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Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
Liver function tests
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Liver function tests

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this is a series of notes on clinical pathology, useful for undergraduate and post graduate pathology students. Notes have been prepared from standard textbooks and are in a format easy to reproduce …

this is a series of notes on clinical pathology, useful for undergraduate and post graduate pathology students. Notes have been prepared from standard textbooks and are in a format easy to reproduce in exams.

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  • 1. 1 Clinical pathology notes LIVER FUNCTION TESTS by Dr. Ashish Jawarkar (M.D. Pathology) Consultant Pathologist Parul Sevashram Hospital Vadodara OVERVIEW 1. Indications of LFT 2. Limitations of LFT 3. Classification of LFTs a. tests that assess excretory function i. bilirubin in serum and urine ii. urobilinogen in urine and feces b. tests that assess synthetic function i. serum protein ii. serum albumin iii. serum albumin:serum globulin ratio iv. Prothrombin time v. Serum protein electrophoresis c. tests that assess metabolic function i. Blood ammonia level d. tests that assess hepatic injury i. ALT/SGPT ii. AST/SGOT iii. Alkaline phosphatase iv. Gamma GGT v. 5-nucleotidase e. tests that assess clearance of exogenous substances i. Bromsulphathelien excretion test 4. Each LFT in detail 5. Interpretation of LFT 6. Approach to a patient with suspected hepatocellular disorder, cholestatic disorder Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 2. 2 * INDICATIONS OF LIVER FUNCTION TESTS 1. Screening of suspected liver disorder 2. to find out type of liver disease a. hepatocellular b. cholestatic c. infiltrative 3. assess the severity and prognosis of liver disease 4. follow up the course of liver disease through the recovery phase * LIMITATIONS OF LIVER FUNCTION TESTS 1. Lack sensitivity Liver has large anatomic and functional reserve; there has to be extensive liver damage for LFTs to derange 2. Lack specificity LFTs are abnormal in various non hepatic conditions: a. raised bilirubin i. hemolysis ii. ineffective erythropoeisis iii. large hematoma b. raised aminotransferases i. muscle injury ii. alcohol abuse iii. MI c. raised alkaline phosphatase i. pregnancy ii. bone disorders d. low serum albumin i. poor nutrition ii. proteinuria iii. malabsorption iv. severe illness causing catabolism Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 3. 3 (i) BILIRUBIN: Serum Bilirubin Types: Indirect Bilirubin (unconjugated) 90% more of total 1. Tightly bound to albumin 2. water insoluble 3. not excreted in urine Direct Bilirubin (conjugated) 10% or less of total 1. includes bilirubin glucoronide, bilirubin diglucoronide and delta bilirubin# 2. water soluble 3. can be excreted in urine # consists of conjugated bilirubin bound to albumin, level is increased in cholestasis, excreted slowly in urine Method (Di azo method): Serum + di azo reagent Serum + diazo reagent + accelerator Pink Azobilirubin + alkaline tartarate Pink azobilirubin +alkaline tartarate Blue azobilirubin Blue azobilirubin Measure absorbance at 600nm Measure absorbance at 600 nm Total bilirubin Direct bilirubin Indirect bilirubin = total bilirubin – direct bilirubin Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 4. 4 Normal Levels: Total Bilirubin Direct Bilirubin 0.3-1.0 mg/dl 0 – 0.2 mg/dl Patterns: Normal Post hepatic type Hepatic type Pre hepatic type Direct 10% of total Direct >50% of total Direct 20-50% of total Direct <15% of total Urine bilirubin Rationale: 1. Presence of bilirubin in urine indicates conjugated hyperbilirubinemia due to obstructive or hepatocellular causes. 2. Bilirubin is absent in urine in hemolytic jaundice because unconjugated bilirubin is not soluble in water. Methods: 1. Foam test 5 ml urine in test tube shake Yellow foam Bilirubin present 2. Gmelin’s test 3 ml conc nitric acid in test tube + pour 3 ml urine slowly over it Play of colors from yellow to violet to blue to green Positive test Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 5. 5 3. Lugol’s iodine 4 ml lugol’s iodine in test tube + 4 drops urine shake Green color indicates positive taste 4. Fouchet’s test 5 ml urine + 2.5 ml 10% BaCl2 Look for ppt formation Obtain ppt on filter paper Add 1 drop fouchet’s reagent Blue green color immediately Bilirubin is present 5. Reagent strips impregnated with diazo reagent Can detect minimum 0.5 mg/dl of bilirubin Patterns: Urine Bilirubin Urobilinogen Prehepatic Absent Increased Hepatic Present Increased Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes Post Hepatic Present Absent
