Tag Archives: Metastasis

Clear Cell Sarcoma of the Foot: A Case Report of Malignant Melanoma of Soft Parts

by Al Kline, DPM 1

The Foot & Ankle Journal 1 (3): 3

A case report is presented describing a clear cell sarcoma of the foot (malignant melanoma of soft parts). Melanoma is most commonly associated with pigmented lesions and nodules of the skin. Clear cell sarcoma (CCS) is an anaplastic tumor consisting of cells derived from melanoblasts not forming melanin in the skin, but rather mitotic changes more consistent with malignant melanoma in subcutaneous tissue, tendons and aponeuroses. The tumor is very rare and can pose clinical challenges in early diagnosis since the tumor lacks pigment and obvious color changes and can clinically appear as a benign soft tissue tumor. A case report including surgical excision, histologic features, and survival prognosis is presented.

Key words: Clear cell sarcoma, malignant melanoma of soft parts, metastasis, skin cancer

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.  It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot & Ankle Journal (www.faoj.org

Published online: March 1, 2008

ISSN: 1941-6806/08/0103-0003
doi: 10.3827/faoj.2008.0103.0003

Malignant melanoma is a relatively rare skin cancer accounting for only 4% of all skin cancers. [1] Clear cell sarcomas account for less than 1% of all melanomas. Clear cell sarcoma (CCS) is an indolent tumor of unknown histogenesis involving subcutaneous tissue, tendon and aponeurosis. CCS is a very rare, malignant soft tissue tumor and often is called ‘malignant melanoma of soft parts’ due to the histologic similarities and lack of observable pigmentation often seen in cutaneous melanoma. It can affect all age ranges including children and young adults.

The tumor is characterized by cytoplasmic melanosomes and melanotic mitotic figures isolated to the soft tissue without skin involvement.

It presents as a soft tissue mass common to tendon and aponeurosis seen in the lower extremity, but can occur anywhere. It has also been reported to occur in other tissues such as the GI tract, kidney and retroperitoneum with clinical features similar to that of malignant ovarian tumors. [2]

Interestingly, there is an increased incidence of lower extremity and foot CCS reported in the literature. It tends to present around the ankles and around the heel and aponeurosis of the plantar fascia.

The tumor is rare, but has over 300 cases reported. Although the tumor is rare and histologically resembles melanoma, it more closely resembles soft tissue sarcoma in that it has a high propensity to lymph node metastasis. [3]

Clear cell sarcomas pose a particular challenge in early detection. The tumor is more common in younger individuals, but can occur at any age. These lesions may start rather innocuously as a small, non-pigmented swelling and lay in situ for many years.

Clear cell sarcomas may show a more rapid growth after laying in situ. In particular, the border of the lesion may become irregular and progress with diameter enlargement. It is common to use the “A,B,C,D,E criteria” for early detection of malignant melanoma and this criteria may also be useful in the differential diagnosis of CCS. (Table 1) [1,12] Early and late tumors may only reveal asymmetry and size changes.

ABCDE Criteria in the diagnosis of MM

A- Asymmetry to outline of the lesion
B- Border irregularity
C- Color variegation
D- Diameter enlargement
E- Evolving/Elevation/Enlargment

Table 1   Clear cell sarcoma (CCS) often meets four of the five criteria of malignant melanoma with asymmetry, border irregularity, diameter enlargement, and evolving changes of the tumor.

Case Report

A 61 year-old female presents with a painful, soft tissue tumor of the right medial heel. The tumor is irregular in shape, non-movable and firm to palpation (Fig. 1). The tumor became bothersome in February 2007. She relates the tumor was present for 12 years and had remained small and non-painful.

Figure 1   The lesion is irregular, firm and non-movable.  It is painful to palpation and measures about 2 cm in diameter.

