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The Liver and the
Biliary Tract
Dr Dinah Parums
Principal Histopathologist
July 2007
Normal Liver
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QuickTimeâ„ĸ and a
TIFF (Uncompressed) decompressor
are needed to see this picture.

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A ver ag e liver weig h t is 1 ,4 0 0
to 1 ,8 0 0 g m s
L ower b or d er can b e felt
u n d er th e r ig h t cost al m ar g in
on d eep in sp ir ation
T h e r ig h t lob e is six tim es th e
size of t h e left
D u al b lood su p p ly - 4 0 %
h ep atic ar t er y - th e r est b y
th e h ep atic p or tal vein
B ile d r ain s in t o th e r ig h t an d
left h ep atic d u ct s, in to th e
com m on h ep atic d u ct wh ich
join s with th e cyst ic d u ct fr om
th e g allb lad d er , t o for m th e
com m on b ile d u ct d r ain in g in
to t h e d u od en u m via th e
A m p u lla of V ater
Normal Liver
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P

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HV

QuickTimeâ„ĸ and a
TIFF (Uncompressed) decompressor
are needed to see this picture.

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H ist olog y of t h e liver sh ows a
solid m ass of p ar en ch ym a
co m p osed of h ep at ocyt es an d
cells lin in g t h e sin u soid s p ier ced
b y p or t al t r act s an d t r ib u t ar ies of
t h e h ep at ic vein s
T h e liver lob u le h as an
ar ch it ect u r e d efin ed b y t h e liver
vascu lat u r e
H V - t h e h ep at ic vein is at t h e
cen t r e of t h e liver lo b u le
( som et im es called t h e C en t r al
V ein )
P - t h e p or t al t r act - con t ain s t h e
p or t al t r iad
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h epat ic ar ter iole,
bile d u ct an d
por t al vein

B lood flow is fr om P t o H V
B ile flow is fr om H V t o P
T h e d ist an ce b et ween t h e H V an d
t h e P is 0.5 m m
Normal Liver

The Kupffer Cell and Sinusoids
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One type of cell lining the hepatic sinusoids, the Kupffer cell, is phagocytic and is a
component of the mononuclear phagocyte system.

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The Kupffer cell helps clear the blood of foreign substances and old erythrocytes.

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The other major type of lining cell is a special endothelial cell containing numerous
pores permitting free passage of plasma macromolecules between hepatocytes and
blood. It is not phagocytic.

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Finally, there are scattered lipocytes that store vitamin A and also are responsible for
collagen synthesis in liver fibrosis.
Normal Liver
Bile

Bile, the exocrine product of the hepatocytes, is initially secreted into intercellular bile
canaliculi and then passes into branches of the bile (hepatic) duct.
The bile canaliculi are tiny passageways between adjacent hepatocytes.
They are difficult to visualize with the light microscope unless they are selectively
stained.
Apart from the connective tissue of the portal triads, the structural framework of
hepatic lobules consists of reticular fibers which are arranged in small bundles
located in the space between the endothelial cells lining the sinusoids and the
hepatocytes. This space is called the space of Disse.
The space of Disse is too narrow to be seen with the light microscope
Hepatic Injury
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Inflammation = hepatitis
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Portal tracts, lobules

Degeneration
Damage from toxic or immunologic insult
īŽ Accumulation of substances, e.g., steatosis
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Cell death
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Fibrosis
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Centrilobular, submassive, massive necrosis
Usually irreversible

Cirrhosis
Bile
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Two major functions
Elimination of bilirubin, excess cholesterol, and
xenobiotics that are insufficiently water soluble to be
excreted in urine
īŽ Emulsification of dietary fat in the gut by bile acids
(cholic acid, chenodeoxycholic acid)
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īŽ
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Unconjugated → Conjugated
Reabsorbed in terminal ileum (enterohepatic
circulation)
Jaundice
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Excessive production of bilirubin
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īŽ
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Hemolytic anemias, ineffective erythropoiesis

Reduced hepatic uptake
Impaired conjugation
Physiologic jaundice of the newborn
īŽ Crigler-Najjar syndromes types I and II
īŽ Gilbert syndrome
īŽ Viral or drug-induced hepatitis, cirrhosis
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Decreased hepatocellular excretion
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Dubin-Johnson syndrome, Rotor syndrome

Impaired bile flow
Cholestasis
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īŽ
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Systemic retention of not only bilirubin but also
other solutes eliminated in bile, particularly bile
salts and cholesterol
Due to hepatocellular dysfunction or biliary
obstruction
Accumulation of bile pigment within the hepatic
parenchyma – Kupffer cells
Bile ductular proliferation
Bile lakes
Portal tract fibrosis
Hepatic Failure
īŽ

īŽ

80% to 90% of hepatic functional capacity must
to destroyed
Massive hepatic necrosis
Fulminant viral hepatitis
īŽ Drugs and chemicals, e.g., acetaminophen, carbon
tetrachloride, mushroom poisoning
īŽ

