bubble_chart Overview

This disease is also known as condyloma acuminatum, genital warts, or sexually transmitted disease warts. It is a sexually transmitted infection caused by human papillomavirus (HPV). There are multiple types of HPV, with the main types causing this disease being HPV1, 2, 6, 11, 16, 18, 31, 33, and 35. Among these, long-term infection with HPV16 and 18 may be associated with the development of cervical carcinoma in women.

bubble_chart Epidemiology

1. Epidemiological Status

Condyloma acuminatum is caused by human papillomavirus (HPV). It is now widely acknowledged that the incidence of this disease is increasing, making it the most common sexually transmitted disease (STD), with a prevalence rate of 0.5–1% among young adults. In the UK, the incidence of condyloma acuminatum rose from 30 per 100,000 in 1970 to 260 per 100,000 in 1988, an almost eightfold increase. Similarly, in the United States, the incidence of this disease increased sixfold from 1966 to 1984. Similar to Acquired Immune Deficiency Syndrome (AIDS), symptomatic condyloma acuminatum represents only the "tip of the iceberg" among infected individuals. Therefore, when subclinical infections are taken into account, HPV infection may rank as the most prevalent sexually transmitted disease. The modes of transmission for this infection include direct and indirect contact, with sexual contact being the most common. Moreover, the more recent the lesions, the higher the infectivity, with an estimated 50% chance of infection per sexual encounter. Other routes include direct non-sexual contact, such as autoinoculation and neonatal infection during delivery, followed by indirect contact through contaminated materials. While transmission via fomites is theoretically possible, it has not been confirmed due to the inability to culture the virus.

2. Risk Factors for Condyloma Acuminatum

(1) Sexual behavior: The number of sexual partners and early sexual debut are factors contributing to HPV infection.

(2) Immunosuppression: HPV infection and HPV-related cancers appear to be advanced-stage complications of chronic immune suppression. The risk of condyloma acuminatum is increased among renal transplant recipients.

(3) HIV infection: HIV-positive individuals have an increased likelihood of HPV infection and HPV-related tumors.

(4) Age and pregnancy: The peak prevalence of HPV detection in gynecological smears occurs between ages 20–40, with a steady decline as age increases. HPV detection rates are higher during pregnancy and decrease postpartum.

bubble_chart Pathogen

HPV causes warts on the skin and proliferative sexually transmitted disease lesions on the pharyngeal, perianal, and genital mucous membranes. The virus type is a small DNA virus. Most HPV infections result in benign lesions that can resolve spontaneously, but there are also cases of malignant progression. For example, there have been reports of squamous cell carcinoma formation on perianal and genital mucous membranes. Additionally, HPV has been detected in cancer cells from rare hereditary skin disorders such as epidermodysplasia verruciformis (EV) and its associated skin cancers.

HPV belongs to the genus Alphapapillomavirus of the Papillomaviridae family. The viral particles are non-enveloped icosahedral capsids with a diameter of 50–55 nm, containing a circular double-stranded DNA of 7,900 base pairs. Under electron microscopy, the size and morphology of HPV particles closely resemble those of oral papillomaviruses. Papillomaviruses (PV) exhibit species specificity, and HPV has not yet been successfully cultured in tissue culture or experimental animal models.

The structural proteins of the virus consist of: 85% of PV particles, as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), revealing a major capsid protein with a molecular weight of 56,000 and a minor capsid protein migrating at 76,000. Additionally, four cellular histones associated with viral DNA have been identified.

The genomic structures of all HPV types are similar. Viral types and subtypes can be determined based on DNA hybridization under stringent conditions. Different HPV types show only 50% cross-hybridization with other viral DNAs. To date, more than 60 HPV types have been identified, and further research is expected to uncover additional novel HPV types.

bubble_chart Pathogenesis

HPV infection of condyloma acuminatum is transmitted through sexual contact, and minor trauma at the contact site can facilitate infection. The three types of squamous epithelium (skin, mucosa, and metaplastic) are all susceptible to HPV infection. Each type of HPV is associated with specific clinical lesions and has its preferred sites on the skin or mucosal squamous epithelium. Infection may occur when desquamated superficial cells or keratin fragments containing a relatively large number of viral particles enter susceptible epithelial fissures. This can happen through direct contact, rare autoinoculation, or contamination via underwear, bathtubs, towels, or toilet seats.

