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Vaginal cancer

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

Synonyms and keywords: Primary vaginal carcinoma, primary vaginal cancer, vaginal carcinoma

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]

Overview

Vaginal cancer is a type of cancer that forms in the tissues of the vagina. The vagina leads from the cervix (the opening of the uterus) to the outside of the body.

Carcinomas of the vagina are uncommon tumors comprising 1% to 2% of gynecologic malignancies. They can be effectively treated, and when found in early stages, are often curable. The histologic distinction between squamous cell carcinoma and adenocarcinoma is important because the two types represent distinct diseases, each with a different pathogenesis and natural history. Squamous cell vaginal cancer (approximately 85% of cases) initially spreads superficially within the vaginal wall and later invades the paravaginal tissues and the parametria. Distant metastases occur most commonly in the lungs and liver.

Adenocarcinoma (approximately 15% of cases) has a peak incidence between 17 and 21 years of age and differs from squamous cell carcinoma by an increase in pulmonary metastases and supraclavicular and pelvic node involvement. Rarely, melanoma and sarcoma are described as primary vaginal cancers. Adenosquamous carcinoma is a rare and aggressive mixed epithelial tumor comprising approximately 1% to 2% of cases.

Classification

Vaginal cancer may be classified according to histopathology into squamous cell carcinoma, adenocarcinoma, and vaginal sarcoma.

Pathophysiology

On gross pathology, an ulcerating or fungating mass , or an annular constricting lesion is characteristic finding of vaginal cancer.

Differential diagnosis

Vaginal cancer must be differentiated from cervical carcinoma, rectal carcinoma, uterine carcinoma, vaginal lymphoma, vaginal cyst, vaginal node of endometriosis, and uterine fibroids.

Epidemiology and Demographics

In 2015, the incidence of vaginal cancer is approximately 2-3 per 100,000 individuals with a death number of 910.

Risk factors

The risk factors of vaginal cancer may include vaginal adenosis, cervical cancer, diethylstilbestrol, human papillomavirus infection, HIV infection, unhealthy lifestyle, and age.

Prognosis

Depending on the extent of the tumor at the time of diagnosis, the prognosis of vaginal cancer may vary. However, the prognosis is generally regarded as good.

History and Symptoms

Common symptoms of vaginal cancer include vaginal bleeding, abnormal vaginal discharge, mass, and pain during intercourse.

Staging

Vaginal cancer may be classified into 4 subtypes based on FIGO or AJCC staging system.

Pelvic MRI

Pelvic MRI may be helpful in the diagnosis of vaginal cancer.

Other Diagnostic Studies

Cystoscopy, ureteroscopy, proctoscopy, lymphangiogram, and cone biopsy may be helpful to detect the spread of vaginal cancer.

Medical therapy

Medical therapies of vaginal cancer include surgery, radiation, and chemotherapy. The optimal therapy depends on the stage at diagnosis.

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]

Overview

Vaginal cancer may be classified according to histopathology into squamous cell carcinoma, adenocarcinoma, vaginal sarcoma and melanoma.

Types of vaginal cancer

Types of vaginal cancer, in order of prevalence, include:

  • Vaginal squamous cell carcinoma:
  • Vaginal adenocarcinoma:
  • Vaginal sarcoma:

Melanoma:

References

  1. ↑ 1.0 1.1 Creasman WT, Phillips JL, Menck HR (September 1998). “The National Cancer Data Base report on cancer of the vagina”. Cancer. 83 (5): 1033–40. PMID 9731908.
  2. ↑ Ikenberg H, Runge M, Göppinger A, Pfleiderer A (September 1990). “Human papillomavirus DNA in invasive carcinoma of the vagina”. Obstet Gynecol. 76 (3 Pt 1): 432–8. PMID 2166263.
  3. ↑ Isaacs JH (September 1976). “Verrucous carcinoma of the female genital tract”. Gynecol. Oncol. 4 (3): 259–69. PMID 964693.
  4. ↑ Herbst AL, Ulfelder H, Poskanzer DC (April 1971). “Adenocarcinoma of the vagina. Association of maternal stilbestrol therapy with tumor appearance in young women”. N. Engl. J. Med. 284 (15): 878–81. doi:10.1056/NEJM197104222841604. PMID 5549830.
  5. ↑ Hanselaar AG, Van Leusen ND, De Wilde PC, Vooijs GP (April 1991). “Clear cell adenocarcinoma of the vagina and cervix. A report of the Central Netherlands Registry with emphasis on early detection and prognosis”. Cancer. 67 (7): 1971–8. PMID 2004313.
  6. ↑ Verloop J, Rookus MA, van Leeuwen FE (June 2000). “Prevalence of gynecologic cancer in women exposed to diethylstilbestrol in utero”. N. Engl. J. Med. 342 (24): 1838–9. doi:10.1056/NEJM200006153422415. PMID 10866558.
  7. ↑ Hilgers RD, Malkasian GD, Soule EH (June 1970). “Embryonal rhabdomyosarcoma (botryoid type) of the vagina. A clinicopathologic review”. Am. J. Obstet. Gynecol. 107 (3): 484–502. PMID 4915719.
  8. ↑ DeMatos P, Tyler D, Seigler HF (July 1998). “Mucosal melanoma of the female genitalia: a clinicopathologic study of forty-three cases at Duke University Medical Center”. Surgery. 124 (1): 38–48. PMID 9663250.
  9. ↑ Frumovitz M, Etchepareborda M, Sun CC, Soliman PT, Eifel PJ, Levenback CF, Ramirez PT (December 2010). “Primary malignant melanoma of the vagina”. Obstet Gynecol. 116 (6): 1358–65. doi:10.1097/AOG.0b013e3181fb8045. PMID 21099603.
Pathophysiology

Pathophysiology

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

Vaginal cancer is a rare type of cancer that affects women. Vaginal intraepithelial neoplasia is a precancerous condition where some cells look abnormal. These cell changes are not cancer, but could become cancer over time. Vaginal intraepithelial neoplasia or VAIN means that the changed cells are only found in the innermost surface layer of the vagina. VAIN is more common in women who have had their uterus removed (hysterectomy) and in those who were treated for cervical cancer or pre-cancer in the past.

Pathophysiology

  • The vagina is a tube-like organ that connects the cervix (the lower part of the uterus) to the vulva (the outside female genitals).
  • The vagina is lined by a layer of flat cells called squamous cells.
  • This layer of cells is also called epithelium because it is formed by epithelial cells.
  • At birth, a baby passes through the vagina as he or she is born, so the vagina is sometimes also known as the birth canal.
  • Vaginal intraepithelial neoplasia is defined by the presence of squamous cell atypia without invasion.
  • The disease is classified according to the depth of epithelial involvement.
  • There are 3 types of VAIN: VAIN1, VAIN2, and VAIN3.
  • Low-grade VAIN (VAIN1) will sometimes go away on its own, but VAIN can sometimes lead to cancer if not treated.
  • Higher-grade VAIN (VAIN2 or VAIN3) is usually treated right away.
  • Two etiologies have been proposed to explain the strong association between VaIN and neoplasia elsewhere in the lower genital tract.
  • One possibility is that women who develop VaIN shortly after surgery for cervical intraepithelial neoplasia (CIN) may simply have vaginal extension of cervical disease that was not detected and treated.
  • VaIN is frequently multifocal, can occur several years after a hysterectomy for neoplasia, is independent of the amount of vaginal cuff excised, and is often observed de novo in the absence of cervical disease[1].
  • A second theory is that lower genital tract neoplasia share common etiologic factors, since approximately one-half of VaIN lesions are associated with concomitant cervical or vulvar neoplasia[2].
  • Tissues of common embryological origin are susceptible to neoplasia from exposure to similar carcinogenic stimuli. In particular, exposure to human papillomavirus (HPV) appears to induce neoplasms in all three locations of the lower female genital tract (cervix, vagina, vulva)[3].
  • HPV infection — HPV-associated lesions are often multifocal (originating within several discrete foci at one anatomic site) and multicentric (involving several distinct anatomic sites of the lower genital tract).
  • Although the relationship between HPV infection and intraepithelial neoplasia of the cervix is well known, there are less data available regarding vaginal neoplasia[4].
  • Several viral subtypes are associated with VaIN (table 1), with HPV 16 and 18 being the most prevalent HPV types [31]. The prevalence of oncogenic HPV subtypes in the vagina is similar in women who have and have not undergone hysterectomy[5].
  • Thus, presence of the cervix does not appear to be necessary for oncogenic HPV to infect the genital tract. (See “Cervical cancer screening tests: Techniques for cervical cytology and human papillomavirus testing”, section on ‘HPV testing’.)
  • The disparity between the relatively high incidence of CIN and rarity of VaIN in women who test positive for HPV may be due to increased susceptibility of the metaplastic transformation zone of the cervix to oncogenic stimuli. By contrast, the mature, stable, squamous epithelium of the vagina may be less vulnerable to the same stimuli[6].
  • Women who have been exposed to diethylstilbestrol (DES) in utero often have squamous metaplasia of the vagina instead of normal columnar epithelium; this observation may explain the increased incidence of VaIN noted in some studies of these women[7].
  • Women who have the human papillomavirus (HPV) are more likely than other women to develop this rare cancer.
  • Women who have been infected with herpes simplex virusare also at higher risk for vaginal cancer.
  • If a woman’s mother took a medicine called diethylstilbestrol (DES) when she was pregnant between 1940 and 1971.
  • Women whose mothers took DES – known as DES daughters – develop clear-cell adenocarcinomaof the vagina or cervix more often than women in the general population.
  • Lesions characteristically arise from the posterior wall of the upper third of the vagina. The common patterns of disease are:

References

  1. ↑ Creasman WT, Rutledge F (March 1972). “Carcinoma in situ of the cervix. An analysis of 861 patients”. Obstet Gynecol. 39 (3): 373–80. PMID 5019309.
  2. ↑ Aho M, Vesterinen E, Meyer B, Purola E, Paavonen J (July 1991). “Natural history of vaginal intraepithelial neoplasia”. Cancer. 68 (1): 195–7. PMID 2049744.
  3. ↑ Sturgeon SR, Curtis RE, Johnson K, Ries L, Brinton LA (March 1996). “Second primary cancers after vulvar and vaginal cancers”. Am. J. Obstet. Gynecol. 174 (3): 929–33. PMID 8633671.
  4. ↑ Matsukura T, Sugase M (March 1995). “Identification of genital human papillomaviruses in cervical biopsy specimens: segregation of specific virus types in specific clinicopathologic lesions”. Int. J. Cancer. 61 (1): 13–22. PMID 7705925.
  5. ↑ Castle PE, Schiffman M, Bratti MC, Hildesheim A, Herrero R, Hutchinson ML, Rodriguez AC, Wacholder S, Sherman ME, Kendall H, Viscidi RP, Jeronimo J, Schussler JE, Burk RD (August 2004). “A population-based study of vaginal human papillomavirus infection in hysterectomized women”. J. Infect. Dis. 190 (3): 458–67. doi:10.1086/421916. PMID 15243917.
  6. ↑ Schneider A, de Villiers EM, Schneider V (September 1987). “Multifocal squamous neoplasia of the female genital tract: significance of human papillomavirus infection of the vagina after hysterectomy”. Obstet Gynecol. 70 (3 Pt 1): 294–8. PMID 2819794.
  7. ↑ Bornstein J, Adam E, Adler-Storthz K, Kaufman RH (January 1988). “Development of cervical and vaginal squamous cell neoplasia as a late consequence of in utero exposure to diethylstilbestrol”. Obstet Gynecol Surv. 43 (1): 15–21. PMID 2829071.
Causes

Causes

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

Causes

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

Differentiating Vaginal cancer from other Diseases

Differentiating Vaginal cancer from other Diseases

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

Vaginal cancer must be differentiated from cervical carcinoma, rectal carcinoma, uterine carcinoma, vaginal lymphoma, vaginal cyst, vaginal node of endometriosis, and uterine fibroids.