īŽ
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Chronic liver disease
Hepatic dysfunction without overt necrosis
Acute fatty liver of pregnancy
īŽ Tetracycline toxicity
īŽ Reye syndrome
īŽ
Clinical Features
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Jaundice
Hypoalbuminaemia
Hyperammonaemia
Fetor hepaticus
Palmar erythaema
Spider angiomas
Hypogonadism
Gynaecomastia
Complications
īŽ
īŽ
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Multiple organ failure
Coagulopathy
Hepatic encephalopathy
Metabolic disorder of the CNS and NMS
īŽ Elevated blood ammonia level and deranged
neurotransmission
īŽ Rigidity, hyperreflexia, seizures
īŽ Asterixis
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Hepatorenal syndrome
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Idiopathic renal failure
Cirrhosis
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Bridging fibrous septa
Parenchymal nodules
Disruption of the architecture of the entire liver
Aetiologies
Alcoholic liver disease 60% to 70%
īŽ Viral hepatitis 10%
īŽ Biliary diseases 5% to 10%
īŽ Hereditary hemochromatosis 5%
īŽ Wilson disease rare
īŽ Cryptogenic cirrhosis 10% to 15%
īŽ
Portal Hypertension
īŽ

Prehepatic
īŽ

īŽ

Occlusive thrombosis, narrowing of the portal vein

Intrahepatic
Cirrhosis
īŽ Schistosomiasis, massive fatty change, diffuse
granulomatous diseases (sarcoidosis, miliary TB)
īŽ

īŽ

Posthepatic
īŽ

Right-sided heart failure, constrictive pericarditis,
hepatic vein outflow obstruction
Clinical Sequelae
īŽ
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Ascites
Portosystemic venous shunts
Oesophageal varices 65% of cases
īŽ Hemorrhoids
īŽ Caput medusae
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īŽ
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Splenomegaly
Hepatic encephalopathy
Drug Induced Liver Disease
īŽ

īŽ
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īŽ

Liver is the major drug metabolizing and
detoxifying organ in the body
Direct toxicity
Hepatic conversion of a xenobiotic to an active
toxin
Immune mechanisms
Alcoholic Liver Disease
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Hepatic steatosis
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Alcoholic hepatitis
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Micro and macrovesicular
Initially centrilobular
Hepatocyte swelling and
necrosis
Mallory bodies
Neutrophilic reaction
Fibrosis

Alcoholic cirrhosis
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Micronodular
Irreversible
Pathogenesis
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Shunting of normal substrates away from
catabolism toward lipid biosynthesis
Induction of cytochrome P-450
Free radicals generated by microsomal ethanol
oxidizing system
Alcohol directly affects microtubular and
mitochondrial function
Acetaldehyde induces lipid peroxidation
Neutrophil infiltration
Immunologic attack of hepatocytes
Causes of Death
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Hepatic failure
Massive GI hemorrhage
Infection
Hepatorenal syndrome
Hepatocellular carcinoma
Nonalcoholic Fatty Liver
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Elevated serum aminotransferase levels
Low risk for development of hepatic fibrosis or
cirrhosis
Associated with obesity, type 2 DM,
hyperlipidemia
Need to exclude other causes
Hemochromatosis
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Primary or hereditary
īŽ

īŽ

HLA-linked autosomal recessive disease

Secondary
Transfusion dependent
īŽ Chronic liver disease
īŽ
Pathogenesis
īŽ
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īŽ

Total body iron pool 2 to 6 gm
Primary defect in regulation of intestinal
absorption of dietary iron, leading to a net iron
accumulation of 0.5 to 1.0 g/yr
HFE gene on 6p
īŽ

īŽ
īŽ
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Interacts with transferrin receptor of intestinal
enterocyte and modulates interaction with
transferrin-iron complexes

C282Y – disulfide bridge disrupted
H63D
Lipid peroxidation, collagen formation, DNA
interactions
Morphology
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īŽ
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Deposition of hemosiderin in the liver, pancreas,
myocardium, pituitary, adrenal, thyroid and parathyroid
glands, joints, and skin
Cirrhosis, micronodular
Pancreatic interstitial fibrosis and parenchymal atrophy
→ DM
Clinical Features
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īŽ
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M:F = 5-7:1
Symptoms usually appear in the fifth to sixth
decades of life.
Classic triad: cirrhosis with hepatomegaly, skin
pigmentation, DM (late in course)
Cardiac dysfunction, e.g., arrhythmias,
cardiomyopathy
Atypical arthritis
Hypogonadism
Tx: phlebotomy, iron chelators
Wilson Disease
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īŽ

īŽ
īŽ
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Autosomal recessive disorder of copper
metabolism
ATP7B on chr 13 ATP-dependent metal ion
transporter on the Golgi of hepatocytes
Failure to excrete copper into bile
Copper causes progressive liver injury
Affects brain, cornea, kidneys, bones, joints, and
parathyroid glands
Dx: ↓ serum caeruloplasmin, ↑ hepatic copper
content, ↑ urinary copper
Morphology
īŽ

Liver – fatty change, acute
hepatitis, chronic hepatitis,
cirrhosis
īŽ
īŽ

īŽ

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Rhodanine stain for copper
Orcein stain for copperassociated protein

Brain – Basal ganglia
(putamen) shows atrophy
and cavitation
Eye – Kayser-Fleischer
rings
Aka hepatolenticular
degeneration
Clinical Features
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Manifestations rare before 6 yrs
Acute or chronic liver disease – most common
Neuropsychiatric manifestations
Copper chelation therapy with D-penicillamine
Liver transplantation
Îą1-Antitrypsin Deficiency
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Autosomal recessive disorder
AAT is a protease inhibitor, particularly
neutrophil elastase released at sites of
inflammation
AAT gene on chr 14
īŽ

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M allele normal, Z allele abnormal → misfolding of
the nascent polypeptide in the hepatocyte ER,
accumulation, degradation

Leads to pulmonary emphysema due to tissue
destructive enzymes
Morphology
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Round to oval
cytoplasmic inclusions of
retained AAT
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Periodic acid-Schiff (PAS)
positive