Over the past 2 years, she states it began to enlarge. There is no history of trauma. Further questioning revealed a history of previous nevi of the abdomen and neck. Multiple lesions had been biopsied in the past, but were negative for malignant transformation. She had a similar nodule on her neck. The patient had seen a dermatologist, who suggested watching the lesion. A differential diagnosis of the tumor includes benign lipoma, dermoid tumor or cyst, dermatofibroma, fibroxanthoma, dermatofibrosarcoma, nodular fibroma, lipoblastoma and giant cell fibroblastoma.

It was decided to take the patient to surgery for excisional biopsy, removing the tumor.

Surgical Removal

The patient was brought to an out-patient operating facility and underwent local removal of the tumor. A curvilinear approach was planned to gain maximum exposure for removal of the tumor. During surgery, it was noted the tumor was nodular and adherent to the underlying epidermal tissue. Blunt dissection was used to remove the tumor. Redundant skin was sectioned and sent with the tumor to pathology for identification (Fig. 2).


Figure 2   The tumor is nodular and adherent to the underlying epidermis extending through the dermis and subcutaneous fat.

Histology Report

The specimen was designated “foot mass.” The gross specimen measured 2.1 x 1.8 x 1.4-cm. (Fig. 3). The gross specimen was described as rubbery, yellow to pink-tan, fibrofatty soft tissue.

Figure 3   The tumor, once removed, is a firm, lobulated mass within subcutaneous fat measuring 2.1 x 1.8 x 1.4 cm.

The specimen is inked and serially sectioned to reveal an edematous, pink to red-tan lobulated mass with a variegated cut surface that measures about 1.5 x 1.4 x 1.2 cm.

Microscopic sections are stained routinely and underwent additional immunostains including Mart-1, CD10, HMB45, S-100, vimentin and pankeratin/cytokeratin. Routine stains show a malignant, predominantly spindle cell, neoplasm that diffusely infiltrates into and between connective tissue bundles and extends into adipose tissue. The neoplastic cells are arranged as vaguely cohesive aggregates which sometimes form ill-defined, loosely associated fascicles of variable size and thickness seen in various planes of section. Other fields show epithelioid-like clusters composed of smaller nests of spindle cells. Individual neoplastic cells contain oval to fusiform nuclei with prominent large macronucleoli.

The nuclear to cytoplasm ratios are elevated. Mitotic figures are frequently encountered. The cytoplasm tends to be clear with some cells showing amphophilic cytoplasm (Fig. 4).


Figure 4   Under simple H&E (Hematoxylin–eosin) stains.  Slide 1 in low power, reveals melanoma cells around a Pacinian corpuscle.  Slide 2 in higher power, shows mitotic figures (arrow) in center with multiple, macronucleolus and fusiform nuclei within the tumor cells.  Slide 3 reveals predominant spindle cells to the neoplasm.  The cells are arranged as loose, cohesive aggregates and epitheliod like clusters of smaller nests of spindle cells.

The battery of immunostains is microscopically evaluated showing conspicuous positive reactions for Mart-1, HMB45, S-100 and vimentin. The pan cytokeratin is negative in the tumor cells with appropriate internal and external positive controls. The CD10 stain shows minimal, nonspecific cystoplasmic decoration. The Mart-1 immunostain uses peroxidase, which stains cancerous cells a brown color. This has been fairly specific for detection of malignant melanoma. (Fig. 5)


Figure 5   Immunoperioxidase stains using Mart-1 is highly specific for melanoma.  Melan-A immunoperoxidase stains melanoma cells brown.  The brown staining on these slides is considered positive for malignant melanoma. 

This case was deferred to M.D. Anderson Cancer Center of Houston and reviewed by Dr. Harry Evans. Submitted stains for S-100, MART-1 and HMB-45 were positive with negative keratin consistent with clear cell sarcoma. The t(12;22) chromosomal translocation was not reported.


This case highlights the challenges of early detection of CCS. This is especially true of the foot. More troubling is the fact that the plantar aspect of the foot is often a common site for malignant melanoma. [4,7] This tumor appears to have been in-situ for many years without radical growth before a more rapid increase in size and associated pain. Any recent change in a soft tissue nodule, change in symmetry of the tumor or any suspicious soft tissue mass along the ankle or foot may present clear cell sarcoma as a differential diagnosis.

