Hepatobiliary and Pancreatic Disorders

Chapter 18 Hepatobiliary and Pancreatic Disorders

I. Laboratory Evaluation of Liver Cell Injury

A. Bilirubin metabolism and jaundice

(1) Senescent RBCs are phagocytosed by splenic macrophages.

18-1: Bilirubin metabolism. Refer to the text for discussion. RBC, red blood cell; UGT, uridine glucuronosyltransferase.

UCB: end-product of heme degradation in splenic macrophages

(2) UCB is the end-product of heme degradation.

• UCB is lipid-soluble (indirect bilirubin).

UCB: lipid soluble

b. UCB combines with albumin in the blood.

(1) UCB is taken up by hepatocytes.

(2) UCB is conjugated to glucuronic acid to produce conjugated bilirubin (CB).

• CB is water soluble (direct bilirubin).

CB: glucuronic acid makes bilirubin water soluble

c. CB is secreted into the intrahepatic bile ducts.

(1) Temporarily stored in the gallbladder

(2) Enters the duodenum via the common bile duct

e. Approximately 20% of UBG is recycled to the liver (90%) and kidneys (10%).

• Color of urine is due to urobilin.

Urobilin: color of stool and urine

2. Jaundice

a. Jaundice is due to an increase in UCB and/or CB.

(1) Jaundice is first noticed in the sclera (Fig. 18-2).

(2) Sclera has a high affinity for bilirubin.

18-2: Scleral icterus. Note the yellowish discoloration of the sclera.

(From Savin J, Hunter JA, Hepburn NC: Diagnosis in Color: Skin Signs in Clinical Medicine. London, Mosby-Wolfe, 1997, Fig. 6.28.)

Viral hepatitis: most common cause of jaundice

b. Classification of causes of jaundice is based on the percentage of CB (Table 18-1).

Table 18-1 Causes of Jaundice

Gilbert’s disease: 2nd most common cause of jaundice; fasting unconjugated hyperbilirubinemia

• Percent CB = CB/total bilirubin

c. Common causes of jaundice (Box 18-1)

B. Summary of liver function tests (Table 18-2)

C. Summary of laboratory findings in selective liver disorders (Table 18-3)

II. Viral Hepatitis

A. Phases of acute viral hepatitis

1. Prodrome

BOX 18-1 Common Causes of Jaundice

In this discussion, the symbol (+) is used to indicate degrees of magnitude. Normal bilirubin metabolism (A) shows liver uptake of lipid-soluble unconjugated bilirubin (UCB) and its conjugation with glucuronic acid to produce water-soluble conjugated bilirubin (CB). CB is secreted into the common bile duct (CBD) and is emptied into the bowel. Intestinal bacteria convert CB to urobilinogen (UBG), which spontaneously oxidizes to the pigment urobilin. Urobilin is responsible for the color of stool. A small percentage of UBG is reabsorbed into the blood. Most of it enters the liver (larger arrow) and a small percentage (smaller arrow) enters the urine (UBG). Urobilin is responsible for the color of urine. All of the normal bilirubin in blood is UCB (CB% < 20%) primarily derived from macrophage destruction of senescent RBCs. UCB does not enter urine, because it is attached to albumin in the blood and is lipid, not water, soluble. CB is never a normal finding in urine because it does not have contact with blood in its metabolism.

In extravascular hemolysis (B) (e.g., hereditary spherocytosis), there is increased macrophage production of UCB causing an increase in serum UCB (++) (CB% < 20%). There is a corresponding increase in uptake and conjugation of UCB, conjugation to CB (++), and conversion of CB in the bowel to UBG (++). This causes darkening of the stool. There is a greater percentage of UBG recycled back to the liver (wider arrow) and urine (wider arrow). The increase in urine UBG (++), darkens the color of urine. Because RBCs contain the enzyme aspartate aminotransferase (AST), hemolysis of RBCs causes an increase in serum AST. Alanine aminotransferase (ALT), alkaline phosphatase (ALP), and γ-glutamyltransferase (GGT) levels are normal.

