The viral nature of genital warts was first recognized in 1907 when Ciuffo induced warts after autoinoculation of cell-free wart extracts.[1] The human papillomavirus (HPV) was identified with the development of molecular biology techniques as the virus responsible for condyloma acuminatum. Zur Hansen proposed that HPV was likely important in the etiology of genital tract neoplasias in the mid 1970s.[2] The DNA of the first genital wart was characterized in 1980. Today, more than 120 distinct HPV subtypes have been identified. This group of viruses is strongly linked to the development of cervical cancer. HPV contributes to 90% of anal cancers and 40% of vulva, vaginal, and penile cancers. Squamous cell carcinoma of the oropharynx is associated with HPV in 50% of cases.[3, 4]
Complete understanding of the natural history of HPV disease has significantly improved over the last 20 years, but key issues remain unanswered. Topics requiring further research include HPV age-specific outcomes, risk of progression and regression of disease, and factors important in the acquisition of immunity following infection.[5]
Genital warts are transmitted by sexual contact. Approximately two thirds of individuals who have sexual contact with an infected partner develop genital warts. The exact incubation time is unknown, but most investigators believe the incubation period is 3 weeks to 8 months.[6, 7]
HPV is a group of double-stranded DNA viruses. The genome encodes 6 early open reading frames (E1, E2, E4, E5, E6, E7) and 2 late open reading frames (L1, L2). The E genes encode proteins important in regulatory function, and the L genes encode for viral capsid proteins. This group of viruses can infect many different sites, including the larynx, skin, mouth, esophagus, and the anogenital tract.
Approximately 40 different types of HPV can infect the anogenital tract. Infection caused by the HPV virus results in local infections and appears as warty papillary condylomatous lesions. HPV infections in the genital area are sexually transmitted.[8, 9, 10]
HPVs associated with genital tract lesions have been divided into low risk and high risk based on each genotype's association with benign or malignant lesions. Most genital condylomata are due to infection by HPV-6 or HPV-11. These HPV types replicate as an episome and rarely incorporate their genetic material into the host DNA. In contrast, HPV-16 and HPV-18 can be recovered in approximately 70% of squamous cell carcinomas of the cervix. These high-risk HPV types, along with types 31, 33, 45, 51, 52, 56, 58, and 59 incorporate a portion of their genetic material into the host DNA. The E6 and E7 genes can produce oncoproteins that alter cell growth regulation. Specifically, E6 oncoprotein inactivates the tumor suppressor gene p53, and the oncoprotein produced by E7 inactivates pRB (retinoblastoma).[11]
Accurate data concerning the frequency of HPV infection in the US population are difficult to ascertain. Studies reporting the diagnosis of HPV by visual inspection of genital condyloma report the lowest prevalence rates. The highest prevalence rates are reported by studies typing HPV from exfoliated genital tract cells. Most researchers believe HPV is the most common sexually transmitted disease (STD) in the United States. An estimated 500,000 to 1 million new cases of genital warts are diagnosed each year. Data indicate that up to 75% of individuals who have sexual contact with an HPV-infected partner will develop external genital warts.[12] In the United States, 20 million individuals are infected with HPV each year.[13, 14, 15, 16, 17] In the United States, young adults aged 15-24 years account for approximately one half of new HPV infections each year.[18]
Condyloma acuminata are clinically apparent in 1% of the sexually active population. Molecular studies indicate 10-20% of men and women aged 15-49 years have been exposed to HPV. The prevalence of HPV is higher in certain populations. A prevalence rate of 4-13% has been reported by STD clinics. Young adults in the United States, ages 15 to 24 years, account for approximately one-half of new HPV infections each year.
The incidence of HPV infection has clearly increased in the last 35 years based on clinical observations. Data from the National Disease and Therapeutic Index, which is a random survey of private physicians indicate in 1966, 169,000 people consulted a physician about genital warts. By 1984, this number had risen to 1,150,000 consultations. Today, researchers believe at least 1 million new cases of genital warts are diagnosed each year.[19, 18]
Several investigators report an increased prevalence of anogenital HPV infections during pregnancy. During pregnancy, the prevalence of condyloma increases from the first to third trimester and decreases significantly in the postpartum period. The risk of condyloma acuminata in pregnancy is 2-fold. Vulvar condyloma can rarely become large enough to obstruct labor. Cesarean delivery decreases, but does not completely prevent, HPV transmission with development of laryngeal papillomas in the infant.[20, 21, 22, 23]
International
Globally, HPV is the most common sexually transmitted infection.[24, 25] A study in Finland in the mid-1980s demonstrated an annual incidence of cytologic cervical HPV infection of 7%.[26] A study of Finnish males found 6.5% had evidence of HPV in exfoliative cells obtained from the urethra and genital epithelium.[27]
Mortality/Morbidity
Condyloma acuminatum is often asymptomatic.
