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HIV/AIDS Kaposi’s Sarcoma
A Practical Approach
Anisa MosamMB ChB( Natal), FC Derm(SA), MMed( Derm)
NRMSOM, UKZN
AWACC1-2 October 2009
ICC
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Epidemiologic Types
• Classic• Endemic• Iatrogenic• Epidemic
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Introduction
• Multicentric tumour originating from vascular and lymphatic endothelial cells
• Sites: – Skin– Lymphatics– Mucosal– Visceral: GIT & Pulmonary
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Cutaneous Features
• Asymptomatic pink to purple or brown
• Patches, papules, plaques, nodules or tumours
• Round, oval, elongated, fusiform• Undiagnosed or overlooked
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Cutaneous Sites
Head and neck, earlobes, occiput
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Cutaneous Sites• upper torso, extremities• Widespread, symmetric, Langers lines
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Mucosal Involvement
• Oral cavity in 20% at diagnosis
• Tongue, hard & soft palate• Associated with GIT KS
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Visceral Involvement: GIT
• >50% clinically• 80% at autopsy• May be asymptomatic• Symptoms: Abd pain, bloody stools,
LOW
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Visceral Involvement: Pulmonary
• 30% clinically• 50% at autopsy• Symptoms: dyspnoea,
cough, effusions• Survival poor
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Lymphatic Involvement
• Lymphadenopathy
• Lymphoedema• Woody hard
induration• Non-pitting
oedema
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KS mimickers
Patch Papules Nodules
Bruises Secondary SyphilisPPE
Pyogenic Granuloma
Purpura Lichen Planus Bacillary Angiomatosis
Haemangiomas Basal Cell Carcinoma Dermatofibroma
Naevi Squamous Cell Carcinoma
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Investigations
• biopsy• CD4 and HIV-1 viral load • CXR• Stool occult blood• Sputa MCS and AFB• If GIT symptoms, endoscopy• If abnormal CXR or symptoms,
bronchoscopy
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Diagnosis
• Proliferation of abnormal vascular spaces, lymphaplasmacytic infiltrates
• Endothelial cells contain HHV 8
• Spindle cells predominant cell
Biopsy: Skin, endoscopic or transbronchial
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Aetiopathogenesis
• HIV Tat protein, angiogenic• Inhalant nitrites and exposure of lymphatic and
vascular endothelium to nitrites in semen• Saliva• HHV 8
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HHV 8 and KS
• Genes homologous to cellular oncogenes
• Alter cell cycle• Inhibit apoptosis• Evade immune mechanisms• Promote angiogenesis
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Direct role of HIV-1 in KS
• Production of the HIV-1 Tat protein– Indirectly increases B-FGF Angiogenesis– Activates HHV 8
•Increases viral loads•Expression of viral oncogenes
–v-GPCR–V-Bcl-2
• Promoting cytokine production– Tumour initiation– Progression
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Staging
• 1988 ACTG: Good risk and Poor risk• T tumour extent• I immune status CD4• S systemic symptoms• Validated by Krown et al• TIS system effectively predicted survival Prior
to HAART• Data from 281 patients from 34 ACTG sites
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Staging Classification- “TIS”
Krown, SE J Clin Oncol 1989; 7:120
Good Risk (All) Poor Risk (Any)
T (Tumor)
T0: 27 mo survivalSkin, minimal oral mucosa, lymph node only
T1: 15 mo Edema or ulcerationExtensive oral mucosaVisceral KS
I (Immune System)
I0: 40 mo
CD4>150
I1: 13 mo
CD4<150
S (Systemic Illness)
S0: 22 mo No OI’s or thrushNo B symptomsKarnofosky >70%
S1: 16 mo Hx of OI’s or thrushB symptoms presentKarnofosky<70%Other HIV related disease
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Staging in HAART era
• Nasti et al, 2003• 211 patients from 2 prospective
Italian cohort studies• 3yr survival:• 85% T0 69% T1 (p=0007)• 83% S0 63% S1 (p=.003)• 83% I0 71% I1 (p=.06)
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3 year survival
• T1S1 53% poor risk
• T0S0 88%• T1S0 80%• T0S1 81% good risk• (p= .0001)
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HAART and KS
• Profoundly influenced natural history of KS• Incidence declined• Lengthened time to rx failure• Improved survival in pulmonary KS with CXT• KS regression
Krown JCO vol 22 no 3 2004:399-402
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HAART and KS
Int Collaboration of HIV and Cancer, Int Collaboration of HIV and Cancer,
J Nat Cancer Inst, 92(22) :1823-30 : J Nat Cancer Inst, 92(22) :1823-30 : 20002000
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HAART and KS
• Decreased HIV Tat and cytokines• Indirectly by CD4 restoration• Restored immunity to HHV 8• PI’s antiangiogenic
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PI’s vs NNRTI’s
