Kaposi Sarcoma is a type of cancer that develops in the soft tissue. A key contributing factor to the development of this disorder is immunosuppression. Patients with immunosuppression, such as AIDS or immunosuppressed from an organ transplant, are more likely to develop Kaposi sarcoma.
It is characterized by the presence of purple lesions on the skin or enlarged lymph nodes. The etiologic cause of all types of Kaposi sarcoma is human herpesvirus-8 (HHV-8). Although it affects HIV-uninfected individuals, this condition occurs more frequently in HIV-infected patients.
Epidemiology
Most patients with classic Kaposi sarcoma are over 50 and of Eastern Mediterranean and European origin, with a male-to-female ratio of 17:1. These patients are more vulnerable to developing secondary cancers. The prevalence of patients with HHV-8 seropositivity was estimated at 10% in the Mediterranean countries and 5 to 20% in the United States.
The seropositivity incidence of HHV-8 varies globally, with 40% in Africa and 2-4% in Northern Europe, the Caribbean, and Southeast Asia. AIDS-related Kaposi sarcoma is the second most prevalent cause of malignancy in HIV patients with CD4 counts below 200 cells/mm3. Homosexual males with HIV are five to ten times more likely to develop Kaposi sarcoma.
This condition can also develop in up to 30% of HIV patients who do not receive antiretroviral therapy. The male-to-female ratio for iatrogenic Kaposi sarcoma is 3:1. Compared to individuals with solid organ transplants, patients with bone marrow or peripheral blood stem cell transplants have a significantly decreased likelihood of developing Kaposi sarcoma.
Anatomy
Pathophysiology
HHV-8 is an encapsulated double-strand DNA virus. It is transmitted through saliva in children and sexually, blood transfusions, and intravenous drug use. Infection also spreads from seropositive family members.
When HHV-8 infects endothelial cells, it activates the mTOR pathway, causes the cells to change into mesenchymal cells, and stimulates abnormal angiogenesis. The HHV-8-infected cells can survive and multiply when the immune system is suppressed and inflamed.
When the latency-associated nuclear antigen (LANA) is expressed, p53 is bound, and apoptosis is suppressed. Additionally, LANA protects against Fas-induced programmed cell death and preserves the viral episome. HHV-8 activates NF-kB and increases cytokine expression. By HHV-8, matrix metalloproteinases are increased.
Etiology
All types of Kaposi sarcoma possess the human herpesvirus-8 (HHV-8). [4] Kaposi sarcoma is caused by HHV-8, which disrupts a variety of typical cell activities and needs cofactors like cytokines or specific proteins to develop.
Primary effusion lymphoma, Castleman disease, intravascular large B cell lymphoma, angiosarcoma, inflammatory myofibroblastic tumor, and other malignancies are associated with HHV-8.
Genetics
Prognostic Factors
About 10-20 % of patients with classic sarcoma have a poor prognosis, while a significantly large percentage of individuals develop life-threatening secondary malignancies.
HIV-related sarcoma depends on the CD4 count and opportunistic infections associated. A worse prognosis is observed in patients involving visceral organs, particularly the lungs.
AIDS-related Kaposi sarcoma (KS)
Take 5 mg orally daily on Days 1 to 21 of each 28-day cycle
Kaposi sarcoma in adults who are HIV-negative
Take 5 mg orally daily on Days 1 to 21 of each 28 days cycle Dosage Modifications Neutropenia (MM)
Discontinue forever, if not able to tolerate dose of 1 mg daily Neutropenia (KS)
Day 1 of cycle: resume on a similar dose
During cycle: Carry on at the current dose Febrile neutropenia (KS)
Discontinue forever, if not able to tolerate dose of 1 mg daily Thrombocytopenia (MM)
Discontinue forever, if not able to tolerate dose of 1 mg daily Thrombocytopenia (KS) H4
If platelet count 25,000 to <50,000/mcl:
Day 1 of cycle: resume on a similar dose
During cycle: Carry on at the current dose
If platelet count <25,000/mcl:
Discontinue forever Renal impairment
Severe
Severe requiring hemodialysis (MM): decrease to 3 mg daily
Severe requiring hemodialysis (KS): decrease to 4 mg daily
Hemodialysis: Undergo sessions of hemodialysis after the procedure has concluded Hepatic impairment Multiple Myeloma
Mild-to-moderate: decrease to 3 mg daily
Severe: decrease to 2 mg daily Kaposi Sarcoma
Mild-to-severe: decrease to 3 mg daily Dosing Considerations
Get two pregnancy tests that are negative and utilize contraception
Kaposi Sarcoma is a type of cancer that develops in the soft tissue. A key contributing factor to the development of this disorder is immunosuppression. Patients with immunosuppression, such as AIDS or immunosuppressed from an organ transplant, are more likely to develop Kaposi sarcoma.
