2. LIVER
• THE LIVER IS THE LARGEST INTERNAL ORGAN, AND THE BODY’S SECOND
LARGEST, AFTER THE SKIN. ITS BOTH AN ORGAN & GLAND, IT HAS FOUR LOBES
AND IS SURROUNDED BY A CAPSULE OF FIBROUS CONNECTIVE TISSUE
CALLED GLISSON’S CAPSULE.
• GLISSON’S CAPSULE IN TURN IS COVERED BY THE VISCERAL PERITONEUM
(TUNICA SEROSA), EXCEPT WHERE THE LIVER ADHERES DIRECTLY TO THE
ABDOMINAL WALL OR OTHER ORGANS. THE PARENCHYMA WITHIN THE
LOBULES IS SUPPORTED ONLY BY FINE RETICULAR FIBRES. CONNECTIVE
TISSUE ENTER THE LIVER THROUGH THE HILUS OR PORTA TO DIVIDE IT INTO
LOBULES.
3. LIVER
• THIS SECTION SHOWS THE STRUCTURE OF
THE LIVER WHICH IS A SOLID ORGAN
COMPOSED OF TIGHTLY PACKED, PINK
STAINING PLATES OF EPITHELIAL CELLS
TERMED HEPATOCYTES. THE OUTER
SURFACE OF THE LIVER IS COVERED BY A
CAPSULE COMPOSED OF COLLAGENOUS
TISSUE C CALLED GLISSON’S CAPSULE
OVER WHICH IS A LAYER OF MESOTHELIAL
CELLS M FROM THE PERITONEUM.
4. LIVER
• SLIDE [B] SHOWS THE OVERALL
ARCHITECTURE OF THE LIVER. THE
LIVER DOES NOT CONTAIN MUCH OF
CONNECTIVE TISSUE. MOST OF THE
COLLAGENOUS CONNECTIVE TISSUE
IN THE LIVER IS IN THE FORM OF THE
PORTAL TRACTS P WHICH CONTAIN
THE MAIN BLOOD VESSELS RUNNING
INTO THE LIVER.
• LESS CONSPICUOUS THAN THE
PORTAL TRACTS ARE THE
CENTRILOBULAR VENULES [HEPATIC
VENULES] V THAT DRAIN THE LIVER.
THESE ARE TRIBUTARIES OF THE
HEPATIC VEIN AND TAKE BLOOD AWAY
FROM THE LIVER. [BARBARA ET AL.,
2006]
5. FUNCTIONS OF THE LIVER
• FAT METABOLISM ; OXIDIZING TRIGLYCERIDES TO PRODUCE ENERGY
• SYNTHESIS OF PLASMA LIPOPROTEINS.
• SYNTHESIS OF CHOLESTEROL AND PHOSPHOLIPID
• CARBOHYDRATE METABOLISM;
• CONVERTING CARBOHYDRATES AND PROTEINS INTO FATTY ACIDS AND TRIGLYCERIDE.
• REGULATION OF BLOOD GLUCOSE CONCENTRATION BY GLYCOGENESIS, GLYCOGENOLYSIS AND
• GLUCONEOGENESIS.
• PROTEIN METABOLISM
• SYNTHESIS OF THE PLASMA PROTEINS, INCLUDING ALBUMIN AND CLOTTING FACTORS.
• SYNTHESIS OF THE NON-ESSENTIAL AMINO ACIDS
• DETOXIFICATION OF METABOLIC WASTE PRODUCTS E;G DEAMINATION OF AMINO ACIDS AND PRODUCTION OF UREA
• STORAGE
• STORAGE OF GLYCOGEN, VITAMINS, IRON.