  • 6. 6 (ii) URINE UROBILINOGEN Rationale: Bile contains conjugated bilirubin Converted by bacterial action in intestines to urobilinogen Enterohepatic circulation Some urobilinogen not taken up by liver is excreted in urine On exposure to air (urine), urobilinogen is converted to urobilin which gives urine its pale yellow color Method: 1. Ehrlich’s aldehyde test 5 ml urine + 0.5 ml Ehrlich’s aldehyde reagent 5 min, room temp Pink color Normal urobilinogen Dark red color Increased urobilinogen Fallacy: This test is positive with urobilinogen, bilirubin and porphobilinogen. If bilirubin is suspected; before adding Ehrlich’s reagent, BaCl2 is added and ppt is removed, which removes the bilirubin and test is performed on the filterate. Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 7. 7 If Porphobilinogen is suspected – Watson-Shwartz test is performed 5ml urine + 0.5 ml Ehrlich’s aldehde reagent Pink / Dark red solution Add chloroform 1-2 ml Pink color in aqueous layer Acqueous layer Chloroform layer Porphobilinogen suspected Pink color in chloroform layer acqueous layer Chloroform layer Urobilinogen confirmed Decant pink acqueous solution Add butanol Pink color in butanol layer Butanol layer Acqueous layer Indicates porphobilinogen Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 8. 8 2. Reagent strip method On reagent strips, test area is impregnated with p-dimethylaminobenzal dehyde or 4methoxy benzene tetrafluoroborate Normal levels: Normal Increased urobilinogen in urine 0.5-4mg in 24 hours Hemolytic jaundice, hemorrhage in tissues Decreased urobilinogen in urine Obstructive jaundice, reduction of intestinal flora Fallacy: False negative results may be obtained if 1. UTI – oxidizes urobilinogen to urobilin 2. antibiotic therapy – eliminates gut bacteria, no urobilinogen produced Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 9. 9 (iii) Prothrombin time Rationale: 1. Most of the clotting factors (except vWF) are synthesized in the liver, hence clotting function would be deranged in liver disorders 2. Vitamin K dependent clotting factors include factor II, VII and IX, and X. PT measures the activity of II, VII and X. Method: Platelet poor plasma + Tissue thromboplastin (activates extrinsic pathway) + Calcium chloride Allowed to clot Note time Causes of raised PT: 1. Hepatocellular disease# 2. Obstructive jaundice# – malabsorption of vitamin K – lack of synthesis of vitamin K dependent clotting factors 3. DIC – exhaustion of coagulation factors 4. Inherited deficiency of coagulation factors # To differentiate raised PT due to hepatocellular disease or obstructive causes, repeat after administration of Vit K Normal values: PT 11 To 16 seconds Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 10. 10 (iv) Serum Proteins 1. Total Proteins Rationale: 1. Liver is the sole site for synthesis of all proteins except gammaglobulins (which is synthesized by plasma cells). 2. Hence measurement of total proteins is a fair indicator of liver function 3. However, the decrease in proteins synthesized by liver is compensated by increased synthesis of gamma globulins by plasma cells. 4. Hence overall value of total serum protein measurement is limited. Methods: 1. Refractometer method: Refractive index of serum is measured and read directly from the refractometer 2. Biuret method: Copper ions in the reagent react with peptide bonds of the protein Violet color compound Color intensity read by colorimeter Normal: Total Protein 5.5 – 8 gm/dl Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 11. 11 2. Serum Albumin Rationale: 1. Albumin consists of 60% of total proteins and is exclusively synthesized in liver. Hence its estimation can help in liver diseases (especially chronic). Serum albumin level is low in chronic liver diseases like cirrhosis and also correlates with severity like progression of ascites. 2. The half life of albumin is 20 days, hence its level does not fall with acute diseases such as acute hepatitis. 