Marked cholestasis with
hepatocyte necrosis in
newborns
Childhood cirrhosis
Chronic hepatitis or
cirrhosis later in life
Tx: liver transplantation
Neonatal Hepatitis
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Not a specific entity
Not necessarily inflammatory
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īŽ

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Extrahepatic biliary atresia (20%), toxic, metabolic
diseases, AAT deficiency (1.5%), idiopathic (50% to
60%)

Neonatal cholestasis (prolonged conjugated
hyperbilirubinemia)
Present with jaundice, dark urine, light or acholic
stools, hepatomegaly
īŽ

Marked bilirubin
stasis in
hepatocytes,
canaliculi, and
Kupffer cells in
neonate with
extrahepatic bile
duct atresia.
Reye Syndrome
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īŽ
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Rare disease characterized by fatty change in the
liver and encephalopathy
Children < 4 yo
3 to 5 days after a viral illness
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īŽ

īŽ
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Associated with salicylate (aspirin) use

Present with vomiting, irritability or lethargy,
hepatomegaly
25% progress to coma
Death due to progressive neurologic
deterioration or liver failure
Tx: symptomatic, supportive
Morphology
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Liver – microvesicular steatosis
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īŽ

Brain – cerebral oedema
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īŽ

EM – mitochondrial enlargement with disruption of
cristae
Astrocytes swollen, mitochondrial changes

Skeletal muscles, kidneys, and heart may have
microvesicular steatosis.
Obstructive Biliary
Tract Disease
Secondary Biliary Cirrhosis
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īŽ
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Most common cause is extrahepatic
cholelithiasis
Biliary atresia, malignancies of the biliary tree
and head of the pancreas, and strictures
Cholestasis
Bile duct proliferation with surrounding
neutrophils
Periportal fibrosis
Primary Biliary Cirrhosis
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īŽ
īŽ

Middle-aged women
M:F = 1:10
Possibly autoimmune
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īŽ
īŽ
īŽ

Autoantibodies to mitochondrial pyruvate
dehydrogenase 90%

Insidious onset, usually presenting with pruritus
Hyperbilirubinemia, jaundice, cirrhosis late
↑ alkaline phosphatase, cholesterol
īŽ

Nonsuppurative,
granulomatous
destruction of
medium-sized
intrahepatic bile
ducts = florid duct
lesion
Primary Sclerosing Cholangitis
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īŽ
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Inflammation, obliterative onion-skin fibrosis,
and segmental dilatation of the obstructed
intrahepatic and extrahepatic bile ducts
String of beads on ERCP
70% associated with inflammatory bowel
disease, particularly ulcerative colitis
M:F = 2:1, third through fifth decades
Progressive fatigue, pruritus, jaundice
Chronic course
Increased risk for cholangiocarcinoma
Circulatory Disorders
Hepatic Artery Inflow
īŽ
īŽ

Liver has dual blood supply.
Thrombosis of hepatic artery in transplanted
liver → loss of organ
Portal Vein Obstruction
īŽ

Extrahepatic
Peritoneal sepsis leads to phlebitis
īŽ Lymphatic metastases to hilar lymph nodes
īŽ Pancreatitis leads to splenic vein thrombosis
īŽ Postsurgical thromboses
īŽ Banti syndrome umbilical vein catheterization
īŽ

īŽ

Intrahepatic thrombus does not cause an
ischemic infarction but results in an area of redblue discoloration (infarct of Zahn).
Invasive carcinoma
īŽ Hepatoportal sclerosis
īŽ
Impaired Blood Flow Through the
Liver
īŽ
īŽ
īŽ

īŽ
īŽ
īŽ

Cirrhosis
Sickle cell disease
DIC – disseminated intravascular coagulation potentially fatal subcapsular haematoma in pts with
eclampsia
Right-sided heart failure → congestion of centrilobular
sinusoids
Left-sided heart failure → hypoperfusion and hypoxia
→ centrilobular necrosis
Peliosis hepatis – primary sinusoidal dilation associated
with anabolic steroids, danazol, and oral contraceptives
Hepatic Vein Thrombosis
īŽ
īŽ

īŽ

īŽ
īŽ

Aka Budd-Chiari syndrome
Hepatomegaly, weight gain, ascites, abdominal
pain
Polycythaemia vera or other myeloprolifera-tive
disorders, pregnancy, the postpartum state, oral
contraceptive use, PNH, intra-abdominal
cancers, esp. HCC
Massive intrahepatic abscess or parasitic cyst
Centrilobular congestion and necrosis
Veno-Occlusive Disease
īŽ
īŽ
īŽ
īŽ

Shortly after bone marrow transplantation
25% incidence
Subendothelial swelling and reticulated collagen
Due to toxic endothelial injury secondary to
chemotherapy and radiation therapy
Hepatic Neoplasms
īŽ

Metastatic carcinomas – most common
Colon
īŽ Lung
īŽ Breast
īŽ

īŽ
īŽ

Benign tumors
Primary liver carcinoma
Hepatocellular carcinoma
īŽ Cholangiocarcinomas
īŽ Hepatoblastoma – children
īŽ Angiosarcoma – associated with vinyl chloride,
arsenic, or Thorotrast exposure
īŽ
Benign Tumors
īŽ