• INTERMEDIARY METABOLISM
• DETOXIFICATION OF VARIOUS DRUGS AND TOXINS, SUCH AS ALCOHOL. [BARBARA ET AL., 2006]
6. CELL TYPES
• TWO MAJOR TYPES OF CELLS POPULATE THE LIVER LOBES;
• 1]PARENCHYMAL CELLS
• HEPATOCYTES
• 2] NON-PARENCHYMAL CELLS
• SINUSOIDAL HEPATIC ENDOTHELIAL CELLS
• KUPFFER CELLS
• HEPATIC STELLATE CELLS
7. HEPATOCYTES
• HEPATOCYTES, ARE LARGE POLYGONAL CELLS, USUALLY TETRAPLOID AND OFTEN
BINUCLEATE IN THE ADULT. EACH NUCLEUS HAS TWO OR MORE NUCLEOLI. THE
AVERAGE LIFE SPAN OF LIVER CELLS IS FIVE MONTHS. THEY CONTAIN ABUNDANT
ROUGH ENDOPLASMIC RETICULUM AND MITOCHONDRIA, LARGE DEPOSITS OF
GLYCOGEN AND LIPID DROPLETS OF VARIOUS SIZES, AND SEVERAL SMALL
ELABORATE GOLGI COMPLEXES. THEY ALSO CONTAIN MANY PEROXISOMES, A
VARIABLE AMOUNT OF SMOOTH ENDOPLASMIC RETICULUM AND LYSOSOMES. IN
STANDARD HISTOLOGICAL PREPARATIONS, LIVER CELLS USUALLY APPEAR
VACUOLATED BECAUSE THE GLYCOGEN AND LIPIDS ARE REMOVED DURING
PROCESSING. LIVER CELLS ARE CAPABLE OF CONSIDERABLE REGENERATION WHEN
LIVER SUBSTANCE IS LOST.
8. HEPATOCYTES
• HEPATOCYTES
• BC : BINUCLEATE CELLS
• S : SINUSOIDS
• THE SINUSOIDS ARE LINED BY FLAT
ENDOTHELIAL LINING CELLS WHICH
ARE READILY DISTINGUISHABLE
FROM HEPATOCYTES BY THEIR
FLATTENED CONDENSED NUCLEI
AND ATTENUATED POORLY STAINED
CYTOPLASM.
9. KUPFFER CELLS
• THE LIVER HAS ITS OWN VERSION
OF MACROPHAGES WHICH IS
KNOWN AS THE KUPFFER CELL
(STAINED BLUE BY UPTAKE OF
TRYPAN BLUE)
10. LIVER LOBULE
• THE HEPATIC LOBULE IS ROUGHLY
HEXAGONAL IN SHAPE AND IS
CENTRE ON A TERMINAL HEPATIC
VANULE V. THE PORTAL TRACTS T
ARE POSITIONED AT THE ANGLES
OF THE HEXAGONAL. THE LOBULE
IS OUTLINED BY BANDS OF
FIBROUS TISSUE C GIVING A WELL
DEFINED STRUCTURAL UNIT.
11. PORTAL TRACT
• THIS SLIDE SHOWS A TYPICAL PORTAL TRACT
CONTAINING THREE MAIN STRUCTURES. THE
LARGEST IS A TERMINAL BRANCH OF THE
HEPATIC PORTAL VEIN PV WHICH HAS A THIN
WALL LINED BY ENDOTHELIAL CELLS. SMALLER
DIAMETER THICK WALLED VESSELS ARE
TERMINAL BRANCHES OF THE HEPATIC ARTERY A
WITH THE STRUCTURE OF ARTERIOLES.
• A NETWORK OF BILE CANALICULI IS LOCATED
WITHIN EACH PLATE OF HEPATOCYTES, THESE
DRAIN INTO BILE COLLECTING DUCTS LINED BY
SIMPLE CUBOIDAL OR COLUMNAR EPITHELIUM,
KNOWN AS THE CANALS OF HERING, WHICH IN
TURN DRAIN INTO THE BILE DUCTULES B.