• PI’s have anti-angiogenic activity• both PI and NNRTI’s similarly improved • HHV 8 immunity to and clearance of
viraemia• No evidence that PI’s regimen of choice• HAART durable HIV VL suppression and CD4
restoration is key
Bourboulia AIDS 18,485-493 2004
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Baseline 8 weeks 12 weeks
16 weeks HAART 20 weeks HAART 48 weeks HAART
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IRIS related oedema
Baseline 2 weeks HAART
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Before 4 Weeks HAART
KS IRIS
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8 weeks post HAART
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KS IRIS• Worsening of existing KS or development
of new lesions on HAART• Associated with rapid decline in HIV VL
and increase in CD4 • Close monitoring required• pulmonary involvement fatal• HAART continued but CXT required• British cohort of 150 KS 6.6% developed
IRIS KS• Higher CD4, KS oedema, PI + NNRTI
regimen
Lipman Curr Opinion Inf Dis 2006;19:20-25Bower J Clin Oncol 2005 Aug 1;23(22):5224-8
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Corticosteroids and KS
• Corticosteroids have been associated with the induction or exacerbation of KS in HIV patients
• Generally, should be avoided • Use only in:
– acute respiratory distress syndrome accompanying HIV-related opportunistic pulmonary infection
– tuberculosis meningitis or pericarditis– immune thrombocytopenic purpura, if necessary
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Treatment
• HAART• Local therapy• Systemic therapy
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Local treatment of KS
• Radiation therapy• Cryotherapy : 80% RR regardless of CD4• Laser surgery • Excisional surgery• Electrocauterization• Intralesional chemotherapy• Topical retinoids
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Systemic cytotoxic therapy
Important factors :
– Extent of KS – performance status– organ function (especially liver and bone
marrow)– Degree of immunosuppression (CD4 count), – Concomitant medications
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Systemic cytotoxic therapy
Indications : • palliation of tumour-related symptoms (pedal or
scrotal oedema)• treatment of pulmonary KS,• progressive mucocutaneous lesions (> 25 lesions)• extensive Kaposi’s sarcoma of the oral cavity• Symptomatic visceral involvement• IRIS
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Combination chemotherapy
• ABV / ABVb • Oral Etoposide• most widely used in poor resource settings • Standard of care in the past• Been replaced by newer drugs• More toxic and less effective than • Liposomal anthracyclines • Paclitaxel• Should only be reserved where Liposomal
anthracyclines and paclitaxel aren't available
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Local Policy
• HIV• CD4• FBC• Histology• On HAART
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Public Sector Policy
• If CD4 >150• Oral Etoposide 50-100 mg for 3
weeks• Repeated for at least 3-6 months• If tumour progression• IVI CXT with AVB• If T progression and good HIV control
and performance….3rd line CXT
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Public Sector Policy
• If CD4 count <150• Continue HAART• Review in 6 months• If local control required/palliation• 8Gy RXT single dose• Max 20-30 Gy esp for oral disease
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Kaposi’s sarcomaBiopsy
HIVCD4
HAART
Localized disease Systemic disease
Etoposide ABV/BV/VRadiotherapyIntralesional drugsCryotherapy
Limited to skin LymphoedemaFungating tumour
BleedingDisseminated
CutaneousLymphedoema
Visceral diseaseIRIS
Large oral lesions
ALGORITHMIC APPROACH TO HIV KS
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Thank You
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Assessing response
• numerous cutaneous lesions• reproducible lesion counts difficult• Estimates of <10;10-50 and >50 used• Photographs of all body areas• 3-5 marker lesions selected • photos and body diagrams• Tumour-assd oedema documented• Checklist of anatomical area
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Complete response (CR) resolution of any detectable disease for 4 weeks.
Partial response (PR) is a 50% or > decrease in number and/or size of all existing lesions for at least 4 weeks, without the appearance of new lesions. A response may be assigned to a diminution in the diameter of all lesions, or to flattening of at least 50% of the lesions. The size of each lesion will be the product of the longest dimension and the maximum dimension perpendicular to it.
Stable disease (SD) response not meeting the criteria for progression or PR
Progression is defined as at least a 25% increase in the size of any lesion or the appearance of any new lesions. Krown J Clin Oncol 1989
ResponseResponse
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