Author Information
Jahan N*, Tiwari N**, Chaudhari HK***.
(* Junior Resident, ** Assistant Professor, *** Associate Professor. Department of Obstetrics and Gynecology, Seth G S Medical College and K E M Hospital, Mumbai, India.)
Abstract
HPV infection can manifest clinically, subclinically or in latent form. HPV infection causes visible genital lesions known as genital warts, which are commonly caused by HPV types 6 and 11, and involves vulva, vagina, cervix, urethra and anus. Oncogenic HPV types 16, 18, 31, 33 and 35 are commonly associated with vulvar (VIN), cervical (CIN) and anal (AIN) intraepithelial neoplasia. The prevalence of HPV infection in the form of visible genital warts is about 1 % in sexually active adults. Here we are presenting a case of genital wart in pregnancy.
Introduction
Human papilloma virus (HPV) is a DNA virus belonging to the Papillomaviridae family. Out of more than 100 types, over 30 types can infect the genital area. These genital types are generally categorized as either “high-risk” types which are associated with high grade squamous intraepithelial lesions and invasive cancer or “low-risk” types causing genital warts, low grade squamous intraepithelial lesions and recurrent respiratory papillomatosis. There is no curative treatment for HPV infection, treatments are directed to abnormal cells infected with HPV rather than the virus itself. The risk factors are early age of first sexual intercourse and male partner's promiscuity. Less consistently identified risk factors include smoking, oral contraceptive use (because of increased unprotected sexual intercourse and impaired metabolism of vitamins and folic acid), nutritional factors and lack of circumcision of male partner.[1] Compromised immunity as in pregnancy also increases susceptibility to HPV infection.
Case Report
A 20 year old gravida 2 spontaneous abortion 1, presented at 35 weeks of gestation with preterm labor for want of a NICU. She had pain in abdomen with leaking per vaginum for 6 hours. She was perceiving good fetal movements. She had already received antenatal steroids for fetal lung maturity. On systemic examination, pulse was 88 beats per minute and blood pressure was 130/80 mm of Hg. On per abdomen examination, uterus was 34 weeks of gestation with vertex presentation with 140 beats/min fetal heart rate. On local examination, there was a single well defined white colored plaque with verrucous surface over right side of the vulva suggestive of a genital wart (figure 1). On vaginal examination, she was in active labor. There was no history of bleeding, ulceration, or discharge from the growth. Dermatology reference was taken. Emergency lower segment cesarean section was advised as vaginal delivery could lead to fetal infection. She was counseled regarding the same but she requested vaginal delivery. Respecting her request, decision to monitor her labor was taken. A male child weighing 2334 g was born whose Apgar score was 9/10 at 1 minute. He was asymptomatic and was followed till 6 weeks. She was advised to follow up with the dermatologist for trichloroacetic acid application.
Jahan N*, Tiwari N**, Chaudhari HK***.
(* Junior Resident, ** Assistant Professor, *** Associate Professor. Department of Obstetrics and Gynecology, Seth G S Medical College and K E M Hospital, Mumbai, India.)
Abstract
HPV infection can manifest clinically, subclinically or in latent form. HPV infection causes visible genital lesions known as genital warts, which are commonly caused by HPV types 6 and 11, and involves vulva, vagina, cervix, urethra and anus. Oncogenic HPV types 16, 18, 31, 33 and 35 are commonly associated with vulvar (VIN), cervical (CIN) and anal (AIN) intraepithelial neoplasia. The prevalence of HPV infection in the form of visible genital warts is about 1 % in sexually active adults. Here we are presenting a case of genital wart in pregnancy.
Introduction
Human papilloma virus (HPV) is a DNA virus belonging to the Papillomaviridae family. Out of more than 100 types, over 30 types can infect the genital area. These genital types are generally categorized as either “high-risk” types which are associated with high grade squamous intraepithelial lesions and invasive cancer or “low-risk” types causing genital warts, low grade squamous intraepithelial lesions and recurrent respiratory papillomatosis. There is no curative treatment for HPV infection, treatments are directed to abnormal cells infected with HPV rather than the virus itself. The risk factors are early age of first sexual intercourse and male partner's promiscuity. Less consistently identified risk factors include smoking, oral contraceptive use (because of increased unprotected sexual intercourse and impaired metabolism of vitamins and folic acid), nutritional factors and lack of circumcision of male partner.[1] Compromised immunity as in pregnancy also increases susceptibility to HPV infection.
Case Report
A 20 year old gravida 2 spontaneous abortion 1, presented at 35 weeks of gestation with preterm labor for want of a NICU. She had pain in abdomen with leaking per vaginum for 6 hours. She was perceiving good fetal movements. She had already received antenatal steroids for fetal lung maturity. On systemic examination, pulse was 88 beats per minute and blood pressure was 130/80 mm of Hg. On per abdomen examination, uterus was 34 weeks of gestation with vertex presentation with 140 beats/min fetal heart rate. On local examination, there was a single well defined white colored plaque with verrucous surface over right side of the vulva suggestive of a genital wart (figure 1). On vaginal examination, she was in active labor. There was no history of bleeding, ulceration, or discharge from the growth. Dermatology reference was taken. Emergency lower segment cesarean section was advised as vaginal delivery could lead to fetal infection. She was counseled regarding the same but she requested vaginal delivery. Respecting her request, decision to monitor her labor was taken. A male child weighing 2334 g was born whose Apgar score was 9/10 at 1 minute. He was asymptomatic and was followed till 6 weeks. She was advised to follow up with the dermatologist for trichloroacetic acid application.