After infecting the human body, the virus can remain latent among basal keratinocytes and replicate in the epidermal cell layer. HPV invades the cell nucleus, causing rapid cell division along with the proliferation and dissemination of viral particles, forming characteristic papillomas. In the advanced stage, gene expression produces structural polypeptides, leading to the assembly of viral particles. The virus is mainly concentrated in the nuclei of cells in the granular layer, with an increase in koilocytes in the epidermal granular layer. Histologically normal epithelial cells may also harbor HPV, and residual DNA after treatment often leads to disease recurrence.

The host's immune response to HPV infection includes both cellular and humoral immunity.

1. Cellular Immunity

The cellular immune status of the body is one of the important factors influencing the occurrence and outcome of CA. Cellular immunity is more critical than humoral immunity. Clinically, CA patients with cellular immune deficiencies often exhibit persistent rashes, increased suppressor T cells in peripheral blood, reduced NK cell function, and decreased production of gamma-interferon and interleukin-2. In contrast, regressing warts often show infiltration of activated T cells and NK cells, with some keratinocytes testing positive for HLA-DR.

Immunosuppression or immunodeficiency increases the incidence of genital HPV infection and HPV-related diseases. In CA, helper T cells are depleted, and the CD4/CD8 ratio is inverted (<1). Peripheral blood of CA patients shows a significant increase in suppressor/cytotoxic T cells and a decrease in the helper/inducer T cell ratio and helper/suppressor T cell ratio. Langerhans cells are markedly reduced in cervical CA and cervical intraepithelial neoplasia (CIN) lesions. NK cells in CA produce less gamma-interferon and interleukin-2. In Bowenoid papulosis and anogenital cancers, NK cell lytic activity against keratinocytes containing HPV-16 is reduced, possibly due to impaired recognition of disease-specific target cells. Keratinocytes in cervical CA do not express MHC class II antigens (HLA-DR), and the lack of antigen presentation may disrupt immune surveillance.

2. Humoral Immunity

Current serological test results indicate: ① The production rate of antibodies against advanced-stage proteins is 25–65%, higher than that against early-stage proteins. ② Detected HPV antibodies appear to be type-specific with no cross-reactivity. ③ Anti-HPV-16E7 antibodies are closely associated with the presence of cervical carcinoma. ④ Anti-HPV-16E4 antibodies are also markers for cervical carcinoma, recurrence, or recent HPV infection. ⑤ The IgG antibody positivity rate is estimated to be similar in adults and children, ranging between 10–75% depending on the type. ⑥ Among patients with HPV-16 or 18 tumor antibodies, only 50–70% test positive for these antibodies.

3. Natural Regression of Condyloma Acuminatum

There is no systematic evaluation of the natural regression of CA. However, placebo-controlled studies have found natural regression rates ranging between 0%, 17%, 18%, and 69%. After regression or cure of CA, 45% of patients still have latent infections, with 67% experiencing recurrence.

bubble_chart Clinical Manifestations

The incubation period ranges from 3 weeks to 8 months, with an average of 3 months. It is most commonly seen in sexually active young and middle-aged men and women, with the peak age of onset being 20–25 years. For male and female patients with an average disease duration of 3–5 months, symptoms may appear shortly after sexual contact, whereas male patients with an average disease duration of 12 months may have sexual partners who do not develop symptoms. Most patients are generally asymptomatic. The size and shape of the lesions vary. They may be limited to a few or appear as numerous pinpoint-sized lesions: in the genital and anal regions, they can grow into large tumor-like masses, causing a sensation of pressure; they may emit a foul odor; sometimes, small warts can cause genital itching and discomfort, and patients may experience hematuria and dysuria; rectal condylomata acuminata may cause pain and hematochezia, while larger rectal warts can lead to a sense of tenesmus.

