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Summary

  1. Top of page
  2. Summary
  3. Introduction
  4. Viral infections
  5. Infestations
  6. Genital manifestations of cutaneous diseases
  7. Balanitis and balanoposthitis
  8. Premalignant and malignant genital tumours

Diseases of the male genitalia range from infectious lesions to inflammatory and neoplastic conditions, including many genital manifestations of more general skin diseases. This review highlights the clinical features, diagnosis and treatment of the most common dermatoses of the male genitalia. Herpes genitalis and infections caused by human papillomavirus (HPV) are increasing, particularly in young sexually active people. Herpes simplex virus infection is the commonest infectious cause of genital ulceration, with evidence that many infections are asymptomatic. HPV infection may be latent, subclinical and clinical. The most common causal agents for condyloma acuminatum are low-risk HPV 6 and 11; high-risk HPV types 16 and 18 are associated with premalignant and malignant lesions. Treatment for genital warts remains unsatisfactory; recurrences are common. Imiquimod, a new topical immunotherapeutic agent, which induces interferon and other cytokines, has the potential to be a first-line therapy for genital warts. Scabies and pediculosis are transmitted by skin-to-skin contact and sexual transmission is common, with the penis and scrotum favourite locations for scabious lesions. Oral ivermectin, a highly active antiparasitic drug, is likely to be the treatment of choice, but until approval is granted it should be reserved for special forms of scabies. Common skin diseases, e.g. psoriasis and lichen planus, may have an atypical appearance in the genital area. The typical psoriatic scale is usually not apparent because of moisture and maceration. Allergic contact dermatitis of the genital area may result from condoms, lubricants, feminine hygiene deodorant spray and spermicides. More often, contact dermatitis is irritant, resulting from persistent moisture and maceration. Lichen sclerosus is a chronic inflammatory disease that occurs as atrophic white patches on the glans penis and foreskin. The penile form is a common cause of phimosis in uncircumcised men; involvement of the urethral meatus may lead to progressive meatal stenosis. Plasma cell balanitis is a benign, idiopathic condition presenting as a solitary, smooth, shiny, red-orange plaque of the glans and prepuce of a middle-aged to older man. Squamous cell carcinoma (SCC) in situ, e.g. erythroplasia of Queyrat and Bowen's disease, cannot be excluded clinically; their apparent clinical benignity may lead to lengthy periods of misdiagnosis and biopsy is required to confirm the diagnosis. SCC is the most common malignancy of the penis and the role of oncogenic HPV-types has been also established in SCC of the penis. Prevention of SCC of the penis presupposes an identification of risk factors, early detection of all pre-cancerous lesions and treatment of phimosis.


Introduction

  1. Top of page
  2. Summary
  3. Introduction
  4. Viral infections
  5. Infestations
  6. Genital manifestations of cutaneous diseases
  7. Balanitis and balanoposthitis
  8. Premalignant and malignant genital tumours

A wide range of infectious, neoplastic and inflammatory dermatoses can affect the male genitalia. Several common diseases may involve the genital region only incidentally, while others present in this region with unusual features. In addition, there are some conditions that are entirely or predominantly confined to these regions.

Viral infections

  1. Top of page
  2. Summary
  3. Introduction
  4. Viral infections
  5. Infestations
  6. Genital manifestations of cutaneous diseases
  7. Balanitis and balanoposthitis
  8. Premalignant and malignant genital tumours

