Falcone T (February 2004). “Laboratory testing for endometriosis”. Clin. Chim. Acta. 340 (1–2): 41–56. PMID 14734195.
      50. ↑ Van Holsbeke C, Van Calster B, Guerriero S, Savelli L, Paladini D, Lissoni AA, Czekierdowski A, Fischerova D, Zhang J, Mestdagh G, Testa AC, Bourne T, Valentin L, Timmerman D (June 2010). “Endometriomas: their ultrasound characteristics”. Ultrasound Obstet Gynecol. 35 (6): 730–40. doi:10.1002/uog.7668. PMID 20503240.
      51. ↑ Filip G, Balzano A, Cagnacci A (November 2018). “Histological evaluation of the prevalence of adenomyosis, myomas and of their concomitance”. Minerva Ginecol. doi:10.23736/S0026-4784.18.04291-0. PMID 30486633.
      52. ↑ Fujino T, Watanabe T, Shinmura R, Hahn L, Nagata Y, Hasui K (December 1992). “Acute abdomen due to adenomyosis of the uterus: a case report”. Asia Oceania J Obstet Gynaecol. 18 (4): 333–7. PMID 1492806.
      53. ↑ Fujino T, Watanabe T, Shinmura R, Hahn L, Nagata Y, Hasui K (December 1992). “Acute abdomen due to adenomyosis of the uterus: a case report”. Asia Oceania J Obstet Gynaecol. 18 (4): 333–7. PMID 1492806.
      54. ↑ Zhou Y, Wu B, Li H (October 1996). “[The value of serum CA125 assays in the diagnosis of uterine adenomyosis]”. Zhonghua Fu Chan Ke Za Zhi (in Chinese). 31 (10): 590–3. PMID 9275451.
      55. ↑ Courtney A. Woodfield, Evan S. Siegelman, Beverly G. Coleman & Drew A. Torigian (2009). “CT features of adenomyosis”. European journal of radiology. 72 (3): 464–469. doi:10.1016/j.ejrad.2008.08.002. PMID 18804933. Unknown parameter |month= ignored (help)
      56. ↑ Mouhajer M, Obed S, Okpala AM (June 2017). “Cervical Ectopic Pregnancy in Resource Deprived Areas: A Rare and Difficult Diagnosis”. Ghana Med J. 51 (2): 94–97. PMC 5611908. PMID 28955106.
      57. ↑ Rathod, Setu; Samal, SunilKumar (2015). “Cervical ectopic pregnancy”. Journal of Natural Science, Biology and Medicine. 6 (1): 257. doi:10.4103/0976-9668.149221. ISSN 0976-9668.
      58. ↑ Tantitamit T, Hamontri S, Rangsiratanakul L (May 2017). “Clear cell adenocarcinoma of the cervix in second generation young women who are without maternal exposure to diethylstilbestrol: A case report”. Gynecol Oncol Rep. 20: 34–36. doi:10.1016/j.gore.2017.02.008. PMC 5328756. PMID 28275694.
      59. ↑ Subrata Pal, Sritanu Jana & Kingshuk Bose (2015). “Clear cell carcinoma of cervix in a postmenopausal woman: A case report”. Journal of mid-life health. 6 (2): 85–87. doi:10.4103/0976-7800.158964. PMID 26167060. Unknown parameter |month= ignored (help)
      60. ↑ Mary G. Dandulakis, Aidas J. Mattis, Andrea R. Hagemann & Ian S. Hagemann (2018). “Cervical clear cell adenocarcinoma with an exceptionally low proliferation index: Report of a case”. Gynecologic oncology reports. 23: 16–19. doi:10.1016/j.gore.2017.12.006. PMID 29326971. Unknown parameter |month= ignored (help)
      61. ↑ 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.
      62. ↑ Lloyd J, Evans DJ, Flanagan AM (July 1999). “Extension of extramammary Paget disease of the vulva to the cervix”. J. Clin. Pathol. 52 (7): 538–40. PMC 501500. PMID 10605411.
      63. ↑ Shaco-Levy R, Bean SM, Vollmer RT, Papalas JA, Bentley RC, Selim MA, Robboy SJ (January 2010). “Paget disease of the vulva: a histologic study of 56 cases correlating pathologic features and disease course”. Int. J. Gynecol. Pathol. 29 (1): 69–78. doi:10.1097/PGP.0b013e3181b1cc5e. PMID 19952933.