Male patients often develop lesions on the frenulum, coronal sulcus, foreskin, urethra, penis, perianal area, and scrotum. Initially, the lesions appear as pale red or dirty red foxtail millet-sized growths, soft in texture, slightly pointed at the tip, and gradually enlarge or multiply. They may develop into papillomatous or cystic forms, with a slightly broad base or a stalk, and a granular surface. In the anal region, they often enlarge, resembling cauliflower, with a moist surface or bleeding, and pus may accumulate between the granules, emitting a foul odor. Scratching can lead to secondary infection. Genital warts in drier, low-humidity areas are often small and flat. Warts in damp, moist areas tend to appear as filiform or papillomatous and may fuse into large masses. Patients with severe liver disease may experience enlarged warts. Pregnancy can cause warts to recur or grow more rapidly.

Subclinical infection refers to lesions that are not visible to the naked eye clinically, but applying 3–5% vinegar acid solution topically or as a wet compress for 5–10 minutes can cause whitening in HPV-infected areas, known as the "vinegar acid whitening phenomenon."

HPV infection and tumor development:

(1) HPV is associated with the development of skin tumors

It appears to play a decisive role in skin cancer and tumors at other anatomical sites. HPV-11, 16, and 18 DNA have been detected in oral benign growths and precancerous lesions, as well as in squamous cell carcinoma tissue of the skin. Cases of HPV-6 papillomas in the larynx transforming into laryngeal cancer have been reported. Epidermodysplasia verruciformis (EV) is evidence of HPV's potential carcinogenic effects, with multiple HPV types detected in EV lesions. HPV-5, 8, 14, 17, and 20 have been identified in patients' cutaneous squamous cell carcinomas, suggesting that these cancers may arise from preexisting viral lesions.

(2) Condylomata acuminata and anogenital cancer

There is a certain relationship between genital cancer and HPV types. DNA hybridization techniques have detected HPV-6, 11, 16, and 18 in genital cancer tissue.

1. Cervical carcinoma: Based on the relationship between HPV and cervical carcinoma, HPV can be divided into two main types: low-risk types, primarily HPV-6 and 11, and high-risk types, such as HPV-16 and 18. Gissmann et al. observed that 57.4% of patients with invasive cervical carcinoma had HPV-16 and 18, a finding corroborated by other researchers. HPV-33 and 35 have also been isolated from invasive cervical carcinoma.

2. Squamous cell carcinoma (SCC) of the skin: Condylomata acuminata (CA) caused by HPV infection may also be precancerous lesions and can develop into anogenital SCC, indicating that HPV is a significant factor in vulvar, penile, and anogenital SCC. CA, giant CA, and verrucous SCC form a spectrum of precancerous and cancerous lesions in the genital region. Some cases of genital cancer have surrounding skin with CA, and sometimes lesions that appear typical of CA under visual inspection may reveal isolated foci of SCC upon histological examination.

3. Bowenoid papulosis: Commonly found on the penis, vulva, or perianal area, HPV-16 DNA has been detected in the lesions.

bubble_chart Auxiliary Examination

1. Vinegar Acid-White Test

Apply 3–5% vinegar acid externally to the wart for 2–5 minutes. The affected area will turn white and slightly raised. Anal lesions may require up to 15 minutes. The principle of this test is the whitening and coagulation of proteins upon contact with acid. The keratin produced by HPV-infected cells differs from that of normal, uninfected epithelial cells, and only the former can be decolorized by vinegar acid. The vinegar acid-white test is highly sensitive for detecting HPV, outperforming conventional histological examinations. However, false positives may occasionally occur in cases of thickened epithelium or traumatic abrasions, where whitening appears indistinct and irregular. The CDC notes that the vinegar acid-white test is not specific and false positives are common.

2. Immunohistochemical Examination

The peroxidase-antiperoxidase (PAP) method is commonly used to reveal viral proteins within warts, confirming the presence of viral antigens in the lesions. When HPV proteins are positive, a faint reddish weakly positive reaction may appear in the superficial epithelial cells of condyloma acuminatum.