There are now specific immunoreactive markers used to delineate clear cell sarcoma. More specifically, S-100 and HMB-45 are used to differentiate clear cell sarcoma from epithelial tumors, and more specifically, synovial sarcoma. Although the absence of keratin with positive S-100 and HMB-45 immunostains is often associated with the primary diagnosis of CCS, faint keratin immunoreactivity has been observed in clear cell sarcoma.

Therefore, keratin positivity does not rule out CCS. [6] More recently, molecular genetic characterization of clear cell sarcoma has shown to be specific for t(12;22) chromosomal translocation which is typically not present in cutaneous malignant melanoma. [5] However, the t(12;22) chromosomal translocation may not always be identifiable in some cases.

In 2002, a CCS was established from a metastatic tumor of a 17-year-old Japanese girl that originated in the left Achilles tendon. A small number of melanosomes were detected in the cytoplasm by electron microscopy. In this particular case, there was no t(12;22) chromosomal translocation identified although Melan-A and HMB-45 were reactive. [8] As demonstrated by cytogenetics and reverse-transcriptase polymerase chain reaction, generally between 70 percent and over 90 percent of clear cell sarcomas have a t(12;22) translocation, fusing the EWS and ATF1 genes on chromosomes 22q12 and 12q13 respectively. [9]

Typically, once clear cell sarcoma is diagnosed, the patient will undergo CT and PET scans. If there is a high suspicion of metastasis, sentinel lymph node biopsy (SLNB) is usually scheduled. Lymph node metastasis has been reported in a high number of cases, so sentinel lymph node biopsy is now indicated with the diagnosis of CCS. [6]

Recently published data suggests that baseline laboratory testing such as LDH, liver function studies and imaging studies such as chest x-rays, CT, MRI, PET and bone scanning is not typically beneficial in early stage melanomas without signs or symptoms of metastasis. However, LDH have been incorporated into the AJCC (American Joint Committee on Cancer) 2002 melanoma staging guidelines for the classification of stage IV or distant disease. Elevated LDH levels are associated with the worst prognosis and survival in this subgroup. [1]

In this particular case, the tumor was initially excised and a larger margin of tissue will need to be removed. This will likely include wide excision with split thickness skin grafting. Sentinel node biopsy is highly recommended in all cases of diagnosed CCS due to the propensity of lymph node metastasis.


In general, CCS has a high propensity of lymph node metastasis and the prognosis is dismal once metastasis occurs. However, it does appear from multiple literature reviews, that tumors less than 2 cm have a generally better long term prognosis. Deenik, et al, reviewed 30 cases of clear cell sarcoma which revealed a 5 year survival rate of 54 percent in 29 patients. [6] Unfortunately, when the sentinel node biopsy is positive, distant metastasis appeared within 2 years, even after radical lymph node dissection in all cases. Chemotherapy has not had an appreciable effect on CCS, but remarkable responses to interferon -2b have been reported. [6,7] In this same study, 7 of 14 patients with tumors greater than 2 cm had a 50 percent survival rate. [6]

In another study, Sara, et al, reported both survival and distant metastasis were correlated with tumor size (P value less than 0.01 for patients with tumors greater than or equal to 5 cm versus less than 5 cm) in 17 cases. Other clinical and pathologic factors had no significant relation to survival or distant metastasis when tumor size was greater than 5 cm. [7]

A Mayo Clinic study of 35 cases showed tumor size and the presence of necrosis as statistically significant predictors of prognosis. Twelve patients with tumors measuring over 5 cm were either living with the disease or died. Eleven of twenty patients with tumors measuring less than 5 cm were alive with no evidence of disease. Tumor necrosis was present in 10 cases; 8 of these patients died of the disease and one was alive with disseminated metastases. [10]

