Dermatologic Manifestations of Kaposi Sarcoma Medication

  • Author: Robert A Schwartz, MD, MPH; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Feb 22, 2012
 

Medication Summary

The authors' preference often is the Klein[50] regimen of weekly outpatient intravenous vinblastine titered against white cell count levels to avoid falling below 4000/µL. The authors recommend intralesional injections of vinblastine for persistent cutaneous nodules and intraarterial vinblastine in certain settings for locally aggressive Kaposi sarcoma (KS). Systemic vinblastine (3.5-10 mg IV weekly with, at times, 1 intralesional injection of 0.1 mg) usually is best for both the patient with classic Kaposi sarcoma and, occasionally, patients with KS-AIDS. Treatment of classic Kaposi sarcoma may also be accomplished with topical imiquimod.[51] Limited experience in Kaposi sarcoma in renal transplant recipients suggested it may be beneficial in at least some of them.[52]

Although the authors prefer low-dose vinblastine, a number of other chemotherapeutic agents may be effective. Drugs with proven efficiency include vincristine, vinblastine, dacarbazine, doxorubicin, and actinomycin D. Alkylating agents (eg, cyclophosphamide, chlorambucil, bleomycin, doxorubicin, etoposide) also may be of value. Multiagent intravenous chemotherapy, rather than single agent usage, is preferred by some for disseminated aggressive Kaposi sarcoma. No particular combination regimen has been established yet. The combination of doxorubicin, bleomycin, vinblastine, and dacarbazine may be effective.

Alternating vincristine and vinblastine in patients with KS-AIDS can be both effective and well tolerated, but leukopenia and a propensity to opportunistic infections makes aggressive chemotherapy difficult. Patients with KS-AIDS usually succumb either to disseminated Kaposi sarcoma or to an intervening opportunistic infection within 3 years of diagnosis, regardless of the form of therapy (except with HAART therapy). All of these therapies (except low-dose vinblastine) are significantly immunosuppressive and, perhaps, accelerate the disease. Combining chemotherapy for Kaposi sarcoma with chemotherapy for HIV is an attractive option. Interferon also may be used in this way. Thus, the combination of zidovudine, interferon, and low-dose intravenous vinblastine may be used for patients with KS-AIDS.

Experimental treatments for Kaposi sarcoma and HHV-8 infections are myriad. Many come under the rubric of immunotherapy, pioneered for Kaposi sarcoma by Klein in the early 1960s. Other agents (in addition to interferon) used for immunomodulation include bovine-thymic extracts, thymosin, Imreg-l, thalidomide, endothelial growth factor inhibitor (SU5416), human chorionic gonadotropin, isoprinosine, thymopoietin, monoclonal antibodies to T-suppressor (T8) cells, BCG vaccine, cord factor, and topically administered halofuginone, an angiogenesis inhibitor that inhibits collagen type-I and matrix metalloproteinases (MMPs).[53]

The value of recombinant interferon alfa and other modalities may depend on the pretreatment immune status of the patient as the best predictor of response. The degree of reduction in the helper-inducer T-cell (T4) subpopulation as manifested in the T4:T8 ratio may correlate highest with prognosis and be a good measure of immune status for this purpose. Thalidomide therapy may be of value in non-AIDS–related Kaposi sarcoma; in 2 of 3 patients, complete remission was achieved after 12 months of treatment.[54]

In iatrogenic Kaposi sarcoma, cessation of immunosuppressive therapy may be the most effective treatment. Patients on immunosuppressive therapy, specifically corticosteroids and cytotoxic drugs, may have partial or complete regression when therapy is discontinued. If possible, immunosuppressive medication doses should be reduced or discontinued before beginning specific therapy for iatrogenic Kaposi sarcoma. Sirolimus has the advantage of decreased risk of malignancies, including Kaposi sarcoma, associated with its use compared with other immunosuppressants, namely calcineurin inhibitors, and possibly Kaposi sarcoma regression.[55, 56]

In some patients, KS-AIDS may resolve clinically with the use of HAART. Resolution of conjunctival Kaposi sarcoma after use of HAART alone has been described.[57] Antiviral therapy with foscarnet may not only reduce progression of Kaposi sarcoma in patients, but may lower its occurrence substantially in patients with HIV disease.

Patients with KS-AIDS, the most common tumor in Zimbabwe, were randomized and evaluated for the effectiveness of supportive care versus 3 intervention approaches, namely oral etoposide, a 3-drug combination, and radiotherapy, using quality of life as the primary measure of success.[58] No patient used antiretroviral therapy. Oral etoposide resulted in a significantly better quality of life and may represent a pragmatic approach to treating epidemic Kaposi sarcoma in an environment where antiretroviral drugs are not universally available.

Paclitaxel and pegylated liposomal doxorubicin were compared in a randomized trial evaluating their efficacy and toxicity.[59] Treatment with both produced significant improvements in pain and swelling in patients with advanced, symptomatic, HIV-associated Kaposi sarcoma. Three fourths of patients had also received highly active antiretroviral therapy.

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Chemotherapy agents

Class Summary

Inhibit cell growth and proliferation. Vincristine 2 mg IV alternating with vinblastine 0.1 mg/kg IV qwk is effective. Doxorubicin, an anthracycline, is used effectively as ABV combination (doxorubicin A=anthracycline [20 mg/m2 IV], B=bleomycin [10 U/m2 IV], V=vincristine [1.4 mg/m2 IV q2wk]). The combination may produce alopecia, neuropathy, neutropenia, nausea and vomiting, oral erosions, or palmoplantar erythrodysesthesia.

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Vinblastine (Alkaban-AQ, Velban)

 

Important vinca alkaloid, which is the salt of a common flowering herb, the periwinkle Vinca rosea. Inhibits microtubule formation, which in turn disrupts the formation of mitotic spindle, causing cell proliferation to arrest at metaphase.

