When A Patient Presents With An Unusual Lesion On The Sole

Pages: 24 - 28
By G. “Dock” Dockery, DPM, FACFAS

A 60-year-old Caucasian female patient presents for consultation to the foot and ankle clinic regarding a one-year history of an erythematous, scaly and irregular lesion on the sole of her right foot. She notes the lesion is entirely asymptomatic. She originally saw a primary care physician about the lesion. The physician told her that she had a case of “athlete’s feet” and recommended an over-the-counter (OTC) antifungal cream. After four weeks of treatment with the antifungal cream, the patient showed no improvement.

The primary care physician then re-diagnosed the lesion as “eczema” and prescribed an intermediate strength topical cortisone cream. However, after two weeks of treatment, the lesion again failed to respond. Since the lesion was not pruritic and did not hurt, the patient simply quit worrying about it. Yet she recently noticed that it appeared to get bigger so she sought a second opinion.

The patient has had no known exposures to any new drugs, chemicals, paints, toxins, irritants or other potential allergens. She is currently taking a thyroid supplement but denies taking any other medications, vitamins or supplements. Her husband recently died due to heart failure and no one else in her household or within her family has any similar conditions.

What The Exam Revealed

Examination of the plantar aspect of the patient’s right foot reveals an obvious lesion that demonstrates a slightly elevated, red, irregular, scaly plaque with surface fissures and some crusts along with well-defined borders on the non-weightbearing surface. The lesion does not involve other parts of the foot or ankle, and there is no involvement of the hands or nails. There are no targetoid lesions or other distinctive skin lesions. There is also no color or inflammatory changes involving the eyes or ears. There are no tongue or oral cavity lesions or discolorations present. The patient has normal vital signs and there is no elevation of the oral temperature. The remaining portion of the physical examination is within normal limits and the patient has no other clinically significant skin conditions.



A Closer Look At Bowen’s Disease

The most likely diagnosis is intraepidermal (in situ) squamous cell carcinoma (Bowen’s disease). Bowen first described this entity in 1912 and described two cases. This squamous cell carcinoma (in situ) is a slow growing and scaly skin patch with a potential for significant lateral spread. The lesion may range from a few millimeters to several centimeters in diameter. Bowen’s disease presents as a single lesion in two thirds of cases. The term “in situ” simply means that the malignant cells are confined to the epidermis. However, there is evidence that the affected cells may migrate deeper into the skin layers and subsequently become a more aggressive form of skin cancer if this goes untreated.

Both chronic sun damage and inorganic arsenic ingestion have been implicated as etiologic factors in the development of Bowen’s disease. Researchers have also documented the human papilloma virus (HPV), especially HPV 16, as a cause of Bowen’s disease. In cases related to chronic UV exposure, the lesions may appear on sun-exposed areas of the head, neck, upper and lower extremities.

When it comes to cases in which Bowen’s disease occurs on areas of the legs and the plantar aspect of the feet, which are protected from the sun, these cases may often be related to inorganic arsenic exposure. This chemical was formerly present in several medications, such as “bromide mixtures,” Fowler’s solution and Gay’s solution, which were used for the treatment of epilepsy, psoriasis and asthma respectively. Inorganic arsenic was also used in occupational agents such as environmental fungicides, pesticides and weed killers. It was also commonly found in well water on many farms throughout the United States.

Studies have shown that up to 50 percent of arsenical cancers reported involve Bowen’s disease. There is typically a lag time of greater than 10 years (often several decades) between exposure and the development of Bowen’s disease. Patients may not recall any previous contact with inorganic arsenic compounds.

In general, Bowen’s disease is more common in women (80 to 85 percent). It has been reported that Bowen’s disease is more prevalent among Caucasian people over the age of 40. Most patients diagnosed with Bowen’s disease are over the age of 60 and about 75 percent of all patients have lesions on the lower leg. Other locations include perianal, palms and soles and subungual locations. Pigmented and verrucous forms have been reported and are frequently misdiagnosed.