Cavernous hemangioma – most common
īŽ

īŽ

Well-circumscribed, subcapsular, < 2 cm

Focal nodular hyperplasia
Young to middle aged adults
īŽ Poorly encapsulated
īŽ Central fibrous scar
īŽ Response to local vascular injury
īŽ
Focal Nodular Hyperplasia
Liver Cell Adenoma
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īŽ
īŽ

īŽ
īŽ

īŽ

Women of childbearing
age who have used oral
contraceptives
Often subcapsular
Sheets and cords of
hepatocytes
Portal tracts are absent
Prominent vessels
throughout
Risk for rupture, esp
during pregnancy
Hepatocellular Carcinoma
īŽ

Annual incidence
Americas, Northern Europe, Australia 3-7
cases/100,000
īŽ Southern Europe 20 cases/100,000
īŽ Southeast China, Taiwan 150 cases/100,000
īŽ

īŽ

īŽ
īŽ
īŽ

HBV carrier since infancy = 200 fold risk

Cirrhosis in 85% to 90% vs 50%
M:F = 3:1 vs 8:1
Sixth to seventh decades vs third to fifth
Pathogenesis
īŽ

Infection with HBV
Genomic instability with integrated HBV DNA
īŽ Integration pattern is clonal
īŽ HBV X-protein disrupts cell cycle control
īŽ Certain HBV proteins inactivate p53
īŽ

īŽ

Chronic liver disease, esp HCV and Etoh
īŽ

īŽ
īŽ

Cirrhosis plays an important role.

Hepatocarcinogens in food (aflatoxins from the
fungus Aspergillus flavus)
Repeated cycles of cell death and regeneration,
i.e., chronic hepatitis, with possible mutations
Morphology
īŽ
īŽ

Unifocal, multifocal, or infiltrative
Strong propensity for vascular invasion
īŽ

īŽ
īŽ
īŽ
īŽ

Portal vein or IVC involvement

Well-differentiated – intracellular bile
Scant stroma → soft
Metastasizes to LN, lung, bone, adrenal
Fibrolamellar carcinoma
20-40 yo, M=F
īŽ No assoc. with cirrhosis or other risk factors
īŽ Tumor cells separated by dense collagen
īŽ Better prognosis
īŽ
HCC
Clinical Features
īŽ
īŽ
īŽ
īŽ
īŽ
īŽ

īŽ

Rapid increase in liver size
Sudden worsening of ascites
Appearance of bloody ascites, fever, pain
↑ serum AFP, esp if > 1000 ng/ml
Median survival 7 months
Death due to GI or esophageal variceal bleeding
or liver failure with hepatic coma
Surgical resection for smaller tumors
īŽ

īŽ

Recurrence rate 60% at 5 yrs

Liver transplantation
Disorders of the
Gallbladder
Cholelithiasis
īŽ
īŽ

Very common
Cholesterol stones
Bile is supersaturated with cholesterol
īŽ Gallbladder stasis
īŽ F>M
īŽ Obesity
īŽ Advancing age
īŽ

īŽ

Pigment stones – calcium bilirubinate salts
Asian more than Western
īŽ Chronic hemolytic syndromes
īŽ
Clinical Features
īŽ
īŽ
īŽ
īŽ

Asymptomatic
Biliary colic
Cholecystitis
Gallstone ileus
Cholecystitis
īŽ

Acute calculous
Obstruction of GB neck or cystic duct
īŽ RUQ pain radiating to right shoulder
īŽ Fever, nausea, leukocytosis
īŽ Potential surgical emergency
īŽ

īŽ
īŽ

Acute acalculous – seriously ill pts
Chronic
Recurrent attacks of pain
īŽ Nausea and vomiting
īŽ Associated with fatty meals
īŽ
Choledocholithiasis
īŽ
īŽ
īŽ

īŽ

Stones within the biliary tree
West – from gallbladder
Asia – primary ductal and intrahepatic stone
formation
Symptoms due to:
Biliary obstruction
īŽ Pancreatitis
īŽ Cholangitis
īŽ Hepatic abscess
īŽ
Cholangitis
īŽ
īŽ
īŽ

Acute inflammation of bile ducts
Due to biliary obstruction, usually
choledocholithiasis
Bacterial infection from gut, i.e., gram negative
aerobes
īŽ

īŽ
īŽ
īŽ

Fever, chills, abdominal pain, jaundice

Latin America and Near East: Fasciola hepatica,
schistosomiasis
Far East: Clonorchis sinensis, Opisthorchis
viverrini
AIDS: cryptosporidiosis
Biliary Atresia
īŽ
īŽ
īŽ

īŽ
īŽ
īŽ
īŽ
īŽ

1/3 of cases of neonatal cholestasis
1 in 10,000 live births
Complete obstruction of bile flow caused by
destruction or absence of all or part of the
extrahepatic bile ducts
Acquired inflammatory disorder
Normal stools to acholic stools
Bile ductular proliferation on liver bx
Cirrhosis by 3 to 6 months of age.
Require liver transplantation
Gallbladder Carcinoma
īŽ
īŽ
īŽ
īŽ
īŽ
īŽ

īŽ

Seventh decade
F>M
Discovered at late stage, usually incidental
Exophytic and infiltrating types
Adenocarcinoma
Local extension into liver, cystic duct,
portahepatic LNs
Mean 5 yr survival 1%
Cholangiocarcinoma
īŽ
īŽ
īŽ
īŽ

īŽ
īŽ
īŽ
īŽ

Older pts
M>F
Painless jaundice, N/V, weight loss
Opisthorchis sinensis (liver fluke), PSC,
inflammatory bowel disease
Tumors usually small at dx yet not resectable
Klatskin tumor – arises at bifurcation
Adenocarcinoma
Mean survival 6 to 18 months
Questions?