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Vincristine (Oncovin, Vincasar PFS)

 

Salt of a common flowering herb, the periwinkle Vinca rosea. Mechanism of action is uncertain. May involve a decrease in reticuloendothelial cell function or an increase in platelet production.

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Bleomycin (Blenoxane)

 

Mixture of cytotoxic glycopeptide antibiotics isolated from a strain of Streptomyces verticillus and freely soluble in water. Glycopeptide antibiotic that inhibits DNA synthesis. For palliative measure in the management of several neoplasms.

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Doxorubicin (Adriamycin, Rubex)

 

Cytotoxic anthracycline antibiotic isolated from cultures of Streptomyces peucetius var caesius. Inhibits topoisomerase II and produces free radicals, which may cause the destruction of DNA. The combination of these 2 events can in turn inhibit the growth of neoplastic cells.

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Daunorubicin (Cerubidine, DaunoXome)

 

Inhibits DNA and RNA synthesis by intercalating between DNA base pairs.

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Paclitaxel (Taxol)

 

Mechanisms of action are tubulin polymerization and microtubule stabilization.

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Interferon alfa 2a

 

Protein product manufactured by recombinant DNA technology. Mechanism of antitumor activity is not understood clearly; however, direct antiproliferative effects against malignant cells and modulation of host immune response may play important roles. Effective option for patients with more extensive cutaneous disease that is not rapidly progressive in whom no need exists for a rapid reduction in lesions and in whom overall functional status is relatively good.

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Retinoids

Class Summary

Decrease cohesiveness of abnormal hyperproliferative keratinocytes and may reduce potential for malignant degeneration. Modulate keratinocyte differentiation. Have been shown to reduce risk of skin cancer formation in renal transplant patients.

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Alitretinoin topical

 

0.1% gel. Topical treatment for cutaneous lesions. Naturally occurring endogenous retinoid. Inhibits growth of Kaposi sarcoma by binding to retinoid receptors.

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Antiviral agents

Class Summary

Active against HHV-8 and represent an important potential intervention and prevention option.

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Foscarnet (Foscavir)

 

Use of this medication appears to be linked to a decreased risk of developing Kaposi sarcoma. Organic analog of inorganic pyrophosphate that inhibits replication of known herpesviruses, including CMV, HSV-1, and HSV-2. Inhibits viral replication at pyrophosphate-binding site on virus-specific DNA polymerases.

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Contributor Information and Disclosures
Author

Robert A Schwartz, MD, MPH  Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi

Disclosure: Nothing to disclose.

Coauthor(s)

W Clark Lambert, MD, PhD  Professor and Head, Dermatopathology, Departments of Pathology and Dermatology, UMDNJ-New Jersey Medical School

W Clark Lambert, MD, PhD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, American Dermatological Association, American Society of Dermatopathology, International Academy of Pathology, Medical Society of New Jersey, Sigma Xi, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Specialty Editor Board

Abby S Van Voorhees, MD  Assistant Professor, Director of Psoriasis Services and Phototherapy Units, Department of Dermatology, University of Pennsylvania School of Medicine, Hospital of the University of Pennsylvania

Abby S Van Voorhees, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, National Psoriasis Foundation, Phi Beta Kappa, Sigma Xi, and Women's Dermatologic Society

Disclosure: Amgen Honoraria Consulting; Abbott Honoraria Consulting; Merck Salary Management position; Abbott Honoraria Speaking and teaching; Amgen Honoraria Review panel membership; Centocor Honoraria Consulting; Leo Consulting; Merck None Other

Michael J Wells, MD  Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Christen M Mowad, MD  Associate Professor, Department of Dermatology, Geisinger Medical Center

Christen M Mowad, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Joel M Gelfand, MD, MSCE  Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania

Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology

Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

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Elderly American man of Armenian origin with characteristic violaceous plaques of the legs, a good example of classic Kaposi sarcoma.
Man who is homosexual and has HIV infection and Kaposi sarcoma.
Man who is homosexual and has HIV infection and Kaposi sarcoma.
Man who is homosexual and has HIV infection and Kaposi sarcoma.
Elderly man of Mediterranean lineage with hyperkeratotic nodule of Kaposi sarcoma on sole of foot.
Man who is homosexual and has HIV infection and Kaposi sarcoma.
Man who is homosexual and has HIV infection and Kaposi sarcoma.
Man who is homosexual and has HIV infection and Kaposi sarcoma.
A 35-year-old man with dome-shaped locally aggressive tumors, an example of exophytic Kaposi sarcoma with cavernous hemangiomalike histology.
Ecchymotic Kaposi sarcoma in a man who is homosexual.
Intermediate lesion showing moderately enlarged spindle cells, some of which line poorly formed blood vessels that open into the interstitium with extravasation of erythrocytes. Erythrophagocytosis by these spindle cells is noted in places (hematoxylin and eosin, magnification X80).
Early lesion showing increased cellularity of the dermis with slightly enlarged spindle cells of focally fine stellate blood vessels that open at their corners into the interstitium (hematoxylin and eosin, magnification X40).
Keloidal Kaposi sarcoma demonstrating features both of keloids and Kaposi sarcoma (hematoxylin and eosin, magnification X80).
Oral Kaposi sarcoma.
Kaposi sarcoma of the leg.
Late lesion showing masses of moderately atypical spindle cells in a haphazard array, some of which line poorly formed blood vessels. Many of the spindle cells show erythrophagocytosis (hematoxylin and eosin, magnification X40).
Late lesion showing atypical spindle cells, some of which are lining poorly formed blood vessels, with prominent erythrophagocytosis by the cells (hematoxylin and eosin, magnification X80).
 
 
 
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