Symposium : Newer Diagnostic Tests
Liver Function Tests and their Interpretation
B.R. Thapa and Anuj Walia
Division of Pediatric Gastroenterology, Hepatology and Nutrition, Post Graduate Institute of Medical Education
and Research, Chandigarh

Liver function tests (LFT) are a helpful screening tool, which are an effective modality to detect hepatic dysfunction. Since the
liver performs a variety of functions so no single test is sufficient to provide complete estimate of function of liver. Often clinicians
are faced with reports that do not tally with the clinical condition of the patient and they face difficulty in interpreting the LFT.
An attempt is being made to study and understand the LFT and simplify their interpretation with algorithms. [Indian J Pediatr
2007; 74 (7) : 663-671]
E-mail: [email protected]
Key words : LFT; Alkaline phosphatase; Albumin; Prothrombin time; Aminotransferases (ALT & AST)
Liver has to perform different kinds of biochemical, Assess severity : They are helpful to assess the severity
synthetic and excretory functions, so no single and predict the outcome of certain diseases like primary biochemical test can detect the global functions of liver.
All laboratories usually employ a battery of tests for Follow up : They are helpful in the follow up of certain
initial detection and management of liver diseases and liver diseases and also helpful in evaluating response to these tests are frequently termed “Liver function tests”, although they are of little value in assessing the liverfunction per se. In spite of receiving a lot of criticism for LIMITATIONS
this terminology, the phrase ‘Liver function tests’ is firmlyentrenched in the medical lexicon. It might be argued that Lack sensitivity: The LFT may be normal in certain liver
‘Liver injury tests’ would be a more appropriate diseases like cirrhosis, non cirrhotic portal fibrosis, terminology. Moreover, the clinical history and physical examination play important role to interpret thefunctions. The role of specific disease markers, Lack specificity : They lack specificity and are not specific
radiological imaging and liver biopsy can not be for any particular disease. Serum albumin may be decreased in chronic disease and also in nephroticsyndrome. Aminotransferases may be raised in cardiacdiseases and hepatic diseases.
Except for serum bile acids the LFT are not specific for The various uses of Liver function tests include: liver diseases and all the parameters may be elevated forpathological processes outside the liver.1,3 Screening : They are a non-invasive yet sensitive
screening modality for liver dysfunction.
Thus, we see that LFT have certain advantages as well Pattern of disease : They are helpful to recognize the
as limitations at the same time. Thus, it is important to pattern of liver disease. Like being helpful in view them keeping the clinical profile of the patient in differentiating between acute viral hepatitis and various cholestatic disorders and chronic liver disease. (CLD).
A. Tests of the liver’s capacity to transport organic
Correspondence and Reprint requests : Prof. B.R. Thapa, Professor
anions and to metabolize drugs- Serum bilirubin, urine
and Head Division of Pediatric Gastroenterology, Hepatology and Nutrition, Post Graduate Institute of Medical Education andResearch, Chandigarh 160012 B. Tests that detect injury to hepatocytes (serum enzyme
tests) –
Aminotransferases, alkaline phosphatase, ã
[Received August 10, 2006; Accepted August 11, 2006]
Indian Journal of Pediatrics, Volume 74—July, 2007 B.R.Thapa and A. Walia
glutamyl transpeptidase, 5 nucleotidase, leucine reacts in 30 minutes after addition of alcohol. Normal range is 0.2-0.9 mg/dl (2-15µmol/L). It is slightly higherby 3-4 µmol/L in males as compared to females. It is this C. Tests of the Liver’s biosynthetic capacity- Serum
factor, which helps to diagnose Gilbert syndrome in proteins, albumin, prealbumin, serum ceruloplasmin, procollagen III peptide, a 1 antitrypsin, a feto protein,prothrombin time etc. ii. Direct Bilirubin : This is the water-soluble fraction.
