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DISEASES OF BLOOD
VESSELS
H.A .MWAKYOMA, MD
BLOOD VESSELS
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Introduction
Atherosclerosis
Aneurysms
Hypertensive vascular disease
Vasculitis
Diseases of veins
Diseases of lymphatics
Tumors (we will not talk much about it except Kaposi’s sarcoma)
Types of blood vessels
1. Arteries:
-
Elastic arteries: Aorta and large arteries.
Muscular arteries: Smaller arteries.
 Atherosclerosis is a disease of large elastic arteries. It
rarely affects muscular arteries and does not affects
arterioles.
2. Arterioles:
-
Smallest elements of arterial system.
 Hypertensive arterial disease is primarily a disease of the
arterioles.
3. Capillaries:
-
Tiniest blood vessels.
 Capillaries are rarely affected by disease, except in
disseminated intravascular coagulation.
Types of blood vessels cont-4. Venules
5. Veins

Venous thrombosis is more common than arterial, because of the slow
blood flow and at a lower pressure.
6. Lymphatics
A. Atherosclerosis
• A disease of large and medium-sized arteries.
 So we are talking about the aorta and its main branches: internal
and external iliac, carotids, & subclavian arteries.
 The organ arteries are rarely affected such as renal, splanchnic,
upper extremity arteries. The intracerebral arteries & lower
extremity arteries are the only exceptions.
 By far the commonest clinical problem you will face because of
atherosclerosis is coronary artery atherosclerosis.
• Accumulation within the intima of smooth
muscle cells and lipids.
• Produces irregular thickening of the wall and
narrowing of the lumen.
General Comments
• Arteriosclerosis
– Thickening and loss of elasticity of arterial
walls
– Hardening of the arteries
– Greatest morbidity and mortality of all human
diseases via;
Narrowing
Weakening
Three patterns of
arteriosclerosis
• Atherosclerosis
– The dominant pattern of arteriosclerosis
– Primarily affects the elastic (aorta, carotid, iliac)
and large to medium sized muscular arteries
(coronary, popliteal)
• Monckeberg medial calcific sclerosis
• Arteriolosclerosis –small arteries and
arterioles (hypertension and DM)
Non-Modifiable Risk Factors
• Age
– A dominant influence
– Atherosclerosis begins in the young, but does not
precipitate organ injury until later in life
• Gender
– Men more prone than women, but by age 60-70 about
equal frequency
• Family History
– Familial cluster of risk factors
– Genetic differences
Modifiable Risk Factors
(potentially controllable)
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Hyperlipidemia
Hypertension
Cigarette smoking
Diabetes Mellitus
Elevated Homocysteine
Factors that affect hemostasis and thrombosis
Infections: Herpes virus; Chlamydia pneumoniae
Obesity, sedentary lifestyle, stress
• Pathogenesis of
atherosclerosis
Normal Artery
Atherosclerosis
• A disease of the intima
• A disease of the intima
• A disease of the intima
• Atheromas, atheromatous/fibrofatty
plaques, fibrous plaques
• Narrowing/occlusion; weakness of wall
ATHEROSCLEROSIS


Steps in atherosclerosis development
•
Fatty streak
•
Fibrous plaque
•
Atherosclerotic plaque
•
Calcification plaque
Complication of atherosclerotic plaques.
ATHEROSCLEROSIS

Fatty streak:


Represents the initial lesion
Results from abnormal accumulation of
lipoproteins in the intima layer

Mainly localized at arterial bifurcations

Appears since first years of life.
ATHEROSCLEROSIS

Fibrous plaque:

Is the most characteristic lesion of
Atherosclerosis, is composed of:

Monocytes

Macrophages

S.M.C. (Smooth Muscle Cells)

“Foam cells”

*** Lipid-rich “Necrotic core”.
Fibrous plaque:
Major components of plaque
• Cells (SMC, macrophages and other WBC)
• ECM –Extracellular Matrix (collagen, elastin, and
PGs)
• Lipid = Cholesterol (Intra/extracellular)
• (Often calcification)
Two major processes in plaque
formation
• Intimal thickening (SMC proliferation and
ECM synthesis)
• Lipid accumulation
ATHEROSCLEROSIS

Atherosclerotic plaque:

Proliferation at the intima layer of:




S.M.C.
Macrophages
“Foam cells”
Conective Tissue elements (CTE)
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