      64. ↑ Casey PM, Long ME, Marnach ML (February 2011). “Abnormal cervical appearance: what to do, when to worry?”. Mayo Clin. Proc. 86 (2): 147–50, quiz 151. doi:10.4065/mcp.2010.0512. PMC 3031439. PMID 21270291.
      65. ↑ Bin Park, Sung; Lee, Jong Hwa; Lee, Young Ho; Song, Mi Jin; Choi, Hye Jeong (2010). “Multilocular Cystic Lesions in the Uterine Cervix: Broad Spectrum of Imaging Features and Pathologic Correlation”. American Journal of Roentgenology. 195 (2): 517–523. doi:10.2214/AJR.09.3619. ISSN 0361-803X.
      66. ↑ Torky, Haitham A. (2016). “Huge Nabothian cyst causing Hematometra (case report)”. European Journal of Obstetrics & Gynecology and Reproductive Biology. 207: 238–240. doi:10.1016/j.ejogrb.2016.10.042. ISSN 0301-2115.
      67. ↑ Okamoto, Yoshikazu; Tanaka, Yumiko O.; Nishida, Masato; Tsunoda, Hajime; Yoshikawa, Hiroyuki; Itai, Yuji (2003). “MR Imaging of the Uterine Cervix: Imaging-Pathologic Correlation”. RadioGraphics. 23 (2): 425–445. doi:10.1148/rg.232025065. ISSN 0271-5333.
      68. ↑ Chiara Molinari, Federica Matteucci, Paola Caroli & Alessandro Passardi (2015). “Biomarkers and Molecular Imaging as Predictors of Response to Neoadjuvant Chemoradiotherapy in Patients With Locally Advanced Rectal Cancer”. Clinical colorectal cancer. 14 (4): 227–238. doi:10.1016/j.clcc.2015.05.014. PMID 26170142. Unknown parameter |month= ignored (help)
      69. ↑ William Hamilton & Deborah Sharp (2004). “Diagnosis of colorectal cancer in primary care: the evidence base for guidelines”. Family practice. 21 (1): 99–106. PMID 14760054. Unknown parameter |month= ignored (help)
      70. ↑ Wolfgang B. Gaertner, Mary R. Kwaan, Robert D. Madoff & Genevieve B. Melton (2015). “Rectal cancer: An evidence-based update for primary care providers”. World journal of gastroenterology. 21 (25): 7659–7671. doi:10.3748/wjg.v21.i25.7659. PMID 26167068. Unknown parameter |month= ignored (help)
      71. ↑ V. Raman Muthusamy & Kenneth J. Chang (2007). “Optimal methods for staging rectal cancer”. Clinical cancer research : an official journal of the American Association for Cancer Research. 13 (22 Pt 2): 6877s–6884s. doi:10.1158/1078-0432.CCR-07-1137. PMID 18006793. Unknown parameter |month= ignored (help)
      72. ↑ Mohammad Sadegh Fazeli & Mohammad Reza Keramati (2015). “Rectal cancer: a review”. Medical journal of the Islamic Republic of Iran. 29: 171. PMID 26034724.
      73. ↑ Jacques Donnez & Marie-Madeleine Dolmans (2016). “Uterine fibroid management: from the present to the future”. Human reproduction update. 22 (6): 665–686. doi:10.1093/humupd/dmw023. PMID 27466209. Unknown parameter |month= ignored (help)
      74. ↑ Mohamed Sabry & Ayman Al-Hendy (2012). “Medical treatment of uterine leiomyoma”. Reproductive sciences (Thousand Oaks, Calif.). 19 (4): 339–353. doi:10.1177/1933719111432867. PMID 22378865. Unknown parameter |month= ignored (help)
      75. ↑ Sahana Gupta, Jude Jose & Isaac Manyonda (2008). “Clinical presentation of fibroids”. Best practice & research. Clinical obstetrics & gynaecology. 22 (4): 615–626. doi:10.1016/j.bpobgyn.2008.01.008. PMID 18372219. Unknown parameter |month= ignored (help)