• LYMPHATICS L ARE ALSO PRESENT IN THE
PORTAL TRACTS. SURROUNDING THE PORTAL
TRACT ARE ANASTOMOSING PLATES OF
HEPATOCYTES H, BETWEEN WHICH ARE THE
HEPATIC SINUSOIDS S RECEIVING BLOOD FROM
BOTH THE HEPATIC PORTAL AND HEPATIC
12. Hepatic cirrhosis
This condition is characterized by aggregates of regenerated hepatic cells that are separated by bands of scar tissue (deposited
collagen tissue). These two processes take place in response to some extent of hepatocyte destruction, resulting in their damage
and subsequent death.
Some causes include:
Chronic alcoholism
Hepatitis B or C infection
Certain autoimmune conditions
Some genetic metabolic diseases that result in an excessive storage of copper and iron
The scar tissue negatively impacts the blood flow from the sinusoids to the hepatocytes, resulting in a decrease in function. As a
result, portal hypertension develops because the blood cannot drain from the portal vein.
Cirrhosis of the liver is one of the ten leading causes of death in the Western world. Irrespective of the etiology, cirrhosis in
general is initiated by hepatocellular necrosis. It represents the irreversible end-stage of several diffuse diseases causing
hepatocellular injury and is characterised by the following 4 features:
1. It involves the entire liver.
2. The normal lobular architecture of hepatic parenchyma is disorganised.
3. There is formation of nodules separated from one another by irregular bands of fibrosis.
4. It occurs following hepatocellular necrosis of varying etiology so that there are alternate areas of necrosis and regenerative
nodules. However, regenerative nodules are not essential for diagnosis of cirrhosis since biliary cirrhosis and cirrhosis in
haemochromatosis have little regeneration.
13. CLASSIFICATION
Cirrhosis can be classified on the basis of morphology and etiology.
A. MORPHOLOGIC CLASSIFICATION. There are 3 morphologic types of cirrhosis—micronodular, macronodular and
mixed. Each of these forms may have an active and inactive form.
An active form is characterised by continuing hepatocellular necrosis and inflammatory reaction, a process that closely
resembles chronic hepatitis.
An inactive form, on the other hand, has no evidence of continuing hepatocellular necrosis and has sharply-defined nodules of
surviving hepatic parenchyma without any significant inflammation.
14. 1. Micronodular cirrhosis.
In micronodular cirrhosis, the nodules are usually regular and small, less than 3 mm in diameter. There is diffuse
involvement of all the hepatic lobules forming nodules by thick fibrous septa which may be portal-portal, portal-central, or
both. The micronodular cirrhosis includes etiologic type of alcoholic cirrhosis (or nutritional cirrhosis or Laennec’s
cirrhosis) and represents impaired capacity for regrowth as seen in alcoholism, malnutrition, severe anaemia and old age.
15. 2. Macronodular cirrhosis.
In this type, the nodules are of variable size and are generally larger than 3 mm in diameter. The pattern of involvement is more
irregular than in micronodular cirrhosis, sparing some portal tracts and central veins, and more marked evidence of regeneration.
Macronodular cirrhosis corresponds to post-necrotic (or posthepatitis) cirrhosis of the etiologic classification.
16. 3. Mixed cirrhosis.
In mixed type, some parts of the liver show micronodular appearance while other parts show macronodular pattern. All the
portal tracts and central veins are not involved by fibrosis but instead some of them are spared. Mixed pattern is a kind of
incomplete expression of micronodular cirrhosis.
17. B. ETIOLOGIC CLASSIFICATION.
Based on the etiologic agent for cirrhosis, various categories of cirrhosis are described as given in Table below
18. 1. Alcoholic Liver Disease and Cirrhosis
Alcoholic liver disease is the term used to describe the spectrum of liver injury associated with acute and chronic alcoholism.
There are three sequential stages in alcoholic liver disease: alcoholic steatosis (fatty liver), alcoholic hepatitis and alcoholic
cirrhosis
1. Post-necrotic Cirrhosis
Post-necrotic cirrhosis, also termed post-hepatitic cirrhosis, macronodular cirrhosis and coarsely nodular cirrhosis, is characterised
by large and irregular nodules with broad bands of connective tissue and occurring most commonly after previous viral hepatitis.