3. Histochemical Examination

A small amount of lesion tissue is smeared onto a slide and stained with specific antibodies against human papillomavirus. If viral antigens are present, antigen-antibody binding occurs. In the PAP method, the nuclei may stain red. This method is highly specific, rapid, and aids in diagnosis.

4. Pathological Examination

The main features include parakeratosis, marked thickening of the prickle cell layer, papillomatous hyperplasia, and elongation of epidermal rete ridges, sometimes resembling pseudoepitheliomatous hyperplasia. There may also be a significant number of mitotic figures in prickle cells and basal cells, mimicking cancerous changes. However, the cells are orderly arranged, and the boundary between hyperplastic epithelium and dermis is clear. A distinctive feature is the presence of vacuolated cells in the granular and upper prickle cell layers. These vacuolated cells are larger than normal, with pale cytoplasm and a large, round, deeply basophilic nucleus. Typically, there is dermal edema, capillary dilation, and dense chronic inflammatory infiltration. In Buschke-Löwenstein giant condyloma acuminatum, the epidermis grows downward extensively, replacing underlying tissue and potentially resembling squamous cell carcinoma, necessitating multiple biopsies. If there is a tendency for slow progression, it may represent a low-grade malignant process, known as verrucous carcinoma.

5. Genetic Diagnosis

To date, HPV cannot be cultured by traditional methods or detected via serological techniques. The primary diagnostic method is nucleic acid hybridization. The PCR method, developed in recent years, offers specificity, sensitivity, simplicity, and speed, providing a new approach for HPV detection.

(1) Specimen Collection and Processing

1. Specimen collection and pretreatment: Use a spatula or saline-moistened swab to collect secretions and cells from the vagina and cervical os. While performing cytological examination, place the specimen in 5 ml of PBS containing 0.05% thimerosal. Wash the sample twice by centrifugation (3000g, 10 min) in PBS, then resuspend the pellet in 1 ml PBS. Extract DNA from 0.5 ml of the cell suspension.

2. Extraction of nucleic acids from specimens: Add 10 volumes of cell lysis buffer (10 mmol/L Tris-HCl, pH 7.4, 10 mmol/L EDTA, 150 mmol/L NaCl, 0.4% SDS, 1.0 mg/ml proteinase K) to 1 volume of cell suspension and incubate at 37°C overnight. Then perform two extractions each with equal volumes of phenol/chloroform (1:1) and chloroform/isoamyl alcohol (24:1). Add 1/10 volume of 3 mol/L NaAc (pH 5.2) and 2.5 volumes of absolute ethanol, and precipitate the DNA at -20°C for 2 hours or overnight. Wash once with 1 volume of ethanol. Dissolve the DNA in 60 μl of TE buffer (10 mmol/L Tris-HCl, pH 8.0, 1.0 mmol/L EDTA) containing RNase (100 μg/ml) and incubate at 37°C for 30 minutes.

(II) PCR Amplification

1. Primer Design and Synthesis: The HPV genome can be divided into the early region (E) and the late region (L), each containing a series of open reading frames (ORFs). Sequence analysis indicates that the non-coding regions as well as the E1, E6, E7, and L1 regions of various HPV types contain conserved sequences. Manos et al. selected conserved sequences from the HPV L1 region to design and synthesize primers MY11 and MY09 (see Table 1). These primers have complementary sequences to HPV types 6, 11, 16, 18, and 33 and can also amplify other HPV types.

Universal primers for HPV L1 designed by Manos et al.

MY11: GCMCAGGGWCATAAYAATGG

MY09: CGTCCMARRGGAWACTGATC

Table 1

M=A+C, R=A+G, W=A+T, Y=C+T

Table 2 lists the oligonucleotide probes designed by Manos et al. The common mixed probe sequences were selected from another conserved region in the HPV L1 region and can hybridize with the various HPV L1 PCR amplification products generated by the MY11 and MY09 primers. Type-specific probes have complementary sequences only to the corresponding HPV types and are used for HPV typing.