Collagen type I
Elastin Fibers
Glycosaminoglycans
Cholesterol uptake

Calcium deposits

Complication of the plaque
ATHEROSCLEROSIS

COMPLICATED PLAQUE:

Ulceration
•
•

Thrombosis
•

Acute ischemia/necrosis
Growth
•

Acute thrombosis with oclussion
Disloging and peripheral embolism
Chronic ischemia
Necrosis
•
Aneurysm development
• PATHOGENESIS OF
ATHEROSCLEROSIS
Response to injury hypothesis
* Injury to the endothelium
(dysfunctional endothelium)
* Chronic imflammatory response
* Migration of SMC from media to intima
* Proliferation of SMC in intima
• Excess production of ECM
• Enhanced lipid accumulation
Response to injury hypothesis (I)
1. Chronic EC (Endothelial Cell) injury
– EC dysfunction
– Increased permeability
– Leukocyte adhesion (via VCAM-1)
– Thrombotic potential
Response to Injury
Response to injury hypothesis (I)
Response to injury hypothesis
(II)
2. Accumulation of LDL (cholesterol)
3. Oxidation of lesional LDL
4. Adhesion & migration of blood
monocytes; transformation into
macrophages and foam cells
5. Adhesion of platelets
6. Release of factors from platelets,
macrophages and ECs
Response to injury hypothesis
(III)
7. Migration of SMC from media to intima
8. Proliferation of SMC
9. ECM production by SMC
10. Enhanced lipid accumulation
Intracellular & Extracellular (SMC and
macrophages)
Initiation of Fatty Streak
Fatty Streak
Fatty Streak-Aorta
Fatty Streak-Coronary Artery
Fibro-fatty Atheroma
Summary of Atherosclerotic Process
• Multifactorial process (risk factors)
• Initiated by endothelial dysfunction
• Up regulation of endothelial and leukocyte adhesion
molecules
• Macrophage diapedesis
• LDL transcytosis
• LDL oxidation
• Foam cells
• Recruitment and proliferation of smooth muscle cells
(synthesis of connective tissue proteins)
• Formation and organization of arterial thrombi
Consequences of plaque formation
Generalized
– Narrowing/Occlusion
– Rupture
– Emboli
– Leading to specific problems:
• Myocardial and cerebral infarcts
• Aortic aneurysms
• Peripheral vascular disease
Consequences of plaque formation
Altered Vessel Function
• Vessel change
- Plaque narrows lumen
– Wall weakened
– Thrombosis
– Breaking loose of
plaque
– Loss of elasticity
• Consequence
– Ischemia, turbulence
– Aneurysms, vessel
rupture
– Narrowing, ischemia,
embolization
– Athero-embolization
– Increase systolic blood
pressure
Fibrous cap
Cholesterol
clefts
Elastin
membrane
destroyed
Neovas.
Calcification
Inflam. cells
Foam Cells/Cholesterol Crystals
Cholesterol Crystals/Foam Cells
Hemorrhage into Plaque
Late Changes
• Calcification
– An example of dystrophic calcification
• Cracking, ulceration, rupture
– Usually occurs at edge of plaque
• Thrombus formation
– Caused by endothelial injury,ulceration, turbulence
– Organization of thrombus
– More thrombus
• Encroachment
– Weakens vessel wall
• Bleeding
– Ulceration, cracking and angiogenesis
Fibrous Plaques
Complicated Lesions
Complicated Lesions
A. Atherosclerosis
•
The major complications of atherosclerosis are
1. ischemic heart disease without MI
2. myocardial infarction the most serious complication
3. Stroke which is cerebrovascular ischemia
4. gangrene of the lower extremities
5.
•
 the upper extremities are rarely affected if it was
due to atherosclerosis however it is common in
other diseases like embolization, vasculitis,
compression, trauma.
Rarely embolization.
Ischemic heart disease is the leading cause of
death in developed countries
while in the developing countries infectious diseases is the
leading cause of death.
Complicated Lesion/Ulceration/Thrombosis
Ulceration/Hemorrhage/Cholesterol
Crystals
Thrombosis/Complicated Lesion
Complicated Lesion/Calcification
B: Aneurysms
 Localized
dilatation of blood vessels
caused by a congenital or acquired
weakness in the media (by infection or
atherosclerosis).
 Classification
may be based on
location, configuration, or etiology.
Classification of Aneurysms by Etiology
1.
2.
Atherosclerotic
 The commonest large artery aneurysms is caused
by atherosclerosis.
 It affects mostly the thoracic aorta, abdominal
aorta, and its large branches.
 Atherosclerosis affecting the arch of aorta or the
ascending aorta is extremely rare.
Syphilitic
 Uncommon, affects the ascending portion of the
aorta .
Classification of Aneurysms by Etiology
3.
Dissecting
we don’t use this term anymore, it
is called “aortic dissection”
necrosis)

