KAPOSI SARCOMA
Presenter: Muluse Chipo Muluti
Moderator: Dr Ngoma
Introduction
• Kaposi sarcoma (KS) is an
angioproliferative malignancy caused by
HHV-8, commonly seen in
immunocompromised individuals,
especially those with HIV/AIDS.
• It is a systemic tumor of endothelial cell
origin.
• It has Four clinical variants
• Responds to radiation and chemotherapy,
Clinical variants of KS
• classic KS
• endemic African KS
• immunosuppressive therapy–related KS
• HIV/AIDS-related KS
Classic KS
• Occurs in elderly males of eastern
European heritage.
• Predominantly arises on the legs but also
occurs in lymph nodes and abdominal
viscera.
• slow progression and has good prognosis
Classic KS
African-Endemic KS
• It occurs in people living in Equatorial Africa.
• HHV-8 infection is much more common in
Africa than in other parts of the world,
increasing the chance of KS developing.
• Males > females
• Has poor prognosis (young adults 5–8
years; young children 2–3 years)
• Four clinical patterns
African KS
African-Endemic KS patterns
a) Nodular type: benign course and resembles classic KS.
b) Florid or vegetating type: more aggressive. Nodular
extend deeply into the subcutaneous fat, muscle, and bone.
c) Infiltrative type: more aggressive has mucocutaneous and
visceral .
d) Lymphadenopathic type: children and young adults.
confined to lymph nodes and viscera, also involves the skin
and mucous membrane.
Iatrogenic Immunosuppression-
Associated KS
• It is rare.
• Most commonly in solid-organ transplant
recipients
• chronic use of immunosuppressive drugs
• Resolves on cessation of immunosuppression.
HIV/AIDS-Associated KS
• AIDS increases risk of KS ( 20,000 times that those
not infected with HIV)
• This occurs more often in men than in women
• Common in homosexual men
• Rapid progression, extensive systemic involvement
• HIV-1 associated Kaposi sarcoma has high
occurrence in homosexual men.
• Most cultures of these tumors yield cells with
properties of hyperplastic endothelial cells
• KS of the bowel and/or lungs is responsible for
numerous deaths
Route of Infection
• KSHV appears to be shed in saliva independent of
subjects immune status
• Viral DNA is detected in breast milk samples in African
patients.
• HHV 8 infects dividing B cells CD45+phase
• Sexually transmitted among men who have sex with
men. Who have higher prevalence ( 30- 60%)
• Infections are common in Africa (>50%) with infections
acquired early in life by nonsexual routes, through
contact with oral secretion
Pathogenesis
• HHV-8 causes KS by infecting endothelial
and immune cells, evading immune
detection, and promoting angiogenesis via
VEGF. It suppresses apoptosis through
LANA-1 and cytokines, leading to
uncontrolled cell growth. Immune
suppression (e.g., HIV, transplant drugs)
creates a favorable environment for KS
development.
Clinical manifestation
• Mucocutaneous lesions are usually
asymptomatic
• lower extremities - edema and moderate
to severe pain
• Urethral or anal canal lesions- obstruction
• Pulmonary KS - bronchospasm, intractable
coughing, shortness of breath, progressive
respiratory failure.
Skin Lesions (Most Common Presentation)
• Color: Pink, red, purple, or brown macules,
plaques, or nodules.
• Distribution: Common on lower limbs, face (nose,
ears), and genitalia.
• Progression: Begins as flat macules, later forming
raised plaques and nodular tumors.
• Usually painless and non-pruritic, but may
ulcerate in advanced cases.
Mucosal Involvement
• Oral KS: Common in AIDS-associated KS,
affecting the hard palate, gingiva, and tongue.
• Symptoms include bleeding, pain, and
difficulty eating.
Oral kaposi sacroma
Lymphatic System Involvement
• Causes lymphedema, especially in the lower
limbs and genitalia.
• Can occur even without visible skin lesions
due to lymphatic obstruction.
Visceral Involvement (Advanced KS)
Gastrointestinal KS
• Symptoms include bleeding, weight loss, abdominal
pain, and diarrhea.
• Endoscopy may reveal red/violaceous lesions in the GI
tract.
Pulmonary KS
• Symptoms include cough, hemoptysis, dyspnea, and
pleural effusion.
• Can be life-threatening if extensive.
Investigations
• Skin biopsy- Vascular channels lined by
atypical endothelial cells.
- extravasated erythrocytes
with hemosiderin deposition
Imaging – abdominal ultrasound, cxr
Differential diagnosis
• Dermatofibroma
• melanocytic nevus
• ecchymosis
• granuloma annulare
• insect bite reactions
Management
Localized Treatment
• Cryotherapy – Effective for superficial
lesions.
• Intralesional chemotherapy (e.g.,
vinblastine) – Used for small symptomatic
lesions.
• Radiotherapy – Preferred for a few
localized lesions, especially in classic KS.
Systemic Treatment
• HAART (Highly Active Antiretroviral Therapy)
The backbone of KS treatment in HIV-positive patients,
often leading to lesion regression.
Chemotherapy
• Liposomal anthracyclines (e.g., doxorubicin,
daunorubicin) – First-line therapy.
• Paclitaxel – Used for refractory or advanced cases.
• Other agents (e.g., vincristine, vinblastine, bleomycin) –
Used in some combination therapies.