Although there have been reports of poor response with chemotherapy, there have also been reports of amputation of the diseased limb, even in the presence of metastasis. In 1983, Eckardt reported 27 patients ranging in age from 9 to 57 years and were followed an average of 7 years. [11] Females outnumbered males by 2 to 1 and the distal extremity location predominated. At presentation, the tumor was localized in 21 patients, regionally metastatic in 5, and disseminated in 1. Surgery was the primary therapy for 26 patients and adjuvant treatment was nonstandardized. Its effectiveness is undetermined. Local recurrence developed in 10 patients, regional metastases in 9, and widespread dissemination in 12. Twelve patients died of the disease from 7 months to 10 years after diagnosis and only 11 patients remained free of disease. They reported that wide excision, or perhaps even radical excision or amputation, is the surgical treatment of choice. [11]


This case describes a solitary, subcutaneous lesion that histologically represents clear cell sarcoma or malignant melanoma of soft parts. The diameter of this tumor is over 2 cm and less than 5 cm. However, more aggressive resection of tissue and lymph node biopsy is required to map the tumor margins and rule out metastasis. This patient had previous nevi and a similar nodule located on the neck that may reveal other malignancy. This patient is presently under further investigation and testing for primary sources of the tumor and evidence of metastasis. At the time of this writing, the PET and CT scans were negative, so the overall, long-term prognosis is promising.


1. Swetter, S.M., et al: Malignant Melanoma. Emedicine online [online].
2. Katabuchi, H, el al: Clear cell sarcoma arising in the retroperitoneum. In J Gynecol Cancer: 12(1): 124-127, Jan-Feb, 2002.
3. Finley, et al: Clear cell sarcoma: the Roswell Park experience: Journal of Surgical Oncology, 77(1):16-20, May 2001.
4. Fortin, PT, et al. Malignant melanoma of the foot and ankle. JBJS (Am), 77:1396-1403, 1995. [PDF]
5. Fujimura, Y., el al: The EWS-ATF-1 gene involved in malignant melanoma of soft parts with t(12;22) chromosome translocation, encodes a constitutive transcriptional activator. Oncogene 12: 159-167, 1996.
6. Deenik, W. et al: Clear cell sarcoma (malignant melanoma) of soft parts: A clinicopathologic study of 30 cases. Cancer 86(6): 969-975, September 1999.
7. Sara, AS, et al: Malignant melanoma of soft parts (clear cell sarcoma). A study of 17 cases, with emphasis on prognostic factors. Cancer, 65 (2): 367-374, January 1990.
8. Moritake, H. et al: Newly established clear cell carcinoma (malignant melanoma of soft parts) cell line expression melanoma-associated Melan-A antigen and overextpressing C-MYC oncogene. Cancer Genet Cytogent, 135(1):48-56, May 2002.
9. Patel, RM, et al: Dual-color, break-aparat fluorescence in situ hybridization for EWS gene rearrangement distinguishes clear cell sarcoma of soft tissue from malignant melanoma. Mod Pathol. 18(12):1585-1590, December 2005.
10. Lucas, et al: Clear cell sarcoma of soft tissues. Mayo Clinic experience with 35 cases. Am J Surg Pathol: 16(12): 1197-1204, December 1992.
11. Eckardt, JJ, et al. Clear cell sarcoma. A clinicopathologic study of 27 cases. Cancer. 52(8): 1482-1488, October 1983.
12. Strayer, S.M., Reynolds, P. Diagnosing skin malignancy: Assessment of predictive clinical criteria and risk factors. The Journal of Family Practice. Vol. 52, No.3, March 2003 [online].

Special thanks to Kenneth Linville, MD and Michael Bailey, MD in preparing the slides. Thanks to Harry Evans, MD from MD Anderson Cancer Center for review of this case.

Case Report Update

Since the patient’s original surgery, the patient was sent to San Antonio, Texas for additional surgery and skin grafting (Fig. 6)


Figure 6  3 months after the patient’s original surgery, she underwent additional wide excision including rotational full thickness graft with STSG of the arch.  