In viral hepatitis (C), there is generalized liver dysfunction involving uptake and conjugation of UCB, secretion of CB into bile ducts, and recycling of UBG. Serum UCB is increased (++) owing to a decrease in uptake and conjugation. Serum and urine CB are increased (++) because of liver cell necrosis and disruption of bile ductules between hepatocytes. Urine UBG is increased (++) because UBG is redirected from the liver (smaller arrow) to the kidneys (larger arrow). Because there is an increase in serum UCB and CB, there is a mixed hyperbilirubinemia with a CB% of 20% to 50%. In viral hepatitis, ALT is higher (+++) than AST (++) and there is a slight increase in ALP and GGT (+). In alcoholic hepatitis, AST is greater than ALT, because alcohol damages mitochondria, which is where AST is normally located.

In obstructive liver disease (D), an increase in serum and urine CB (++) is due to obstruction of intrahepatic or extrahepatic bile flow (stone in the CBD in this case). This causes increased pressure in the intrahepatic bile ductules leading to rupture and egress of CB into sinusoidal blood. There is absence of UBG in the stool (light-colored) and urine. CB% > 50% and there is a marked increase in serum ALP and GGT (+++) and only a slight increase in serum AST and ALT (+).

Table 18-2 Liver Function Tests

Table 18-3 Summary of Laboratory Findings in Selected Liver Disorders

Phases acute hepatitis: prodrome, jaundice, recovery

a. Fever

b. Painful hepatomegaly; distaste for alcohol/cigarettes

c. Serum transaminases increase steadily.

Transaminases: peak before jaundice

• Peak just before jaundice occurs

d. Atypical lymphocytosis

2. Jaundice

a. Variable finding depending on the type of hepatitis

b. Increased urine bilirubin and urine UBG

3. Recovery

• Jaundice resolves.

B. Microscopic findings in acute viral hepatitis

1. Lymphocytic infiltrate with destruction of hepatocytes (see Fig. 2-9)

• Apoptosis of hepatocytes (Councilman bodies; see Fig. 1-12)

2. Persistent inflammation and fibrosis is an unfavorable sign.

• Sign of chronic hepatitis progressing to postnecrotic cirrhosis

C. Epidemiology of viral hepatitis (Table 18-4)

Table 18-4 Viral Hepatitis: Transmission and Clinical Findings

Hepatitis A: most common viral cause of jaundice

D. Serologic studies in viral hepatitis

1. Hepatitis A virus (HAV)

HAV: anti-HAV-IgM indicates infection; anti-HAV-IgG indicates recovery/vaccination

a. Anti-HAV-IgM indicates active infection.

b. Anti-HAV-IgG indicates recovery from infection or vaccination.

Extravascular hemolysis: ↑↑ UBG, no UB

• Protective antibody

2. Hepatitis B virus (HBV) (Fig. 18-3 and Table 18-5)

a. Hepatitis B surface antigen (HBsAg)

(1) Appears within 2 to 8 weeks after exposure

• First marker of infection

18-3: Serologic markers in hepatitis B. Anti-HBc, anti-HBV core antigen; anti-HBe, anti-HBV e antigen; anti-HBs, anti-HBV surface antibody; HBsAg, hepatitis B surface antigen; HBeAg, hepatitis B e antigen; HBV, hepatitis B virus; IgG, immunoglobulin G; IgM, immunoglobulin M.

Table 18-5 Serologic Studies in Hepatitis B Virus (HBV)

HBsAg: first antigen to arrive and last one to leave with recovery

(2) Persists up to 4 months in acute hepatitis

• HBsAg longer than 6 months defines chronic HBV.

b. Hepatitis B e antigen (HBeAg) and HBV-DNA

HBeAg and HBV-DNA: infective particles

(1) Infective particles

(2) Appear after HBsAg and disappear before HBsAg

c. Anti-HBV core antibody IgM (anti-HBc-IgM)

(1) Nonprotective antibody

• Remains positive in acute infections

(2) Persists during “window phase” or “serologic gap”

Anti-HBc-IgM: only marker present during window phase

• HBsAg, HBV DNA, and HBeAg are absent.

(3) Converts entirely to anti-HBc-IgG by 6 months

Anti-HBc-IgG: present after 6 months

d. Anti-HBV surface antibody (anti-HBs)

(1) Protective antibody

Anti-HBs: protective antibody; immunization or recovery from past infection

(2) Marker of immunization after HBV vaccination

e. Chronic HBV

(1) Persistence of HBsAg longer than 6 months

HBsAg > 6 months defines chronic HBV

• Anti-HBc-IgM converts to anti-HBc-IgG.