In regard to Bowen’s disease, one would primarily diagnose this disease via clinical features and dermatohistological confirmation is generally necessary. A shave biopsy or punch biopsy that incorporates any follicular structures is helpful. It is common to perform these procedures in the office with a local anesthesia. It is best to obtain the pathological analyses from board-certified dermatopathologists as opposed to general pathologists. The prognosis of Bowen’s disease is generally favorable. Around 3 percent of reported cases advance to invasive squamous cell carcinoma and metastases are even more rare.

The differential diagnosis includes psoriasis, eczematous dermatitis, tinea pedis, actinic keratosis, superficial basal cell carcinoma and lichen simplex chronicus among other conditions.





A Guide To The Differential Diagnosis

Psoriasis. This chronic condition affects many different parts of the body, including the palms and soles, and the typical plaque formation may appear similar in clinical presentation to Bowen’s disease, especially on the lower legs. Careful examination of the entire body may be helpful in finding other typical lesions. This condition is difficult to treat effectively and one can diagnose it with a punch biopsy.

Eczematous dermatitis. Next to tinea pedis, this is the second most misdiagnosed condition. The word eczema is derived from the Greek term ekzein, meaning “to boil out.” This term aptly describes the swollen, wet, oozy, bubbly appearance of acute eczema. When pruritic skin has been rubbed and scratched for weeks, it lichenifies into the dry, thick, scaly plaques of chronic eczema. Chronic plantar nummular and other eczematous dermatoses may look very similar to Bowen’s disease, and a biopsy will differentiate these conditions.

Tinea pedis. This is the most common misdiagnosis when the lesion is on the foot but one can see this concurrently with Bowen’s disease. Since most cases of Bowen’s disease occur on the lower leg, one should not often see this diagnosis.

Actinic keratosis. This condition is more common on sun-exposed areas of the body and rarely occurs on the plantar aspect of the feet. However, this condition may be very similar to Bowen’s disease when it presents on the lower legs. The distinction between the two is a matter of degree (the extent of the lesion) as opposed to differences in individual cells. One will often see marked hyperkeratosis and areas of parakeratosis with loss of the granular layer. A dense inflammatory infiltrate is usually present. The case has been made that actinic keratosis is the earliest manifestation of squamous cell carcinoma and one should regard it as such rather than as a precancerous lesion. Biopsy of the lesion will help confirm the diagnosis.

Superficial basal cell carcinoma (BCC). This variety of BCC appears as scaly patches or papules that are pink to reddish-brown, and often have central clearing. A threadlike border is common. Erosion is less common in superficial BCC than in nodular BCC. Superficial BCC is common on the trunk and has little tendency to become invasive. The papules may mimic Bowen’s disease, psoriasis or eczema, but they are not prone to fluctuate in appearance. Numerous superficial BCCs may indicate arsenic exposure. Biopsy is essential in the diagnosis.

Lichen simplex chronicus (LSC). This occurs on skin regions accessible to chronic rubbing and scratching. Pruritus provokes rubbing that produces clinical lesions but the underlying pathophysiology is unknown. Some skin types are more prone to lichenification. One example is skin that is more susceptible to eczematous conditions (i.e., atopic dermatitis, atopic diathesis). The possible interplay among primary lesions, psychic factors and the intensity of pruritus additively influences the extent and severity of LSC.





Key Insights On Preventing And Treating Bowen’s Disease

Preventative measures include protection of the solar exposed areas of the body with proper clothing and headgear as well as the use of a broad spectrum sunscreen at all times when outside. Early detection of skin lesions with regular evaluations by a physician is highly recommended.

The treatment for Bowen’s disease depends upon the size and location of lesions, the number of lesions to be treated, and the preference of the physician.

Topical therapy with administration of 5-fluorouracil under occlusion reportedly is effective for the treatment of Bowen’s disease. Patients would apply this cytotoxic cream once or twice daily as a 5% cream for one to eight weeks. Patients may also use imiquimod 5% cream, a topical immune response modifier, which they would apply three to five days per week for six to 16 weeks.