This is measured by the reaction with diazotized
The clinical significance of LFT is given in Table 1 sulfanilic acid in 1 minute and this gives estimation of A. Tests of the liver’s capacity to transport organic
conjugated bilirubin. Normal range 0.3mg/dl( 5.1µmol/ anions and to metabolize drugs
iii. Indirect bilirubin: This fraction is calculated by the
difference of the total and direct bilirubin and is ameasure of unconjugated fraction of bilirubin.1,5 Bilirubin is an endogenous anion derived from The diazo method of bilirubin estimation is not very hemoglobin degradation from the RBC. The classification accurate especially in detecting low levels of bilirubin.
of bilirubin into direct and indirect bilirubin are based on Direct bilirubin over estimates bilirubin esters at low the original van der Bergh method of measuring bilirubin levels and under estimates them at high bilirubin. Bilirubin is altered by exposure to light so concentration. Thus slight elevation of unconjugated serum and plasma samples must be kept in dark before bilirubin not detected, which is of value in detecting measurements are made. When the liver function tests are abnormal and the serum bilirubin levels more than17µmol/L suggest underlying liver disease.4 A newer highly accurate method of estimation involves alkaline methanolysis of bilirubin followed by chloroform extraction of bilirubin methyl esters and later i. Total bilirubin: This is measured as the amount, which
separation of these esters by chromatography and TABLE 1. Clinical Significance of Liver Function Tests in Children
Associated liver
Mild elevations: Liver diseases,
Moderate elevations: EHBA, IHBA, drugs,
viral hepatitis, inherited hyperbilirubinemias
Marked elevations: Hepatitis, autoimmune,
Mild elevations: Liver disease
Moderate elevations: EHBA, IHBA,
infiltrating disorders, granulomatoushepatitis EHBA/biliary obstruction- responsiveto Vit K Indian Journal of Pediatrics, Volume 74—July, 2007 Liver Function Tests and their Interpretation
spectrophotometric determination at 430 nm.1 Other causes of extreme hyperbilirubinemia includesevere parenchymal disease, septicemia and renal a. Diagnostic value of bilirubin levels : Bilirubin in body
is a careful balance between production and removal ofthe pigment in body. Hyperbilirubinemia seen in acute 2. URINE BILIRUBIN
viral hepatitis is directly proportional to the degree ofhistological injury of hepatocytes and the longer course of The presence of urine bilirubin indicates hepatobiliary disease. Unconjugated bilirubin is tightly bound to Hyperbilirubinemia: It results from overproduction /
albumin and not filtered by the glomerulus and thus not impaired uptake, conjugation or excretion / regurgitation present in urine. Measurable amounts of conjugated of unconjugated or conjugated bilirubin from hepatocytes bilirubin in serum are found only in hepatobiliary to bile ducts.Approach to jaundice in neonatal period is Because the renal threshold for conjugated bilirubin is low and the laboratory methods can detect low levels of bilirubin in urine so conjugated bilirubin may be found inurine when the serum bilirubin levels are normal. This isthe case in early acute viral hepatitis.1, 6 Tests strips impregnated with diazo reagent are easy to use and detect as little as 1-2µ mol bilirubin/L.5 3. UROBILINOGEN
An increase in the urobilinogen in urine is a sensitive indicator of hepatocellular dysfunction. It is a good indication of alcoholic liver damage, well compensated cirrhosis or malignant disease of the liver. In viral Fig. 1. Algorithm to Approach Hyperbilirubinemia in Neonatal
hepatitis it appears early in urine. It is markedly increased In cholestatic jaundice urobilinogen disappears from Increased unconjugated bilirubin: This results from
urine. It may be intermittently present in case of overproduction/impaired uptake, conjugation Increased conjugated bilirubin: Impaired intrahepatic
Urobilinogen gives a purple reaction to Ehrlich’s excretion / regurgitation of unconjugated or conjugated aldehyde reagent. A dipstick containing this reagent bilirubin from hepatocytes of bile ducts.4 allows rough and ready quantification. Freshly voided Serum bilirubin could be lowered by drugs like salicylates, sulphonamides, free fatty acids which displace B. Tests that detect injury to hepatocytes( serum enzyme
bilirubin from its attachment to plasma albumin. On the tests) : The liver contains thousands of enzymes and these
contrary it could be elevated if the serum albumin enzymes have no function and behave as serum proteins.