Genital warts

These lesions are caused by infection with human papillomavirus (HPV); the incidence of genital HPV infection among sexually active people aged 15–25 years has been estimated at 1%. However, the prevalence of virologically detectable subclinical or latent infection may be as high as 30–50%[1,2]. The prevalence of HPV DNA in healthy men is estimated to be 5%, with a peak of 8–11% occurring at 16–35 years of age [2,3]. Currently there are over 90 different HPV types, with genital types characterized as either low- or high-risk [4]. Common genital warts are usually the manifestation of infection with low-risk HPV types, most commonly types 6 and 11. HPV 6 and 11 have a strong tendency to induce condyloma, but are rarely associated with genital cancer. HPV types 16, 18, 31, 33, 39, 42 and 51–54 are linked with cervical carcinoma and termed ‘high-risk’[5]. HPV 16 and 18 are more likely to be present in subclinical infection, and are the types most commonly associated with genital cancer. Genital warts are predominantly a sexually transmitted disease although other modes of HPV transmission exist. The infectivity of HPV between sexual partners is estimated to be 60%[6]. There are three major types of anogenital warts: condyloma acuminata are pedunculated, cauliflower-like, skin-coloured to reddish verrucous papules [7]; genital warts may also manifest as dome-shaped, usually flesh-coloured papules; flat warts are flat-topped papules which may vary in colour from pink-red to reddish-brown [1,3]. Lesions are frequently multifocal. Areas with increased friction are most commonly affected by condylomas; the commonest location of primary infection in uncircumcised men is the subpreputial region. Other sites of predilection are the glans penis, coronal sulcus, frenulum, prepuce, shaft and the scrotum (Fig. 1). They may also occur on the urethral meatus and can be intraurethral (Fig. 2). The urethra is involved in 10–28% of patients [1,8]; condom users often have suprapubic warts.

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Figure 1. Multiple papular pigmented condylomata acuminata on the penile shaft.

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Figure 2. Numerous whitish condylomata acuminata on the tip of the penis.

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Subclinical lesions are detected by applying 3–5% acetic acid to the genital area for up to 5 min [6]. The acetic acid produces white changes in HPV infected areas. However, aceto-whitening is not a specific method for diagnosis, with false-positive results in up to 25%[6]. Subclinical involvement is especially common in uncircumcised men. Treatment options for genital warts are [3,9]:

  • • 
    Podophyllotoxin 0.5% solution or gel;
  • Bichloroacetic or trichloroacetic acid 35–85%;
  • • 
    Cryotherapy with liquid nitrogen;
  • • 
    Electrofulguration;
  • • 
    CO2 laser;
  • • 
    Imiquimod 5% cream.

Treatment is not confirmed to reduce transmission to sexual partners nor to prevent progression to dysplasia or cancer. Treatments with antiviral or immunomodulatory agents are associated with much lower rates of recurrence [5]. It is estimated that 10–30% of genital warts resolve spontaneously within 3 months as a result of cell-mediated immunity [6].

Genital herpes

Herpes simplex virus (HSV) is the most common cause of genital ulceration [10]. Genital herpes simplex is predominantly caused by HSV type 2, although HSV-1 is responsible for 5–30% of cases of first-episode genital herpes [10,11]. After infection, the viral genome remains in a latent state in the nuclei of sensory neurones for the life of the host [11]. Genital HSV-1 infections are usually less severe and less prone to recur than those caused by HSV-2. Genital herpes caused by HSV-1 is characterized by lower rates of asymptomatic shedding and transmission. From seroprevalence studies, genital herpes has increased by ≈ 30% during the last two decades [10]. Transmission of HSV occurs through both symptomatic lesions and asymptomatic viral shedding. In 50–90% of transmissions the infected partner is unaware of the herpes infection [10]. A recent study showed that condom use offers significant protection against HSV-2 infection in susceptible women [12].