(2) “Healthy” chronic carrier

(a) Presence of HBsAg and anti-HBc-IgG

“Healthy” carrier: HBsAg, anti-HBc-IgG

(b) Absence of DNA and e antigen

(3) Infective chronic carrier

Infective carrier: HBsAg, HBeAg, HBV-DNA, anti-HBc-IgG

(a) Presence of HBsAg, anti-HBc-IgG, and infective particles (DNA and e antigen)

(b) Increased risk for postnecrotic cirrhosis and hepatocellular carcinoma

3. Hepatitis C virus (HCV)

a. Screen with enzyme immunoassay (EIA)

(1) Presence of anti-HCV-IgG indicates active infection or recovery.

• Sensitivity > 97%

(2) It does not differentiate among acute, chronic, or resolved infection.

(3) It is not a protective antibody.

HCV testing: screen with EIA; confirm with RIBA and HCV RNA

b. Confirmatory tests

(1) Recombinant immunoblot assay (RIBA)

(a) Supplemental test if EIA is positive

(b) More specific but less sensitive than EIA

(2) HCV RNA using polymerase chain reaction

HCV RNA: gold standard test

(a) Gold standard test for diagnosing HCV

(b) Detects virus as early as 1 to 2 weeks after infection

(3) Positive RIBA and HCV RNA indicate active infection.

(4) Positive RIBA and negative HCV RNA indicate recent recovery.

4. Hepatitis D virus (HDV)

a. Presence of anti-HDV-IgM or IgG indicates active infection.

b. IgG is not a protective antibody.

HCV, HDV: no protective antibodies

5. Hepatitis E virus (HEV)

a. Presence of anti-HEV-IgM indicates active infection.

b. Anti-HEV-IgG indicates recovery (protective antibody).

E. Other laboratory test findings (see Box 18-1C)

1. CB 20% to 50% (mixed hyperbilirubinemia)

a. Decreased uptake/conjugation of UCB

b. CB gains access to blood via damaged bile ductules.

2. Increased urine UBG and urine bilirubin

a. CB is water soluble and is filtered in the kidneys.

b. UBG recycled back to inflamed liver is redirected to the kidneys.

Viral hepatitis: urine UBG ++, urine bilirubin ++

3. Increased serum transaminases

a. Serum ALT is greater than AST.

Serum ALT: last enzyme to return to normal

b. Serum ALT is the last liver enzyme to return to normal.

III. Other Inflammatory Disorders

A. Summary of important infectious diseases (Table 18-6 and Fig. 18-4)

B. Autoimmune hepatitis

1. Epidemiology

a. Two types

(1) Type 1 is the predominant form in the United States and worldwide (80%).

Table 18-6 Infectious Diseases of the Liver

18-4: Hydatid cyst. A single cyst in the liver shows numerous daughter cysts containing larval forms.

(From MacSween R, Burt A, Portmann B, et al: Pathology of the Liver, 4th ed. London, Churchill Livingstone, 2002, p 388, Fig. 8-35.)

Autoimmune hepatitis: type 1 most common in the United States

(2) Type 2 is uncommon in the United States (not discussed).

b. Occurs most often in young women

c. Range of presentations

(1) Symptomatic with increased transaminases

(2) Fulminant hepatitis

(3) Cirrhosis

d. Human leukocyte antigen (HLA) DR3 and DR4 association

e. Other autoimmune associations

• Examples—Hashimoto’s thyroiditis, Graves’ disease

2. Clinical findings

a. Fever

b. Jaundice

c. Hepatosplenomegaly

Autoimmune hepatitis: + serum ANA, + anti–smooth muscle antibodies

3. Laboratory findings for type 1

a. Positive serum antinuclear antibody (ANA) test (>60%)

b. Anti–smooth muscle antibodies (>85%)

c. Increased serum transaminases

d. Decreased serum albumin in severe disease

e. Prolonged prothrombin time in severe disease

4. Treatment

a. Initial treatment with corticosteroids + azathioprine

b. Liver transplantation if resistant to therapy

C. Neonatal hepatitis

1. Epidemiology

a. Idiopathic

b. Associated with congenital infections

• Example—cytomegalovirus

c. Associated with inborn errors of metabolism

• Example—α₁-antitrypsin deficiency

2. Biopsy shows multinucleated giant cells.

Neonatal hepatitis: multifactorial; biopsy shows multinucleated giant cells

• “Giant cell” hepatitis

D. Reye syndrome

1. Epidemiology

a. Postinfectious triad:

(1) Encephalopathy

(2) Microvesicular fatty change

(3) Transaminase elevation

b. Uncommon since the role of aspirin was elucidated

c. Usually develops in children < 4 years old

Reye syndrome: association with aspirin and infection (chickenpox, influenza)

• Often follows a chickenpox or influenza infection

2. Pathogenesis

a. Mitochondrial damage (? virus, salicylates)

b. Disruption of the urea cycle

• Increase in serum ammonia

c. Defective β-oxidation of fatty acids

3. Microvesicular fatty change (? salicylate effect)

a. Small cytoplasmic globules without nuclear displacement

b. No inflammatory infiltrate

4. Clinical findings

Reye syndrome: encephalopathy, fatty change in liver, ↑ transaminases

a. Initially afebrile, quiet, lethargic, sleepy, and vomiting

• Hepatomegaly and liver dysfunction present

b. Encephalopathy findings in progression

Reye syndrome: sleepy but respond → stuporous → obtundation → coma

• Signs and symptoms related to cerebral edema and increasing pressure

(1) Sleepy but respond; vomiting

(2) Stuporous, seizures, decorticate rigidity, intact papillary reflexes

(3) Deepening coma, decerebrate rigidity, fixed pupils

(4) Coma, loss of deep tendon reflexes, fixed dilated pupils, flaccidity/decerebrate

(5) Death

5. Laboratory findings

a. Transaminasemia

Reye syndrome: ↓ transaminases, bilirubin, PT, ammonia; ↓ glucose

b. Normal to slight increase in total bilirubin

c. Increased serum ammonia and prothrombin time (PT)

• Levels predict degree of severity

d. Hypoglycemia

e. Cerebrospinal fluid usually normal

6. Treatment

a. Supportive

b. Mannitol, glycerol, or hyperventilation to reduce cerebral edema

7. Approximately 25% to 50% mortality rate

E. Acute fatty liver of pregnancy

1. Abnormality in β-oxidation of fatty acids (FAs)

Fatty liver of pregnancy: dysfunction in β-oxidation FAs; deliver baby

2. Fatal to mother and fetus unless the baby is delivered

F. Preeclampsia (refer to Chapter 21)

1. Hypertension, proteinuria, dependent pitting edema in third trimester

2. Liver cell necrosis around portal triads (zone 1)

Preeclampsia: periportal triad liver cell necrosis; HELLP syndrome

• Increased serum transaminases

3. HELLP syndrome

a. Hemolytic anemia with schistocytes (refer to Chapter 11)

b. Elevated serum transaminases

c. Low platelets

• Due to disseminated intravascular coagulation (refer to Chapter 14)

G. Fulminant hepatic failure

• Acute liver failure with encephalopathy within 8 weeks of hepatic dysfunction

1. Causes

Fulminant hepatic failure: viral hepatitis most common overall cause

a. Viral hepatitis (most common overall cause)

b. Drugs (e.g., acetaminophen most common cause)

c. Reye syndrome

2. Gross and microscopic findings

Fulminant hepatitis: acetaminophen most common drug cause

a. Wrinkled capsular surface due to loss of hepatic parenchyma

b. Dull red to yellow necrotic parenchyma with blotches of green (bile)

3. Clinical findings

• Hepatic encephalopathy (see section VII), jaundice

4. Laboratory findings

Fulminant hepatic failure: ↑ transaminases, ↑ PT and ammonia

a. Decrease in transaminases

• Liver parenchyma is destroyed.

b. Increase in PT and ammonia

5. Treatment (refer to section VII, Cirrhosis)

IV. Circulatory Disorders

A. Prehepatic obstruction to blood flow

• Obstruction of blood flow to the liver (i.e., hepatic artery, portal vein)

1. Hepatic artery thrombosis with infarction

Hepatic artery infarction: uncommon due to dual blood supply

a. Liver infarction is uncommon because of a dual blood supply.