Differential diagnosis

For large lesions consider invasion of the vagina by:

Malignant involvement of the vagina from metastatic spread is much more common, and except for isolated reports of metastases from extragenital cancers, the most common cause of metastatic disease is direct local invasion from the female urogenital tract. Therefore some authors state the diagnosis of primary vaginal carcinoma should be diagnosed only if other gynecologic malignancies have been excluded.

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
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: Syed Musadiq Ali M.B.B.S.[2]

      Overview

      In 2015, the incidence of vaginal cancer is approximately 2-3 per 100,000 individuals with a death number of 910.

      Epidemiology and Demographics

      • New cases: 4,070.
      • Deaths: 910.
      • New cases: 2,210.
      • Deaths: 760.

      References

      1. ↑ Gadducci A, Fabrini MG, Lanfredini N, Sergiampietri C (March 2015). “Squamous cell carcinoma of the vagina: natural history, treatment modalities and prognostic factors”. Crit. Rev. Oncol. Hematol. 93 (3): 211–24. doi:10.1016/j.critrevonc.2014.09.002. PMID 25476235.
      2. ↑ Siegel RL, Miller KD, Jemal A (2015). “Cancer statistics, 2015”. CA Cancer J Clin. 65 (1): 5–29. doi:10.3322/caac.21254. PMID 25559415.
      3. ↑ Shah CA, Goff BA, Lowe K, Peters WA, Li CI (May 2009). “Factors affecting risk of mortality in women with vaginal cancer”. Obstet Gynecol. 113 (5): 1038–45. doi:10.1097/AOG.0b013e31819fe844. PMC 2746762. PMID 19384118.
      4. ↑ Alemany L, Saunier M, Tinoco L, Quirós B, Alvarado-Cabrero I, Alejo M, Joura EA, Maldonado P, Klaustermeier J, Salmerón J, Bergeron C, Petry KU, Guimerà N, Clavero O, Murillo R, Clavel C, Wain V, Geraets DT, Jach R, Cross P, Carrilho C, Molina C, Shin HR, Mandys V, Nowakowski AM, Vidal A, Lombardi L, Kitchener H, Sica AR, Magaña-León C, Pawlita M, Quint W, Bravo IG, Muñoz N, de Sanjosé S, Bosch FX (November 2014). “Large contribution of human papillomavirus in vaginal neoplastic lesions: a worldwide study in 597 samples”. Eur. J. Cancer. 50 (16): 2846–54. doi:10.1016/j.ejca.2014.07.018. PMID 25155250.
      5. ↑ Daling JR, Madeleine MM, Schwartz SM, Shera KA, Carter JJ, McKnight B, Porter PL, Galloway DA, McDougall JK, Tamimi H (February 2002). “A population-based study of squamous cell vaginal cancer: HPV and cofactors”. Gynecol. Oncol. 84 (2): 263–70. doi:10.1006/gyno.2001.6502. PMID 11812085.
      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.
      Risk Factors

      Risk Factors

      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

      The risk factors of vaginal cancer may include vaginal adenosis, cervical cancer, diethylstilbestrol, human papillomavirus infection, HIV infection, unhealthy lifestyle, and age.

      Risk factors

      Clinical data has suggested that the development of vaginal cancer is related to several factors.

      • Clinical research suggest that having adenosis increases the risk of developing clear cell carcinoma. Although it is very small, many doctors feel that any woman with adenosis should have very careful screening and follow-up[1].
      • HIV infection:
      • Unhealthy lifestyle:
      • Age:
      • Approximately 85 percent of the cases of vaginal cancer occur in women who are over the age of 40, and nearly 50 percent of cases occur in women age 70 or older[7].

