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Therapeutic Strategies

Kaposi's Sarcoma

Timothy Berger Bruce Wintroub

Saturday, January 01, 2011


Kaposi's sarcoma (KS) results from endothelial cell proliferation caused by infection with human herpesvirus 8 and occurs in four settings: classic KS, African (endemic) KS, immunosuppressive-associated KS, and AIDS-associated KS. The therapy of each form is discussed separately.

Classic Kaposi's sarcoma (Mediterranean Kaposi's Sarcoma)

Classic KS affects primarily elderly males of Mediterranean or Eastern European Jewish extraction. Although visceral involvement is found in up to 70% of patients (primarily in the GI tract), this is usually asymptomatic, and only 20% of patients with classic KS die of their disease. For this reason, therapy is often palliative and directed at control of local symptoms. Progressive disease may require more aggressive therapy.

First Steps

  1. For localized or limited disease, local or extended-field radiotherapy is highly efficacious. Doses as low as 800 rads may be effective in a single dose. Fractionated doses at 1,200-3,000 rads are also effective. Extended- field radiotherapy will control edema as well as local lesions.
  2. Solitary or a few lesions may be treated with local destruction by cryotherapy or intralesional injections with vinblastine or vincristine 0.2-0.5 mg/ml.
  3. Alitretinoin 0.1% gel may be used for thin local lesions, although it may not be more effective than the significantly cheaper alternatives of cryotherapy or intralesional vinca alkaloids.
  4. Lymphedema may precede or accompany KS. Control of the lymphedema with elevation and support stockings is important for patients with lower-extremity lesions. Ulceration and secondary infection are not infrequent, and they require aggressive therapy with antibiotics for infection or cellulitis and local dressings.
  5. Low-dose interferon-alpha, 3 million units three times weekly, is well tolerated and over several months may lead to marked improvement and clinical remissions.
  6. For debilitating extensive cutaneous disease, symptomatic visceral involvement, and relapses after radiation therapy, systemic chemotherapy with single agents such as liposomal anthracyclines (doxorubicin and daunorubicin), low-dose paclitaxel, or combinations of vincristine and bleomycin, or doxorubicin, vincristine, and bleomycin, may be considered.

African Kaposi's sarcoma

African KS occurs in three forms in adults and children: localized cutaneous disease, localized aggressive disease (which may extend to underlying bone), and generalized disease. In areas endemic for HIV infection, AIDS-associated KS also occurs (see below).

First Steps

  1. Localized cutaneous disease is managed like localized classic KS, with radiotherapy, cryotherapy, or local vinca alkaloids injection.
  2. Localized aggressive disease and generalized disease require systemic chemotherapy.
  3. For debilitating extensive cutaneous disease, symptomatic visceral involvement, and relapses after radiation therapy, systemic chemotherapy with single agents such as liposomal anthracyclines (doxorubicin and daunorubicin), low-dose paclitaxel, or combinations of vincristine and bleomycin, or doxorubicin, vincristine, and bleomycin, may be considered. Unfortunately, many African KS patients present with quite advanced disease. Amputation may be required in patients with local cutaneous or locally aggressive disease.

Immunosuppressive associated Kaposi's sarcoma

Iatrogenic immunosuppression for connective tissue disease, malignancy, organ transplantation, or other immunosuppressive conditions have been associated with the development of KS or the worsening of stable endemic KS.

First Steps

  1. For localized disease, local measures such as radiation therapy, cryotherapy, or intralesional vinca alkaloid injections (see above), are effective.
  2. Reduce the doses of immunosuppressive agents to the minimum required. If immunosuppressives can be significantly reduced or discontinued, the KS will usually gradually regress (over many months).

Subsequent Steps

Progressive, disseminated life-threatening KS may be treated with systemic chemotherapy (see above). This is difficult in the already-immunosuppressed individual.