4.
5.
(cystic medial
This will not produce an aneurysm but narrowing
of the aorta and occlusion.
Mycotic
Congenital
Congenital Aneurysm
“Berry Aneurysm”
They are so called Berry aneurysm because
they look like small berries ‫توت‬
 Cerebral arteries.
 Congenital defect in arterial wall.
 Is a cause of subarachnoid or intracerebral
hemorrhage.
 Usually participated by hypertension
-
Congenital Aneurysm
“Berry Aneurysm”
saccular or berry aneurysms
Unruptured berry aneurysm of
middle cerebral artery
A ruptured berry aneurysm with subarachnoid
hemorrhage leads to sudden onset of an
excruciating headache.
Hemorrhagic stroke - SAH (Berry
Aneurysm)
Dissecting Aneurysms
A
form of hematoma within the
vessel wall.
 History of
hypertension or have a
weakening in the vessels wall.
 Cystic
medial necrosis.
 Clinical features.
 Treatment.
Dissecting Aneurysm
Dissecting Aneurysm
Dissecting Aneurysm
Atherosclerotic Aneurysms
 Abdominal
aorta and common iliac
arteries.
 Usually fusiform.
 May contain a mural thrombosis.
 Micro: destruction of arterial wall.
 Clinical features
Aortic Aneurysm
Aortic Aneurysm
Aneurysms
Aortic Aneurysm
Pulsatile abdominal mass
Abdominal pain
Bleeding
Atheroembolization
Narrowing of lumen
Usually not a problem

Syphilitic Aneurysms
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


Uncommon, but some studies are suggesting that
syphilis is coming back specially in the developing
countries.
 Aetiology of syphilis: bacterial spirochetes
“Treponema pallidum”
 Treatment: penicillin
Thoracic Aorta
Syphilitic Aortitits - “tree bark” appearance
Obliterative endarteritis and plasma cell
infiltration
Syphilitic Aneurysms
• In tertiary syphilis, inflammation of the
adventitia and the vasa vasorum of the aorta
lead to weakening of the media and gradual
aneurysm formation.
• These aneurysms typically affect the arch of
the aorta, and may involve the root of the
aorta, leading to incompetence of the aortic
valve.
• Complications include compression or
erosion of adjacent structures as well as
rupture
Syphlitic Aneurysm of the Aortic
Arch
Aortic Aneurysm with Thrombus
Mycotic Aneurysms
• Result of microbial infection (it doesn’t have
to be fungal infection, it could be any other
infection) and weakening of vessel wall.
• Can rupture.
• Aorta, cerebral vessels, splanchnic
arteries.
C: Vasculitis
Inflammation and with or without necrosis of
blood vessels, including arteries, veins and
capillaries.
 May also be known as angiitis.
 Many of these disorders involve immune
mechanisms such as immune complex
deposition, circulating antibodies and
various forms of cell-mediated immunity

Classification of Vasculitis
• Large Vessel Vasculitis:
– Giant cell arteritis: Granulomatous arteritis of aorta
and large branches. Patients older than 50
– Takayasu arteritis: Granulomatous inflammation of
aorta & large branches. Patients younger than 50
• Medium-sized vessel Vasculitis
– Polyarteritis nodosa (classic):
– Kawasaki disease: Usually children; coronary artery
involvement
Classification of Vasculitis
• Small Vessel Vasculitis very common
 It involves the dermal blood vessels and the renal blood
vessels
– Wegener’s granulomatosis: Upper & lower respiratory
tracts & kidneys.> ANCA present
– Churg Strauss syndrome: Lower respiratory tract; asthma;
blood eosinophilia
– Leukocytoclastic vasculitis: Hypersensitivity vasculitis
involving skin
– Henoch Schonlein purpura: IgA dominant immune complex
deposition in skin, gut & kidney
– Microscopic polyarteritis:
Classification according to
pathogenesis
• Infectious: Bacterial, viral, fungal, rickettsial
• Immunologic: commonest
- Immune complex mediated:Henoch Schonlein; Lupus
vasculitis.
Immune complex nephritis is very important,
we can see it in purpura or SLE.
- Direct antibody attack: Goodpasture’s syndrome it’s a
disease that will attack the lungs and the kidney;
Kawasaki disease
- ANCA associated disorder of the muscles:
- Wegener’s granulamatose which is a disease of the
lung and the kidney
- microscopic PAN, Churg Strauss
So they are
termed as
vasculitis
that present
pulmonaryrenal
syndrome
Classification according to pathogenesis –
cont--
• Unknown:
- Giant cell(temporal) arteritis
- Takayasu disease
- Classic Polyarteritis nodosum
1.
Polyarteritis Nodosa