Pruritus or occasional bleeding may lead the patient to seek medical care.
Patients who do not develop immunity to HPV can develop potentially serious sequelae.
HPV infection of the vulva can result in the development of vulvar intraepithelial neoplasia (dysplasia) or squamous cell carcinoma of the vulva. Most research indicates that HPV infection is strongly associated with the development of cervical dysplasia and cervical carcinoma. HPV confers more than 99% of the attributable risk for the development of cervical dysplasia.[28] Vaginal dysplasia and vaginal cancer are also associated with HPV exposure.
Race
Most studies indicate that no racial predilection exists for the acquisition of genital warts. Dinh and associates analyzed data from the 1999-2004 National Health and Nutrition Examination Surveys which collect data from a random sample of the United States civilian population. These investigators reported that non-Hispanic whites had a higher prevalence of genital warts when compared with other racial/ethnic groups.[29] One US survey reported that among women, the prevalence of HPV infection due to any HPV type was 39% for non-Hispanic blacks, and 24% for non-Hispanic whites and Mexican Americans.[30]
Sex
The prevalence of condyloma acuminata seems to be similar in men and women. One study from an STD clinic in Washington State found that 13% of men and 9% of women had condyloma acuminata (US Department of Health and Human Services, 1996).[13] HPV infections have been reported in approximately one third of US college females.[31] This incidence is higher than in the male population. This presumed higher incidence of HPV infection in females may be the result of detection of HPV infection in cytologic smears performed for cervical cancer screening. Females seek medical care for genital warts more frequently than men.[16]
Age
The highest rates of genital HPV infection are in sexually active females aged 18-25 years. This incidence is independent of the number of lifetime sexual partners. Most of these infections (90%) are transient.[32, 33, 34] An estimated 5.6% of sexually active adults in the United States aged 18-59 years have been diagnosed with genital warts by a medical provider.[29] The prevalence of genital warts in children younger than 18 years is unknown.[35]
A cytologic screening of the cervix in more than 400,000 women supports a higher incidence of HPV in young women. This study found that the rate of HPV infection is twice as frequent in women younger than 30 years than it is in women older than 30 years.[36] The prevalence of HPV in a representative sample of US females aged 14-59 years was 26.8%. Women aged 20-24 years had a prevalence rate of 44.8%.[37]
The reason for the higher prevalence in younger women is not completely understood. Some investigators hypothesize that older women have fewer sexual partners and, consequently, less exposure to the HPV. An alternative theory is that by age 30 years, women have acquired immunity to HPV.[38]
The presence of genital condyloma in the pediatric population presents a diagnostic and therapeutic challenge. Vertical transmission of HPV can occur via in utero exposure to amniotic fluid or transmission of HPV from the maternal genital tract. An incubation period of several months is usually required between virus infection at delivery and clinical manifestations in the infant. The average latency period is 3 months, but periods as long as 20 months have been reported.[39] Cases of childhood condylomata outside a reasonable incubation period after vertical transmission should arouse the suspicion of child abuse. Treatment of condyloma in the infant includes excision under general anesthesia or the use of podophyllin.[40]
Inspection of the female genital area requires good lighting.
Typical condyloma are usually discrete, papillary, cauliflowerlike lesions that involve multiple sites on moist surfaces.
Keratotic warts are often seen on dry surfaces like the labia majora.
Subclinical infection is another common presentation of condyloma. Tiny, slightly raised areas can be felt or visualized on the vagina or cervix.
These flat warts are best visualized using 3-5% acetic acid and a colposcope. Areas infected with HPV appear acetowhite.
Often, a biopsy is needed to distinguish these lesions from cervical squamous intraepithelial lesions or vaginal intraepithelial lesions.
The sexual partner or partners of a woman with condyloma should be examined by a physician and treated if indicated. Often the examination of the male fails to reveal any visible condyloma.
Patients who present with condyloma acuminata do not necessarily need other laboratory studies. Patients who are diagnosed with condyloma are at an increased risk for other STDs.