3. Serum albumin measurement is not specific because albumin also falls in a. Malnutrition b. Malabsorption c. Decreased sythesis – liver disease, chronic infection d. Increased catabolism – thyrotoxicosis, malignancies, infection e. Increased loss i. Nephrotic syndrome ii. Burns iii. Protein loosing enteropathy f. Increased blood volume (dilution – false low) i. Pregnancy ii. CCF Method: BROMOCRESOL GREEN METHOD; Serum + Bromo cresol green Binds to albumin Blue color Measured colorimetrically Normal Values: Serum albumin 3.5 – 5 gm/dl (60% of total proteins) Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 12. 12 3. Serum albumin : Serum globulin ratio Rationale: 1. The total serum plasma protein level is affected by compensatory increase of gamma globulins as albumin falls 2. The ratio of serum albumin to globulin gives a better idea of the liver function Normal: Normal albumin:globulin ratio >1:5 4. Serum Protein electrophoresis Following pattern can be observed on electrophoresis: Normal: Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 13. 13 Cirrhosis of liver: When liver function is sufficiently diminished, protein synthesizing capacity is compromised and concentrations of albumin and proteins in the alpha and beta bands are decreased. An additional common finding is beta-gamma bridging due to increased IgA. Beta-gamma bridging Alb α1 α2 β γ The Nephrotic Syndrome -1. Renal disease involving the glomeruli is always associated with increased urinary protein loss. When protein loss is greater than 3-4 g/day, the protein synthesizing capacity of the liver is exceeded and hypoproteinemia, accompanied by anasarca, develops to cause the nephrotic syndrome. 2. The massive urine protein loss is due to increased permeability of glomeruli to protein. The permeability increase may be minimal so that only albumin and other smaller molecular weight proteins are selectively filtered (selective nephrosis, as in Minimal Change Disease) or may be greater so that larger proteins are also filtered (nonselective nephrosis, as in membranous golmerulonephritis) as is the case in the example shown. 3. Alpha-2-macroglobulin is sufficiently large so that it is not filtered and increased synthesis (from the general hepatic protein synthesis) causes its accumulation. 4. Lipoproteins are also sufficiently large to accumulate and hyperlipidemia is a characteristic of the nephrotic syndrome, although lipoproteins are not stained with the protein stain used in visualizing proteins. Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 14. 14 Normal Abnormal Alb α1 α2 β γ Alpha-1-Antitrypsin Deficiency: A genetic defect causes a deficiency of alpha-1-antitrypsin. The antiprotease deficiency results in a propensity to develop emphysema. Since alpha-1-antitrypsin is the major component of the alpha-1 band, deficiency is suggested by a reduced alpha-1 band. Deficiency is confirmed by specific immunochemical quantification. Normal Abnormal Alb α1 α2 β γ Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 15. 15 Acute Inflammation The alpha-1 and alpha-2 bands are increased during the inflammatory response from increased hepatic synthesis of acute phase reactant proteins. Normal Abnormal Alb α1 α2 β γ Chronic Inflammation -Immunoglobulin synthesis by antigen activated B lymphocytes transformed to plasma cells is demonstrated by the increased polyclonal gamma band. Normal Abnormal Alb α1 α2 β γ Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 16. 16 Immunoglobulin Deficiency -Deficient immunoglobulin synthesis is revealed by a markedly diminished gamma band. Effected individuals are prone to recurrent infection Monoclonal Gammopathy -1. An unusually sharp band in the gamma region strongly suggests the presence of a homogeneous immunoglobulin and, thus, the malignant proliferation of plasma cells from a single cell (multiple myeloma) in contrast to the broad, heterogeneous, or polyclonal, gamma band as exhibited above in chronic inflammation from immunoglobulin synthesis by many different clones of plasma cells. 2. Homogeneous immunoglobulins are also found in Waldenstrom's macroglobulinemia (where the sharp gamma band is always IgM). Specimens which exhibit a narrow gamma band are further examined by immunofixation electrophoresis as described below Alb α1 α2 β γ Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 17. 