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Dr Dinah Parums. Principal Pathologist. Liver and Biliary Tract Pathology. Teaching Handout.

  • 1. The Liver and the Biliary Tract Dr Dinah Parums Principal Histopathologist July 2007
  • 2. Normal Liver īŽ īŽ īŽ īŽ QuickTimeâ„ĸ and a TIFF (Uncompressed) decompressor are needed to see this picture. īŽ A ver ag e liver weig h t is 1 ,4 0 0 to 1 ,8 0 0 g m s L ower b or d er can b e felt u n d er th e r ig h t cost al m ar g in on d eep in sp ir ation T h e r ig h t lob e is six tim es th e size of t h e left D u al b lood su p p ly - 4 0 % h ep atic ar t er y - th e r est b y th e h ep atic p or tal vein B ile d r ain s in t o th e r ig h t an d left h ep atic d u ct s, in to th e com m on h ep atic d u ct wh ich join s with th e cyst ic d u ct fr om th e g allb lad d er , t o for m th e com m on b ile d u ct d r ain in g in to t h e d u od en u m via th e A m p u lla of V ater
  • 3. Normal Liver īŽ P īŽ HV QuickTimeâ„ĸ and a TIFF (Uncompressed) decompressor are needed to see this picture. īŽ īŽ H ist olog y of t h e liver sh ows a solid m ass of p ar en ch ym a co m p osed of h ep at ocyt es an d cells lin in g t h e sin u soid s p ier ced b y p or t al t r act s an d t r ib u t ar ies of t h e h ep at ic vein s T h e liver lob u le h as an ar ch it ect u r e d efin ed b y t h e liver vascu lat u r e H V - t h e h ep at ic vein is at t h e cen t r e of t h e liver lo b u le ( som et im es called t h e C en t r al V ein ) P - t h e p or t al t r act - con t ain s t h e p or t al t r iad īŽ īŽ īŽ īŽ īŽ īŽ h epat ic ar ter iole, bile d u ct an d por t al vein B lood flow is fr om P t o H V B ile flow is fr om H V t o P T h e d ist an ce b et ween t h e H V an d t h e P is 0.5 m m
  • 4. Normal Liver The Kupffer Cell and Sinusoids īŽ One type of cell lining the hepatic sinusoids, the Kupffer cell, is phagocytic and is a component of the mononuclear phagocyte system. īŽ The Kupffer cell helps clear the blood of foreign substances and old erythrocytes. īŽ The other major type of lining cell is a special endothelial cell containing numerous pores permitting free passage of plasma macromolecules between hepatocytes and blood. It is not phagocytic. īŽ Finally, there are scattered lipocytes that store vitamin A and also are responsible for collagen synthesis in liver fibrosis.
  • 5. Normal Liver Bile Bile, the exocrine product of the hepatocytes, is initially secreted into intercellular bile canaliculi and then passes into branches of the bile (hepatic) duct. The bile canaliculi are tiny passageways between adjacent hepatocytes. They are difficult to visualize with the light microscope unless they are selectively stained. Apart from the connective tissue of the portal triads, the structural framework of hepatic lobules consists of reticular fibers which are arranged in small bundles located in the space between the endothelial cells lining the sinusoids and the hepatocytes. This space is called the space of Disse. The space of Disse is too narrow to be seen with the light microscope
  • 6. Hepatic Injury īŽ Inflammation = hepatitis īŽ īŽ Portal tracts, lobules Degeneration Damage from toxic or immunologic insult īŽ Accumulation of substances, e.g., steatosis īŽ īŽ Cell death īŽ īŽ Fibrosis īŽ īŽ Centrilobular, submassive, massive necrosis Usually irreversible Cirrhosis
  • 7. Bile īŽ Two major functions Elimination of bilirubin, excess cholesterol, and xenobiotics that are insufficiently water soluble to be excreted in urine īŽ Emulsification of dietary fat in the gut by bile acids (cholic acid, chenodeoxycholic acid) īŽ īŽ īŽ Unconjugated → Conjugated Reabsorbed in terminal ileum (enterohepatic circulation)
  • 8. Jaundice īŽ Excessive production of bilirubin īŽ īŽ īŽ Hemolytic anemias, ineffective erythropoiesis Reduced hepatic uptake Impaired conjugation Physiologic jaundice of the newborn īŽ Crigler-Najjar syndromes types I and II īŽ Gilbert syndrome īŽ Viral or drug-induced hepatitis, cirrhosis īŽ īŽ Decreased hepatocellular excretion īŽ īŽ Dubin-Johnson syndrome, Rotor syndrome Impaired bile flow
  • 9. Cholestasis īŽ īŽ īŽ īŽ īŽ īŽ Systemic retention of not only bilirubin but also other solutes eliminated in bile, particularly bile salts and cholesterol Due to hepatocellular dysfunction or biliary obstruction Accumulation of bile pigment within the hepatic parenchyma – Kupffer cells Bile ductular proliferation Bile lakes Portal tract fibrosis