increases and the bilirubin may shift from tissue sites tocirculation.1 A. ENZYMES THAT DETECT HEPATOCELLULAR
b. Prognostic value of bilirubin levels
Bilirubin may be of prognostic value in conditions likefulminant hepatic failure where deep jaundice isassociated with increased mortality.2,4 The aminotransferases (formerly transaminases)are themost frequently utilized and specific indicators of Hyperbilirubinemia and Hemolysis
hepatocellular necrosis. These enzymes- aspartate Bilirubin itself is not soluble in water and is bound to aminotransferase(AST, formerly serum glutamate albumin and thus does not appear in urine. Hemolysis oxaloacetic transaminase-SGOT) and alanine amino with overproduction of bilirubin and concomitant transferase( ALT, formerly serum glutamic pyruvate reduced GFR cause decreased excretion and can lead to transaminase-SGPT) catalyze the transfer of the á amino high bilirubin levels.1 Bilirubin levels in excess of 25 mg/ acids of aspartate and alanine respectively to the á keto dl may be seen in hemolysis in association with liver group of ketoglutaric acid. ALT is primarily localized to the liver but the AST is present in a wide variety of tissues Indian Journal of Pediatrics, Volume 74—July, 2007 B.R.Thapa and A. Walia
like the heart, skeletal muscle, kidney, brain and liver. 4, 2 AST : alanine + α ketoglutarate = oxaloacetate + Algorithm to approach mild and sustained rise of aminotransferases is given in Fig. 2.
ALT: alanine + α ketoglutarate = pyruvate + Large increases in mitochondrial AST occur in serum after extensive tissue necrosis. Because of this, assay ofmitochondrial AST have been advocated in myocardial Whereas the AST is present in both the mitochondria infarction. Mitochondrial AST is also increased in chronic and cytosol of hepatocytes, ALT is localized to the cytosol.2,3 The cytosolic and mitochondrial forms of ASTare true isoenzymes and immunologically distinct.7 Their activity in serum at any moment reflects the relative rate at which they enter and leave circulation. Of About 80% of AST activity in human liver is the numerous methods used for measuring their levels, contributed by the mitochondrial isoenzyme, whereas the most specific method couples the formation of most of the circulating AST activity in normal people is pyruvate and oxaloacetate- the products of the Fig. 2. Algorithm to Approach Mild but Sustained Rise of Aminotransferases
Indian Journal of Pediatrics, Volume 74—July, 2007 Liver Function Tests and their Interpretation
aminotransferase reactions to their enzymatic reduction Mitochondrial AST: Total AST ratio : This ratio is
characteristically elevated in alcoholic liver disease.
Abstinence from alcohol improves this ratio. It is also Virtually no aminotransferases are present in the urine or bile and hepatic sinusoids are the primary site for theirclearance. 11, 12 Falsely low aminotransferase levels : They have been
seen in patients on long term hemodialysis probably
secondary to either dialysate or pyridoxine deficiency.