The patient underwent a single surgery including sentinel node biopsy (groin) and wide excision with rotational skin flap and split thickness skin graft. This was performed by a surgical oncologist and plastic surgeon. The initial wide excision was performed by the surgical oncologist who noted the tumor tissue extending into the longitudinal arch. The plastic surgeon, on the same day of surgery, performed the rotational flap and STSG to cover the defect. Sentinel node biopsy was positive and the patient refused additional surgery to remove all the inguinal lymph nodes. About 2 months after surgery, she underwent radiation treatment to the foot. Complications of treatment included slight infection of the graft edges and “blisters” of the foot.

The heel portion of the rotational graft was sensitive and took some time to desensitize. She was placed in a total contact cast during this recovery period. Since that time, she has had some residual swelling of the foot and ankle that is responding to local compression bracing.

Her long term prognosis is hopeful. It has already been one year since the initial surgery and additional node biopsies are still a consideration.

Address correspondence to: Dr. Al Kline, DPM, 3130 South Alameda, Corpus Christi, Texas 78404. Email: Al@Kline.net 

1Adjunct Clinical Faculty, Barry University School of Podiatric Medicine. Private practice, Chief of Podiatry, Doctors Regional Medical Center. Corpus Christi, Texas, 78411.

© The Foot & Ankle Journal, 2008

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Kaposi’s Sarcoma of the Foot: A Case Report

by Al Kline, DPM 1

The Foot & Ankle Journal 1 (3): 1

A case of ulcerated, classic Kaposi Sarcoma (KS) of the foot is described. This is a tumor of vascular endothelial origin which most commonly present in men 50-70 years of age. This case report includes presentation and discussion of differential diagnosis, surgical removal, histopathology interpretation, incidence of metastasis and treatment.

Key words: Kaposi’s Sarcoma, Metastasis, Ulcerated KS, Classic KS, Pedunculated KS

This is an Open Access article distributed under the terms of the Creative Commons Attribution License. It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot & Ankle Journal (www.faoj.org)

Published online: March 1, 2008

ISSN: 1941-6806/08/0103-0001
doi: 10.3827/faoj.2008.0103.0001

Kaposi’s sarcoma (KS) was first described by Hungarian dermatologist Moritz Kaposi in 1872. [1,2] Kaposi first described the lesions as “idiopathic, multiple pigmented sarcoma of the skin”. Kaposi’s sarcoma is a spindle cell tumor of endothelial origin. It is commonly associated with the endothelial lining of blood vessels. In the early 1980’s, KS was commonly associated with the AIDS epidemic. Four types of Kaposi’s sarcoma have been described that include epidemic AIDS related Kaposi’s Sarcoma, Immunocompromised KS, Endemic African KS and Classic KS. The classic KS is the only form not associated with the AIDS epidemic. In the past two decades, with the improvement in AIDS medication and treatment, the incidence of AIDS related KS has decreased by 90%. [1]

Classic KS was first described as most prevalent in elderly Jewish, Mediterranean men between the ages of 50-70 years. [1,3] The ratio of KS in men to women is 15:1. [1] The highest incidence of KS is reported in Sicily.

In the lower extremity, the lesion is most commonly associated with venous stasis and lymphedema. However, lesions on the plantar surface of the foot are rarely associated with edema which complicates this classic description. The lesions are usually violasceous, red to pink in color. Almost all cutaneous lesions are raised, non-pruritic and symmetrical. The histopathology of KS reveals excessive spindle-cell proliferation throughout the endothelium. Human Herpes Virus 8 (HHV-8) has been identified in over 90% of all KS tumors, suggesting a causative role. [2] The incidence of KS of the foot is rarely reported. This report describes a case of ulcerated, classic Kaposi’s sarcoma of the foot is described.