Table 2 Probes for HPV L1 PCR Products Designed by Manos et al.

H=A+C+T, R=A+G, W=A+T, Y=C+T

2. PCR reaction reagents: Taq DNA polymerase (2U/ml), 10mmol/L dNTP stock solution (10mmol/L each of dATP, dCTP, dGTP, dTTP), 10×PCR buffer (500mmol KCl, 40mmol/L MgCl2, 100mmol/L Tris-HCl, pH 8.5), 100μmol/L MY11 and MY09 stock solutions, distilled water prepared with a sterilized glass distiller.

3. PCR amplification method and procedure: The amplification reaction is performed in sterile 0.5 ml siliconized plastic centrifuge tubes with a 100 μl PCR reaction mixture.

(1) Prepare and aliquot the premixed reaction reagents before the experiment. The premixed reaction reagents include all PCR reaction reagents except for the sample DNA. The PCR reaction reagents contained in each reaction tube are shown in Table 3.

Table 3    PCR reaction reagents in each reaction tube

(2) Add 10 μl of sample and 90 μl of premixed reaction reagents sequentially to each reaction tube.

(3) Add 80–100 μl of mineral oil and centrifuge briefly in a benchtop centrifuge for a few seconds to collect all reaction reagents under the oil layer. Currently, PCR reagents are commercially available with a reaction volume of 25 μl. Only the sample DNA needs to be added during use.

(4) Place the reaction tubes in the PCR amplifier with the following cycling parameters: 95°C for 30 s, 55°C for 40 s, and 72°C for 50 s for 35 cycles, followed by a final extension at 72°C for 5 min.

4. Each experiment should include positive and negative controls. Use recombinant plasmids carrying HPV (100 pg per reaction) or DNA from HPV-containing cell lines (e.g., Caski, HeLa) as positive controls, and DNA from HPV-free human cell lines as negative controls.

(3) Detection and analysis of amplification products

1. Gel electrophoresis: After the amplification reaction is completed, remove the reaction tube and cool it to room temperature. Take 10 μl of the amplification product and perform electrophoresis using 5-7% polyacrylamide gel or 1.5% agarose gel. Stain with ethidium bromide and analyze the results under a UV analyzer. A distinct DNA band should appear at approximately 450 bp.

2. Nucleic Acid Hybridization: If the gel electrophoresis does not show clear DNA bands or if the specificity of the DNA bands needs to be confirmed, labeled common mixed probes and/or type-specific probes can be used for Southern blot hybridization or dot blot verification.

Prepare 32P ATP-labeled oligonucleotide probes according to standard methods, aiming for a specific activity of approximately 10^7 cpm/pmol. The hybridization solution should contain 2×10⁶–5×10⁶ cpm of probe per ml. Hybridize at 55°C with gentle shaking for 2–3 hours, followed by a quick rinse of the hybridization membrane with washing buffer (2×SSC, 0.1% SDS) at 30–55°C to remove excess probe. Then, perform membrane washing under conditions that vary depending on the probe used: - For common mixed probes: Wash the membrane at 55°C for 10 minutes. - For MY12, MY13, and MY16 probes: Wash at 56–57°C for 10 minutes, then repeat with fresh buffer. - For MY14 and WD74 probes: Wash at 58–59°C for 10 minutes, also repeating with fresh buffer.

PCR-based detection of HPV is superior to nucleic acid hybridization. It offers higher sensitivity: GP-PCR with direct gel electrophoresis analysis can detect as few as 200 copies of HPV DNA in a sample. If nucleic acid hybridization is used to detect PCR products, the sensitivity increases further, enabling the detection of 10 copies of HPV DNA.