Low levels have also been seen in uremia 15,16 Other enzymes tests of hepatocellular necrosis
1. Severe ( > 20 times, 1000 U/L) : The AST and ALT
None of these tests have proved to be useful in practice levels are increased to some extent in almost all liver than the aminotransferases.These include glutamate diseases. The highest elevations occur in severe viral dehydrogenase, isocitrate dehydrogenase, lactate hepatitis, drug or toxin induced hepatic necrosis and circulatory shock. Although enzyme levels may reflectthe extent of hepatocellular necrosis they do not correlate b. Enzymes that detect cholestasis
with eventual outcome. In fact declining AST and ALTmay indicate either recovery of poor prognosis in 1. ALKALINE PHOSPHATASE
2. Moderate (3-20 times): The AST and ALT are
Alkaline phosphatases are a family of zinc moderately elevated in acute hepatitis, neonatal hepatitis, metaloenzymes, with a serine at the active center; they chronic hepatitis, autoimmune hepatitis, drug induced release inorganic phosphate from various organic hepatitis, alcoholic hepatitis and acute biliary tract orthophosphates and are present in nearly all tissues. In obstructions. The ALT is usually more frequently liver, alkaline phosphatase is found histochemically in the increased as compared to AST except in chronic liver microvilli of bile canaliculi and on the sinusoidal surface disease. In uncomplicated acute viral hepatitis, the very of hepatocytes. Alkaline phosphatase from the liver, bone high initial levels approach normal levels within 5 weeks and kidney are thought to be from the same gene but that of onset of illness and normal levels are obtained in 8 from intestine and placenta are derived from different genes.5 Approach to elevated alkaline phosphatase isgiven in Fig. 3.
For reasons, which are not, understood AST levels appear disproportionately low in patients with Wilson In liver two distinct forms of alkaline phosphatase are also found but their precise roles are unknown. In healthypeople most circulating alkaline phosphatase originates 3. Mild (1-3 times) : These elevations are usually seen in
sepsis induced neonatal hepatitis, extrahepatic biliaryatresia (EHBA), fatty liver, cirrhosis, non alcoholic steato The internationally recommended reference method hepatitis(NASH), drug toxicity, myositis, duchenne uses p- nitrophenol phosphate as substrate, in al alkaline muscular dystrophy and even after vigorous exercise.1,4 buffer. Fresh unhemolysed serum is the specimen ofchoice for the estimation. Heparinized plasma may also One third to one half of healthy individuals with an be used. The test should not be done on plasma if citrate, isolated elevation of ALT on repeated testing have been oxalate or EDTA were used as anticoagulants, they form a complex with zinc and the alkaline phosphatase, AST: ALT ratio
causing irreversible enzyme inactivation.5 The ratio of AST to ALT is of use in Wilson disease, CLD Average values of alkaline phosphatase vary with age and alcoholic liver disease and a ratio of more than 2 is and are relatively high in childhood and puberty and usually observed. The lack of ALT rise is probably due to lower in middle age and higher again in old age. Males pyridoxine deficiency. In NASH the ratio is less than one usually have higher values as compared to females. The in the absence of fibrosis on liver biopsy.4 levels correlate with person’s weight and inversely withthe height of person. 18 In viral hepatitis the ratio is usually less than one. The ratio invariably rises to more than one as cirrhosis Not uncommonly isolated elevated levels of alkaline develops possibly because of reduced plasma clearance of phosphatase in otherwise healthy persons return to AST secondary to impaired function of sinusoidal cells.14 ALT exceeds AST in toxic hepatitis, viral hepatitis, Highest levels of alkaline phosphatase occur in chronic active hepatitis and cholestatic hepatitis 5 cholestatic disorders. Elevations occur as a result of both Indian Journal of Pediatrics, Volume 74—July, 2007 B.R.Thapa and A. Walia
Fig. 3. Algorithm to evaluate Marked Rise of Alkaline Phosphatase