Consider testing for chlamydia, gonorrhea, syphilis, hepatitis B, hepatitis C, herpes, and HIV depending on the clinical situation.
These patients need a Papanicolaou test of the cervix in accordance with the guidelines of the American College of Obstetricians and Gynecologists.
Histologic examination of the vulvar lesions to detect vulvar condyloma is sometimes difficult.
Non-HPV conditions, such as vestibular papillomatosis and inflammatory squamous metaplasia, may be difficult to distinguish from condyloma with light microscopy.
The pathologist may report microscopic features from a biopsy of the vulva that are suggestive, but not diagnostic, of HPV.
When the histologic diagnosis of condyloma is questionable, HPV testing may be useful.
A wide variety of methods to detect HPV have been used since 1983.
Currently, the 2 most accurate methods use 2 consensus primer polymerase chain reaction (PCR) systems. The commercially available system is the Hybrid Capture II system with differential testing for 9 high-risk HPV types and 5 low-risk HPV types. No genotype-specific information is obtained from this test. Newer HPV tests that are being developed include DNA chip, Linear Array, and cycle sequencing.[41]
Testing for HPV confirmation of equivocal vulvar histology results provides an objective method for confirming a diagnosis of condyloma.
Patients who present with typical appearing condyloma acuminata usually do not need a vulvar biopsy. A biopsy is recommended for the following scenarios:
Women with a history of vulvar dysplasia
Postmenopausal women
Women who fail medical therapy
Clinical doubt about the diagnosis
Biopsy technique
The base of the lesion is injected with 1% lidocaine.
A biopsy can be performed easily with an alligator mouth biopsy forceps.
Silver nitrate applied to the base of the biopsy site controls any bleeding.
Rarely, a suture is required to obtain hemostasis.
Biopsy of the vulvar skin associated with condyloma shows evidence of hyperkeratosis, acanthosis, and parakeratosis. A chronic inflammatory infiltrate is often observed within the dermis. Koilocytosis, which is perinuclear cytoplasmic halos, is commonly observed in the superficial epithelial cells. Other microscopic findings include basilar hyperplasia with binucleated and multinucleated cells and enlarged parabasal cells with a foamy nuclear chromatin.
A variety of medical treatments are available to remove condyloma acuminata; no single treatment regimen is superior. Patients should be informed that genital warts resolve spontaneously in 20-30% of women within 3 months.[12]
The treatment strategy is to eliminate as many of the visible lesions as possible until the host immune system can control viral replication.
Treatment is reserved for patients with visible vulvar condyloma.
The type of treatment is influenced by previous therapies, pregnancy status, sexual behavior, immune status, and the patient's willingness to comply with therapy.
Development of a therapeutic vaccine against HPV is currently being investigated. Two published trials demonstrated either a clinical complete response or a clinical partial response in women with vulvar or vaginal dysplasia.[42, 43]
Patients who are HIV positive or immunosuppressed due to immunosuppressive drugs usually require more than 1 treatment method. Often, the condyloma in these patients is refractory to therapy.
Regardless of the mode of therapy chosen, recurrence rates are high for any patient with condyloma acuminata. This can result in a high level of frustration for the patient and the physician.
Medical therapy should be the first option for most patients. The authors' prefer the following 4 options for patient-applied therapy.[44]
Podofilox: Our first choice, in a nonpregnant patient, is Podofilox gel or solution. This agent is applied twice daily for 3 consecutive days and repeated for up to 4 weeks. Side effects are minimal.
Imiquimod: This is our second choice in a nonpregnant woman with vulvar condyloma. Application is 3 times weekly at bedtime for up to 16 weeks. Imiquimod should be washed off 8 hours after application.[45] Several randomized trials have demonstrated that application of imiquimod 5% cream can result in complete resolution of genital warts in up to 50% of patients. Recurrence rates range from 19-23% at 6 months.[46] The primary side effect is erythema, itching, and burning. This drug is expensive and is often not a treatment option in many health insurance plans.