AIDS-associated KS

Kaposi's sarcoma may occur as an initial or later complication of HIV infection. It may appear in patients with a relatively high helper T-cell count and no other evidence of immunosuppression, or in those with advanced HIV disease. In the terminal phase of HIV infection, KS may progress rapidly. Reduction of the HIV viral load and improvement of the helper T-cell count associated with combinations of antiretroviral agents (Highly Active Antiretroviral Therapy or HAART) frequently lead to improvement or resolution of KS lesions. Visceral involvement is common, but often asymptomatic, and does not always require therapy, except in the case of pulmonary KS.

First Steps

  1. Establish the diagnosis. Skin lesions are an excellent source of diagnostic material. Biopsy the thickest nonulcerated lesion. Punch, excision, or shave biopsies (of exophytic nodules) are adequate. Do not biopsy at the edge of skin lesions, but rather in the center.
  2. Evaluate the overall status of the patient. Determine the helper T-cell count and HIV viral load, and look for HIV-associated infections and complications. Treat any treatable conditions. Institute HAART treatment. This alone is often adequate to treat AIDS-associated KS.
  3. Determine the extent and rate of progression of the HIV-associated KS. The following staging system may be used:

    Stage I: Localized cutaneous (fewer than 10 lesions, or one anatomic region);

    Stage II: Disseminated cutaneous (more than 10 lesions, or more than one anatomic area);

    Stage III: Visceral only;

    Stage IV: Cutaneous and visceral or pulmonary.

    The above stages may be further classified using these subtypes:

    Subtype A: No signs or symptoms;

    Subtype B: Systemic symptoms (fever or weight loss).

  4. For stable cutaneous disease stages I and II, A or B:
    1. Intralesional vinblastine or vincristine 0.2-0.5 mg/cc. Use 0.1-0.5 cc/lesion, not to exceed 2 mg/treatment session. Treatments may be repeated biweekly.
    2. For flat (macular) or slightly infiltrated lesions, especially those less than 1 cm in maximum diameter, cryotherapy with two freeze-thaw cycles (20-30 seconds thaw time) may be efficacious. Cryotherapy will also treat the residual lesions following radiation therapy or intralesional injection. Several treatments may be required for each lesion.
    3. Alternatively, radiation therapy is quite effective in a single dose of 800 rads or fractionated in doses of 1,000-3,000 rads. This is especially useful for painful or disfiguring lesions of the feet, penis, or face.
    4. Alitretinoin gel 0.1% may be applied to macular lesions.
    5. Subsequently, for patients with stage II-A disease and helper T-cell counts over 200/mm3, intramuscular or subcutaneous α2 interferon 30 x 06 IU/m2 three times a week results in tumor regression in slightly more than 50% of patients.
  5. For localized lymphatic and mucosal disease, radiation therapy in fractionated doses may help to control lymph node disease and the associated lymphedema. Patients with mucosal disease may require significant fractionation, as mucositis is a common complication of oropharyngeal radiation therapy for AIDS-associated KS.
  6. For systemic, visceral, or pulmonary disease stages II-B, III-A and B, and IV-A and B, systemic chemotherapy with single agents such as liposomal anthracyclines (doxorubicin and daunorubicin), low-dose paclitaxel, vinca alkaloids, or combinations of vincristine and bleomycin, or doxorubicin, vincristine, and bleomycin, may be considered. Patients without systemic symptoms (subgroup A) have a much higher response rate. Immunosuppressive effects of these agents are a significant concern. Toxicity often limits therapy.


  1. Confirm KS by tissue biopsy, especially if skin lesions are present. KS is not a clinical diagnosis.
  2. KS is rarely life-threatening, and therapy is palliative. Do not interfere with the overall health of the patient by overzealous treatment of KS.
  3. Cryotherapy may lead to local scarring and hypopigmentation.
  4. Large lesions of KS injected with vinca alkaloids may ulcerate. Ulcerated lesions heal with scarring.
  5. Hyperpigmentation may occur after vinca alkaloid injections. Cryotherapy will reduce this side effect.
  6. α-Interferon therapy frequently produces systemic symptoms (fever, chills, myalgias); these are transient.

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