      References

      1. ↑ Vessey MP (1989). “Epidemiological studies of the effects of diethylstilboestrol”. IARC Sci. Publ. (96): 335–48. PMID 2680951.
      2. ↑ Jain G, Sabeena S, Vasudeva A, Mundkur A, Srinivas SP, Arunkumar G, Kumar P (December 2018). “A report of human papilloma virus-16 associated vaginal carcinoma after thirty-two years of successful radiation therapy for cervical cancer”. Virusdisease. 29 (4): 537–539. doi:10.1007/s13337-018-0479-8. PMID 30539058.
      3. ↑ Huo D, Anderson D, Palmer JR, Herbst AL (September 2017). “Incidence rates and risks of diethylstilbestrol-related clear-cell adenocarcinoma of the vagina and cervix: Update after 40-year follow-up”. Gynecol. Oncol. 146 (3): 566–571. doi:10.1016/j.ygyno.2017.06.028. PMID 28689666.
      4. ↑ Pham T, Bi X, Hoang H, Ishizaki A, Nguyen M, Nguyen CH, Nguyen HP, Pham TV, Ichimura H (November 2018). “Human Papillomavirus Genotypes and HPV16 E6/E7 Variants among Patients with Genital Cancers in Vietnam”. Jpn. J. Infect. Dis. 71 (6): 419–426. doi:10.7883/yoken.JJID.2018.206. PMID 29962490. Vancouver style error: initials (help)
      5. ↑ Davies O, Rajamanoharan S, Balachandran T (November 2015). “Cervical screening in HIV-positive women in the East of England: recent CD4 as the predictive risk factor”. Int J STD AIDS. 26 (13): 945–50. doi:10.1177/0956462414563624. PMID 25505037.
      6. ↑ Santoso JT, Crigger M, English E, Wan J, Likes W (June 2012). “Smoking cessation counseling in women with genital intraepithelial neoplasia”. Gynecol. Oncol. 125 (3): 716–9. doi:10.1016/j.ygyno.2012.02.018. PMID 22366589.
      7. ↑ Strander B, Hällgren J, Sparén P (January 2014). “Effect of ageing on cervical or vaginal cancer in Swedish women previously treated for cervical intraepithelial neoplasia grade 3: population based cohort study of long term incidence and mortality”. BMJ. 348: f7361. doi:10.1136/bmj.f7361. PMC 3898577. PMID 24423603.
      Screening

      Screening

      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 no general screening programme for vaginal cancer because it’s a very rare condition.
      • When you have a cervical screening test, the doctor or nurse does a routine examination of your vagina at the same time. They can pick up pre cancerous conditions such as vaginal intraepithelial neoplasia (VAIN). Treatment for VAIN prevents vaginal cancer from developing.
      • Screening is done by means of vaginal Pap smears in women who had previously undergone a hysterectomy for benign gynecologic disease.[1]
      • In the United States, annual vaginal Pap smears have been recommended for the possible detection of vaginal cancer even for women who have previously undergone a hysterectomy, despite the fact that evidence of the value of such screening in this group of patients is virtually nonexistent[2].
      • In 1995, the American College of Obstetricians and Gynecologists recommended that such women be screened periodically, yet it acknowledged that no data were available to support the recommendation.[3]
      • The relationship between the human papillomavirus (HPV) and malignancies of the uterine, cervix, vagina, and vulva has been established.
      • The prevalence of oncogenic HPV subtypes in cervical cancers has been the most studied, but prevalence has also been established for vaginal and vulvar cancers. Clinical trials demonstrate impressive efficacy in disease prevention as well as excellent safety and tolerability. Screening cervical cancer can reduce the risk of vaginal cancer[4].