Sinecatechins (Veregen): A third option is Veregen ointment for medical treatment of anogenital warts. Several randomized, double-blind, placebo-controlled trials demonstrated a 58% clearance of external genital warts. A trial of 502 male and female patients with anogenital warts were treated 3 times per week for a maximum of 16 weeks. Complete clearance of all baseline and newly occurring warts was obtained in 57% of patients treated with 15% sinecatechins ointment.[47] The primary side effects were erythema, pruritus, and pain.[48]
5-fluorouracil: Another option is 5-fluorouracil (Efudex) cream. This agent is applied to genital warts to cause a chemical desquamation. A meta-analysis of 6 trials involving 645 women concluded that topical treatment with 5-fluorouracil has a therapeutic effect. The data were unclear on the risks and benefits and further studies were recommended.[49] Protection of the normal surrounding skin is imperative to prevent pain, burning, and ulceration. This therapy is often not tolerated by patients. Use of this agent should be limited.
Other options include the following:
Podophyllin: Podophyllin is applied directly to warts but no more than 0.5 mL should be used with one treatment. Systemic absorption, ulceration, and pain are potential side effects of this therapy. Podophyllin is contraindicated in pregnancy. The authors of this article prefer Podofilox to podophyllin. Podofilox results in less toxicity and can be self-administered by the patient.
Interferon: Intralesional injection of interferon has been used to treat condyloma. Locally-injected interferon appears to be more effective than systemic injection of interferon. A meta-analysis of 7 randomized controlled trials comparing interferon and placebo for the treatment of genital warts reported complete response rate of 45% and 16%, respectively. Recurrence rates were 21% for interferon and 34% for patients in the placebo group.[50] Side effects including flu-like symptoms, fatigue, and pain. Interferon is contraindicated in pregnancy.
Trichloroacetic acid (TCA): TCA, using 80-90% concentration, is the author's first choice to treat vulvar/vaginal condyloma in pregnant women. TCA should be applied to the condyloma after pretreatment of the surrounding normal skin with petroleum jelly. This treatment usually requires weekly application for 4-6 weeks. The principle side effect is pain and burning if the TCA comes in contact with the normal skin.
Surgical removal of warts is appropriate if the condyloma do not respond to medical therapy, if there are numerous, bulky condyloma, or if the condyloma are associated with vulvar dysplasia. Several options are available.
Simple excision
Simple excision is usually performed in an outpatient surgical suite.
The individual lesions are removed with a knife after general or regional anesthesia is administered.
This procedure is reserved for refractory cases or extensive disease. The surgical specimen should be submitted for microscopic analysis.
Reports in the literature indicate that within one year of surgery, complete wart clearance occurs in 35-72% of individuals treated with surgical excision. One report found surgical excision as effective as laser surgery.[51]
Patients with a few small lesions can have vulvar condyloma removed in the office. The underlying skin should be anesthetized with 1% Xylocaine and the condyloma removed with a #15 knife blade. One or 2 sutures may be needed to reapproximate the healthy skin.
Carbon-dioxide laser therapy[51, 52, 53]
Laser treatment of vulvar condyloma acuminata effectively destroys the condyloma while sparing adjacent healthy tissue.
This procedure is performed in outpatient surgery with general or regional anesthesia.
The amount of energy needed to remove a condylomatous lesion with the laser depends on parameters controlled by the surgeon. These parameters include the amount of wattage, the length of time the beam is fired, and the spot size on the tissue. Some researchers calculate the power density, which equals the power (watts)/area (cm2). No exact power density is needed to remove vulvar or vaginal condyloma. The surgeon needs to be flexible in the application of the laser for each patient. If the laser is calibrated to 20 watts, continuous mode, the spot size can be adjusted easily to provide the proper power density.[54]
Most patients experience significant discomfort beginning 24 hours after surgery and require narcotic analgesia.
Laser therapy should be reserved for recalcitrant cases of condyloma or extensive disease.
Complete wart clearance after laser surgery has been reported to occur in 23-52% of patients within 3 years of surgery.
The recurrence rates are similar to surgical excision.
Electrosurgery[55]
For isolated lesions unresponsive to topical therapy, electrosurgical techniques can be performed in the office with local anesthesia.
The most popular method is to use a loop electrode that removes the lesion or lesions.
Pain after surgery is common and can be treated with narcotic analgesics. Topical analgesics, such as lidocaine jelly, can be beneficial to some patients.
A recurrence rate in one trial was 22% compared with 44% for podophyllin resin.
Cryotherapy[56, 57]
Cryotherapy is our treatment of choice for pregnant women when TCA fails to eliminate vulvar condyloma. This therapy is most effective for small lesions that can be treated with a small cryoprobe.