Based on epidemiologic and serologic studies, the following factors have been implicated in the etiology of post-necrotic cirrhosis:
• Viral hepatitis. About 25% of patients give history of recent or remote attacks of acute viral hepatitis followed by chronic viral
hepatitis. Most common association is with hepatitis B and C; hepatitis A is not known to evolve into cirrhosis. It is estimated
that about 20% cases of HBV chronic hepatitis and about 20-30% cases of HCV chronic hepatitis go to develop cirrhosis over
20-30 years.
• Drugs and chemical hepatotoxins. A small percentage of cases may have origin from toxicity due to chemicals and drugs such
as phosphorus, carbon tetrachloride, mushroom poisoning, acetaminophen and α-methyl dopa.
• Others. Certain infections (e.g. brucellosis), parasitic infestations (e.g. clonorchiasis), metabolic diseases (e.g. Wilson’s disease
or hepatolenticular degeneration) and advanced alcoholic liver disease may produce a picture of post-necrotic cirrhosis.
• Idiopathic. After all these causes have been excluded, a group of cases remain in which the etiology is unknown
19. Biliary Cirrhosis
Biliary cirrhosis is defined as a chronic disorder characterised by clinical, biochemical and morphological features of
longcontinued cholestasis of intrahepatic or extrahepatic origin. Biliary cirrhosis is of following types:
Primary biliary cirrhosis in which the destructive process of unknown etiology affects intrahepatic bile ducts.
Secondary biliary cirrhosis resulting from prolonged mechanical obstruction of the extrahepatic biliary passages.
Primary sclerosing cholangitis and autoimmune cholangiopathy causing biliary cirrhosis.
ETIOLOGY. The etiology of these forms of biliary cirrhosis is distinctive:
A. Primary biliary cirrhosis. The etiology of this type remains unknown. However, a few factors have been implicated:
1. The condition is predominant in middle-aged women (male: female ratio = 1:9) and has led to the suggestion of a possible
endocrine origin.
2. Familial incidence has been observed suggesting the role of some genetic influence and certain HLA types.
3. There is elevated cholesterol level with appearance of xanthoma and xanthelasma. Hepatomegaly and chronic liver disease are
late features of the disease.
4. However, presently the most widely accepted hypothesis is autoimmune origin of the disease. In support are the following
observations:
20. A. Primary biliary cirrhosis. The etiology of this type remains unknown. However, a few factors have been implicated:
1. The condition is predominant in middle-aged women (male: female ratio = 1:9) and has led to the suggestion of a possible
endocrine origin.
2. Familial incidence has been observed suggesting the role of some genetic influence and certain HLA types.
3. There is elevated cholesterol level with appearance of xanthoma and xanthelasma. Hepatomegaly and chronic liver disease are
late features of the disease.
4. However, presently the most widely accepted hypothesis is autoimmune origin of the disease. In support are the following
observations:
- Increased incidence of associated autoimmune diseases (e.g. scleroderma, Sjögren’s syndrome, CREST syndrome, and
autoimmune thyroiditis),
- Circulating anti-mitochondrial antibody of IgG class detected in more than 90% cases;
- Elevated levels of immunoglobulins, particularly of IgM
- Increased levels of circulating immune complexes;
- Decreased number of circulating T-cells; and
- Accumulation of T cells around bile ducts.
21. B. Secondary biliary cirrhosis.
Most cases of secondary biliary cirrhosis result from prolonged obstruction of extrahepatic biliary passages. These causes
include the following:
1. Extrahepatic cholelithiasis, most common
2. Biliary atresia
3. Cancer of biliary tree and of head of pancreas
4. Postoperative strictures with superimposed ascending cholangitis.
C. Cirrhosis due to primary sclerosing cholangitis. Primary or idiopathic sclerosing cholangitis is a chronic cholestatic syndrome
of unknown etiology. It is characterised by progressive, inflammatory, sclerosing and obliterative process affecting the entire
biliary passages, both extrahepatic and intrahepatic ducts. Although etiology remains unknown, various mechanisms have been
postulated which include viral and bacterial infections, immunologic injury, toxins, and genetic predisposition.