      Screening Guidelines

      American Cancer Society (ACS), American Society for Colposcopy and Cervical Pathology (ASCCP), and American Society for Clinical Pathology U.S. Preventive Services Task Force (USPSTF) American College of Obstetricians and Gynecologists (ACOG)
      When to start screening Age 21. Women aged <21 years should not be screened regardless of the age of sexual initiation or other risk factors Age 21. (A recommendation) Recommend against screening women aged <21 years (D recommendation) Age 21 regardless of the age of onset of sexual activity. Women aged <21 years should not be screened regardless of age at sexual initiation and other behavior-related risk factors (Level A evidence)
      Statement about annual screening Women of any age should not be screened annually by any screening method Individuals and clinicians can use the annual Pap test screening visit as an opportunity to discuss other health problems and preventive measures. Individuals, clinicians, and health systems should seek effective ways to facilitate the receipt of recommended preventive services at intervals that are beneficial to the patient. Efforts also should be made to ensure that individuals are able to seek care for additional health concerns as they present In women aged 30–65 years, annual cervical cancer screening should not be performed. (Level A evidence) Patients should be counseled that annual well-woman visits are recommended even if cervical cancer screening is not performed at each visit
      Screening method and intervals
      Cytology (conventional or liquid based) 21–29 years Every 3 years Every 3 years (A recommendation) Every 3 years (Level A evidence)
      30–65 years Every 3 years Every 3 years (A recommendation) Every 3 years (Level A evidence)
      HPV co-test (cytology + HPV test administered together) 21–29 years HPV co-testing should not be used for women aged <30 years Recommend against HPV co-testing in women aged <30 years (D recommendation) HPV co-testing should not be performed in women aged <30 years. (Level A evidence )
      30–65 years Every 5 years; this is the preferred method. For women who want to extend their screening interval, HPV co-testing every 5 years is an option (A recommendation) Every 5 years; this is the preferred method (Level A evidence)
      Primary hrHPV f testing (as an alternative to cotesting or g cytology alone) For women aged 30–65 years, screening by HPV testing alone is not recommended in most clinical settings Recommend against screening for cervical cancer with HPV testing (alone or in combination with cytology) in women aged <30 years (D recommendation) Not addressed
      When to stop screening Aged >65 years with adequate negative prior screening* and no history of CIN2 or higher within the last 20 years Aged >65 years with adequate screening history* and are not otherwise at high risk for cervical cancer (D recommendation) Aged >65 years with adequate negative prior screening* results and no history of CIN 2 or higher (Level A evidence)
      When to screen after age 65 years When to screen after age 65 years Aged >65 years with a history of CIN2 CIN2, CIN3, or adenocarcinoma in situ, routine screeningk should continue for at least 20 years Women aged >65 years who have never been screened, do not meet the criteria for adequate prior screening, or for whom the adequacy of prior screening cannot be accurately accessed or documented.l Routine screeningk should continue for at least 20 years after spontaneous regression or appropriate management of a high-grade precancerous lesion, even if this extends screening past age 65 years. Certain considerations may support screening in women aged > 65 years who are otherwise considered high risk (such as women with a highgrade precancerous lesion or cervical cancer, women with in utero exposure to diethylstilbestrol, or women who are immunocompromised) Women aged >65 years with a history of CIN2, CIN3, or AIS should continue routine agebased screeningk for at least 20 years (Level B evidence)
      Screening post-hysterectomy Women who have had a total hysterectomy (removal of the uterus and cervix) should stop screening.Women who have had a supra-cervical hysterectomy (cervix intact) should continue screening according to guidelines Recommend against screening in women who have had a hysterectomy (removal of the cervix) (D recommendation) Women who have had a hysterectomy (removal of the cervix) should stop screening and not restart for any reason, (Level A evidence)
      The need for a bimanual pelvic exam Not addressed in 2012 guidelines but was addressed in 2002 ACS guidelines Addressed in USPSTF ovarian cancer screening recommendations (draft) Addressed in 2012 well-woman visit recommendations.Aged <21 years, no evidence supports the routine internal examination of the healthy, asymptomatic patient. An “external-only” genital examination is acceptable. Aged ≥21 years, no evidence supports or refutes the annual pelvic examination or speculum and bimanual examination. The decision whether or not to perform a complete pelvic examination should be a shared decision after a discussion between the patient and her health care provider. Annual examination of the external genitalia should continue
      Screening among those immunized against HPV 16/18 Women at any age with a history of HPV vaccination should be screened according to the age specific recommendations for the general population The possibility that vaccination might reduce the need for screening with cytology alone or in combination with HPV testing is not established. Given these uncertainties, women who have been vaccinated should continue to be screened Women who have received the HPV vaccine should be screened according to the same guidelines as women who have not been vaccinated (Level C evidence)

      HPV = human papillomavirus; CIN = cervical intraepithelial neoplasia; AIS=adenocarcinoma in situ; hrHPV = high-risk HPV.