It is called like this because it is segmental and produces small
aneurysms that looks like nodes.

An acute, necrotizing vasculitis affecting medium
and smaller, muscular arteries.
Patchy involvement of arteries.
Fibrinoid necrosis, acute inflammation, eosinophils.
Thrombosis
Small aneurysms because of the weakening of the wall.
Clinical features: it affects many vessels (polyarteritis)
– Kidneys, heart, skeletal muscle, skin, intestine, lung
– Association with Hepatitis B
– Responds to Steroids and Cyclophosphamide


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
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2.
-


Angiitis means an inflammation of an artery.
Group of vascular disorders thought to be in
response to exogenous substances, e.g., bacterial
products or drugs.
Cutaneous lesions - leukocytoclastic vasculitis.



Hypersensitivity Angiitis
Due to this many of the vasculitis patients go to dermatology.
Systemic lesions - microscopic polyarteritis,
inflammation restricted to the smallest arteries
and arterioles.
May be a feature of other systemic diseases such
as Lupus Erythematosus.
3.



Allergic granulomatosis and
Angiitis
(Churg-Strauss Syndrome
Systemic vasculitis with prominent
eosinophilia
Young persons with history of asthma
Widespread necrotizing vascular lesions
of small and medium-sized arteries,
arterioles, and veins
4.



Giant Cell Arteritis (Temporal
Arteritis, Granulomatous Arteritis)
Focal,
chronic,
granulomatous
inflammation of temporal arteries and/or
other cranial arteries.
 The patient will come complaining of
headaches and tenderness at the temporal
region, so it will produce pain while
wearing a hat.
 you don’t have to wait for testing, it needs to
be treated with steroids immediately.
Disease of elderly individuals (60 – 70 yrs
old).
Artery is cord-like and nodular.
4. Giant Cell Arteritis (Temporal Arteritis,
Granulomatous Arteritis) cont- Thrombus
in lumen.
 Granulomatous
inflammation
of
arterial wall so the artery becomes really hard.
 Presenting symptoms of headache
and temporal pain.
 Visual symptoms in 50% of patients.
 Common
symptoms: +/- fever, pain,vessel is very
hard, very tender.
5.




Wegener’s Granulomatosis
Systemic vasculitis involving nasal sinuses,
lungs and kidneys( pulmonary-renal syndrome.)
Anti-neutrophilic cytoplasmic antibodies –
ANCA.
Necrosis, granulomatous inflammation,
vasculitis of small arteries and veins.
Persistent
sinusitis,
pneumonitis,
hematuria and proteinuria.
6.
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
Takayasu Arteritis
Aortic arch, large arteries.
Unknown cause, may be auto-immune.
Worldwide distribution affecting young
women.
Intimal thickening, obliteration of lumen,
thrombosis.
Pulseless disease.
7.
Kawasaki Disease
-
It attacks the small vessels or the lymph nodes.

Muco-cutaneous lymph node syndrome,
because patients have enlarged lymph nodes.
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Infancy and childhood.
Unknown cause.
Fever, rash, conjunctival and oral lesions.
Lymphadenitis.
Necrotizing vasculitis.
Coronary artery aneurysms rare.
8.
Thrombo-Angiitis Obliterans
-
You can tell from the name that the patient have thrombosis, obliteration, and
vasculitis. Angiitis could affect either arteries or veins.

Also referred as

Buerger disease.
Occlusive, inflammatory disease of blood vessels.
Smoking usually in males.
Intermittent claudication.

Can lead to gangrene of the lower limps.