22. Hepatocellular Carcinoma (HCC)
HCC is ranking as the 6th position of human cancers, is the most common type of primary liver cancer, followed by
cholangiocarcinoma. Importantly, HCC represents the main complication of cirrhosis, and shows a growing incidence worldwide
related to the increased prevalence of the various risk factors of chronic liver diseases, such as hepatitis infection with hepatitis C
and B viruses, and more recently Fatty Liver Diseases which are mostly associated with metabolic syndrome. Although most
HCC develop in the background of chronic liver disease, some may occur on normal liver and usually correspond to specific
types, including fibrolamellar HCC mostly encountered in young population, or malignant transformation of hepatocellular
adenomas. Overall, HCC is still associated with a poor prognosis depending on delayed diagnosis, the clinical status of the
patient but also tumor behavior showing a great propensity for angioinvasion. Liver tumor classification has recently been
reviewed according to the 2010 WHO classification
Pathological analysis of HCC is an overall procedure able to provide its accurate diagnosis and prognosis by evaluating both
tumor macroscopic (including tumor size, growth pattern of development…) and microscopic features (including grade of
differentiation, vascular invasion…), and aspect of nontumoral liver, especially the identification of preneoplastic changes. At
last, pathogenesis of HCC is complex, involving different molecular pathways that may reflect both underlying etiologies and
biological tumor behavior.
Hepatocellular Carcinoma Associated with Chronic Liver Diseases HCC represents one of the main complications of chronic
liver diseases. As a result, most HCCs develop in the background of advanced liver fibrosis and cirrhosis, highlighting the
multistep process of liver carcinogenesis through the progressive malignant transformation of cirrhotic nodules and premalignant
lesions.
24. Histology of Hepatocellular Carcinoma
On histology, the main hallmark of HCC is its resemblance to the normal liver both in its plate-like growth and its cytology. HCC
is usually a hypervascularized tumor showing different degrees of hepatocellular differentiation ranging from well to poorly
differentiated, that are based upon the architectural and cytologic features. Different histological patterns may be seen:
(1) the trabecular pattern of growth where tumoral hepatocytes are arranged in plates of various thickness, separated by sinusoid
vascular spaces.
(2) the acinar or pseudoglandular pattern showing gland-like dilatation of the canaliculi between tumor cells (lumens can contain
bile) or central degeneration of trabeculae (lumen containing mainly fibrin).
(3) the compact or solid pattern composed of thick trabeculae compressed into a compact mass.
25. Histologic features of Hepatocellular carcinoma: a Well-differentiated HCC with trabecular architecture,
few pseudoglandular structures are present. b HCC showing steatotic tumor cells. c Poorly differentiated
HCC with increased mitotic figures. d Glypican-3 immunostaining showing cytoplasmic positivity in most
of tumor cells.
26. Hepatocellular Carcinoma Without Cirrhosis
Although the large majority of HCC arise in patients with advanced chronic liver diseases, HCC may be observed without
advanced liver fibrosis or even in underlying normal liver. Altogether, such HCC appear to have a better prognosis, mainly
related to the absence of advanced damages in the background liver.
Hepatocellular Carcinoma Associated with Chronic Liver Diseases
HCC may occur early in the process of chronic liver diseases before the stage of advanced fibrosis and cirrhosis. Although this
situation may be observed whatever the etiological cause, it is especially encountered in the context of hepatitis B viral infection
and metabolic syndrome (MS). Due to the increase in the prevalence of MS worldwide, HCC associated with MS will become a
major concern. Fatty liver diseases, which represent the liver manifestation of MS, encompass a large spectrum of liver changes,
from simple steatosis to steatohepatitis that may progress to fibrosis. Although, and as in other chronic liver diseases, the
presence of cirrhosis may promote per se development of HCC in such patients, diabetes and obesity, as factors of MS, also
appear to be independent risk factors in liver carcinogenesis. Interestingly, several studies reported significant number of cases of
HCC in patients with non-advanced liver fibrosis. These data support the hypothesis that liver carcinogenesis related to MS may
follow distinct molecular pathways of tumorigenesis, independently from the usual multistep process-fibrosis-cirrhosis-HCC at
least in some cases. A small subset of these HCC, mainly occurring in male patients, develops from the malignant transformation
of preexisting hepatocellular adenoma. Morphologically, these HCC present as larger and better differentiated tumors compared
to those diagnosed in a background of cirrhosis.