Clinically, true primary genital herpes appears as macules and papules, followed by vesicles, pustules and ulcers [7]. Systemic complaints including fever, myalgias and lethargy may be present, but are rare in men. Patients will often have accompanying tender lymphadenitis. Recurrent episodes of genital herpes are characteristically less severe and undergo rapid involution, healing within 5–10 days [10,11]. Recurrent male genital infection may present as three to five vesicles on the shaft of the penis. Of those with a symptomatic first episode of HSV-2 genital infection will recur in 80–90% within the following year, but many patients will have unrecognized recurrent infections with asymptomatic viral shedding [13]. Asymptomatic shedding occurs most commonly in the first year after the primary episode. The diagnosis of ulceration caused by herpes may be highly suggestive when the usually grouped blisters rupture and form coalescent grouped erosions (Fig. 3). However, atypical clinical manifestations including deep, persistent ulcerations may occur in immunocompromised patients, especially in those who are co-infected with HIV [14]. Recently, a first clinical episode of genital herpes presenting as non-gonococcal urethritis was described [15]. A diagnosis of genital herpes infection can be confirmed by virus isolation in cell culture or PCR detection of HSV DNA [10,11]. Serologic diagnosis of HSV infection is of value only to determine past exposure. Serological tests that distinguish between HSV-1 and HSV-2 will soon be commercially available. The treatment given depends on several factors, including the frequency and severity of recurrences, and the infection status of the sexual partner. Because the herpes virus cannot be eliminated from neurones treatment is aimed at controlling the mucocutaneous expression of the disease. The regimens for treating genital herpes are summarized in Table 1[10,11].

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Figure 3. Genital herpes; grouped vesicles and erosions are located on the penis shaft and scrotum.

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Table 1.  Recommendations for treating genital herpes
Patient/stateTreatment, mg, ×/day, duration in days
Immunocompetent  First episodeoral acyclovir 200, ×5, 5
oral valacyclovir 500, ×2, 5
oral famciclovir 250, ×3, 5
Recurrent episodeoral acyclovir 200, ×5, 5
oral valacyclovir 500, ×2, 5
oral famciclovir 125, ×2, 5
Continuous suppressionoral acyclovir 400, ×2
oral valacyclovir 500, ×1
oral famciclovir 250, ×2
Immunocompromised  patientsoral aciclovir, 200–400, ×5, 10
oral acyclovir 400, ×5, 7–14
oral acyclovir 500, ×2
oral famciclovir 250, ×3

Infestations

  1. Top of page
  2. Summary
  3. Introduction
  4. Viral infections
  5. Infestations
  6. Genital manifestations of cutaneous diseases
  7. Balanitis and balanoposthitis
  8. Premalignant and malignant genital tumours

Scabies

Scabies is an infestation with a mite, Sarcoptes scabiei var hominis. The mites burrow tunnels into the horny layer of the epidermis. The female lays 2–3 eggs in the tunnels each day; within 3–5 days the eggs hatch into larvae which transform into nymphs, and these in turn metamorphose into adults [6]. Classic areas of infestation include the web spaces of the hands, axillae, and the flexor surfaces of the wrists [16]. Burrows are small, crooked lines 4–6 mm long most frequently found in the web spaces of the fingers, sides of the hands and flexor surfaces of the wrist. With the development of the immune response to scabies, the patient develops erythematous papules and nodules. Non-specific secondary, eczematous lesions are very common [16]. Multiple typical scabetic burrows and papules are often present on the glans penis, scrotum and penis shaft [7]. Elsewhere on the skin the lesions may be few or many, but it is very rare not to have penile lesions in scabies (Fig. 4). The chief clinical symptom is pruritus, that is usually worse at night or after hot baths. Patients with very good hygiene have fewer specific lesions, making the diagnosis of scabies more difficult [6]. Generalized crusted scabies is found in immunocompromised or physically incapacitated individuals; it has been reported in patients with HIV infection and in organ-transplant recipients. These patients present with widespread crusting and psoriasis-like scaling, especially around and under the nails. Crusts and scales contains tremendous numbers of mites. Pruritus may be minimal in crusted scabies. Scabies occurs in at least 2–4% of patients with HIV infection. Burrow scraping is the best technique for detecting mites. The preferred treatment for scabies is permethrin 5% cream applied from neck to the feet, with particular attention given to the perianal and genital areas, and to the free nail edge and folds; the cream is rinsed off after 8–14 h [16]. Lindane 1% lotion or cream is another recommended medication for scabies. Ivermectin, an oral semisynthetic derivative of a family of macrocyclic lactones, is a promising new therapeutic agent [16,17]; it interrupts the γ−aminobutyric acid-induced neurotransmission of many parasites, including scabies mites, and is given as a single dose of 200 µg/kg. However, in severe cases two or three doses at 1 or 2 week intervals should be given. Topical ivermectin 1% solution, in two doses of 400 µg/kg applied weekly, was highly effective, with complete cure and no signs of recurrence 6 weeks after completing therapy [18]. All household members of the scabetic patient, and any sexual partners, should be treated concomitantly.

