Tuesday, February 14, 2012

Kaposi Sarcoma

Kaposi sarcoma is a tumor caused by Human herpesvirus 8.  It has been known widely as the Aids defining illness in the 1980's.  Persons with a severely weakened immune system are easily susceptible to this sarcoma.

                                                     Kaposi Sarcoma on skin

                                                        Kaposi Sarcoma of the mouth

The viral cause for this cancer was discovered in 1994.  There is widespread lack of awareness of this even among persons at risk for KSHV/HHV-8 infection. 
It was originally described by Moritz Kaposi (KA-po-she), a Hungarian dermatologist practicing at the University of Vienna 1872.
Since Moritz Kaposi first described this malignant neoplasm, the disease has been reported in five separate clinical settings, with different presentations, epidemiology, and prognoses

1. Classic Kaposi Sarcoma
2. African cutaneous Kaposi sarcoma
3. African lymphadenopathic Kaposi sarcoma
4. AIDS-associated Kaposi sarcoma
5. Immunosuppression-associated Kaposi sarcoma

KS lesions are nodules or blotches that may be red, purple, brown, or black, and are usually papular (i.e., palpable or raised).
They are typically found on the skin, but spread elsewhere is common, especially the mouth, gastrointestinal tract and respiratory tract. Growth can range from very slow to explosively fast, and is associated with significant mortality and morbidity.

Blood tests to detect antibodies against KSHV have been developed and can be used to determine whether a patient is at risk for transmitting infection to their sexual partner, or whether an organ is infected prior to transplantation. However, these tests are not available except as research tools, and, thus, there is little screening for persons at risk for becoming infected with KSHV, such as transplant patients.

If you have been diagnosed with KSHV by biopsy and the tissue is prepared by a histologist and read under the microscope by a pathologists.  CD4 and viral loads are performed on blood samples.

CD4 cells are a type of lymphocyte (white blood cell). They are an important part of the immune system. CD4 cells are sometimes called T-cells. There are two main types of CD4 cells. T-4 cells, also called CD4+, are "helper" cells. They lead the attack against infections. T-8 cells (CD8+) are "suppressor" cells that end the immune response. CD8 cells can also be "killer" cells that kill cancer cells and cells infected with a virus.
Researchers can tell these cells apart by specific proteins on the cell surface. A T-4 cell is a T-cell with CD4 molecules on its surface. This type of T-cell is also called "CD4 positive," or CD4.

The viral load test is a quantitative measurement of HIV nucleic acid (RNA) that provides important information that is used in conjunction with the CD4 cell count:
  • to monitor the status of HIV disease,
  • to guide recommendations for therapy, and
  • to predict the future course of HIV.
Evidence shows that keeping the viral load levels as low as possible for as long as possible decreases the complications of HIV disease, slows the progression from HIV infection to AIDS, and prolongs life.
There are several methods for testing viral load; results are not interchangeable so it is important that the same method be used each time.

you have Kaposi's sarcoma, your doctor will try to determine how far it has spread by examining you and asking you several questions:
  • Do you have a cough, or are you short of breath? (This could indicate that the cancer has reached the lungs.)
  • Do your legs swell up? (This suggests the cancer has reached lymph nodes.)
  • Do you experience nausea, vomiting, or abdominal pain? Do you have blood in your stool? (This suggests the cancer is affecting the gastrointestinal tract.)

Expected Duration

There is no cure for Kaposi's sarcoma. It is a lifelong condition. However, the symptoms will improve with treatment (such as HAART for people with HIV/AIDS.)

http://www.drugs.com/health-guide/kaposi-s-sarcoma.html or   http://www.wikipedia.org

No comments:

Post a Comment