27. Hepatocellular Carcinoma on Normal Liver
In fact, very few HCC are observed in patients with strictly normal liver. They correspond to distinct variants of tumors,
occurring either in specific population or in specific context. Such situation may partly explain their better prognosis compared
to HCC arising in patients with advanced chronic liver diseases.
Hepatitis
Hepatitis is defined as inflammation of the liver that can result from a variety of causes such as heavy alcohol use, autoimmune,
drugs, or toxins. However, the most frequent cause of hepatitis is due to a viral infection and is referred to as viral hepatitis. The
most common types of viral hepatitis are Hepatitis A, Hepatitis B, and Hepatitis C. The other types of viral hepatitis are
hepatitis D and E and are less frequently encountered. Based on the etiology of hepatitis, the severity can range from mild and
self-limiting to severe illness requiring liver transplantation.
Hepatitis can be further classified into acute and chronic based on the duration of the inflammation/insult to the liver. If
inflammation of the liver lasts for less than 6 months, then it is termed as acute hepatitis and if it lasts longer than 6 months, it
is termed as chronic hepatitis. Acute hepatitis is usually self-resolving but can cause fulminant liver failure depending on the
etiology. In contrast, chronic hepatitis can cause liver damage that includes liver fibrosis, cirrhosis, hepatocellular carcinoma,
and features of portal hypertension leading to significant morbidity and mortality.
28. AUTOIMMUNE HEPATITIS
Autoimmune hepatitis is a severe type of chronic hepatitis associated with circulating autoantibodies and elevated serum
immunoglobulins. The disorder may appear at any age; 70% of cases occur in women.
VIRAL HEPATITIS
Viral hepatitis is used to describe infection of the liver caused by hepatotropic viruses. Currently there are 5 main varieties of these
viruses and a sixth poorly characterised virus, causing distinct types of viral hepatitis:
Hepatitis A virus (HAV), causing a faecally-spread selflimiting disease.
Hepatitis B virus (HBV), causing a parenterally transmitted disease that may become chronic.
Hepatitis C virus (HCV), previously termed non-A, non-B (NANB) hepatitis virus involved chiefly in transfusion related hepatitis.
Hepatitis delta virus (HDV) which is sometimes associated as superinfection with hepatitis B infection.
Hepatitis E virus (HEV), causing water-borne infection.
Hepatitis G virus (HGV), is a recently discovered transfusion-transmitted hepatotropic virus but is not known to cause hepatitis.
All these human hepatitis viruses are RNA viruses except HBV, which is a DNA virus.
29. Hepatitis A Infection with HAV causes hepatitis A (infectious hepatitis). Hepatitis A is usually a benign, self-limiting disease and
has an incubation period of 15-45 days. The disease occurs in epidemic form as well as sporadically. It is usually spread by
faeco-oral route. Parenteral transmission is extremely rare. The spread is related to close personal contact such as in
overcrowding, poor hygiene and poor sanitation. Most frequently affected age is 5-14 years; adults are often infected by spread
from children. HEPATITIS A VIRUS (HAV). HAV infection can be transmitted to primates and the virus can be cultivated in
vitro. Inactivation of viral activity can be achieved by boiling for 1 minute, by ultraviolet radiation, or by contact with
formaldehyde and chlorine. The virus is present in the liver cells, bile, stool and blood during the incubation period and in pre-
icteric phase but viral shedding diminishes after the onset of jaundice. Chronic carriers have not been identified for HAV
infection.