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Figure 4. Scabies; multiple erythematous papules.

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Pediculosis pubis

Pediculosis pubis, caused by the ectoparasite Phthirus pubis, also known as the crab louse, is a sexually transmitted infection that frequently coexists with other sexually transmitted diseases [6,16]. Therefore, a search for other sexually transmitted diseases, including HIV, should be initiated. Pediculosis pubis is a likely diagnosis for any patient who complains of pruritis of the pubic area. The lice are 1–2 mm long, appearing as brown or grey specks, and are attached to the hair base [7,16]. Maculae caeruleae are bluish-grey macules that represent the feeding sites of the louse. Rarely, the axillae and eyelashes are also involved. Pediculosis and scabies may coexist in the same individual. Treatment of pediculosis pubis is with topical permethrin or lindane [16]. Permethrin shampoo should be applied to the pubic area for 10 min and then washed off. Sexual partners should also be treated to prevent recurrent infestation.

Genital manifestations of cutaneous diseases

  1. Top of page
  2. Summary
  3. Introduction
  4. Viral infections
  5. Infestations
  6. Genital manifestations of cutaneous diseases
  7. Balanitis and balanoposthitis
  8. Premalignant and malignant genital tumours

Psoriasis

Psoriasis is the most common inflammatory reaction that affects the male genitalia. In many cases, male genital involvement with psoriasis is part of a more generalized cutaneous disorder. The lesions manifest as well-demarcated, bright red plaques, with no scale in the inguinal folds and intergluteal cleft, known as inverse psoriasis [19]. Occasionally, the entire scrotum and penis are involved. Psoriasis may occur solely on the penis (Fig. 5). Usually, in circumcised males red scaly patches are present on the glans and corona [7]. In uncircumcised individuals, well-defined non-scaling plaques are most common under the prepuce and on the proximal glans. The diagnosis of genital psoriasis can usually be made from the local clinical findings. Occasionally, patients may have a coincidental fungal infection in the flexures, and it is always wise to take samples to rule out Tinea or Candida. The presence of typical red scaly patches, particularly in such areas as the elbows, knees and scalp, help to establish the clinical diagnosis. The management of genital psoriasis can sometimes be a vexing problem; control may be satisfactory with low-potency corticosteroid creams. A preparation of 3% liquor carbonis detergens in 1% hydrocortisone cream may be very helpful [7]. Topical vitamin D analogues such as calcipotriene or tacalcitol can be tried as monotherapy or combined with topical steroids. A common side-effect of calcipotriene treatment is the development of an irritant contact dermatitis. Treatment regimens in which topical vitamin analogues and corticosteroids are both used may minimize the side-effects of either agent, while maximising the beneficial effects.

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Figure 5. Psoriasis; red scaly patches on the glans penis.

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Lichen planus

The male genitalia are involved in 25% of cases of this condition and the glans penis is most commonly affected, with annular lesions frequently present [7,19]. Typically, the patient presents with violaceous flat-topped papules on the glans and shaft of the penis (Fig. 6). The lesions may also develop as arcuate groupings of individual papules that develop rings or peripheral extension of clustered papules with central clearing. Fine white streaks are usually visible on the surface, so-called Wickham's striae. Usually the glans penis is involved as a part of a more generalized disorder with typical lichen planus lesions at other sites. However, it may occur as the initial or sole manifestation. Rarely, lesions may become eroded similar to the erosive lichen planus of the oral mucosa. The diagnosis is helped by the finding of typical lichen planus papules, particularly on the wrists, hands, forearms, shins, ankles and lumbosacral region. Oral lesions are common and occur either as white reticulate streaks or as erosive lesions. In atypical cases biopsy may be necessary to confirm the diagnosis. Most cases of genital lichen planus respond to short courses of mild topical glucocorticoids [7].