intrahepatic and extrahepatic obstruction to bile flow and associated specifically with intrahepatic disease as the degree of elevation does not help to distinguish between the two. Alkaline phosphatase levels are likely tobe very high in EHBA.4 Hepatic and bony metastasis can also cause elevated levels of alkaline phosphatase. Other diseases like The mechanism by which alkaline phosphatase infiltrative liver diseases, abscesses, granulomatous liver reaches the circulation is uncertain; leakage from the bile disease and amyloidosis may also cause a rise in alkaline canaliculi into hepatic sinusoids may result from leaky phosphatase. Mildly elevated levels of alkaline tight junctions. 5,20 and the other hypothesis is that the phosphatase may be seen in cirrhosis and hepatitis of damaged liver fails to excrete alkaline phosphatase made Low levels of alkaline phosphatase occur in In acute viral hepatitis, alkaline phosphatase is usually hypothyroidism, pernicious anemia, zinc deficiency and either normal or moderately increased. Hepatitis A may congenital hypophosphatasia.22 Wilson’s disease present a cholestatic picture with marked and prolonged complicated by hemolysis and FHF may also have very itching and elevation of alkaline phosphatase. Tumours low levels of alkaline phosphatase. Ratio of alkaline may secrete alkaline phosphatase into plasma and there phosphatase and bilirubin is low in fulminant Wilson are tumour specific isoenzymes such as Regan, Nagao disease. This might be the result of replacement of cofactor zinc by copper and subsequent inactivation of Elevated serum levels of intestinal alkaline alkaline phosphtase.23 regardless of the cause of acute phosphatase have been found in patients with cirrhosis, hepatic failure a low ratio of alkaline phosphatase to particularly those with blood group type O, and may be bilirubin is associated with a poor prognosis.24 Indian Journal of Pediatrics, Volume 74—July, 2007 Liver Function Tests and their Interpretation
Drugs like cimetidine, frusemide, phenobarbitone and 1. SERUM PROTEINS
phenytoin may increase levels of alkaline phosphtase.5 The liver is the major source of most the serum proteins.
The parenchymal cells are responsible for synthesis of 2. γ GLUTAMYL TRANSPEPTIDASE
albumin, fibrinogen and other coagulation factors and γ Glutamyl transpeptidase(GGT) is a membrane bound glycoprotein which catalyses the transfer of γ glutamyl Albumin : Albumin is quantitatively the most important
group to other peptides, amino acids and water.
protein in plasma synthesized by the liver and is a useful Large amounts are found in the kidneys, pancreas, indicator of hepatic function. Because the half life of liver, intestine and prostate. The gene for γ glutamyl albumin in serum is as long as 20 days, the serum transpeptidase is on chromosome 22. The levels of ã albumin level is not a reliable indicator of hepatic protein glutamyl transpeptidase are high in neonates and infants synthesis in acute liver disease. Albumin synthesis is up to 1 yr and also increase after 60 yr of life. Men have affected not only in liver disease but also by nutritional higher values. Children more than 4 yr old have serum status, hormonal balance and osmotic pressure. Liver is values of normal adults. The normal range is 0-30IU/L 1,5 In acute viral hepatitis the levels of γ glutamyl The serum levels are typically depressed in patients transpeptidase may reach its peak in the second or third with cirrhosis and ascites. In patients with or without wk of illness and in some patients they remain elevated ascites, the serum albumin level correlates with for 6 weeks. In EHBA GGT is markedly elevated.5 prognosis.27 In addition the rate of albumin synthesis hasbeen shown to correlate with the Child- Turcotte or Often clinicians are faced with a dilemma when they see elevated alkaline phosphatase levels and are unable todifferentiate between liver diseases and bony disorders Normal serum values range from 3.5g/dl to 4.5 g/dl.
and in such situations measurement of γ glutamyl The average adult has approximately 300 to 500 g of transferase helps as it is raised only in cholestatic albumin. The serum levels at any time reflect its rate of synthesis, degradation and volume of distribution.