      76. ↑ “ACOG practice bulletin, clinical management guidelines for obstetrician-gynecologists, number 65, August 2005: management of endometrial cancer”. Obstet Gynecol. 106 (2): 413–25. August 2005. PMID 16055605.
      77. ↑ Boruta DM, Gehrig PA, Fader AN, Olawaiye AB (October 2009). “Management of women with uterine papillary serous cancer: a Society of Gynecologic Oncology (SGO) review”. Gynecol. Oncol. 115 (1): 142–153. doi:10.1016/j.ygyno.2009.06.011. PMID 19592079.
      78. ↑ Bokhman JV (February 1983). “Two pathogenetic types of endometrial carcinoma”. Gynecol. Oncol. 15 (1): 10–7. PMID 6822361.
      79. ↑ Felix AS, Weissfeld JL, Stone RA, Bowser R, Chivukula M, Edwards RP, Linkov F (November 2010). “Factors associated with Type I and Type II endometrial cancer”. Cancer Causes Control. 21 (11): 1851–6. doi:10.1007/s10552-010-9612-8. PMC 2962676. PMID 20628804.
      80. ↑ Vera Silva, Paulo Correia, Nuno Oliveira & Luis Sa (2015). “Primary Vaginal Non-Hodgkin’s Lymphoma: Report of a Rare Clinical Entity”. Clinics and practice. 5 (4): 821. doi:10.4081/cp.2015.821. PMID 26918105. Unknown parameter |month= ignored (help)
      81. ↑ Feng Wang, Xuquan Jing, Bo Liu, Xue Meng, Xindong Sun, Yongsheng Gao, Linlin Wang & Zheng Fu (2018). “Primary non-Hodgkin’s lymphoma of the vagina: A case report”. Oncology letters. 15 (3): 3504–3507. doi:10.3892/ol.2018.7805. PMID 29556272. Unknown parameter |month= ignored (help)
      82. ↑ Salvatore Guastafierro, Amando Tedeschi, Clelia Criscuolo, Maria Celentano, Luigi Cobellis, Raffaele Rossiello & Umberto Falcone (2012). “Primary extranodal non-Hodgkin’s lymphoma of the vagina: a case report and a review of the literature”. Acta haematologica. 128 (1): 33–38. doi:10.1159/000337336. PMID 22584110.
      83. ↑ A. I. al-Nafussi, G. Rebello, D. Hughes & K. Blessing (1992). “Benign vaginal polyp: a histological, histochemical and immunohistochemical study of 20 polyps with comparison to normal vaginal subepithelial layer”. Histopathology. 20 (2): 145–150. PMID 1302457. Unknown parameter |month= ignored (help)
      84. ↑ Sunil Kumar Samal, Setu Rathod & Seetesh Ghose (2015). “Fibroepithelial Polyps of the Vagina in Pregnancy”. Journal of clinical and diagnostic research : JCDR. 9 (10): QJ01–QJ02. doi:10.7860/JCDR/2015/13329.6656. PMID 26557576. Unknown parameter |month= ignored (help)
      85. ↑ M. Petrova, J. Laco, K. Cervicek & M. Tomsova (2015). “[Tubulo-squamous polyp of the vagina]”. Ceska gynekologie. 80 (3): 173–175. PMID 26087210. Unknown parameter |month= ignored (help)
      86. ↑ Alexis Heller, Adanna Ukazu & Qing Wang (2017). “Pseudosarcomatous Vaginal Polyp”. International journal of surgical pathology. 25 (1): 54–55. doi:10.1177/1066896916666676. Unknown parameter |month= ignored (help)
      87. ↑ Marguerite B. Vigliani (2017). “A Report of Two Cases of Age-Related Changes in Cervical Morphology in Postmenopausal Women with Vaginal Adenosis”. Case reports in obstetrics and gynecology. 2017: 9523853. doi:10.1155/2017/9523853. PMID 28316850.
      88. ↑ Tiantian Han, Ying Jin, Yan Li, Yalan Bi & Lingya Pan (2018). “Clinicopathologic features and outcomes of primary vaginal adenosis as a dermatologic and gynecologic burden: A retrospective study”. Medicine. 97 (49): e13470. doi:10.1097/MD.0000000000013470. PMID 30544435. Unknown parameter |month= ignored (help)
      Epidemiology and Demographics