Antineutrophil Cytoplasmic Antibodies
(ANCA)
-
We assess and evaluate the immunological findings like ANCA which is
important whenever there is vasculitis.
• A heterogeneous group of autoantibodies against
enzymes mainly in neutrophil granules.
• C-ANCA
seen in Wegener’s.
• p-ANCA
seen in microscopic polyarteritis and
Churg-Strauss.
D: Varicose Veins
• Enlarged tortuous veins
• Risk factors for varicose veins of the legs:
– Increasing age
– Female sex and has fair skin
– Hereditary predisposition
– Obesity
– Posture specially for long hours travelers by car
– Increased venous pressure
Like pregnancy, intra-abdominal tumor,
track drivers, surgeons.
Varicose Veins
• Pathology: dilatation of veins, valvular deformity so the
blood will become static, just dilate and becomes engorged.
 Aetiology : Weakening of the vein or a deformity
• Clinical features: swelling and dull pain
• Complications: besides the ugly appearance
– stasis dermatitis
Stasis of the blood for a long time will produce a form
of dermatitis,so the skin above the vessel becomes
reddish & inflamed.
– stasis ulcers
Varicose Veins At Other Sites



Hemorrhoids in the anal canal.
Esophageal Varices.
 Associated with upper GI bleeding & shock.
 They are usually seen as a complication of
portal hypertension secondary to a chronic
cirrhosis.
Varicocele in the scrotum.
 The engorged veins and the stasis of blood
raises the the temperature of the scrotum, this
may result in infertility or low sperm count.
VASCULAR TUMOURS AND
TUMOUR-LIKE LESIONS
1.
BENIGN
Haemangioma
Granuloma
pyogenicum
Glomus
tumour
2.
BORDERLINE/
INTERMEDIATE
Haemangioendothe
lioma
3.
MALIGNANT
Angiosarcoma
Haemangiopericyto
ma
Kaposi’s sarcoma
TUMOURS OF
LYMPHATIC SYSTEM
•Lymphangiomacapillary, cavernous
•Lymphangiosarcoma
KAPOSI’S SARCOMA
– First described by Moriz Kaposi in 1872 on
five patients presenting with ‘sarcoma
idiopathicum multiple hemorrhagicum’
– In 1912 Sternberg termed this disease
Kaposi’s sarcoma-now referred as classical
KS
• An indolent tumour seen typically in men of
mediterranean or east European Jewish origin
Kaposis Sarcoma
• In 1914 Hallenberg described the first
case of African or endemic KS
• In 1960 the first report of KS following
organ transplant and immuno-suppressive
therapy
• In 1981 Hymes described the epidemic
form associated with AIDS
Kaposis Sarcoma
• The conditions were KS and PCP
• The defined social group was homosexual
male community
• By 1998 nearly 57000 people in the USA
had developed KS as a result of HIV
• Swiss cohort study showed a significant
decrease of KS in mid 90s due to HAART
Kaposis Sarcoma
HHV-8 Associated Diseases
First identified in 1995.
 Kaposi’s Sarcoma: Accounts for 80% of all cancers in
AIDS patients.