In liver disease γ glutamyl transpeptidase activity Corticosteroids and thyroid hormone stimulate correlates well with alkaline phosphatase levels but rarely albumin synthesis by increasing the concentration of the γ glutamyl transpeptidase levels may be normal in intra hepatic cholestasis like in some familial intrahepatic The serum albumin levels tend to be normal in diseases like acute viral hepatitis, drug related Other conditions causing elevated levels of γ glutamyl hepatotoxicity and obstructive jaundice. Albumin levels transpeptidase include uncomplicated diabetes mellitus, below 3g/dl in hepatitis should raise the suspicion of acute pancreatitis and myocardial infarction. Drugs like chronic liver disease like cirrhosis which usually reflects phenobarbitone, phenytoin, paracetamol, tricyclic decreased albumin synthesis. In ascites there may be antidepressants may increase the levels of γ glutamyl normal synthesis but the levels may appear reduced because of increased volume of distribution. 30,31 Non-hepatic causes of increased levels of the enzyme Hypoalbuminemia is not specific for liver disease and include anorexia nervosa, Gullian barre syndrome, may occur in protein malnutrition, nephrotic syndrome hyperthyroidism, obesity and dystrophica myotonica. 5 and chronic protein losing enteropathies. 1 As a diagnostic test the primary usefulness of γ 2. PREALBUMIN
glutamyl transpeptidase is limited to the exclusion ofbone disease, as γ glutamyl transpeptidase is not found inbone. 1 The serum prealbumin level is 0.2- 0.3 g/L. these levelsfall in liver disease presumably due to reduced synthesis.
Because of its short half life, changes may precedealteration in serum albumin. Determination of These are the other enzymes that are not routinely prealbumin has been considered particularly useful in 5 Nucleotidase
Leucine aminopeptidase
Normal plasma levels are 0.2-0.4g/L. It is synthesized in C. Tests of the Liver’s biosynthetic capacity.
the liver and is an acute phase protein. The plasma Indian Journal of Pediatrics, Volume 74—July, 2007 B.R.Thapa and A. Walia
concentration rise in infections, rheumatoid arthiritis, major site of synthesis of 11 blood coagulation proteins: pregnancy, non Wilson liver disease and obstructive fibrinogen, prothrombin, labile factor, stable factor, christmas factor, stuart prowe factor, prekallikrein andhigh molecular wt kininogen.1 This is an important diagnostic marker in Wilson disease, in which the plasma level is usually low. Low Most of these are present in excess and abnormalities levels may also be seen in neonates, Menke’s disease, of coagulation only result when there is substantial kwashiorkor, marasmus, protein losing enteropathy, impairment in the ability of the liver to synthesize these copper deficiency and aceruloplasminemia.
The standard method to assess is the one stage 4. PROCOLLAGEN III PEPTIDE
prothrombin time of quick, which evaluate the extrinsiccoagulation pathway. 4 The serum concentration of this peptide appears to The results of this test may be expressed in sec or as a increase not only with hepatic fibrosis but also with ratio of the plasma prothrombin time to control plasma inflammation and necrosis. Serial measurement of time. Normal control usually is in the range of 9-11 procollagen III may be helpful in the follow up of chronic seconds. A prolongation of more than 2 seconds is The prolonged PT is not specific for liver diseases and 5. α 1 ANTITRYPSIN
is seen in various deficiencies of coagulation factors, DIC,and ingestion of certain drugs.
α 1 antitrypsin is a glycoprotein synthesized by the liver In acute and chronic hepatocellular disease the PT and is an inhibitor of serine proteinases, especially may serve as a prognostic indicator. In acute elastase. Its normal concentration is 1- 1.6g/L. it is an hepatocellular disease worsening of PT suggests an acute phase protein, serum levels increase with increased likelihood of acute hepatic failure. The PT is a inflammatory disorders, pregnancy and after oral predictor of outcome in cases of acetoaminophen over dosage and acute alcoholic hepatitis. Prolongation of PT The various alleles coded are M,F,S,Z and null forms.
is also suggestive of poor long-term outcome in chronic PiZZ homozygotes are associated with neonatal hepatitis.