Data from several clinical trials report a 63-88% clearance 3 months after therapy. A trial comparing cryotherapy to cryotherapy combined with podophyllotoxin failed to demonstrate an improved outcome with the combination therapy.[58]
The recurrence rate of 22% is similar to electrosurgery.
The primary drawbacks are discomfort, ulceration, or scabbing at the treatment site.
No one curative treatment exists for condyloma acuminata.[59] Simple topical therapies are the initial treatments of choice for most patients. They are cost effective and result in minimal toxicities. Most result in a 30-90% success rate in eliminating visible condyloma. Many clinical studies using topical therapies are not well designed, making comparisons between therapies difficult.
Clinical Context:
Treatment results in necrosis of visible wart tissue. Exact mechanism of action is unknown. Great variability exists in the potency of podophyllin between batches. American podophyllum contains one-fourth the amount of the Indian source. Warts visible after 6 treatments usually do not respond to further therapy.[60]
Clinical Context:
Topical antimitotic that can be synthesized chemically or purified from plant families Coniferae and Berberidaceae (eg, Juniperus and Podophyllum species).
Active agent of podophyllin resin and is available as a 0.5% solution. Can apply solution to warts at home.
Clinical Context:
Interferes with DNA synthesis by blocking methylation of deoxyuridylic acid, inhibiting thymidylate synthetase and, subsequently, cell proliferation. Limited data exist concerning the efficacy of this therapy for genital warts. Three case series indicate wart clearance in 10-50% of participants.[61] Experimental treatments injecting 5-FU with epinephrine and bovine collagen currently are in trials.
Clinical Context:
Cauterizes skin, keratin, and other tissues. Although caustic, causes less local irritation and systemic toxicity than others in the same class; however, response often is incomplete and recurrence occurs frequently.[62]
Clinical Context:
Interferons have been used in the United States for the treatment of genital warts in various doses and preparations. Topical, intralesional, and systemic therapy have been used. Currently, no convincing evidence suggests that topical or systemic therapy is better than placebo.[64, 65, 4, 66]
First vaccine indicated to prevent cervical cancer, genital warts (condyloma acuminata), and precancerous genital lesions (eg, cervical adenocarcinoma in situ; cervical intraepithelial neoplasia grades 1, 2, and 3; vulvar intraepithelial neoplasia grades 2 and 3; vaginal intraepithelial neoplasia grades 2 and 3) due to HPV types 6, 11, 16, and 18. Vaccine efficacy mediated by humoral immune responses following immunization series. Indicated for prevention of condyloma acuminata caused by HPV types 6 and 11 in boys, men, girls, and women aged 9-26 years.
A human papillomavirus (HPV) quadrivalent vaccine is now available for prevention of HPV-associated dysplasias and neoplasias, including cervical cancer, genital warts (condyloma acuminata), and precancerous genital lesions. The immunization series should be completed in boys and girls, and young men and women aged 9-26 years.
Clinical Context:
Botanical topical drug product consisting of extract from green tea leaves. Mode of action unknown but does elicit antioxidant activity in vitro. Indicated for topical treatment of external genital and perianal warts (condylomata acuminatum) in immunocompetent patients.
Patients who complete therapy for condyloma acuminata should have a clinical examination 3 months and 6 months after treatment.
Most patients who develop recurrent or persistent disease are diagnosed within 6 months of therapy.
If the patient appears disease free at the 6-month visit, yearly visits are recommended.
The sexual partner or partners of a woman with condyloma should be examined by a physician and treated if indicated. Often, the examination of the male fails to reveal any visible condyloma.
Because genital warts are sexually transmitted, the risk of acquiring HPV is primarily dependent on several factors related to sexual activity.
These factors include the number of sexual partners, frequency of sexual intercourse, and the presence of genital warts on the sexual partners. In most studies, cigarette smoking is a risk factor after controlling for sexual behavior.
Latex condoms offer some, but not complete, protection in the transmission of HPV.
Women should avoid skin-to-skin contact with partners if genital warts are visible.
