Medical Care

Because the natural history of Kaposi sarcoma (KS) is variable, assessment of therapy may be difficult. Treatment usually is based on the extent of disease and the patient's immune status. The optimal therapy of KS-AIDS is yet to be determined. The challenge is to treat KS-AIDS effectively without immunocompromising the patient further, or better, with reconstitution of the immune system.

Management modalities for Kaposi sarcoma include nonintervention, surgical removal of skin nodules or severely affected areas (eg, areas of the extremities, intussuscepted bowel), laser surgery, conventional and megavoltage radiotherapy, chemotherapy, immunotherapy, antiviral drugs, and cessation of immunosuppressive therapy in iatrogenically immunosuppressed patients.

Indolent skin tumors in elderly white patients may not require specific therapy early in the course of the disease; however, systemic vinblastine (or other chemotherapy) attacks both cutaneous and visceral lesions.

Localized nodular disease may respond well to surgical excision, radiotherapy, and intralesional and outpatient low-dose vinblastine chemotherapy. The latter combination of local and systemic regimens may be preferable. The authors usually inform patients that this is a multicentric disease that has silent gut lesions that also may regress with the systemic approach. Although the authors prefer intralesional vinblastine, intralesional vincristine as first-line therapy for nodules in classic Kaposi sarcoma has also been recommended.^[67]

The efficacy of taxanes (eg, paclitaxel, docetaxel), as agents with antiangiogenic properties, has been shown for patients with AIDS-associated Kaposi sarcoma and in those with refractory or life-threatening Kaposi sarcoma without HIV infection.^[68]Pegylated liposomal doxorubicin is now being used as a second-line therapy in the treatment of patients with advanced classic Kaposi sarcoma.^[69]

Limited experience for classic and HIV-related cutaneous Kaposi sarcoma treated with 0.1% topical timolol gel has shown that it can be beneficial.^[70]

Radiotherapy is an option for some Kaposi sarcoma patients. Radiotherapy often produces good therapeutic results with classic nodular Kaposi sarcoma but tends to be only palliative in patients with Kaposi sarcoma and AIDS. In localized nodular Kaposi sarcoma, conventional radiotherapy is highly effective.

Electron-beam radiotherapy, which has limited penetration beyond the dermis, may be a good modality for superficial lesions.

Deeper or unresponsive Kaposi sarcoma may be treated using standard non–electron-beam radiation or other options.

Initial response to radiotherapy usually is complete or demonstrates marked regression of the nodules. The more extensive the involvement, the less responsive it tends to be.

Radiotherapy may be more effective on new, rather than chronic, lesions and may provide local Kaposi sarcoma control in patients with KS-AIDS.

Radioisotope scanning using technetium Tc 99m may detect occult Kaposi sarcoma infiltration in the subcutaneous and muscular tissues and draining lymph nodes. This allows improved efficiency of large-field radiotherapy.

Argon laser photocoagulation therapy also may be beneficial in classic Kaposi sarcoma lesions. Similarly, classic Kaposi sarcoma may favorably respond to long-pulse neodymium-doped yttrium aluminum garnet laser therapy.^[71]

Surgical Care

Solitary Kaposi sarcoma lesions may be excised surgically or removed using laser surgery.

Consultations

Treating patients with advanced Kaposi sarcoma often requires a team approach, as follows:

Medical oncologists often administer systemic chemotherapy.
Radiation oncologists tend to favor radiotherapy options.
Infectious diseases/HIV specialists may be needed for HIV and opportunistic infections.

Prevention

Reducing the HHV-8 infection rate prevents Kaposi sarcoma development.

Suggestions have been made that some antiherpetic agents, particularly foscarnet, may lower the HHV-8 infection rate.

Screening transplant recipients for HHV-8 infection may be beneficial.^{[72, 73, 74, 75, 76]}Testing donors and recipients for HHV-8 is difficult, as there are no validated commercial serology kits available; however, limited HHV-8 antibody testing is available through some US reference laboratories and the US Centers for Disease Control and Prevention.^[77]Many US donors originate from groups at high risk of HHV-8 transmission to recipients.

Use of the highly active anti-HIV therapy (ie, HAART) appears to significantly reduce the risk of developing new Kaposi sarcoma.^[30]

Long-Term Monitoring

Careful follow-up monitoring is essential for patients with Kaposi sarcoma (KS).

Medication

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Media Gallery

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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Author

Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Professor of Pediatrics, Professor of Medicine, Rutgers New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, New York Academy of Medicine, Royal College of Physicians of Edinburgh, Sigma Xi, The Scientific Research Honor Society

Disclosure: Nothing to disclose.

Coauthor(s)

W Clark Lambert, MD, PhD Clinical Professor of Pathology, Clinical Professor of Medicine (Professor of Dermatology), Rutgers New Jersey Medical School; Professor of Pathology, Rutgers Graduate School of Biomedical Sciences

W Clark Lambert, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, American Dermatological Association, American Federation for Clinical Research, American Society of Dermatopathology, College of American Pathologists, Dermatological Society of New Jersey, Institute of Electrical and Electronics Engineers, International Academy of Pathology, International Federation of Pigment Cell Societies, International Society of Dermatopathology, Medical Society of New Jersey, Sigma Xi, The Scientific Research Honor Society, Society for Investigative Dermatology, Xeroderma Pigmentosum Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Michael J Wells, MD, FAAD Dermatologic/Mohs Surgeon, The Surgery Center at Plano Dermatology

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

Disclosure: Nothing to disclose.

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

Christen M Mowad, MD is a member of the following medical societies: Alpha Omega Alpha, Noah Worcester Dermatological Society, Pennsylvania Academy of Dermatology, American Academy of Dermatology, Phi Beta Kappa

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

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

Disclosure: Nothing to disclose.

Additional Contributors

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, Women's Dermatologic Society, National Psoriasis Foundation, American Medical Association, Phi Beta Kappa, Sigma Xi, The Scientific Research Honor Society

Disclosure: Received honoraria from Amgen for consulting; Received honoraria from Abbott for consulting; Partner received salary from Merck for management position; Received honoraria from Abbott for speaking and teaching; Received honoraria from Amgen for review panel membership; Received honoraria from Centocor for consulting; Received honoraria from Leo for consulting; Received none from Merck for other.