• Hepatic artery and portal vein tributaries normally empty blood into the sinusoids.

b. Causes

(1) Liver transplant rejection

Hepatic artery infarction: liver transplant rejection, PAN

(2) Vasculitis due to polyarteritis nodosa (PAN)

2. Portal vein thrombosis

a. Causes

(1) Pylephlebitis (inflammation of portal vein)

(a) Most often due to acute appendicitis

(b) Air in portal vein from bacterial gas

(2) Polycythemia vera

(3) Hepatocellular carcinoma

• Tumor invasion of the portal vein

b. Clinical findings

Portal vein thrombosis: ascites, portal hypertension, no hepatomegaly; air in portal vein

(1) Portal hypertension, ascites, splenomegaly

(2) No hepatomegaly

B. Intrahepatic obstruction to blood flow

• Intrahepatic obstruction to sinusoidal blood flow

1. Causes

a. Cirrhosis (see section VII)

Intrahepatic obstruction to blood flow: cirrhosis most common cause

b. Centrilobular hemorrhagic necrosis

c. Peliosis hepatis

d. Sickle cell disease (see Chapter 11)

2. Centrilobular hemorrhagic necrosis

a. Most often due to left-sided heart failure (LHF) and right-sided heart failure (RHF)

Centrilobular necrosis: combined LHF and RHF; “nutmeg” liver

(1) LHF decreases cardiac output causing hypoperfusion of the liver.

• Causes ischemic necrosis of hepatocytes located around central vein (refer to Chapter 1)

(2) RHF causes a backup of systemic venous blood into the central veins and sinusoids.

b. Enlarged liver with a mottled red appearance (“nutmeg” liver) (Fig. 18-5)

(1) Congestion of central veins and sinusoids

(2) Necrosis of hepatocytes around the central vein

c. Clinical findings

(1) Painful hepatomegaly with or without jaundice

(2) Increased transaminases caused by ischemic necrosis

(3) May progress to cardiac cirrhosis

• Fibrosis around central veins

18-5: Centrilobular hemorrhagic necrosis (“nutmeg” liver). The liver has a mottled cut surface. Dark areas represent congested central veins and sinusoids.

(From Damjanov I, Linder J: Pathology: A Color Atlas. St. Louis, Mosby, 2000, p 146, Fig. 8-8.)

Centrilobular necrosis: may progress to cardiac cirrhosis

d. Treatment

• Treat heart failure

3. Peliosis hepatis

a. Sinusoidal dilation due to blood

b. Causes

Peliosis hepatis: anabolic steroids, Bartonella henselae

(1) Anabolic steroids

(2) Bartonella henselae causing bacillary angiomatosis (refer to Chapter 9)

• Occurs in AIDS

c. Potential for intraperitoneal hemorrhage

C. Posthepatic obstruction to blood flow

• Obstruction of blood flow out of the liver (e.g., hepatic vein)

1. Causes

a. Hepatic vein thrombosis

b. Veno-occlusive disease

2. Hepatic vein thrombosis

a. Causes

Polycythemia vera: most common cause of hepatic vein thrombosis

(1) Polycythemia vera

• Most common cause (up to 40% of cases)

(2) Hypercoagulable state (20% of cases)

(a) Oral contraceptive pills

(b) Protein C/S deficiency

(3) Hepatocellular carcinoma (<5% of cases)

• Invades hepatic vein

b. Clinical findings

Hepatic vein thrombosis: hepatomegaly, portal hypertension, ascites

(1) Enlarged, painful liver

(2) Portal hypertension, ascites, splenomegaly

(3) High mortality rate

c. Laboratory findings

(1) Increased transaminases

(2) Increased PT

d. Diagnosis

(1) Ultrasound with pulsed Doppler first-line test

(2) MRI

e. Treatment

(1) Anticoagulation

(2) In situ thrombolysis

(3) Stenting, various shunts

f. Prognosis

• Approximately 75% mortality rate in first year

3. Veno-occlusive disease

a. Complication of bone marrow transplantation

Veno-occlusive disease: complication of bone marrow transplantation

b. Collagen develops around the central veins.

D. Hematobilia

• Blood in the bile in patients with trauma to the liver

Hematobilia: blood in bile from liver trauma

A. Alcohol-related disorders

1. Risk factors for alcohol-related liver disease (refer to Chapter 6)

2. Pathways for alcohol metabolism (refer to Chapter 6)

3. Types of liver disease

Alcohol liver disease: fatty change, hepatitis, cirrhosis

a. Fatty change is the most common type of disease (see **Fig. 1-8).

(1) Substrates of alcohol metabolism are used to synthesize liver triglyceride.

(2) Clinical findings

• Tender hepatomegaly without fever or neutrophilic leukocytosis

(3) Treatment

• Alcohol rehabilitation

b. Alcoholic hepatitis

(1) Pathogenesis

(a) Genetic predisposition is likely.