Given the high sensitivity of PCR technology, using exfoliated cells from the genital tract as samples is sufficient to meet experimental requirements, eliminating the need for biopsy collection and complex tissue grinding procedures. In most cases, PCR amplification products can be directly diagnosed by observing the DNA bands via gel electrophoresis. Therefore, PCR-based HPV detection is characterized by a short experimental cycle, simplicity, and rapid results.

bubble_chart Diagnosis

1. History of unclean sexual intercourse.

2. Typical skin lesions manifest as papules, papillomatous, cauliflower-like, or cockscomb-like fleshy growths in moist areas such as the genital or perianal regions, with a rough, keratinized surface.

3. Positive vinegar white test, and pathological sections show dyskeratosis and koilocytes.

4. Nucleic acid hybridization can detect HPV-DNA-related sequences, and PCR testing reveals specific HPV-DNA amplification bands.

bubble_chart Treatment Measures

Since there are currently no specific antiviral drugs, the treatment of condyloma acuminatum must adopt a comprehensive approach.

(1) Treating underlying causes: (excessive leucorrhea, phimosis, gonorrhea).

(2) Enhancing the body's immunity.

(3) Applying antiviral medications. Generally, as long as regular comprehensive treatment is adhered to, a cure can be achieved.

1. Surgical therapy

For single, small-area warts, surgical excision can be performed; for large condyloma acuminatum, Mohs surgery can be used, with frozen section examination during the procedure to ensure complete removal of the lesion.

2. Cryotherapy

Utilizing liquid nitrogen at -196°C, the pressure-freezing method is employed to treat condyloma acuminatum, promoting necrosis and shedding of the wart tissue. This method is suitable for warts that are few in number and small in area, with 1–2 treatments possible at weekly intervals.

3. Laser therapy

Typically, CO₂ lasers are used, employing the cauterization method to treat condyloma acuminatum. This therapy is most suitable for warts on the female genitalia, penis, or perianal area. Single or a few multiple warts can be treated in one session, while multiple or large-area warts may require 2–3 treatments, usually spaced one week apart.

4. Electrocautery

High-frequency electric needles or electrosurgical knives are used to remove warts. Method: Local anesthesia is applied, followed by electrocautery. This therapy is suitable for warts that are few in number and small in area.

5. Microwave therapy

Using a microwave surgical device, lidocaine is administered for local anesthesia, and the tip of the rod-shaped radiation probe is inserted into the base of the condyloma acuminatum. When the wart shrinks, darkens in color, and hardens, thermal radiation coagulation is complete, and the probe can be withdrawn. The coagulated lesion can then be removed with forceps. To prevent recurrence, the residual base can be coagulated again.

6. β-ray therapy

We have achieved relatively satisfactory results using β-rays to treat condyloma acuminatum. This method is highly effective, painless, non-injurious, has few side effects, and a low recurrence rate, making it clinically valuable for widespread use.

7. Drug therapy

(1) Podophyllin: This therapy is suitable for moist-area warts, such as those on the glans penis or perineum in cases of phimosis without circumcision. However, cervical condyloma acuminatum cannot be treated with podophyllin. Apply 20% podophyllin tincture to the lesion or, before application, protect the surrounding normal skin or mucous membrane with an oily antibacterial medicinal paste. After 4–6 hours, wash with 30% boric acid solution or soapy water. Repeat the treatment after 3 days if necessary. This drug is the primary treatment for this condition abroad, often curing with a single application. However, it has many drawbacks, such as high tissue destructiveness, potential local ulcers if misused, and significant toxicity, manifesting as nausea, intestinal obstruction, leukopenia, thrombocytopenia, tachycardia, anuria, or oliguria. Thus, caution is required during use, and the drug should be discontinued immediately if the above reactions occur.

(2) Antiviral drugs: 5% phthiobuzone cream or 0.25% idoxuridine ointment can be applied topically twice daily. Acyclovir can be taken orally five times a day, 200mg each time, or its ointment can be applied externally. α-interferon can be injected at 3 million units daily for five days a week. Alternatively, 3 million units of interferon can be injected into the base of the wart twice weekly for 2–3 weeks. The main side effects are flu-like syndrome, while topical application has fewer and milder side effects.