      Epidemiology and Demographics

      Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Monalisa Dmello, M.B,B.S., M.D. [2] Syed Musadiq Ali M.B.B.S.[3]

      Overview

      The incidence of vulvar cancer was estimated to be 2.4 per 100,000 females in the United States. The incidence of vulvar cancer increases with age; the median age at diagnosis is 68 years. Vulvar cancer is more prevalent in the caucasian race.[1]

      Epidemiology and Demographics

      Incidence

      The overall age adjusted incidence rate of vulvar cancer among females is approximately 2.4 per 100,000 individuals in the United States.[1]

      Age

      • The incidence of vulvar cancer increases with age; the median age at diagnosis is 68 years.[1]
      Age <20 20-34 35-44 45-54 55-64 65-74 75-84 >85
      Incidence 0.2% 2% 6.1% 15.3% 19.8% 19.8% 22.1% 14.9%

      Race

      • Vulvar cancer is more prevalent in the caucasian race.[1]
      Race All Races White Black Asian/Pacific Islander American Indian/Alaska Native Hispanic Non-Hispanic
      Incidence 2.4 per 100,000 2.6 per 100,000 1.8 per 100,000 0.9 per 100,000 2.0 per 100,000 1.7 per 100,000 2.5 per 100,000

      References

      1. ↑ 1.0 1.1 1.2 1.3 SEER Stat Fact Sheets: Vulvar Cancer. Surveillance, Epidemiology, and End Results Program. http://seer.cancer.gov/statfacts/html/vulva.html Accessed on September 21, 2015
      Risk Factors

      Risk Factors


      Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Monalisa Dmello, M.B,B.S., M.D. [2] Syed Musadiq Ali M.B.B.S.[3]

      Overview

      Common risk factors in the development of vulvar cancer are human papilloma virus (HPV), human immunodeficiency virus, vulvar intraepithelial neoplasia, and lichen sclerosus.

      Risk factors

      Known risk factors

      • Human immunodeficiency virus (HIV)
        • Scientists found that HIV can damage the body’s immune system and make women more susceptible to persistent HPV infections.
      • Vulvar intraepithelial neoplasia (VIN)
        • Clinical data suggest that women with VIN have an increased risk of developing invasive vulvar cancer.[6]
      • Personal history of vulvar skin conditions
        • Women with a history of vulvar skin conditions have an increased risk of vulvar cancer. These conditions include lichen sclerosus, which is a benign condition of the vulva that causes chronic inflammation of the skin. Having a vulvar skin condition can cause damage to the skin of the vulva over the long term. This damage may be what increases the risk for vulvar cancer.[7]
      • Personal history of cervical, vaginal or anal cancer
        • Women diagnosed with cancer of the cervix, vagina or anus have a higher risk of developing vulvar cancer. This may be because these cancers have similar risk factors, such as HPV infection.

      Possible risk factors

      • Smoking
        • Studies suggest that smoking increases a woman’s risk of developing vulvar cancer.
      • Personal history of melanoma
        • Studies suggest that women with a personal or family history of melanoma have a higher risk of developing melanoma of the vulva.
      • Northern European ancestry

      References

      1. ↑ Risk factors for vulvar cancer. Canadian Cancer Society. http://www.cancer.ca/en/cancer-information/cancer-type/vulvar/risks/?region=ns Accessed on September 27, 2015
      2. ↑ de Koning MN, Quint WG, Pirog EC (March 2008). “Prevalence of mucosal and cutaneous human papillomaviruses in different histologic subtypes of vulvar carcinoma”. Mod. Pathol. 21 (3): 334–44. doi:10.1038/modpathol.3801009. PMID 18192968.
      3. ↑ Halec G, Alemany L, Quiros B, Clavero O, Höfler D, Alejo M, Quint W, Pawlita M, Bosch FX, de Sanjose S (April 2017). “Biological relevance of human papillomaviruses in vulvar cancer”. Mod. Pathol. 30 (4): 549–562. doi:10.1038/modpathol.2016.197. PMID 28059099.
      4. ↑ Weberpals JI, Lo B, Duciaume MM, Spaans JN, Clancy AA, Dimitroulakos J, Goss GD, Sekhon HS (August 2017). “Vulvar Squamous Cell Carcinoma (VSCC) as Two Diseases: HPV Status Identifies Distinct Mutational Profiles Including Oncogenic Fibroblast Growth Factor Receptor 3”. Clin. Cancer Res. 23 (15): 4501–4510. doi:10.1158/1078-0432.CCR-16-3230. PMID 28377483.
      5. ↑ Brinton LA, Thistle JE, Liao LM, Trabert B (May 2017). “Epidemiology of vulvar neoplasia in the NIH-AARP Study”. Gynecol. Oncol. 145 (2): 298–304. doi:10.1016/j.ygyno.2017.02.030. PMC 5629039. PMID 28236455.
      6. ↑ Bigby SM, Eva LJ, Fong KL, Jones RW (November 2016). “The Natural History of Vulvar Intraepithelial Neoplasia, Differentiated Type: Evidence for Progression and Diagnostic Challenges”. Int. J. Gynecol. Pathol. 35 (6): 574–584. doi:10.1097/PGP.0000000000000280. PMID 26974999.
      7. ↑ van de Nieuwenhof HP, Bulten J, Hollema H, Dommerholt RG, Massuger LF, van der Zee AG, de Hullu JA, van Kempen LC (February 2011). “Differentiated vulvar intraepithelial neoplasia is often found in lesions, previously diagnosed as lichen sclerosus, which have progressed to vulvar squamous cell carcinoma”. Mod. Pathol. 24 (2): 297–305. doi:10.1038/modpathol.2010.192. PMID 21057461.
      Screening

      Screening

      Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Monalisa Dmello, M.B,B.S., M.D. [2] Syed Musadiq Ali M.B.B.S.[3]

      Overview

      Screening for vulvar cancer is not recommended.