Hepatitis B (serum hepatitis) caused by HBV infection has a longer incubation period (30-180 days) and is transmitted
parenterally such as in recipients of blood and blood products, intravenous drug addicts, patients treated by renal dialysis and
hospital workers exposed to blood, and by intimate physical contact such as from mother to child and by sexual contact. The
disease may occur at any age. HBV infection causes more severe form of illness that includes: acute hepatitis B, chronic
hepatitis, progression to cirrhosis, fulminant hepatitis and an asymptomatic carrier stage. HBV plays some role in the
development of hepatocellular carcinoma. HEPATITIS B VIRUS (HBV). The etiologic agent for hepatitis B, HBV, is a DNA
virus which has been extensively studied.
30. Hepatitis D Infection with delta virus (HDV) in the hepatocyte nuclei of HBsAg-positive patients is termed hepatitis D. HDV is a
defective virus for which HBV is the helper. Thus, hepatitis D develops when there is concomitant hepatitis B infection. HDV
infection and hepatitis B may be simultaneous (coinfection), or HDV may infect a chronic HBsAg carrier (superinfection).
With coinfection, acute hepatitis D may range from mild to fulminant hepatitis but fulminant hepatitis is more likely in such
simultaneous delta infection. Chronicity rarely develops in coinfection.
With superinfection (incubation period 30-35 days), chronic HBV infection gets worsened indicated by appearance of severe and
fulminant acute attacks, progression of carrier stage to chronic delta hepatitis or acceleration towards cirrhosis. Occurrence of
hepatocellular carcinoma is, however, less common in HBsAg carriers with HDV infection.
HEPATITIS C VIRUS (HCV).
Hepatitis C has an incubation period of 20-90 days (mean 50 days). Clinically, acute HCV hepatitis is milder than HBV hepatitis
but HCV has a higher rate of progression to chronic hepatitis than HBV. Persistence of infection and chronic hepatitis are the key
features of HCV. Occurrence of cirrhosis after 5 to 10 years and progression to hepatocellular carcinoma are other late
consequences of HCV infection. Currently, HCV is considered more important cause of chronic liver disease worldwide than
HBV.
Hepatitis E
Hepatitis E is an enterically-transmitted virus, previously labelled as epidemic or enterically transmitted variant of nonA non-B
hepatitis. The infection occurs in young or middleaged individuals, primarily seen in India, other Asian countries, Africa and
central America. The infection is generally acquired by contamination of water supplies such as after monsoon flooding.
However, compared with HAV, secondary person-to-person infection does not occur with HEV. Thus HEV has some common
epidemiologic features with HAV. HEV infection has a particularly high mortality in pregnant women but is otherwise a self-
limited disease and has not been associated with chronic liver disease.
31. Hepatitis G
A virus distinct from the foregoing hepatitis viruses has been designated separately as hepatitis G (HGV).
HGV infection has been found in blood donors, patients on haemodialysis and as coinfection with HIV. However, unlike HCV,
HGV is cleared from the plasma in majority of individuals while a small percentage of cases have chronic HGV infection who do
not develop hepatitis, nor does infected blood require screening for HGV RNA.
HEPATITIS G VIRUS (HGV).
HGV is a single-stranded RNA virus. The virus has been identified by PCR amplification technique. CLINICOPATHOLOGIC
SPECTRUM Among the various etiologic types of hepatitis, evidence linking HBV and HCV infection with the spectrum of
clinicopathologic changes is stronger than with other hepatotropic viruses. The typical pathologic changes of hepatitis by major
hepatotropic viruses are virtually similar. HAV and HEV, however, do not have a carrier stage nor cause chronic hepatitis. The
various clinical patterns and pathologic consequences of different hepatotropic viruses can be considered under the following
headings:
Carrier state
Asymptomatic infection
Acute hepatitis
Chronic hepatitis
Fulminant hepatitis (Submassive to massive necrosis)
