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422    SECTION II  Diseases of Organ Systems


                             (iii)  AST on the other hand is also found in heart and muscle. Normal value is
                               0–40 IU/L.
                            (iv)  Aminotransferase  levels  are  useful  in  differentiating  between  hepatocellular
                               and obstructive jaundice.
                            (v)  Marked  elevation  is  seen  in  severe  viral  hepatitis  (Hepatitis  A,  B  and  C),
                               drug-induced injury (acetominaphen toxicity) and circulatory abnormalities
                               (shock liver).
                            (vi)  Mild elevation is seen in neonatal hepatitis, extrahepatic biliary atresia, fatty
                               liver, cirrhosis, NASH (nonalcoholic steatohepatitis) and drug toxicity.
                         (b)  Alkaline phosphatase or ALP (indicator of cholestasis)
                             (i)  Serum ALP activity is primarily derived from liver and bone. Normal level is
                               3–13 KA units.
                            (ii)  In hepatocellular	jaundice, very little ALP is liberated from the cells and the
                               rise in ALP is less than three folds.
                            (iii)  In obstructive	jaundice, due to obstruction of biliary tract, all the new ALP that is
                               synthesized, escapes into the blood. Hence, serum ALP levels are markedly raised.
                           Causes of raised ALP:
                           •	 Obstructive jaundice
                           •	 Metastatic bone tumours
                           •	 Hyperparathyroidism
                           •	 Paget disease
                           •	 Pregnancy
                           •	 Rickets
                           •	 Tumours of GIT
                         (c)  Gamma-glutamyl transpeptidase or GGTP (indicator of cholestasis)
                            (i)  If  the  source  of  ALP  is  not  clear,  the  levels  of  two  enzymes,  gamma-
                               glutamyltransferase	and 5’	nucleotidase can be determined (more specific
                               for liver). Raised levels occur in biliary obstruction and parenchymal damage.
                             (ii)  Serum levels rise in acute and chronic alcoholism (raised levels suggest pro-
                               longed intake of more than 60 g alcohol/day).
                       5.  Plasma	proteins	(indicator	of	synthetic	ability):
                         (a)  Albumin is synthesized in liver. Normal serum albumin level is 3.5–4.5 g/dL. In
                           chronic liver diseases like cirrhosis and chronic active hepatitis, serum albumin is
                           low (,3 g/dL).
                         (b)  Globulins are synthesized by the reticuloendothelial system. Normal serum globu-
                           lin level is 1.5–3 g/dL. Their levels rise in chronic liver disease. IgG is raised in
                           chronic active hepatitis and cryptogenic cirrhosis. IgA is raised in alcoholic liver
                           disease. IgM is raised in primary biliary cirrhosis.
                       6.  Coagulation	factors	(indicator	of	synthetic	ability):
                         (a)  Liver synthesizes 11 coagulation factors and activates some in the presence of vitamin K.
                         (b)  Prothrombin time (PT) is prolonged in liver disease (PT depends on factors I, II, V,
                           VII and X, and gets prolonged when the plasma concentration of any one of these
                           falls below 30% of the normal).
                       7.	 Bromsulphthalein	 (BSP)	 clearance:  BSP  clearance  is  delayed  in  Dubin–Johnson
                        syndrome.
                       8.  Other	tests	for	liver	function:
                         (a)  Serology for viral hepatitis (B and C, CMV and EBV)
                         (b)  Autoantibody screen for autoimmune hepatitis and biliary cirrhosis (antimitochondrial
                           antibody, antismooth muscle antibody and antinuclear antibody)
                         (c)  Serum ferritin and transferrin saturation for haemachromatosis
                          (d)  a-fetoprotein levels for hepatocellular carcinoma
                         (e)  Copper/ceruloplasmin levels for Wilson disease
                         (f)  a-1 antitrypsin levels for a-1 antitrypsin deficiency
                         (g)  Noninvasive tests like ultrasound and CT that help in detecting structural abnor-
                           malities
                          (h)  Doppler test can be used to assess vasculature-related abnormalities
                         (i)  Liver biopsy for definitive histopathological diagnosis of inflammatory and neo-
                           plastic pathology



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