  • 10. Hepatic Failure īŽ īŽ 80% to 90% of hepatic functional capacity must to destroyed Massive hepatic necrosis Fulminant viral hepatitis īŽ Drugs and chemicals, e.g., acetaminophen, carbon tetrachloride, mushroom poisoning īŽ īŽ īŽ Chronic liver disease Hepatic dysfunction without overt necrosis Acute fatty liver of pregnancy īŽ Tetracycline toxicity īŽ Reye syndrome īŽ
  • 12. Complications īŽ īŽ īŽ Multiple organ failure Coagulopathy Hepatic encephalopathy Metabolic disorder of the CNS and NMS īŽ Elevated blood ammonia level and deranged neurotransmission īŽ Rigidity, hyperreflexia, seizures īŽ Asterixis īŽ īŽ Hepatorenal syndrome īŽ Idiopathic renal failure
  • 13. Cirrhosis īŽ īŽ īŽ īŽ Bridging fibrous septa Parenchymal nodules Disruption of the architecture of the entire liver Aetiologies Alcoholic liver disease 60% to 70% īŽ Viral hepatitis 10% īŽ Biliary diseases 5% to 10% īŽ Hereditary hemochromatosis 5% īŽ Wilson disease rare īŽ Cryptogenic cirrhosis 10% to 15% īŽ
  • 14. Portal Hypertension īŽ Prehepatic īŽ īŽ Occlusive thrombosis, narrowing of the portal vein Intrahepatic Cirrhosis īŽ Schistosomiasis, massive fatty change, diffuse granulomatous diseases (sarcoidosis, miliary TB) īŽ īŽ Posthepatic īŽ Right-sided heart failure, constrictive pericarditis, hepatic vein outflow obstruction
  • 15. Clinical Sequelae īŽ īŽ Ascites Portosystemic venous shunts Oesophageal varices 65% of cases īŽ Hemorrhoids īŽ Caput medusae īŽ īŽ īŽ Splenomegaly Hepatic encephalopathy
  • 16. Drug Induced Liver Disease īŽ īŽ īŽ īŽ Liver is the major drug metabolizing and detoxifying organ in the body Direct toxicity Hepatic conversion of a xenobiotic to an active toxin Immune mechanisms
  • 17. Alcoholic Liver Disease īŽ Hepatic steatosis īŽ īŽ īŽ Alcoholic hepatitis īŽ īŽ īŽ īŽ īŽ Micro and macrovesicular Initially centrilobular Hepatocyte swelling and necrosis Mallory bodies Neutrophilic reaction Fibrosis Alcoholic cirrhosis īŽ īŽ Micronodular Irreversible
  • 18. Pathogenesis īŽ īŽ īŽ īŽ īŽ īŽ īŽ Shunting of normal substrates away from catabolism toward lipid biosynthesis Induction of cytochrome P-450 Free radicals generated by microsomal ethanol oxidizing system Alcohol directly affects microtubular and mitochondrial function Acetaldehyde induces lipid peroxidation Neutrophil infiltration Immunologic attack of hepatocytes
  • 19. Causes of Death īŽ īŽ īŽ īŽ īŽ Hepatic failure Massive GI hemorrhage Infection Hepatorenal syndrome Hepatocellular carcinoma
  • 20. Nonalcoholic Fatty Liver īŽ īŽ īŽ īŽ Elevated serum aminotransferase levels Low risk for development of hepatic fibrosis or cirrhosis Associated with obesity, type 2 DM, hyperlipidemia Need to exclude other causes
  • 21. Hemochromatosis īŽ Primary or hereditary īŽ īŽ HLA-linked autosomal recessive disease Secondary Transfusion dependent īŽ Chronic liver disease īŽ
  • 22. Pathogenesis īŽ īŽ īŽ Total body iron pool 2 to 6 gm Primary defect in regulation of intestinal absorption of dietary iron, leading to a net iron accumulation of 0.5 to 1.0 g/yr HFE gene on 6p īŽ īŽ īŽ īŽ Interacts with transferrin receptor of intestinal enterocyte and modulates interaction with transferrin-iron complexes C282Y – disulfide bridge disrupted H63D Lipid peroxidation, collagen formation, DNA interactions
  • 23. Morphology īŽ īŽ īŽ Deposition of hemosiderin in the liver, pancreas, myocardium, pituitary, adrenal, thyroid and parathyroid glands, joints, and skin Cirrhosis, micronodular Pancreatic interstitial fibrosis and parenchymal atrophy → DM
  • 24. Clinical Features īŽ īŽ īŽ īŽ īŽ īŽ īŽ M:F = 5-7:1 Symptoms usually appear in the fifth to sixth decades of life. Classic triad: cirrhosis with hepatomegaly, skin pigmentation, DM (late in course) Cardiac dysfunction, e.g., arrhythmias, cardiomyopathy Atypical arthritis Hypogonadism Tx: phlebotomy, iron chelators
  • 25. Wilson Disease īŽ īŽ īŽ īŽ īŽ īŽ Autosomal recessive disorder of copper metabolism ATP7B on chr 13 ATP-dependent metal ion transporter on the Golgi of hepatocytes Failure to excrete copper into bile Copper causes progressive liver injury Affects brain, cornea, kidneys, bones, joints, and parathyroid glands Dx: ↓ serum caeruloplasmin, ↑ hepatic copper content, ↑ urinary copper
  • 26. Morphology īŽ Liver – fatty change, acute hepatitis, chronic hepatitis, cirrhosis īŽ īŽ īŽ īŽ īŽ Rhodanine stain for copper Orcein stain for copperassociated protein Brain – Basal ganglia (putamen) shows atrophy and cavitation Eye – Kayser-Fleischer rings Aka hepatolenticular degeneration