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Figure 6. Lichen planus; numerous annular violaceous papules on the glans penis.

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Penile lichen sclerosus

Lichen sclerosus of the male genitalia is a chronic inflammatory disorder presenting as a chronic, sclerosing atrophic process of the glans and foreskin, leading to meatal stenosis and acquired phimosis. Most authors consider lichen sclerosus of the penis synonymous with balanitis xerotica obliterans [20]. However, the latter can be a consequence of other scarring dermatoses such as lichen planus and bullous disorders. The incidence of genital lichen sclerosus in young boys with phimosis has been estimated at ≈ 15%, but the exact frequency in men is unknown [20,21]. Of 357 patients referred for diagnosis of genital skin disease, 52 had lichen sclerosus [22]. Penile lichen sclerosus is most common in middle-aged uncircumcised men. In a prospective study of 43 men with narrowing of the prepuce referred for circumcision, lichen sclerosus was present in 32%[23]. Only 21% of the men had been clinically diagnosed as having lichen sclerosus. The initial lesions of lichen sclerosus are white, polygonal and flat-topped papules or plaques. The lesions progress to ivory-coloured atrophic and sclerotic white plaques. In men, the glans and foreskin are usually affected, but not the perianal region. However, the frenulum, urethral meatus and the anterior urethra may also be involved [7,20,21]. Uncommonly, lichen sclerosus involves only the shaft of the penis. If the glans is involved, haemorrhage is common. In addition, haemorrhagic bullae, erosions and fissures may also be present [7,20]. A very typical finding is the presence of a sclerotic white ring at the tip of the prepuce (Fig. 7). With disease progression, the sclerotic lesions lead to contraction of the genital mucosa with subsequent paraphimosis or phimosis with inability to retract the prepuce. Gradual narrowing of the external meatus results in varying degrees of stricture and urinary flow may be obstructed [1,24]. Presenting symptoms are pruritus, burning, painful erections, difficulty in retracting the foreskin, dysuria, and a poor urinary stream. The aetiopathology of lichen sclerosus is still unknown but genetic factors, an association with auto-immunity, several infective agents such as borrelia, and local factors are postulated. The course of penile lichen sclerosus is chronic. The association between lichen sclerosus and squamous cell carcinoma (SCC) is a well-known phenomenon in women, and it has been observed in 3–6% of patients with vulvar involvement. There are anecdotal reports of men developing penile SCC in association with lichen sclerosus. In a retrospective study of 86 uncircumcised patients with lichen sclerosus, five (6%) developed malignant changes [25]. Three patients had SCC, one had in situ carcinoma and one had verrucous carcinoma. The presence of HPV 16 was shown by PCR in four of the five cases. In a recent study of 20 patients with penile SCC, half had histological evidence of lichen sclerosus [26]. Periodic follow-up of patients with lichen sclerosus is advisable, including biopsy of any clinically suspicious lesions. A potent or ultra-potent topical steroid is the treatment of choice for adults and children [21,27]. Topical clobetasol proprionate 0.05% was helpful in ameliorating the symptoms and lesions of lichen sclerosus. In men and young boys the most frequent surgical procedure required is circumcision for a phimosis.

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Figure 7. Lichen sclerosus; a typical white sclerotic ring at the tip of foreskin.