Cirrhosis in adults has been found with ZZ, MZ, SZ and If the PT returns to normal or improves by at least 30% within 24 hr of a single parenteral injection of vitamin K1 Liver disease is usually seen with deficiency of α 1 (5-10 mg), it may be surmised that parenchymal function antitrypsin, an inherited disorder. Deficiency should be is good and that hypovitaminosis K was responsible for confirmed by quantitative measurement.
the original prolongation of PT. Patients withparenchymal disease by contrast will show only minimal 6. α FETO PROTEIN
improvement. Most patients with extra hepaticobstruction like EHBA would respond promptly to asingle injection of vitamin K1.1 This protein, the principal one in fetal plasma in earlygestation is subsequently present at very low levels.( The PT is particularly important in the management of <25µg/L) It is increased in hepatocellular carcinoma patients with liver disease. It is important to perform (HCC)and more than 90% of such patients have raised before procedures like liver biopsy and kidney biopsy levels. Raised values are also found in other liver diseases and it permits an assessment of the tendency to bleed. In like chronic hepatitis, in regeneration phase of acute many centers the International normalized ratio (INR) is hepatitis and in hepatic metastasis. This is also raised in adenomas associated with tyrosinemia.
To assess the severity of liver disease the Child Pugh α feto protein elevation is less frequent when HCC scoring was in use and proved very good to predict the arises in non cirrhotic liver. Serial determination is of outcome of the disease. Now with the upsurge of liver value in cirrhotic patients and rise in the values should transplantation the model for end stage liver disease (MELD) and pediatric end stage liver disease (PELD)scoring system is being followed to prioritize the 7. PROTHROMBIN TIME (PT)
Because of the shortcomings of the biochemical liver Clotting is the end result of a complex series of enzymatic function tests, the quantitative function tests are used and reactions that involve at least 13 factors. The liver is the are shown to be very sensitive but their utility in pediatric Indian Journal of Pediatrics, Volume 74—July, 2007 Liver Function Tests and their Interpretation
aminotransferases. CRC Crit Rev Clin Lab Sci 1985; 21 : 99-103.
11. Dunn M et al the disappearance rate of glutamic oxaloacetic A single liver function test is of little value in screening transaminase from the circulation and its distribution in the for liver disease as many serious liver diseases may be body’s fluid compartments and secretions. J Lab Clin Med 1958; associated with normal levels and abnormal levels might be found in asymptomatic healthy individuals. The use of 12. Frankl HD, Merrit JH. Enzyme activity in the serum and common bile duct. Am J Gastroenterol 1959; 31 : 166-169.
battery of liver function tests, however constitutes a 13. Katkov WN, Friedman LS Cody H et al. Elevated serum highly sensitive procedure. The number of false negatives alanine aminotransferases levels in blood donors; the must be reduced by this technique. The use of battery of contribution of hepatitis C virus. Ann Intern Med 1991; 115 : liver tests is also associated with high specificity especially when more than one test is abnormal. The 14. Park GJH, Lin BPC, Ngu MC et al. Aspartate amino- transferases: alanine aminotransferases ratio in chronic pattern of enzyme abnormality, interpreted in the context hepatitis C infection : is it a predictor of cirrhosis? 2000; 15 : of the patient’s characteristics, can aid in directing the subsequent diagnostic work-up. Awareness of the 15. Yasuda K, Okuda K, Endo N et al. Hypoaminotransferasemia prevalence of determined liver disease in specific in apatients undergoing long term hemodialysis: clinical and populations and of possible hepatic involvement during biochemical appraisal. Gastroenterology 1995; 109 : 1295-1299.
16. Cohen GA, Goffinet JA, Donabedian RK et al. Observations on systemic illnesses or drug therapies may help the clinician decreased serum glutamic oxaloacetic transaminase (SGOT) identify the cause of alterations efficiently.
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17. Hagerstrand I : distribution of alkaline phosphatase activity in healthy and diseased human liver tissue. Acta Pathol Microbiol REFERENCES
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