Surgical care can include cryotherapy or curettage. In both of these cases, an accurate diagnosis following biopsy is required before treatment begins. Simple excision with conventional margins of 4 mm is the most common and preferred treatment for smaller lesions and those that are not in challenging areas of the body.

Mohs micrographic surgery is an excellent method for larger lesions, recurrent lesions or those in areas where tissue sparing is vital. This technique uses the systematic surgical removal of skin cancer with very small margins of normal tissue and subsequent frozen section pathology examination. This offers the highest cure rate of all treatment modalities. Since one is removing relatively small borders around the lesion, this is considered a tissue sparing procedure.

Whatever the chosen treatment, one can often cure Bowen’s disease. Occasionally, the lesions come back at the same site but physicians can usually treat these again effectively. Following the successful treatment of Bowen’s disease, one should reevaluate the patient every three to six months.

A failure to recognize Bowen’s disease or to perform a lesion biopsy can lead to delayed treatment. A high degree of suspicion is needed in both sun-exposed and non-sun-exposed areas of the skin. One should send all biopsy specimens of suspected skin lesions to a board certified dermatopathologist for further diagnostic evaluation.









Suggested Reading
1. Bowen JT: Precancerous dermatoses: a study of two cases of chronic atypical epithelial proliferation. J Cutan Dis. 1912; 30:241-255.
2. Cox NH, Eedy DJ, Morton CA: Guidelines for management of Bowen’s Disease: 2006 Update. Br J Dermatol. 2007; 156(1):11-21.
3. Dockery GL: Premalignant and Malignant Tumors, ch. 7, pp 125-135. In: Cutaneous Disorders of the Lower Extremity. W.B. Saunders Co., Philadelphia, July, 1997
4. Dockery GL, Bakotic B: Biopsy Techniques. Ch. 11, pp 85-96, In: Dockery G. L., Crawford, M.E. (Eds): Lower Extremity Soft Tissue & Cutaneous Plastic Surgery, Elsevier Science Limited (Saunders), Oxford-Philadelphia, January 2006.
5. Lemont H, Haas R: Subungual pigmented Bowen’s disease in a nineteen-year-old black female. J Am Podiatr Med Assoc 1994; 84(1):39-40.
6. Liu GT, Lovell MO, Steinberg JS: Digital syndactylization for the treatment of interdigital squamous cell carcinoma in situ (Bowen disease), J Foot Ankle Surg. 2004; 43(6):419-422.
7. Mitsuishi T, Kawashima M, Sata T: Human papillomavirus associated Bowen’s disease of the foot: unique clinical features mimicking a common wart. Eur J Dermatol. 2001; 11(5):463-465.
8. Mohs FE: Mohs micrographic surgery. A historical perspective. Dermatol Clin 1989 Oct; 7(4): 609-11.
9. Moreno G. Chia AL, Lim A, Shumack S: Therapeutic options for Bowen’s disease. Australas J Dermatol. 2007; 48(1):1-8.
10. Ooi CG, James CL, Huilgol SC: Metastatic Bowen carcinoma. Australas J Dermatol. 2006; 47(4):277-280.
11. Patel MJ, Stockfleth E: Does progression from actinic keratosis and Bowen’s disease end with treatment: diclofenac 3% gel, an old drug in a new environment? Br J Dermatol 2007; 156 (Suppl):3:53-56.
12. Rosen T, Harting M, Gibson M: Treatment of Bowen’s disease with topical 5% imiquimod cream: retrospective study. Dermatol Surg. 2007; 33(4):427-431.
13. Techner LM, Eannace RJ: Squamous cell carcinoma in situ (Bowen’s disease). A case report. J Am Podiatr Med Assoc. 1987; 77(12):662-664.
14. Welch ML: Bowen Disease. eMedicine, update February 2007. Available at: www.emedicine.com/derm/topic59.htm
15. Yu HS, Liao WT, Chai CY: Arsenic carcinogenesis in the skin. J Biomed Sci. 2006; 13(5):657-666.



Very nice site!

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