(b) Due to acetaldehyde damage to hepatocytes

Alcoholic hepatitis: acetaldehyde damages hepatocytes

• Perivenular fibrosis

(2) Microscopic findings

(a) Fatty change with neutrophil infiltration

(b) Mallory bodies

• Damaged cytokeratin intermediate filaments in hepatocytes (see Fig. 1-7)

Alcoholic hepatitis: fatty change, neutrophil infiltration, Mallory bodies

(3) Clinical findings

(a) Painful hepatomegaly

(b) Fever, neutrophilic leukocytosis, ascites, hepatic encephalopathy

(4) Laboratory findings

(a) Absolute neutrophilic leukocytosis

(b) Serum aspartate aminotransferase (AST) > alanine aminotransferase (ALT)

• Serum GGT disproportionately increase to ALP (see Table 18-2)

(d) Thrombocytopenia in some cases

(e) Hypoglycemia in some cases

(5) Treatment

(a) Mandatory to stop drinking

(b) Corticosteroids helpful in some cases

c. Cirrhosis (see section VII)

4. Laboratory findings (refer to Chapter 6; see Fig. 6-1)

B. Chemical- and drug-induced liver disease (Table 18-7)

Table 18-7 Drug- and Chemical-Induced Liver Diseases

Intrahepatic fibrosis: methotrexate, amiodarone

VI. Obstructive (Cholestatic) Liver Disease

2. Extrahepatic cholestasis

Extrahepatic cholestasis: most commonly caused by a stone in CBD

a. Blockage of common bile duct (CBD)

b. Causes

(1) Stone usually originating from the gallbladder

(2) Primary sclerosing cholangitis

(3) Extrahepatic biliary atresia

(4) Carcinoma head of pancreas

B. Gross and microscopic

1. Enlarged, greenish liver

2. Bile ducts distended with bile (Fig. 18-6), bile lakes, bile infarcts

C. Clinical findings

1. Jaundice with pruritus

• Pruritus due to bile salts deposited in skin

2. Malabsorption

• Bile salts do not enter the small intestine.

3. Cholesterol deposits in skin

a. Due to cholesterol in bile

b. Example—xanthelasma (see Fig. 9-2B)

4. Light-colored stools

• Due to a lack of urobilin

D. Laboratory findings (see Box 18-1D)

1. CB > 50%

2. Bilirubinuria

3. Absent urine UBG

18-6: Cholestasis. Note the dilated bile ductules filled with yellowish-green bile.

(From Klatt E: Robbins and Cotran’s Atlas of Pathology. Philadelphia, WB Saunders, 2006, p 199, Fig. 8-11.)

Cholestasis: urine UBG 0, urine bilirubin ++

4. Increase in serum ALP and GGT

5. Increase in serum cholesterol (present in bile)

E. Benign intrahepatic cholestasis of pregnancy

1. Due to estrogen inhibition of intrahepatic bile secretion

Cholestasis in pregnancy: effect of estrogen on intrahepatic bile secretion

2. Not dangerous to the fetus or mother

F. Extrahepatic biliary atresia

1. Cause of jaundice in newborns

Extrahepatic biliary atresia: jaundice in newborn

2. Inflammatory destruction of all or part of the extrahepatic bile ducts

3. Bile duct proliferation in the triads

4. Common indication for liver transplantation in a child

G. Primary sclerosing cholangitis (PSC)

1. Epidemiology

a. Obliterative fibrosis of intrahepatic and extrahepatic bile ducts

PSC: obliterative fibrosis intrahepatic and extrahepatic bile ducts

b. Primary disease

(1) Genetic predisposition

• Association with HLA-DR52a (100%) and HLA-Cw7 (86%)

(2) Male dominant (70%); usually <45 years old

(3) Associations

(a) Inflammatory bowel disease (70%)

• Ulcerative colitis > Crohn’s disease

(b) Other sclerosing disorders

• Retroperitoneal and mediastinal sclerosing fibrosis

(4) Complications

(a) Cirrhosis

(b) Cholangiocarcinoma

PSC: strong association with ulcerative colitis > Crohn’s disease

PSC: cirrhosis, cholangiocarcinoma

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Jun 25, 2017 | Posted by admin in PATHOLOGY & LABORATORY MEDICINE | Comments Off

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