      Screening

      Screening for vulvar cancer is not recommended.[1]

      References

      1. ↑ What Should I Know About Screening? Gynecologic Cancers. http://www.cdc.gov/cancer/vagvulv/basic_info/screening.htm Accessed on September 30, 2015
      Natural History, Complications and Prognosis

      Natural History, Complications and Prognosis

      Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Monalisa Dmello, M.B,B.S., M.D. [2] Syed Musadiq Ali M.B.B.S.[3]


      Overview

      If left untreated, patients with vulvar cancer may progress to develop ulcer on vulva or wart-like patches on vulva and chronic pruritus of the vulva. Common complications of vulvar cancer include fistula and metastasis. Prognosis is generally good, and the 5 year survival rate of patients with vulvar cancer is approximately 71.2%.

      Natural history

      • Patient has early symptoms like ulcer on vulva, chronic pruritus of the vulva, and wart-like patches on vulva.[1]
      • As the tumor grows larger, patient may notice symptoms like unusual bleeding or discharge from the lesion, large mass on the vulva, dysuria, and dyspareunia.
      • In advanced disease, metastases may be present in the abdomen and lungs.
      • The patient may present with dyspnea, cough with blood-stained sputum, persistent pain or discomfort in the chest, edema hands/feet, and inguinal lymphadenopathy.
      • Once the cancer spreads to the other organs, it is most likely fatal.[2]

      Complications

      Common complications of valvular cancer include:[3][4]

      Prognosis

      Stage 5-year relative survival (%)
      I 93%
      II 79%
      III 53%
      IV 29%

      References

      1. ↑ Sykes P, Eva L, van der Griend R, McNally O, Blomfield P, Brand A, Tristram A, Bergzoll C, Petrich S, Kenwright D, Payne K, Kellow M, Innes C, Harker D, Perrin L, Cohen P, Jaaback K, Simcock B (February 2019). “Pathological process has a crucial role in sentinel node biopsy for vulvar cancer”. Gynecol. Oncol. doi:10.1016/j.ygyno.2019.02.012. PMID 30814024.
      2. ↑ Koh WJ, Greer BE, Abu-Rustum NR, Campos SM, Cho KR, Chon HS, Chu C, Cohn D, Crispens MA, Dizon DS, Dorigo O, Eifel PJ, Fisher CM, Frederick P, Gaffney DK, Han E, Higgins S, Huh WK, Lurain JR, Mariani A, Mutch D, Nagel C, Nekhlyudov L, Fader AN, Remmenga SW, Reynolds RK, Tillmanns T, Ueda S, Valea FA, Wyse E, Yashar CM, McMillian N, Scavone J (January 2017). “Vulvar Cancer, Version 1.2017, NCCN Clinical Practice Guidelines in Oncology”. J Natl Compr Canc Netw. 15 (1): 92–120. PMID 28040721.
      3. ↑ Dass PH, Kuper-Hommel MJ (November 2017). “A review of squamous cell vulvar cancers in Waikato region, New Zealand”. N. Z. Med. J. 130 (1465): 19–28. PMID 29121621.
      4. ↑ Wiggans A, Coleridge S, Bryant A, Morrison J (April 2019). “Relationship between vulvar symptoms and incidence of vulvar cancer in women referred to a rapid access clinic”. Int J Gynaecol Obstet. doi:10.1002/ijgo.12818. PMID 30932169.
      5. ↑ Survival statistics for vulvar cancer. Vulvar cancer. http://www.cancer.ca/en/cancer-information/cancer-type/vulvar/prognosis-and-survival/survival-statistics/?region=ns Accessed on October 1, 2015
      Diagnosis

      Diagnosis

      Staging | History and Symptoms | Physical Examination | Laboratory Findings | X Rays | CT | MRI | Ultrasound | Other Imaging Findings | Other Diagnostic Studies

      Treatment

      Treatment

      Medical therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

      Case Studies

      Case Studies

      Case #1

      External links
      1. Information from the National Cancer Institute

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