It is characterized by the presence of purple lesions on the skin or enlarged lymph nodes. The etiologic cause of all types of Kaposi sarcoma is human herpesvirus-8 (HHV-8). Although it affects HIV-uninfected individuals, this condition occurs more frequently in HIV-infected patients.
Most patients with classic Kaposi sarcoma are over 50 and of Eastern Mediterranean and European origin, with a male-to-female ratio of 17:1. These patients are more vulnerable to developing secondary cancers. The prevalence of patients with HHV-8 seropositivity was estimated at 10% in the Mediterranean countries and 5 to 20% in the United States.
The seropositivity incidence of HHV-8 varies globally, with 40% in Africa and 2-4% in Northern Europe, the Caribbean, and Southeast Asia. AIDS-related Kaposi sarcoma is the second most prevalent cause of malignancy in HIV patients with CD4 counts below 200 cells/mm3. Homosexual males with HIV are five to ten times more likely to develop Kaposi sarcoma.
This condition can also develop in up to 30% of HIV patients who do not receive antiretroviral therapy. The male-to-female ratio for iatrogenic Kaposi sarcoma is 3:1. Compared to individuals with solid organ transplants, patients with bone marrow or peripheral blood stem cell transplants have a significantly decreased likelihood of developing Kaposi sarcoma.
HHV-8 is an encapsulated double-strand DNA virus. It is transmitted through saliva in children and sexually, blood transfusions, and intravenous drug use. Infection also spreads from seropositive family members.
When HHV-8 infects endothelial cells, it activates the mTOR pathway, causes the cells to change into mesenchymal cells, and stimulates abnormal angiogenesis. The HHV-8-infected cells can survive and multiply when the immune system is suppressed and inflamed.
When the latency-associated nuclear antigen (LANA) is expressed, p53 is bound, and apoptosis is suppressed. Additionally, LANA protects against Fas-induced programmed cell death and preserves the viral episome. HHV-8 activates NF-kB and increases cytokine expression. By HHV-8, matrix metalloproteinases are increased.
All types of Kaposi sarcoma possess the human herpesvirus-8 (HHV-8). [4] Kaposi sarcoma is caused by HHV-8, which disrupts a variety of typical cell activities and needs cofactors like cytokines or specific proteins to develop.
Primary effusion lymphoma, Castleman disease, intravascular large B cell lymphoma, angiosarcoma, inflammatory myofibroblastic tumor, and other malignancies are associated with HHV-8.
About 10-20 % of patients with classic sarcoma have a poor prognosis, while a significantly large percentage of individuals develop life-threatening secondary malignancies.
HIV-related sarcoma depends on the CD4 count and opportunistic infections associated. A worse prognosis is observed in patients involving visceral organs, particularly the lungs.