Figure 1. Genital wart.
Discussion
The tumor-like masses in HPV infection whose sizes range between few mm to 2 cm are called condyloma acuminata (CA), and are also known as warts. Lesions may be flat, papular or pedunculated growths on the genital mucosa. Genital warts are usually asymptomatic. They can present as painful, friable or pruritic lesions over the genital mucosa. Diagnosis of genital warts is made by visual inspection and confirmed by biopsy. The application of 3-5 % acetic acid usually turns HPV infected genital mucosal tissue to a whitish color.
HPV types 16, 18, 31, 33, and 35 are found occasionally in visible genital warts and have been associated with external genital (vulvar, penile, and anal) squamous intraepithelial neoplasia. Patients having visible genital warts are found to have simultaneous infection with multiple HPV types.
Genital warts respond to various treatment modalities. Factors that might affect response to therapy include the presence of immunosuppression and compliance with therapy.[2] Effect of treatment on future transmission of infection is uncertain and there is a possibility of spontaneous resolution of infection, thus in milder cases one can wait for spontaneous resolution of the disease.
In pregnancy, the natural immune suppressive state worsens the HPV induced lesions. There may be dramatic increase in size of warts so as to obstruct urinary and reproductive passage. The presence of genital warts does not make cesarean section the recommended mode of delivery. There is a rare possibility of laryngeal papillomatosis in children born by vaginal delivery. The risk of neonatal infection can be reduced by avoiding invasive procedures during vaginal delivery. Pregnant woman with genital warts should be counseled about the known risks of cesarean section like wound infection, need of blood transfusion, delayed recovery etc. The only clinical indication for cesarean section is the presence of extensive vaginal warts blocking the birth canal as it can cause profuse bleeding.[3]
Rates of transmission of HPV in subclinical cases of HPV during pregnancy to the neonate range from 1–18 %. In women who had clinically detectable HPV or positive HPV cervical smears during pregnancy, HPV transmission rates ranged from 5–72%. Clinical manifestation in infants born to infected mother are conjunctivitis, anogenital warts and laryngeal papillomatosis.[4] Newborn may be asymptomatic at birth but laryngeal papillomas may develop within 2–5 years of life resulting in hoarse voice and airway obstruction in children.[3] This possibility of fetal exposure should be well followed up. Infants on follow up rarely showed persistence for HPV-DNA positivity.
There is no single definitive treatment for HPV infection in pregnancy. In pregnant women, 80% to 90% trichloroacetic acid (TCA) can be applied topically. For small lesions cryotherapy with liquid nitrogen is a reasonable first line treatment. It is not used for vaginal lesions due to risk of vaginal perforation and fistula formation. Laser therapy with carbon dioxide is recommended in patients with large or multiple lesions or with lesions refractory to treatment with TCA or cryotherapy.[5] Surgical removal is the method of choice in pregnancy specially for giant vaginal warts. Interferon therapy or intralesional or systemic chemotherapy can be given in nonpregnant women before surgical excision. Radiotherapy may also increase the success rate of the therapy in non pregnant women.[6] Imiquimod 5% cream, podophyllin and antiviral drugs are not used in pregnancy.[5,7]
Conclusion
Cesarean section is not the preferred mode of delivery in pregnant women with genital warts. It depends on wart size, number, anatomic site, patient preference and provider experience. There are rare chances of perinatal infection in a baby born to a woman with genital warts .
References
- Kjellberg L, Hallmans G, Ahren AM, Johansson R, Bergman F, Wadell G et al. Smoking, diet, pregnancy and oral contraceptive use as risk factors for cervical intra-epithelial neoplasia in relation to human papillomavirus infection Br J Cancer. 2002, 82(7): 1332- 1338.
- Castellsagué X, Muñoz N. Cofactors in human papillomavirus carcinogenesis-role of parity, oral contraceptives, and tobacco smoking. Journal of the National Cancer Institute Monographs. 2003:31:20–28.
- Singhal P, Naswa S, Marfatia YS. Pregnancy and sexually transmitted viral infections. Indian J Sex Transm Dis AIDS. 2009 Jul;30(2):71-8.
- Rombaldi RL, Serafini EP, Mandelli J, Zimmermann E, Losquiavo KP. Perinatal transmission of human papilomavirus DNA. Virol J. 2009:21;6:83.
- Workowski KA, Bolan GA. Sexually transmitted diseases treatment guidelines, 2015. MMWR Recomm Rep. 2015;64(RR-03):1-137.
- Safi F, Bekdache O, Al-Salam S, Alashari M, Mazen T, El-Salhat H. Management of peri-anal giant condyloma acuminatum--a case report and literature review. Asian J Surg. 2013;36(1):43-52.
- Snoeck R, Bossens M, Parent D, Delaere B, Degreef H, Van Ranst M, et al. Phase II double-blind, placebo-controlled study of the safety and efficacy of cidofovir topical gel for the treatment of patients with human papillomavirus infection. Clin Infect Dis. 2001;33(5):597-602.
Jahan N, Tiwari N, Chaudhari HK. Genital Wart In Pregnancy. JPGO 2019. Volume 6 No. 3. Available from: https://www.jpgo.org/2019/03/genital-wart-in-pregnancy.html