Page 612 - Textbook of Pathology, 6th Edition

596 hepatic cholestasis which result in vitamin K deficiency due iii) Hepatitis Be antigen (HBeAg) can be found in chronic
to impaired lipid absorption, are associated with prolonged varieties of hepatitis B.
prothrombin time. However, parenteral injection of vitamin iv) Amoeba antibodies to Entamoeba histolytica develop in
K will normalise prothrombin time if the prolongation was patients with amoebic liver abscess.
due to obstruction, but there will be no improvement in
prothrombin time if there is extensive hepatocellular disease. V. ANCILLARY DIAGNOSTIC TESTS
iv) Serum ammonia. High blood levels of ammonia are In addition to laboratory tests described above, two ancillary
found in acute fulminant hepatitis, cirrhosis and hepatic tests which are invariably done by the physician are
encephalopathy. The rise in serum ammonia is due to ultrasonography and percutaneous liver biopsy and/or
inability of severely damaged liver to convert ammonia to FNAC.
urea. Thus, urea synthesis is reduced in chronic liver disease.
1. ULTRASONOGRAPHY. Ultrasound (US) examination
2. LIPID AND LIPOPROTEIN METABOLISM. Lipids of the liver is indicated in the following situations:
synthesised in the liver include cholesterol and cholesterol i) Cholestasis of various etiologies to see the dilated intra-
esters, phospholipids and triglycerides. These lipids are and extrahepatic canalicular tree.
insoluble in water and are carried in circulation with three ii) Space-occupying lesions (SOLs) within the liver to
major types of lipoproteins which contain apoproteins. These determine whether they are neoplasms or non-neoplastic
are: high density lipoproteins (HDL), low density cysts.
lipoproteins (LDL) and very low density lipoproteins
(VLDL). iii) To provide US-guidance for FNAC or liver biopsy.
Blood lipids. Estimations of total serum cholesterol, 2. FNAC AND/OR PERCUTANEOUS LIVER BIOPSY.
triglycerides and lipoprotein fractions are frequently done Lastly, FNAC and percutaneous liver biopsy are employed
in patients with liver disease. to examine the microscopic changes of hepatic morphology
There is rise in total serum cholesterol in cholestasis, in various diseases. Both these tests are done after evaluation
probably due to retention of cholesterol which is normally of signs of obstruction since these tests are contraindicated
excreted in the bile (normal < 200 mg/dl). Serum triglyceride in cholestasis. FNAC and liver biopsy are otherwise easily
is also elevated in cholestasis. performed bedside tests of value. Their main indications are
Values are lowered in acute and chronic diffuse liver as follows:
diseases and in malnutrition. i) hepatocellular disease of unknown cause;
SECTION III
ii) suspected cases of chronic hepatitis;
3. CARBOHYDRATE METABOLISM. The liver plays a iii) hepatomegaly of various etiologies;
central role in carbohydrate metabolism. Blood glucose level iv) splenomegaly of unknown cause;
is lowered in fulminant acute hepatic necrosis. In chronic v) fever of unknown cause; and
liver disease, there is impaired glucose tolerance and relative vi) SOLs visualised in radiologic examination
insulin resistance.
JAUNDICE—GENERAL
IV. IMMUNOLOGIC TESTS
Jaundice or icterus refers to the yellow pigmentation of the
Liver diseases are associated with various immunologic skin or sclerae by bilirubin (page 42). Bilirubin pigment has
abnormalities which may be nonspecific immunologic reac- high affinity for elastic tissue and hence jaundice is
tions or may be antibodies against specific etiologic agents.
Systemic Pathology
particularly noticeable in tissues rich in elastin content.
1. NONSPECIFIC IMMUNOLOGIC REACTIONS. These Jaundice is the result of elevated levels of bilirubin in the
include the following: blood termed hyperbilirubinaemia. Normal serum bilirubin
i) Smooth muscle antibody to actin component of muscle is concentration ranges from 0.3-1.3 mg/dl, about 80% of which
formed in certain hepatic disorders with hepatic necrosis. It is unconjugated. Jaundice becomes clinically evident when
appears that hepatocytes have a protein which is the total serum bilirubin exceeds 2 mg/dl. A rise of serum
immunologically similar to actin. bilirubin between the normal and 2 mg/dl is generally not
ii) Mitochondrial antibody develops in patients with primary accompanied by visible jaundice and is called latent jaundice.
biliary cirrhosis. Before considering the features and types of jaundice, it
iii) Antinuclear antibody is present in some patients of chro- is essential to review the normal bilirubin metabolism.
nic hepatitis. The LE cell test may be positive in these cases.
NORMAL BILIRUBIN METABOLISM
2. ANTIBODIES TO SPECIFIC ETIOLOGIC AGENTS.
These vary according to the etiologic agent causing the liver Normal metabolism of bilirubin can be conveniently
cell injury. described under 4 main headings—source, transport, hepatic
i) Hepatitis B surface antigen (HBsAg) can be demonstrated phase and intestinal phase as illustrated schematically earlier
in cases of serum hepatitis. A confirmed positive test for in Chapter 12 (see Fig. 12.9, page 291).
HBsAg is definite proof of hepatitis B infection. 1. SOURCE OF BILIRUBIN. About 80-85% of the bilirubin
ii) Hepatitis B core antibody (HBc) can be detected in all is derived from the catabolism of haemoglobin present in
patients with hepatitis B. senescent red blood cells. The destruction of effete