Case Report

A 71 year old male presents to our office on consultation with a “growth” to the bottom of the left foot. (Figs. 1abc)


Figures 1abc The Kaposi’s tumor measuring 30mm in diameter.  This circular soft tissue tumor of endothelial origin is macerated from occlusive dressings placed over the lesion.  A smaller lesion is noted along the plantar, medial border of the foot along the first MPJ.

The patient and family report he has had this lesion for a number of years. It recently became more macerated with ‘bleeding’ due to its size and location on the bottom of the foot. The patient has no history of allergies. His medications include Gabapentin, Metformin, Trental, Glipizide, Metaprolol and Lisinopril. He has type 2 diabetes, hypertension and has undergone previous vein stripping. His physical examination reveals a well nourished male with palpable pulses. Minimal edema was noted to his extremities with some pretibial pitting edema.

The patient has been covering the growth with a large, occlusive bandage that caused significant maceration of the lesion. The patient also had a smaller lesion along the medial distal foot. The patient had the lesion on the bottom of the foot for over two years without discomfort. The lesion is macerated and vascular in appearance, pedunculated and attached to a ‘stalk’. (Fig. 2) MRI of the foot revealed a cutaneous soft tissue growth not extending into subcutaneous fat. (Fig. 3) The patient was taken to surgery to remove both lesions by simple excision.

Figure 2 The tumor is attached to a stalk or pedicle.

Figure 3 The pedunculated tumor is located in the acral skin with nodular proliferation of the dermis.

The patient was brought to the operating room and under local, IV sedation, the lesions were elipsed and removed. Simple horizontal mattress sutures were used to close the excision sites. A simple dressing was dispensed and the region healed without complication. To date, there has been no recurrence of the tumors.


The histological characteristic of KS does not vary between the different clinical types, but the progressive nature of the tumor varies. Early lesions show spindle cell proliferation within the interstitium of the upper dermis close to the vascular plexus. [4] Nodular lesions are characteristic of older and more progressive tumors.

The surgical specimens were sent in formalin-filled containers. Microscopic sections and step-sections show a biopsy of acral skin and ulceration. In the dermis, there is a nodular dermal proliferation of atypical spindle cells arranged in nests and fascicles. (Fig. 4) Within the spindle cell proliferation, there are slit-like vascular spaces with extravasation of red blood cells. (Fig. 5)

Figure 4 Under simple H&E (Hematoxylin–eosin) stain, magnification x 20.  Lesional cells stained positive with CD31 and focally with CD34.

Figure 5 High power view of lesional cells.  Note extravasation of red blood cells in slit-like spaces, magnification x 400.

Slit-like vascular spaces containing erythrocytes are typical of the histologic characteristics of KS. These split-like spaces with extravasation sporadically display features of lymphangioma. [4] Immunoperoxidase stains consisting of HHV-8 and S-100 were performed at the Baylor College of Medicine reference laboratory. This report confirms atypical spindle cells demonstrating nuclear positivity for HHV-8 and negative for S-100. This renders the final diagnosis as ulcerative Kaposi’s sarcoma.


Our case describes an isolated, pedunculated and ulcerated classic Kaposi’s sarcoma of the foot with a smaller secondary lesion. The ulcerated type of KS appears to be rare with infrequent reports in the literature. The etiology of this type of lesion is unknown. The tumor has been associated with venous stasis and lymphedema. Our patient had signs of venous congestion and lymphedema, but the tumors location is atypical of this association. In recent studies, the tumor is now associated with human herpesvirus- 8 (HVV-8) or commonly called Kasposi sarcoma herpesvirus (KSHV). [2,4]

It is one of the few viruses now proven to be associated with tumorigenesis in humans. [4] The lesions also appear to be associated with immunosuppression. It could be theorized that classic KS arises in elderly men from some form of immunosuppression or compromise. For example, patients who undergo organ transplants and take rejection drugs to suppress the immune system are 150-200 times more likely to ‘acquire’ Kaposi’s sarcoma. [1]