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Allergic and irritant dermatitis

Clinically, genital allergic contact dermatitis is characterized by erythema and marked oedema and, in time, with microvesiculation and exudation. Acute contact dermatitis of the penis is usually associated with marked oedema because the skin covering the genitalia is thin and elastic [7,20]. Sensitisation to applied medicaments, contraceptives, lubricants, feminine hygiene deodorant spray, or industrial or other contact agents transferred by hand, may be responsible, especially if the scrotum and thighs are also involved [19,20]. The list of possible sensitising agents is long. Allergy to latex contraceptive products can manifest as a contact urticaria which occurs within an hour of exposure as a result of immediate IgE-mediated hypersensitivity to natural rubber latex. Immediate reactions may be life-threatening [28]. Anaphylaxis has been reported from contact with condoms. Men with latex allergy may present with oedematous, weeping eruption of acute contact dermatitis, which is a delayed-type hypersensitivity to latex or to chemicals added to natural rubber latex during manufacturing. Other frequently involved contact allergens are lubricants from condoms, feminine hygiene deodorants, local anaesthetics such as benzocaine, and spermicides. Elimination of the suspected offending allergen and appropriate treatment with topical corticosteroids usually serve to manage patients with allergic contact dermatitis. Mild cases can be treated with low potency corticosteroid creams. Severe cases of allergic contact dermatitis may require treatment with systemic corticosteroids. The identification of the contact allergen depends on history and usually requires ‘patch’ testing. This procedure is especially indicated for cases in which inflammation persists despite avoiding the suspected allergens and after appropriate topical therapy. Irritant contact dermatitis results from non-immunological physical or chemical damage to the skin. The eruption primarily occurs in the area of contact with irritants, and may develop from the use of certain soaps, detergents or topical medications. In the acute phase the lesions are erythematous and may be weeping and crusted. With recurrent or prolonged exposure to irritants the skin becomes lichenified, hyperkeratotic and inflamed.

Fixed-drug eruptions

Fixed-drug eruptions are relatively common and distinctive; they characteristically recur in the same site each time the drug is administered. Usually just one drug is involved, although independent lesions from more than one drug have been described. Clinically, the lesions present as sharply marginated, round or oval dusky erythematous and oedematous plaques [7,19,20]. A central bulla may be present within the lesion. The lesions heal with time, leaving a hyperpigmented patch. The penis is a frequent site for fixed-drug eruption (Fig. 8). The lesions usually develop within a few days of drug administration. Fixed-drug eruptions have been reported in association with several drugs, the most frequently implicated being barbiturates, sulphonamides, salicylates, phenazones and tetracyclines. In a study of 450 patients with fixed-drug eruption, 20% had genital lesions; in 73% cotrimoxazole was the commonest incriminated drug [29].

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Figure 8. Fixed drug eruption caused by ingestion of trimethoprim-sulphamethoxazole, showing the dusky erythematous solitary lesion.

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Balanitis and balanoposthitis

  1. Top of page
  2. Summary
  3. Introduction
  4. Viral infections
  5. Infestations
  6. Genital manifestations of cutaneous diseases
  7. Balanitis and balanoposthitis
  8. Premalignant and malignant genital tumours

Plasma cell balanitis

Plasma cell balanitis or balanitis circumscripta plasmacellularis, originally described by Zoon [30] in 1952, is a benign chronic balanitis of unknown origin. Plasma cell balanitis is characterized by a solitary red-orange plaque of the glans and prepuce [7,20]. The condition usually manifests in middle-aged or elderly uncircumcised men. The plaque surface is shiny and smooth, reddish brown, slightly moist and stippled with minute red specks, i.e. ‘cayenne pepper’ surface spotting (Fig. 9). The disease tends to be chronic and may persist for months to years. It is important to verify the diagnosis by biopsy. The histopathology is characteristic showing a band-like infiltrate of plasma cells. Clinically, plasma cell balanitis may be confused with an erythroplasia of Queyrat (SCC in situ), but a case of penile carcinoma preceded by Zoon's balanitis has been reported [31]. The treatment of choice for plasma cell balanitis is circumcision. A topical antibiotic cream (e.g. fusidic acid or mupirocin) can be helpful. Temporary relief is usually achieved by a topical steroid. Resistant cases can be treated with the carbon dioxide laser or erbium-YAG laser ablation.