THE END

kaposi sarcoma at the cancer disease Hospital

  • 1.
    KAPOSI SARCOMA Presenter: MuluseChipo Muluti Moderator: Dr Ngoma
  • 2.
    Introduction • Kaposi sarcoma(KS) is an angioproliferative malignancy caused by HHV-8, commonly seen in immunocompromised individuals, especially those with HIV/AIDS. • It is a systemic tumor of endothelial cell origin. • It has Four clinical variants • Responds to radiation and chemotherapy,
  • 3.
    Clinical variants ofKS • classic KS • endemic African KS • immunosuppressive therapy–related KS • HIV/AIDS-related KS
  • 4.
    Classic KS • Occursin elderly males of eastern European heritage. • Predominantly arises on the legs but also occurs in lymph nodes and abdominal viscera. • slow progression and has good prognosis
  • 5.
  • 7.
    African-Endemic KS • Itoccurs in people living in Equatorial Africa. • HHV-8 infection is much more common in Africa than in other parts of the world, increasing the chance of KS developing. • Males > females • Has poor prognosis (young adults 5–8 years; young children 2–3 years) • Four clinical patterns
  • 8.
  • 9.
    African-Endemic KS patterns a)Nodular type: benign course and resembles classic KS. b) Florid or vegetating type: more aggressive. Nodular extend deeply into the subcutaneous fat, muscle, and bone. c) Infiltrative type: more aggressive has mucocutaneous and visceral . d) Lymphadenopathic type: children and young adults. confined to lymph nodes and viscera, also involves the skin and mucous membrane.
  • 10.
    Iatrogenic Immunosuppression- Associated KS •It is rare. • Most commonly in solid-organ transplant recipients • chronic use of immunosuppressive drugs • Resolves on cessation of immunosuppression.
  • 11.
    HIV/AIDS-Associated KS • AIDSincreases risk of KS ( 20,000 times that those not infected with HIV) • This occurs more often in men than in women • Common in homosexual men • Rapid progression, extensive systemic involvement • HIV-1 associated Kaposi sarcoma has high occurrence in homosexual men. • Most cultures of these tumors yield cells with properties of hyperplastic endothelial cells • KS of the bowel and/or lungs is responsible for numerous deaths
  • 12.
    Route of Infection •KSHV appears to be shed in saliva independent of subjects immune status • Viral DNA is detected in breast milk samples in African patients. • HHV 8 infects dividing B cells CD45+phase • Sexually transmitted among men who have sex with men. Who have higher prevalence ( 30- 60%) • Infections are common in Africa (>50%) with infections acquired early in life by nonsexual routes, through contact with oral secretion
  • 13.
    Pathogenesis • HHV-8 causesKS by infecting endothelial and immune cells, evading immune detection, and promoting angiogenesis via VEGF. It suppresses apoptosis through LANA-1 and cytokines, leading to uncontrolled cell growth. Immune suppression (e.g., HIV, transplant drugs) creates a favorable environment for KS development.
  • 14.
    Clinical manifestation • Mucocutaneouslesions are usually asymptomatic • lower extremities - edema and moderate to severe pain • Urethral or anal canal lesions- obstruction • Pulmonary KS - bronchospasm, intractable coughing, shortness of breath, progressive respiratory failure.
  • 15.
    Skin Lesions (MostCommon Presentation) • Color: Pink, red, purple, or brown macules, plaques, or nodules. • Distribution: Common on lower limbs, face (nose, ears), and genitalia. • Progression: Begins as flat macules, later forming raised plaques and nodular tumors. • Usually painless and non-pruritic, but may ulcerate in advanced cases.
  • 16.
    Mucosal Involvement • OralKS: Common in AIDS-associated KS, affecting the hard palate, gingiva, and tongue. • Symptoms include bleeding, pain, and difficulty eating.
  • 17.
  • 18.
    Lymphatic System Involvement •Causes lymphedema, especially in the lower limbs and genitalia. • Can occur even without visible skin lesions due to lymphatic obstruction.
  • 19.
    Visceral Involvement (AdvancedKS) Gastrointestinal KS • Symptoms include bleeding, weight loss, abdominal pain, and diarrhea. • Endoscopy may reveal red/violaceous lesions in the GI tract. Pulmonary KS • Symptoms include cough, hemoptysis, dyspnea, and pleural effusion. • Can be life-threatening if extensive.
  • 20.
    Investigations • Skin biopsy-Vascular channels lined by atypical endothelial cells. - extravasated erythrocytes with hemosiderin deposition Imaging – abdominal ultrasound, cxr
  • 21.
    Differential diagnosis • Dermatofibroma •melanocytic nevus • ecchymosis • granuloma annulare • insect bite reactions
  • 22.
    Management Localized Treatment • Cryotherapy– Effective for superficial lesions. • Intralesional chemotherapy (e.g., vinblastine) – Used for small symptomatic lesions. • Radiotherapy – Preferred for a few localized lesions, especially in classic KS.
  • 23.
    Systemic Treatment • HAART(Highly Active Antiretroviral Therapy) The backbone of KS treatment in HIV-positive patients, often leading to lesion regression. Chemotherapy • Liposomal anthracyclines (e.g., doxorubicin, daunorubicin) – First-line therapy. • Paclitaxel – Used for refractory or advanced cases. • Other agents (e.g., vincristine, vinblastine, bleomycin) – Used in some combination therapies.
  • 24.