  • 27. Clinical Features īŽ īŽ īŽ īŽ īŽ Manifestations rare before 6 yrs Acute or chronic liver disease – most common Neuropsychiatric manifestations Copper chelation therapy with D-penicillamine Liver transplantation
  • 28. Îą1-Antitrypsin Deficiency īŽ īŽ īŽ Autosomal recessive disorder AAT is a protease inhibitor, particularly neutrophil elastase released at sites of inflammation AAT gene on chr 14 īŽ īŽ M allele normal, Z allele abnormal → misfolding of the nascent polypeptide in the hepatocyte ER, accumulation, degradation Leads to pulmonary emphysema due to tissue destructive enzymes
  • 29. Morphology īŽ Round to oval cytoplasmic inclusions of retained AAT īŽ īŽ īŽ īŽ īŽ Periodic acid-Schiff (PAS) positive Marked cholestasis with hepatocyte necrosis in newborns Childhood cirrhosis Chronic hepatitis or cirrhosis later in life Tx: liver transplantation
  • 30. Neonatal Hepatitis īŽ īŽ Not a specific entity Not necessarily inflammatory īŽ īŽ īŽ Extrahepatic biliary atresia (20%), toxic, metabolic diseases, AAT deficiency (1.5%), idiopathic (50% to 60%) Neonatal cholestasis (prolonged conjugated hyperbilirubinemia) Present with jaundice, dark urine, light or acholic stools, hepatomegaly
  • 31. īŽ Marked bilirubin stasis in hepatocytes, canaliculi, and Kupffer cells in neonate with extrahepatic bile duct atresia.
  • 32. Reye Syndrome īŽ īŽ īŽ Rare disease characterized by fatty change in the liver and encephalopathy Children < 4 yo 3 to 5 days after a viral illness īŽ īŽ īŽ īŽ īŽ Associated with salicylate (aspirin) use Present with vomiting, irritability or lethargy, hepatomegaly 25% progress to coma Death due to progressive neurologic deterioration or liver failure Tx: symptomatic, supportive
  • 33. Morphology īŽ Liver – microvesicular steatosis īŽ īŽ Brain – cerebral oedema īŽ īŽ EM – mitochondrial enlargement with disruption of cristae Astrocytes swollen, mitochondrial changes Skeletal muscles, kidneys, and heart may have microvesicular steatosis.
  • 35. Secondary Biliary Cirrhosis īŽ īŽ īŽ īŽ īŽ Most common cause is extrahepatic cholelithiasis Biliary atresia, malignancies of the biliary tree and head of the pancreas, and strictures Cholestasis Bile duct proliferation with surrounding neutrophils Periportal fibrosis
  • 36. Primary Biliary Cirrhosis īŽ īŽ īŽ Middle-aged women M:F = 1:10 Possibly autoimmune īŽ īŽ īŽ īŽ Autoantibodies to mitochondrial pyruvate dehydrogenase 90% Insidious onset, usually presenting with pruritus Hyperbilirubinemia, jaundice, cirrhosis late ↑ alkaline phosphatase, cholesterol
  • 38. Primary Sclerosing Cholangitis īŽ īŽ īŽ īŽ īŽ īŽ īŽ Inflammation, obliterative onion-skin fibrosis, and segmental dilatation of the obstructed intrahepatic and extrahepatic bile ducts String of beads on ERCP 70% associated with inflammatory bowel disease, particularly ulcerative colitis M:F = 2:1, third through fifth decades Progressive fatigue, pruritus, jaundice Chronic course Increased risk for cholangiocarcinoma
  • 39.
  • 41. Hepatic Artery Inflow īŽ īŽ Liver has dual blood supply. Thrombosis of hepatic artery in transplanted liver → loss of organ
  • 42. Portal Vein Obstruction īŽ Extrahepatic Peritoneal sepsis leads to phlebitis īŽ Lymphatic metastases to hilar lymph nodes īŽ Pancreatitis leads to splenic vein thrombosis īŽ Postsurgical thromboses īŽ Banti syndrome umbilical vein catheterization īŽ īŽ Intrahepatic thrombus does not cause an ischemic infarction but results in an area of redblue discoloration (infarct of Zahn). Invasive carcinoma īŽ Hepatoportal sclerosis īŽ
  • 43. Impaired Blood Flow Through the Liver īŽ īŽ īŽ īŽ īŽ īŽ Cirrhosis Sickle cell disease DIC – disseminated intravascular coagulation potentially fatal subcapsular haematoma in pts with eclampsia Right-sided heart failure → congestion of centrilobular sinusoids Left-sided heart failure → hypoperfusion and hypoxia → centrilobular necrosis Peliosis hepatis – primary sinusoidal dilation associated with anabolic steroids, danazol, and oral contraceptives
  • 44. Hepatic Vein Thrombosis īŽ īŽ īŽ īŽ īŽ Aka Budd-Chiari syndrome Hepatomegaly, weight gain, ascites, abdominal pain Polycythaemia vera or other myeloprolifera-tive disorders, pregnancy, the postpartum state, oral contraceptive use, PNH, intra-abdominal cancers, esp. HCC Massive intrahepatic abscess or parasitic cyst Centrilobular congestion and necrosis
  • 45. Veno-Occlusive Disease īŽ īŽ īŽ īŽ Shortly after bone marrow transplantation 25% incidence Subendothelial swelling and reticulated collagen Due to toxic endothelial injury secondary to chemotherapy and radiation therapy
