Kaposi Sarcoma
Also written as KS.
The AIDS-defining cancers are Kaposi sarcoma, certain lymphomas and cervical cancer.
Treatment at a glance
- Start or optimise ART
Kaposi Sarcoma (KS)
- Vascular neoplasm caused by human herpesvirus 8 (HHV8) — also known as Kaposi sarcoma herpesvirus (KSHV)
- By far most common in AIDS patients ; its presence is used as a criterion for AIDS diagnosis
- Virtually all KS lesions infected by HHV8 — a γ-herpesvirus like EBV
- Transmitted sexually and via oral secretions/cutaneous exposures
- HHV8 lytic infection: virally encoded G protein induces VEGF → endothelial growth; cytokines from inflammatory cells create proliferative milieu
Read this in VASCULAR PATHOLOGY — Must-Know Notes
Kaposi Sarcoma
- Causative virus: Human herpesvirus 8 ( HHV8 , also called Kaposi sarcoma-associated herpesvirus/KSHV) — a γ-herpesvirus
- HHV8 molecular pathogenesis:
- Four epidemiological/clinical forms:
- AIDS-associated KS was the most common malignancy in HIV-positive individuals before the advent of antiretroviral therapy (ART).
- Three morphologic stages (progressive):
Read this in VASCULAR PATHOLOGY — Must-Know Comprehensive Notes
What our notes say
- The AIDS-defining cancers are Kaposi sarcoma, certain lymphomas and cervical cancer. (Internal Medicine (MBIM 4100) main exam, Paper One: 3 July 2019)
- Pseudomembranous candidiasis, hairy leukoplakia and Kaposi's sarcoma are all non-ulcerative, so the question has three possible answers. (Internal Medicine 4th Year 1st Semester CAT: HIV and the gut, liver disease and )
- Kaposi's sarcoma (a purple plaque or nodule) is the clearest non-ulcerative lesion. (Internal Medicine 4th Year 1st Semester CAT: HIV and the gut, liver disease and )
- This describes Kaposi sarcoma, which is causally linked to HHV-8, especially in immunocompromised/HIV-positive patients. (Skin & Breast Pathology MCQs: Dermatological Lesions & Diseases)
- Viruses: HPV 16/18 (cervical Ca — E6/E7 degrade p53/RB), Hep B/C (HCC), EBV (Burkitt lymphoma, nasopharyngeal Ca), HTLV-1 (adult T-cell leukaemia), HHV-8 (Kaposi sarcoma) (Oncopathology Explained CAT : Cancer Hallmarks, Carcinogens & Tumors)
- Acute lymphoblastic leukaemia, chronic myeloid leukaemia, Kaposi sarcoma and malignant ovarian teratomas account for about 50% of all cancer cases globally (Oncopathology MCQs: Test Your Knowledge on Cancer Pathology)
Study material on Kaposi Sarcoma
- VASCULAR PATHOLOGY — Must-Know Comprehensive Notes
- VASCULAR PATHOLOGY — Must-Know Notes
- VIROLOGY SEM 3 CRASHED
- Internal Medicine 4th Year 1st Semester CAT: HIV and the gut, liver disease and pancreatitis, 30 MCQs and 2 short answers
- Oncopathology MCQs: Test Your Knowledge on Cancer Pathology
- Medical Virology: Hepatitis, Viral Carcinogenesis & Oncogenic Viruses
- MCQ: Here are all 40 questions rewritten with **even A/B/C/D spread and no consecutive same-let
Practice questions on Kaposi Sarcoma
Which virus causes Kaposi sarcoma and through what molecular mechanism does latent infection promote tumour growth?
- HIV — reverse transcriptase integrates into endothelial genome activating proto-oncogenes directly
- EBV — latent membrane protein LMP1 activates NF-κB promoting endothelial proliferation
- CMV — UL16 protein activates VEGF receptor signalling in infected endothelial cells
- HHV8 — viral cyclin D homologue disrupts cell cycle controls and viral proteins inhibit p53
Answer: D. HHV8 (KSHV) causes KS. During latent infection, a viral cyclin D homologue disrupts cell cycle checkpoints and viral proteins inhibit p53, providing infected cells with growth and survival advantages. ---
A prepubertal child in sub-Saharan Africa has Kaposi sarcoma with extensive lymph node and visceral involvement. What is the expected prognosis?
- Excellent — paediatric KS responds better to chemotherapy than adult forms
- Intermediate — 50% 5-year survival with aggressive multiagent chemotherapy
- Good — visceral KS in children regresses spontaneously as immune maturation occurs
- Poor — nearly 100% mortality within 3 years for this severe endemic African form in children
Answer: D. The severe endemic African KS in prepubertal children with lymph node and visceral involvement carries nearly 100% mortality within 3 years — one of the most aggressive forms of KS. ---
A renal transplant patient on tacrolimus develops Kaposi sarcoma with mucosal and visceral involvement. What is the most appropriate first management step?
- Initiate HAART therapy targeting HHV8 replication in the transplant setting
- Start full-dose systemic chemotherapy with liposomal doxorubicin immediately
- Reduce or withdraw immunosuppression, accepting the risk of allograft rejection
- Administer interferon-γ monotherapy targeting viral replication in infected cells
Answer: C. Transplant-associated KS is driven by T-cell immunosuppression. The first step is reducing or withdrawing immunosuppression — lesions may regress spontaneously, though organ rejection is a risk. ---
The three progressive morphologic stages of Kaposi sarcoma are patch, plaque, and nodule. What does the nodular stage specifically herald?
- Transformation to frank angiosarcoma requiring different chemotherapy regimens
- Regression through immune surveillance in Classic KS as HHV8 viral load decreases
- Development of HHV8 drug resistance mutations reducing antiviral therapy response
- Lymph node and visceral involvement signalling progression from localised to systemic disease
Answer: D. The nodular stage — sheets of plump spindle cells with slitlike vascular spaces — heralds lymph node and visceral involvement, marking progression to systemic disease. ---