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Figure 9. Balanitis circumscripta plasmacellularis Zoon; a well-circumscribed, shiny red plaque.

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Balanitis circinata

Balanitis circinata is a mucocutaneous manifestation of Reiter's syndrome, a multisystem disease, that is clinically characterized by the triad of nongonococcal urethritis, arthritis and conjunctivitis [20]. Balanitis circinata has been reported in 12–70% of men with Reiter's disease. Circinate balanitis manifests as a well-demarcated, moist, erythematous plaque with a ragged or scalloped white border on the glans penis (Fig. 10). In circumcised patients the lesions are dry and hyperkeratotic, and may appear as psoriasiform plaques [7]. The initial lesion is an erythematous macule developing into a small papule and pustule with hyperkeratotic appearance. Lesions are frequently present around the urethra, and are not necessarily annular or circinate. The histopathological findings may be indistinguishable from psoriasis.

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Figure 10. Balanitis circinata; well-demarcated, erythematous plaque with a ragged border on the glans penis.

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Premalignant and malignant genital tumours

  1. Top of page
  2. Summary
  3. Introduction
  4. Viral infections
  5. Infestations
  6. Genital manifestations of cutaneous diseases
  7. Balanitis and balanoposthitis
  8. Premalignant and malignant genital tumours

Giant condyloma (Buschke-Löwenstein tumour)

Giant carcinoma-like condyloma was described in 1925 by Buschke and Löwenstein [32]. This variant of condyloma is characterized by deep growth, causing local destruction of underlying tissue. Patients frequently have a history of balanitis, ulceration or phimosis. The tumour may enlarge to 5 cm in diameter and tends to occur in uncircumcised men, usually involving the penile glans and prepuce, but these tumours may involve the groin, urethra and anal canal. Lesions may ulcerate and form fistulous tracts. Most cases are caused by infection with low-risk HPV 6 and 11 [1,4,20]. The tumours also have been termed giant malignant condyloma, verrucous carcinoma, and carcinoma-like condyloma. In most cases Buschke-Loewenstein tumours represent a subtype of low-grade SCC. Although true giant condylomas exist, the histological features of benign condyloma and foci of frank SCC may occur concomitantly in some tumours. Because of the clinical overlap in the appearance of giant condyloma and verrucous squamous carcinoma, the presence of rapidly proliferating large warty lesions requires multiple, large and deep biopsy specimens. Recently it was postulated that giant condyloma and verrucous SCC are separate and different pathological lesions.

Bowenoid papulosis

Bowenoid papulosis is characterized by flat, skin-coloured, pink or often hyperpigmented papules with the histological features of Bowen's disease [1,33,34]. The condition is strongly associated with HPV 16, but other HPV types, e.g. 18 and 31, may be involved. The disease occurs mainly in young sexually active adults, with lesions on the glans penis and prepuce. The papules are often multiple and tend to coalesce into plaques; they are often more pigmented on the penis shaft and scrotum (Fig. 11). Brownish or greyish-white lesions occur on the inner side of the foreskin, and the lesions are 2–10 mm. The natural course of bowenoid papulosis is not well defined. The papules may increase, decrease or the lesions may disappear with time. However, coexistence of bowenoid papulosis with and transmission into invasive carcinoma have been reported. Bowenoid papulosis should be differentiated from flat condylomas, lichen planus and psoriasis. Bowenoid papulosis represents a high risk for neoplasia and should be treated, the most effective treatment being excision of the papules. However, cryosurgery with liquid nitrogen and carbon dioxide laser are the most frequently used methods. The recurrence rate after treatment with a laser is 0–33%[9]. Imiquimod, an immune-response modifier, may be tried but the efficacy against bowenoid papulosis has not been evaluated in large studies [35].

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Figure 11. Bowenoid papulosis; multiple flat pigmented papules.