  • 46. Hepatic Neoplasms īŽ Metastatic carcinomas – most common Colon īŽ Lung īŽ Breast īŽ īŽ īŽ Benign tumors Primary liver carcinoma Hepatocellular carcinoma īŽ Cholangiocarcinomas īŽ Hepatoblastoma – children īŽ Angiosarcoma – associated with vinyl chloride, arsenic, or Thorotrast exposure īŽ
  • 47. Benign Tumors īŽ Cavernous hemangioma – most common īŽ īŽ Well-circumscribed, subcapsular, < 2 cm Focal nodular hyperplasia Young to middle aged adults īŽ Poorly encapsulated īŽ Central fibrous scar īŽ Response to local vascular injury īŽ
  • 49. Liver Cell Adenoma īŽ īŽ īŽ īŽ īŽ īŽ Women of childbearing age who have used oral contraceptives Often subcapsular Sheets and cords of hepatocytes Portal tracts are absent Prominent vessels throughout Risk for rupture, esp during pregnancy
  • 50. Hepatocellular Carcinoma īŽ Annual incidence Americas, Northern Europe, Australia 3-7 cases/100,000 īŽ Southern Europe 20 cases/100,000 īŽ Southeast China, Taiwan 150 cases/100,000 īŽ īŽ īŽ īŽ īŽ HBV carrier since infancy = 200 fold risk Cirrhosis in 85% to 90% vs 50% M:F = 3:1 vs 8:1 Sixth to seventh decades vs third to fifth
  • 51. Pathogenesis īŽ Infection with HBV Genomic instability with integrated HBV DNA īŽ Integration pattern is clonal īŽ HBV X-protein disrupts cell cycle control īŽ Certain HBV proteins inactivate p53 īŽ īŽ Chronic liver disease, esp HCV and Etoh īŽ īŽ īŽ Cirrhosis plays an important role. Hepatocarcinogens in food (aflatoxins from the fungus Aspergillus flavus) Repeated cycles of cell death and regeneration, i.e., chronic hepatitis, with possible mutations
  • 52. Morphology īŽ īŽ Unifocal, multifocal, or infiltrative Strong propensity for vascular invasion īŽ īŽ īŽ īŽ īŽ Portal vein or IVC involvement Well-differentiated – intracellular bile Scant stroma → soft Metastasizes to LN, lung, bone, adrenal Fibrolamellar carcinoma 20-40 yo, M=F īŽ No assoc. with cirrhosis or other risk factors īŽ Tumor cells separated by dense collagen īŽ Better prognosis īŽ
  • 53. HCC
  • 54. Clinical Features īŽ īŽ īŽ īŽ īŽ īŽ īŽ Rapid increase in liver size Sudden worsening of ascites Appearance of bloody ascites, fever, pain ↑ serum AFP, esp if > 1000 ng/ml Median survival 7 months Death due to GI or esophageal variceal bleeding or liver failure with hepatic coma Surgical resection for smaller tumors īŽ īŽ Recurrence rate 60% at 5 yrs Liver transplantation
  • 56. Cholelithiasis īŽ īŽ Very common Cholesterol stones Bile is supersaturated with cholesterol īŽ Gallbladder stasis īŽ F>M īŽ Obesity īŽ Advancing age īŽ īŽ Pigment stones – calcium bilirubinate salts Asian more than Western īŽ Chronic hemolytic syndromes īŽ
  • 58. Cholecystitis īŽ Acute calculous Obstruction of GB neck or cystic duct īŽ RUQ pain radiating to right shoulder īŽ Fever, nausea, leukocytosis īŽ Potential surgical emergency īŽ īŽ īŽ Acute acalculous – seriously ill pts Chronic Recurrent attacks of pain īŽ Nausea and vomiting īŽ Associated with fatty meals īŽ
  • 59.
  • 60. Choledocholithiasis īŽ īŽ īŽ īŽ Stones within the biliary tree West – from gallbladder Asia – primary ductal and intrahepatic stone formation Symptoms due to: Biliary obstruction īŽ Pancreatitis īŽ Cholangitis īŽ Hepatic abscess īŽ
  • 61. Cholangitis īŽ īŽ īŽ Acute inflammation of bile ducts Due to biliary obstruction, usually choledocholithiasis Bacterial infection from gut, i.e., gram negative aerobes īŽ īŽ īŽ īŽ Fever, chills, abdominal pain, jaundice Latin America and Near East: Fasciola hepatica, schistosomiasis Far East: Clonorchis sinensis, Opisthorchis viverrini AIDS: cryptosporidiosis
  • 62. Biliary Atresia īŽ īŽ īŽ īŽ īŽ īŽ īŽ īŽ 1/3 of cases of neonatal cholestasis 1 in 10,000 live births Complete obstruction of bile flow caused by destruction or absence of all or part of the extrahepatic bile ducts Acquired inflammatory disorder Normal stools to acholic stools Bile ductular proliferation on liver bx Cirrhosis by 3 to 6 months of age. Require liver transplantation
  • 63. Gallbladder Carcinoma īŽ īŽ īŽ īŽ īŽ īŽ īŽ Seventh decade F>M Discovered at late stage, usually incidental Exophytic and infiltrating types Adenocarcinoma Local extension into liver, cystic duct, portahepatic LNs Mean 5 yr survival 1%
  • 64.
  • 65. Cholangiocarcinoma īŽ īŽ īŽ īŽ īŽ īŽ īŽ īŽ Older pts M>F Painless jaundice, N/V, weight loss Opisthorchis sinensis (liver fluke), PSC, inflammatory bowel disease Tumors usually small at dx yet not resectable Klatskin tumor – arises at bifurcation Adenocarcinoma Mean survival 6 to 18 months
  • 66.