The development of a vaccine to prevent HPV infection has been the focus of extensive research over the last 2 decades. A quadrivalent vaccine against HPV types 6, 11, 16, and 18 has been approved by the FDA. This vaccine is approved for females aged 9-26 years in a 3-dose schedule with the second and third doses administered 2 and 6 months after the first dose. Currently, vaccination is recommended for females aged 11-12 years with catch-up vaccinations for females aged 13-26.[67]
A randomized double-blinded trial in more than 2,000 young females given placebo or HPV-16 vaccine indicates potential efficacy of vaccine protection against HPV infection. The females in the vaccine group did not develop HPV-16 infection or cervical dysplasia during the study period. The seroconversion rate with antibody titers to HPV-16 was almost 100%. In comparison, 41 females in the placebo group developed HPV-16 infection; cervical dysplasia was diagnosed in 9 of these females.[68]
A quadrivalent HPV vaccine to HPV types 6, 11, 16, and 18 has been tested in a double-blinded placebo-controlled trial. This study enrolled 277 young females who were observed on average for 3 years. Women who received the vaccine had a 90% reduction in HPV infection with types 6, 11, 16, and 18 compared with females who received placebo.[69] The safety of the vaccine and longevity of immune responses to the vaccine are still needed. Routine use of this vaccine will reduce the incidence of HPV-associated anogenital diseases in young women. In 2009, a sexual health center in Australia reported a rapid and marked reduction in the incidence of genital warts among vaccinated women. This benefit was conferred to heterosexual males as fewer men presented to this health center with genital warts.[70] This vaccine is not intended or proven to treat patients with genital warts.[71]
For a summary of the referenced article, see HPV Vaccine and Anogenital Diseases.
Patients who develop condyloma acuminata have usually been exposed to low-risk HPV types such as HPV-6 and HPV-11. These HPV infections are associated with mild dysplasia that is often transient in nature.
Many patients with mild dysplasia of the vulva, vagina, or cervix experience spontaneous regression of these lesions.
Patients who are exposed to high-risk HPV types, such as HPV-16 or HPV-18, usually do not develop condyloma. These patients are at risk for developing high-grade dysplasia or angiogenital carcinoma.
The prognosis of immunocompetent women diagnosed with condyloma acuminata is excellent.
HPV infections are transient in most of these women.
Unless the woman is constantly exposed to different HPV types, the infection eventually abates when the host immune system stops viral replication.
Women who are immunocompromised due to immunosuppressive drugs or HIV infection are at higher risk of developing persistent disease. These women have a higher incidence of developing dysplasia or cancer of the vulva, vagina, or cervix.
Robert V Higgins, MD, Clinical Associate Professor, Department of Obstetrics/Gynecology, University of North Carolina School of Medicine; Residency Program Director, Vice-Chairman of Academic Affairs, Associate Director of Gynecologic Oncology, Department of Obstetrics/Gynecology, Carolinas Medical Center
Disclosure: Nothing to disclose.
Coauthor(s)
James Hall, MD, Director, Division of Gynecologic Oncology, Blumenthal Cancer Center, Carolinas Medical Center; Clinical Professor, Department of Obstetrics and Gynecology, University of North Carolina
Disclosure: merck Honoraria Speaking and teaching; GSK Honoraria Speaking and teaching; orthobiotek Honoraria Speaking and teaching
R Wendel Naumann, MD, Clinical Assistant Professor of Obstetrics and Gynecology, University of North Carolina at Chapel Hill; Director, Minimally Invasive Surgery in Gynecologic Oncology; Associate Director, Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, Carolinas Medical Center
Disclosure: Nothing to disclose.
Specialty Editors
Steven David Spandorfer, MD, Assistant Professor, Department of Obstetrics and Gynecology, New York Presbyterian Hospital, Weill Cornell Medical College
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
David Chelmow, MD, Leo J Dunn Distinguished Professor and Chair, Department of Obstetrics and Gynecology, Virginia Commonwealth University Medical Center
Disclosure: Nothing to disclose.
Frederick B Gaupp, MD, Consulting Staff, Department of Family Practice, Hancock Medical Center
Disclosure: Nothing to disclose.
Chief Editor
David Chelmow, MD, Leo J Dunn Distinguished Professor and Chair, Department of Obstetrics and Gynecology, Virginia Commonwealth University Medical Center
Disclosure: Nothing to disclose.
References
Ciuffo G. Imnesto positiv con filtrado di verrucae volgare. Giorn Ital Mal Venereol. 1907;48:12-17.
zur Hansen H. Condyloma acuminata and human genital cancer. Cancer Res. 1976;36:530.
Basita CS, Atallah AN, Saconato, da Silva EMK. 5-FU for genital warts in non-compromised individuals. In: Cochrane Database of Systematic Reviews. 4. John Wiley and Sons, Ltd; 2010.