Commonly, the cutaneous lesions of KS are more diffuse and violasceous in color and distribution. However, the clinical presentation can vary greatly. The differential diagnosis should include acroangiodermatitis, port wine stains of the extremities, Sturge Weber Syndrome, nodular malignant melanoma, angiosarcoma, hemangioma, dermatofibroma, pyogenic granuloma or purpura. [1,2,3]

Treatment of classic KS can vary from simple surgical removal of the lesions to radiation treatment. If lesions are solitary, as in this case, surgical excision of the lesion is the best form of treatment. Brenner, et al, reported 52 patients who underwent primary excision for solitary lesions, 56% had no recurrence of lesions in a median of 15 months. [8] If the classic KS is diffuse, irradiation of water while the legs are submerged in a water tank appears to be an accepted treatment. [3] However, recurrence of lesions seems to be more common when the lesions are diffuse. Isolated lesions are best treated by excision, laser and surgical cauterization. Intralesional interferon injection is still considered controversial. [4] Cryotherapy can be used for superficial lesions but are likely to recur. [3]

In one report, cyrotherapy has been shown to be 70% effective for superficial lesions. [4] Occasionally, the lesions and disease may regress spontaneously. [7]

Incidence of metastasis varies in the literature. Some report that classic KS rarely metastasize. [1] Another report suggests that up to one-third of patients with classic KS develop a secondary primary malignancy, most often non-Hodgkins lymphoma. [3] Other reports suggest that over 35% of patients with the disease of more than 15 years may develop secondary malignancies such as leukemia, myeloma and lymphomas. [4,5,6] It appears that cases should be handled individually and risk should be assessed by the number of lesions and their location. Classic KS rarely disseminate and cause visceral or mucous membrane tumors. Dissemination is seen in less than 10% of the patients with KS. [4] Certainly, if widespread visceral involvement is diagnosed, combination treatment including Chemotherapy, radiation treatment, surgical excision of lesions and conservative care is recommended. [4]

This report describes an unusual case of ulcerated Kaposi’s sarcoma of the foot. Simple excision of the lesion was recommended without further cutaneous or systemic treatment. A smaller lesion on the foot was also removed which was consistent with KS. The surgeon has a variety of options for treatment of such lesions. In this case, surgical excision was the procedure of choice and the region healed without complication. (Fig. 6)

Figure 6   A few weeks after excision of tumor.

Inspection of the patients mucous membranes revealed no other suspected, discolored or violasceous plaques. We have recommended the patient undergo routine colonoscopy to rule out any visceral involvement.


1. American Cancer Society: What is Kaposi Sarcoma, [online], 2008.
2. Fishman, A., Sparano, D.: Kaposi Sarcoma. eMedicine [online], 2008.
3. Dubilier, L.D., Joffe, E.: Case report: Classic Kaposi’s sarcoma, JAAPA, 18 (7), July, 2005. [PDF]
4. Phillips, T.J.: Kaposi’s Sarcoma,Wounds 13 (6): 237-240, 2001. [Online]
5. Piette WW. The incidence of second malignancies in subsets of Kaposi’s sarcoma. J Am Acad Dermatol :16:855, 1987.
6. Safai B, Goo RA. Kaposi’s sarcoma: A review and recent developments. Cancer: 44:419-33. 1981.
7. Chang Y, Cesarman E, Pessin MS, et al. Identification of herpesvirus-like DNA sequences in AIDS-associated Kaposi’s sarcoma. Science 266: 1865-1869, 1994.
8. Brenner B, Rakowsky E, Katz A, Gutman H, et al. Tailoring treatment for classical Kaposi’s sarcoma: Comprehensive clinical guidelines. Int j Oncol: 14 (6), 1097-1102, 1999.

Address correspondence to: Dr. Al Kline, DPM, 3130 South Alameda, Corpus Christi, Texas 78404. Email: Al@Kline.net 

1Adjunct Clinical Faculty, Barry University School of Podiatric Medicine. Private practice, Chief of Podiatry, Doctors Regional Medical Center. Corpus Christi, Texas, 78411.

© The Foot & Ankle Journal, 2008

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