Kaposi’s Sarcoma

Kaposi’s sarcoma otherwise known as (KS) is a low-grade tumor associated with the vascular. It derives or is from human herpesvirus 8 (HHV-8) which is also known as KS-associated herpesvirus (KSHV). There are currently four recognized forms of Kaposi’s sarcoma.

  1. Class Kaposi’s sarcoma known to be an indolent cutaneous proliferative disease that seems to affect older men of Mediterranean and Jewish origins.
  2. Endemic or African Kaposi’s sarcoma. This isn’t associated with an immune deficiency and is found in all parts of equatorial Africa, in particular, sub-Saharan Africa.
  3. Organ transplant associated Kaposi’s sarcoma occurs after an organ transplant. It is possible for the transplant process to be responsible for the HHV-8 infection.
  4. AIDS-associated or epidemic Kaposi’s sarcoma. KS or kaposi’s sarcoma is the most usual type of tumor to pop in HIV-infected persons and marks itself as an AIDS-defining illness according to the Centers for Disease Control and Prevention (CDC) guidelines. KS is 20,000 more times likely in one with AIDS. KS is also 300 times more common in AIDS patients than other immunodeficient hosts such as renal transplant patients.

KS is not as common in women than it is in men. Numbers indicated that men are showing KS both classic and AIDS-related 15 times more than woman. Those also more associated with KS will be homosexual and bisexual men. In other words, AIDS-related KS is not found as much in heterosexual injection users, transfusion recipients, women or children and hemophiliacs.

Interesting statistics prove:

  1. Due to safer sexual practices between 1983 to 1988 in gay and bisexual AIDS patients, KS decreased from 40 percent to 13 percent respectively.
  2. Changes in incident rates of KS have been recorded for the years from 1973 to 1998. In 1973 there were 0.5 people infected per 100,000 to 31.3 and 33.3 from 1987 and 1991 but ending at 2.8 per 100,000 in 1998.
  3. With patients on HAART therapy, KS has decreased significantly in HIV patients. A ratio considering incidence standardized showed a rate of 22,100 without HAART therapy that decreased to 3,640 with HAART therapy.

However, in San Francisco, the prevalence of KS remained constant from 1978/79 through 1984/85 and 95/96 with an average infection rate of 27.5 percent. When considering Europe, Australia and North America with 47,936 HIV persons total, the incidence rates for KS fell from 15.2 to 4.9 situations per 1000 person years between 1992-1996 and 1997-1999 respectively.

One is more likely to become KS infected if they are

  1. HIV infected
  2. Have increasing anti-HHV-8 antibody titers
  3. Present with HHV-8 viremia
  4. Lack neutralizing antibodies

The best marker for likely Kaposi’s sarcoma with HHV-8 is one’s HIV status. Risk was determined in San Francisco when 593 men who have sex with men had a 38 percent infection rate compared to not one case in 195 heterosexual men. Patients with both HIV and HHV-8 had a 50 percent chance of developing Kaposi’s sarcoma within 10 years. Ten-year risk was lower at 30 percent for individuals with only HIV and no HHV-8 at baseline. No cases of KS were seen in those without HIV, making Kaposi’s sarcoma primarily an infection of gay HIV positive men.

A progressive positive relationship between CD4 count and development for Kaposi’s sarcoma exists. Counts below 200 in 70 patients had a rate of 18.9 while those with CD4 counts between 200 and 349 had a rate of 3.6 and those with a CD4 count of 350-499 cells/mm3 had a rate of 4.1.

Progression to Kaposi’s sarcoma in was discovered in 336 HIV positive patients. The study showed higher antibody titers to HHV-8 as more likely to come down with Kaposi’s sarcoma unless these patients have other AIDS-defining diseases. In addition, if HHV-8 is found within the peripheral blood, a 10 fold relationship exists for likely hood to develop Kaposi’s sarcoma. A lack of  neutralizing antibodies to HHV-8 is also found among Kaposi’s sarcoma infected HIV individuals.

Histology associated three traits of Kaposi’s sarcoma: angiogenesis, inflammation and proliferation. To see pictures of what Kaposi’s sarcoma looks like click here on Kaposi’s sarcoma pictures.

Lesions generally display two major differences: whorls of spindle-shaped cells with leukocytic infiltration and neovascularization with aberrant proliferation of small vessels.
These small vessels lack a basement membrane and display leaky behavior with microhemorrhages and hemosiderin deposition. As the disease goes on, it changes from patches to plaques and eventually into a nodular form.

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