(3) Corrosive or disinfectant: Commonly used are 30-50% trichloroacetic acid or saturated dichloroacetic acid, or 18% peracetic acid. A mixed solution of 10% salicylic acid in glacial acetic acid or 40% formaldehyde, 2% liquefied phenol, and 75% ethanol in 100ml of distilled water can be applied topically to the affected area. This is used for condylomata on the glans penis or perianal region, once daily or every other day, with excellent results. Disinfectants such as 20% iodine tincture can be applied externally, or 2.5-5% iodine tincture can be injected into the base of the wart, 0.1-1.5ml each time. Alternatively, benzalkonium bromide can be applied externally or used as a 0.1-0.2% dressing, with the latter requiring combination with systemic therapy.

(4) Anticancer Drugs

① 5-Fluorouracil (5-FU): Generally applied as a 5% ointment or cream twice daily for a 3-week course. For treating penile or perianal condyloma acuminatum, a 2.5%~5% 5-FU solution can be used for wet compresses, applied for 20 minutes once daily for 6 sessions. Alternatively, a suppository can be prepared using polyethylene glycol as a base mixed with 5% 5-FU powder to treat urethral condyloma acuminatum in both men and women. Intralesional injection of 5-FU can also be administered, with multiple injections for extensive lesions.

② Thiotepa: Primarily used for urethral condyloma acuminatum that fails 5-FU treatment. A suppository (15mg each) can be used daily for 8 days. Alternatively, 60mg of the drug can be dissolved in 10–15ml of sterile water and instilled into the urethra weekly, retained for half an hour. Side effects include urethritis. For penile or coronal sulcus condyloma, a solution of 10mg in 10ml can be used to soak the affected area three times daily for half an hour each, mainly for residual or recurrent lesions after other treatments. The solution can also be diluted twofold for local soaking to prevent recurrence.

③ Colchicine: A 2–8% saline solution can be applied topically twice, 72 hours apart, for penile condyloma. Superficial erosions may occur after application.

④ Bleomycin or Pingyangmycin: A 0.1% saline solution can be injected intralesionally, with a total dose limited to 1ml (1mg), often achieving cure in a single session. Pingyangmycin, a successor to bleomycin, is used similarly. Alternatively, 10mg of pingyangmycin can be dissolved in 20ml of 10% procaine for injection.

8. Immunotherapy

① Autologous Vaccine Method: The patient’s own wart tissue homogenate (cryo-inactivated virus) is heated (56°C for 1 hour), and the supernatant is collected for injection. This is used for refractory perianal condyloma.

② Interferon Inducers: Poly I:C and tilorone can be used. Poly I:C is injected at 2ml daily for 10 days, followed by a 1–2 month break before resuming. Tilorone is taken orally at 300mg three times daily, with a 4-day break, or 600mg every other day.

③ Combination Therapy: Interferon, interleukin-2, prodigiosin, and lebailly used together show superior efficacy.

bubble_chart Prevention

Controlling sexually transmitted diseases is the best way to prevent CA. Detect and treat patients and their sexual partners; conduct health education and control sexual behavior; condoms can help prevent HPV infection, but there is currently no effective vaccine.

bubble_chart Differentiation

1. Genital squamous cell carcinoma: More common in individuals over 40 years of age or the elderly, the skin lesion infiltrates downward, forming an ulcer, with characteristic changes in histopathology.
2. Condyloma latum: Multiple moist papules coalesce into patchy lesions, often found around the anus, where Treponema pallidum can be detected, and syphilis serological tests show positive reactions.
3. Pearly penile papules: Arranged along the coronal sulcus, these are skin-colored or pale pink papules the size of a pinhead or foxtail millet grain. Histopathology shows no koilocytes.
4. Pseudocondyloma: Lesions are confined to the labia minora, appearing as foxtail millet-sized, fish-egg-like pale red small papules or villous changes, with a smooth surface, negative vinegar white test, and no diagnostically significant koilocytes on pathology.
5. Bowenoid papulosis: Presents as brownish-red or pigmented small papules, with histopathology revealing atypical squamous cells and tissue patterns resembling carcinoma in situ.