Lesions are flat or raised areas of red to purple to
brown discoloration.
 May be confused with hemangioma or hematoma.
– Strong male predominance.
– 2/3 of affected patients present oral lesions
– Oral lesions are initial presentation in 20% of patients.
– Progressive malignancy that may disseminate widely.
– Oral lesions are a major source of morbidity and frequently
require local therapy.
Kaposis Sarcoma
• KS associated with gamma-2 herpes virus
known as HHV-8(KSHV)
• Virus identified using PCR-based
techniques in all forms of KS
– Classical
– Endemic african
– Paediatric
– Epidemic(HIV related)
Kaposi’s Sarcoma
• HHV-8 transmitted in saliva
• In homosexual men rate of HHV-8 is
related to the number of sexual partners
• Recent evidence from africa on HHV-8
prevalence in children suggests infection
is acquired through normal social contacts
within the family
Clinical features
• Classic lesion of KS is a raised macule
purplish in colour
• Lesions may coalesce into plaques and may
ulcerate and bleed
• KS may develop at sites of previous trauma
• Oedema is almost always a feature
• Visceral
Clinical features
Clinical features
AIDS patient with intraoral Kaposi’s
sarcoma of the hard palate
AIDS patient with intraoral Kaposi’s
sarcoma
Scrotal skin- KS
Endemic Kaposi’s Sarcoma,
nodular form
Extensive symmetric tumor lesions of
Kaposis’s sarcoma in an AIDS patient.
STAGING OF KS
• Stage I represents localized nodular KS, with
more than 15 cutaneous lesions or
involvement restricted to 1 bilateral anatomic
site, and few, if any, gut nodules.
• Stage II includes both exophytic destructive
lesions and locally infiltrative cutaneous
lesions as locally aggressive KS.
• Stage III (generalized lymphadenopathic KS)
has widespread lymph node involvement,
with or without skin lesions, but with no
visceral involvement.
STAGING OF KS
• Stage IV (disseminated visceral KS) has
widespread KS, usually progressing from
Stage II or Stage III, with involvement of
multiple visceral organs.
• A: Associated opportunistic infection(s)
• B: Patient is HIV-I seropositive.
• C: Cutaneous anergy or other evidence of
severe immunodeficiency is present
• EPIDEMIOLOGIC VARIETIES
(TYPES) OF KS
Classic Kaposi's sarcoma
• older men of Eastern European, Mediterranean,
or Jewish descent.
• The male/female ratio :(15:1 -3:1).
–
–
–
–
Bluish-red
macules  papulesplaquesnodules
edema
on the distal lower extremities are often the first sign
of KS.
– The process is slow and the course is benign.
– Visceral or mucosal involvement is found in 10% of
patients.
Endemic Kaposi's sarcoma
(African)
• male to female ratio similar to that of classic KS
and a mean age of onset of 48 years exept
lymphadenopathic type
• 1.nodular variant = classic KS.
• 2.florid / infiltrative are aggressive.
• 3.lymphadenopathic form is particularly
common among the young Bantu children . –
 Rapid visceral involvement can cause early
death.
 Skin lesions are sparse
Iatrogenic Kaposi's sarcoma
• especially true for male patients of Eastern
European, Mediterranean, or Jewish origin.
• The lesions typically appear several years after
transplantation in transplant recipients.
• the lesions commonly regress when the
medications are reduced or discontinued.
• HHV-8 been reported in transplant recipients.
Epidemic Kaposi's sarcoma
(aids associated)
• most common AIDS-associated malignancy
• early lesions commonly appear on the face,
especially on the nose, eyelids, and ears.
• trunk lesions may follow the lines of cleavage.
• reddish to pink macules and papules.
• Only in prolonged courses do the macules and
papules sufficiently coalesce to form plaques
Epidemic Kaposi's sarcoma
(aids associated)
• The lymph nodes and the
gastrointestinal tract are commonly
involved.
• The oral mucosa is the initial site of
disease in 10% to 15% of patients,
(palate)
Other HHV 8 associated diseases
• 1-Primary effusion lymphoma
rare.. DNA copy number is extremely high
IN HIV B cell lymphoma
• 2.Multicentric Castleman's disease
IL6 IN HIV
Fever+ anemia+ hypergammaglobulinemia
• 3.POEMS syndrome
(polyneuropathy, organomegaly, endocrinopathy,
multiple myeloma, skin changes)
Mortality/Morbidity
• Usually die with not from KS
• The mean survival rate of patients with
KS-AIDS has been approximately 15-24
months (without treatment)
• Fatality: gut perforation, cardiac
tamponade, massive pulmonary
obstruction or, rarely, brain metastases
• Patients with iatrogenic KS tend to have
gut bleeding resulting from KS
lab
• Serum glucose levels may reflect an
increased incidence of diabetes mellitus in
patients with classic KS.
• Immunohistochemical detection of
human herpes virus-8
• Eosinophilia
• cytopenia
• Anemia
• PCR
CONT.
• CT chest
• Endoscopy GI
• angiography may demonstrate KS.
• Radionucleotide scans may be USEFUL
• Markers for endothelial cells:
 Factor VIII–related antigen,
 Human leukocyte antigen DR (HLA-DR),
 von Willebrand factor, and
 The lectin Ulex europaeus I is highly suggestive.
• CD34 antigen,
(TISSUE BIOPSY): KS - MICROSCOPIC
• KS tends to demonstrate increased spindle cells
with
• vascular slits and vascular structures with a
predominance of endothelial cells.
• Extravasated erythrocytes and hemosiderinladen macrophages often are evident.
• Some spindle cells may show nuclear
pleomorphism.
• Early KS may resemble granulation tissue with a
diffuse chronic inflammatory infiltrate and
capillaries dilated and increased in number.
KS - MICROSCOPIC
KS - MICROSCOPIC