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Erythroplasia of Queyrat

Erythroplasia of the glans penis, described in 1911 by Queyrat [36], is a carcinoma in situ presenting as a sharply demarcated, slightly raised erythematous plaque on the glans penis or the inner side of the foreskin [1]. An individual lesion may be 10–15 mm in diameter, and solitary or multiple lesions occur; they are usually bright red, glistening and not tender. Their surface may be somewhat smooth, scaly to frankly warty. Patients usually complain of pruritus, pain, bleeding and difficulty in retracting the foreskin. With time clinical ulceration may occur and tends to correlate with histological evidence of invasive SCC. Most patients are in their fifth decade or older. In one series of 100 patients, 90% of cases occurred in men with a median age of 51 years. Erythroplasia is usually seen in uncircumcised men, who account for 80–90% of reported cases. A definite diagnosis is made by a biopsy showing the typical histological picture of intra-epidermal carcinoma in situ. Early invasion should be excluded by obtaining several biopsies. Transformation of erythroplasia into SCC has been reported to occur in 10–33% of cases [37]. Surgical excision is the treatment of choice, but topical 5-fluorouracil and the CO2 laser may also be used.

Bowen's disease

Bowen's disease refers to SCC in situ and may arise anywhere on the skin. Bowens’ disease of the glans penis is termed erythroplasia of Queyrat [1] and is usually found on the shaft of the penis as a solitary, sharply defined plaque of scaly erythema. Clinical variants include crusted and ulcerated plaques, keratotic plaques and elevated flesh-coloured plaques. The skin of the inguinal and suprapubic areas may also be involved. Patients may have more than one lesion. Bowen's disease may be confused with bowenoid papulosis, nummular eczema, psoriasis and superficial basal cell carcinoma. Lesions may sometimes be heavily pigmented and thus may resemble melanoma in these cases. Biopsy is required to confirm the diagnosis. If untreated, invasive SCC may arise in ≈ 5% of cases. Surgical excision is the best treatment option for small lesions [9], preferably by cryosurgery or CO2 laser; both methods have been used for many years with excellent results.

Penile SCC

Of all cancers affecting the penis 95% are SCC; the disease is rare, with age-standardized incidence rates of 0.3–1.0/100 000 men. However, the incidence rates are 10–20% in some countries of Africa and South America [37]. The age at the onset of penile SCC has a wide range (20–90 years) with a peak around the fifth decade. Risk factors are phimosis, lack of circumcision, chronic inflammatory conditions, multiple sexual partners and HPV infection [33,38]. Penile SCC is extraordinarily rare in circumcised males; the relative risk for developing penile cancer in uncircumcised compared with those circumcised at birth is 3.2. Phimosis has been reported to be present in 44–85% of men with penile SCC [38]. In a series of studies, HPV DNA was identified in 40–50% of cases with penile cancer, most being of high-risk HPV 16 [2,38]. Prevention of SCC includes early detection and treatment of pre-cancerous lesions. The clinical appearance of penile SCC varies from erythematous plaque, induration to more verrucous and exophytic lesions that may coalesce into an irregularly shaped mass (Fig. 12). As it increases in size, superficial ulceration, necrosis and bleeding may become evident; it may become large, developing into a locally destructive mass [37]. The primary lesion may occur on the glans or may be hidden under the foreskin. Primary tumour pathological staging and grading, and the involvement of pelvic and inguinal lymph nodes, are the main factors used to predict the prognosis of patients with penile SCC. The treatment of penile SCC depends on tumour staging and includes surgery, radiotherapy, laser surgery and chemotherapy [39]. Moh's micrographic surgery has been used to advantage.

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Figure 12. Penile SCC presenting as an erythematous, nodular, erosive lesion on the glans penis.

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References

Abbreviations
HPV

human papillomavirus

HSV

herpes simplex virus

SCC

squamous cell carcinoma.

Prof Dr S. Buechner, Department of Dermatology, University of Basel, Petersgraben 4, CH-4031 Basel, Switzerland. e-mail: Stanislaw.buechner@hin.ch