AIDS-related Kaposi sarcoma (KS)
Take 5 mg orally daily on Days 1 to 21 of each 28-day cycle
Kaposi sarcoma in adults who are HIV-negative
Take 5 mg orally daily on Days 1 to 21 of each 28 days cycle Dosage Modifications Neutropenia (MM)
Discontinue forever, if not able to tolerate dose of 1 mg daily Neutropenia (KS)
Day 1 of cycle: resume on a similar dose
During cycle: Carry on at the current dose Febrile neutropenia (KS)
Discontinue forever, if not able to tolerate dose of 1 mg daily Thrombocytopenia (MM)
Discontinue forever, if not able to tolerate dose of 1 mg daily Thrombocytopenia (KS) H4
If platelet count 25,000 to <50,000/mcl:
Day 1 of cycle: resume on a similar dose
During cycle: Carry on at the current dose
If platelet count <25,000/mcl:
Discontinue forever Renal impairment
Severe
Severe requiring hemodialysis (MM): decrease to 3 mg daily
Severe requiring hemodialysis (KS): decrease to 4 mg daily
Hemodialysis: Undergo sessions of hemodialysis after the procedure has concluded Hepatic impairment Multiple Myeloma
Mild-to-moderate: decrease to 3 mg daily
Severe: decrease to 2 mg daily Kaposi Sarcoma
Mild-to-severe: decrease to 3 mg daily Dosing Considerations
Get two pregnancy tests that are negative and utilize contraception
Kaposi Sarcoma is a type of cancer that develops in the soft tissue. A key contributing factor to the development of this disorder is immunosuppression. Patients with immunosuppression, such as AIDS or immunosuppressed from an organ transplant, are more likely to develop Kaposi sarcoma.
It is characterized by the presence of purple lesions on the skin or enlarged lymph nodes. The etiologic cause of all types of Kaposi sarcoma is human herpesvirus-8 (HHV-8). Although it affects HIV-uninfected individuals, this condition occurs more frequently in HIV-infected patients.
Most patients with classic Kaposi sarcoma are over 50 and of Eastern Mediterranean and European origin, with a male-to-female ratio of 17:1. These patients are more vulnerable to developing secondary cancers. The prevalence of patients with HHV-8 seropositivity was estimated at 10% in the Mediterranean countries and 5 to 20% in the United States.
The seropositivity incidence of HHV-8 varies globally, with 40% in Africa and 2-4% in Northern Europe, the Caribbean, and Southeast Asia. AIDS-related Kaposi sarcoma is the second most prevalent cause of malignancy in HIV patients with CD4 counts below 200 cells/mm3. Homosexual males with HIV are five to ten times more likely to develop Kaposi sarcoma.
This condition can also develop in up to 30% of HIV patients who do not receive antiretroviral therapy. The male-to-female ratio for iatrogenic Kaposi sarcoma is 3:1. Compared to individuals with solid organ transplants, patients with bone marrow or peripheral blood stem cell transplants have a significantly decreased likelihood of developing Kaposi sarcoma.
HHV-8 is an encapsulated double-strand DNA virus. It is transmitted through saliva in children and sexually, blood transfusions, and intravenous drug use. Infection also spreads from seropositive family members.
When HHV-8 infects endothelial cells, it activates the mTOR pathway, causes the cells to change into mesenchymal cells, and stimulates abnormal angiogenesis. The HHV-8-infected cells can survive and multiply when the immune system is suppressed and inflamed.
When the latency-associated nuclear antigen (LANA) is expressed, p53 is bound, and apoptosis is suppressed. Additionally, LANA protects against Fas-induced programmed cell death and preserves the viral episome. HHV-8 activates NF-kB and increases cytokine expression. By HHV-8, matrix metalloproteinases are increased.
All types of Kaposi sarcoma possess the human herpesvirus-8 (HHV-8). [4] Kaposi sarcoma is caused by HHV-8, which disrupts a variety of typical cell activities and needs cofactors like cytokines or specific proteins to develop.
Primary effusion lymphoma, Castleman disease, intravascular large B cell lymphoma, angiosarcoma, inflammatory myofibroblastic tumor, and other malignancies are associated with HHV-8.
About 10-20 % of patients with classic sarcoma have a poor prognosis, while a significantly large percentage of individuals develop life-threatening secondary malignancies.
HIV-related sarcoma depends on the CD4 count and opportunistic infections associated. A worse prognosis is observed in patients involving visceral organs, particularly the lungs.
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