      References

      1. ↑ Noller KL (November 1996). “Screening for vaginal cancer”. N. Engl. J. Med. 335 (21): 1599–600. doi:10.1056/NEJM199611213352111. PMID 8900096.
      2. ↑ “ACOG committee opinion. Recommendations on frequency of Pap test screening. Number 152–March 1995. Committee on Gynecologic Practice. American College of Obstetricians and Gynecologists”. Int J Gynaecol Obstet. 49 (2): 210–1. May 1995. PMID 7649335.
      3. ↑ Wright TC, Sun XW, Koulos J (February 1995). “Comparison of management algorithms for the evaluation of women with low-grade cytologic abnormalities”. Obstet Gynecol. 85 (2): 202–10. doi:10.1016/0029-7844(94)00373-L. PMID 7824231.
      4. ↑ Diaz ML (August 2010). “Prevention of cervical, vaginal, and vulval cancers: role of the quadrivalent human papillomavirus (6, 11, 16, 18) recombinant vaccine”. Int J Womens Health. 1: 119–29. PMC 2971720. PMID 21072282.
      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: Syed Musadiq Ali M.B.B.S.[2]

      Overview

      Depending on the extent of the tumor at the time of diagnosis, the prognosis of vaginal cancer may vary. However, the prognosis is generally regarded as good.The 5-year survival rate can also depend on the type of vaginal cancer. For squamous cell carcinoma of the vagina, the 5-year survival rate is 54%. For adenocarcinoma of the vagina, the rate is about 60%. Symptoms are related to local extension of disease, urinary symptoms (eg, frequency, dysuria, hematuria), or gastrointestinal complaints (eg, tenesmus, constipation, melena)

      Natural History

      Complications

      Prognosis

      • Data from a United States National Cancer Database showed an increased risk of mortality in women with vaginal cancer with stage II or greater disease and/or tumor size >4 cm (five-year survival 65 versus 84 percent in tumors ≤4 cm)[4].
      • Mortality was 51 percent higher in women with melanoma compared with squamous vaginal cancer.
      • Patient prognosis depends primarily on the stage of disease, but survival is reduced among those who are older than 60 years, are symptomatic at the time of diagnosis.
      • In addition, the length of vaginal wall involvement has been found to be associated with survival and stage of disease in vaginal Squamous cell cancer(SCC) patients.
      • Non–DES-associated adenocarcinomas generally have a worse prognosis than Squamous cell cancer(SCC) tumors, but DES-associated clear cell tumors have a relatively good prognosis[5].

      References

      1. ↑ Choo YC, Anderson DG (August 1982). “Neoplasms of the vagina following cervical carcinoma”. Gynecol. Oncol. 14 (1): 125–32. PMID 7095583.
      2. ↑ Herbst AL, Ulfelder H, Poskanzer DC (April 1971). “Adenocarcinoma of the vagina. Association of maternal stilbestrol therapy with tumor appearance in young women”. N. Engl. J. Med. 284 (15): 878–81. doi:10.1056/NEJM197104222841604. PMID 5549830.
      3. ↑ Nori D, Hilaris BS, Stanimir G, Lewis JL (October 1983). “Radiation therapy of primary vaginal carcinoma”. Int. J. Radiat. Oncol. Biol. Phys. 9 (10): 1471–5. PMID 6629889.
      4. ↑ Beller U, Sideri M, Maisonneuve P, Benedet JL, Heintz AP, Ngan HY, Pecorelli S, Odicino F, Creasman WT (2001). “Carcinoma of the vagina”. J Epidemiol Biostat. 6 (1): 141–52. PMID 11385773.
      5. ↑ Hellman K, Lundell M, Silfverswärd C, Nilsson B, Hellström AC, Frankendal B (2006). “Clinical and histopathologic factors related to prognosis in primary squamous cell carcinoma of the vagina”. Int. J. Gynecol. Cancer. 16 (3): 1201–11. doi:10.1111/j.1525-1438.2006.00520.x. PMID 16803507.
      Diagnosis

      Diagnosis

      History and Symptoms | Physical Examination | Staging | Laboratory Findings | X Ray | 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

      Related Chapters


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