17 ImmunoFixation Electrophoresis Immunofixation electrophoresis (IFE) is used to demonstrate that a narrow gamma band is due to a homogeneous immunoglobulin. IFE has superceded immunoelectrophoresis, results from which are considerably more difficult to interpret, for the purpose of evaluating monoclonal gammopathy. In the illustration below, 6 replicates of the specimen are loaded on to separate lanes of an IFE gel. Following electrophoresis, the protein in each lane is stained differently. The first lane (SP) is stained for total protein. The protein in each of the other lanes is "stained" with specific antisera for immunoglobulin heavy and light chains, respectively, as illustrated in the figure. The finding of the preponderance of only one light chain associated with a predominantly staining heavy chain confirms the molecular homogeneity of the immunoglobulin and also provides identification. IFE identifies the narrow band as monoclonal IgG, lambda. Sometimes malignant plasma cells synthesize excess light chains and less frequently only light chains are synthesized. Almost never is excess heavy chain or only heavy chain synthesized. Excess free lambda light chain is exhibited in the illustration. Serum IFE in monoclonal gammopathy Free light chains are readily filtered by the glomeruli and often are not detectable in serum specimens. Excess light chain synthesis results in proteinuria, which exhibits a narrow band upon electrophoresis. The identity of the narrow band is determined by IFE and is here seen to be free lambda light chain. (A trace of monoclonal IgG,lambda is also present in the urine specimen). The bottom-most band is albumin. Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 18. 18 Urine IFE in monoclonal gammopathy Polyclonal Gammopathy. An IFE of a serum specimen with a polyclonal gamma increase is shown for the sake of comparison. Serum IFE Broad bands are present for both IgG and IgA and corresponding kappa and lambda light chain bands. The light chains appear to be present at the normal kappa/lambda ratio of about 2. Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 19. 19 (v) Blood Ammonia Level Rationale: 1. Ammonia is detoxified and converted to ammonia in liver, estimation of blood ammonia is an indicator of metabolic function of the liver. 2. Estimation of blood ammonia helps in knowing the cause in patients of coma of unknown origin 3. Very nonspecific because it is also raised in a. Reyes syndrome b. Shunting of portal to systemic blood c. GI hemorrhage – increased production of ammonia d. Inherited deficiency of urea cycle enzymes Normal: Ammonia 9-33 micromol/l Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 20. 20 (vi) Serum aminotransferases (SGOT (AST) & SGPT (ALT)) ALT (cytosol) GGT Canalicular surface and microsomes Canalicular surface 5’ nucleotidase ALP LDH (cytosol) AST (mito and cytosol) Location of liver enzymes Rationale: Normally these enzymes are present in serum at low levels When necrosis or cell death occurs, these are released into the blood Levels correlate with extent of tissue damage Normal levels: AST / SGOT ALT / SGPT AST:ALT 5-40 U/L 5-42 U/L 0.7-1.4 Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 21. 21 Patterns: >15 times increase 5-15 times increase 1. 2. 3. 1. 2. 3. 4. Gradual decrease in enzymes Hepatocellular jaundice AST and ALT increase >500 U/L Acute viral hepatitis Toxin induced hepatocellular damage (CC l4) Centrilobular necrosis due to ischemia (like CCF) Chronic hepatitis Autoimmune hepatitis Alcoholic hepatitis Drug induced hepatitis Recovery from acute hepatitis Vs Massive liver necrosis Cholestatic jaundice AST and ALT increase <200 U/L Alcoholic hepatitis AST:ALT > 2 Acute viral hepatitis AST:ALT <1 Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 22. 22 (vii) Serum Alkaline Phosphatase (ALP) Rationale: 1. Alkaline phosphatase is present in canalicular surface of hepatocytes Hence diseases that affect hepatocyte secretion have elevated ALPs It is used primarily to differentiate between hepatocellular and cholestatic jaundice No increased ALP Increased ALP 2. It is non specific – also secreted from a. bones b. intestine c. kidneys d. placenta Causes of raised ALP: Cholestasis Increased >3 times 1. Bile duct obstruction a. Ca head pancreas b. Bile duct strictures c. Biliary atresia 2. Biliary cirrhosis 3. PSC 4. infiltrative diseases of liver (granulomas, amyloid cysts) Bone diseases 1. Active bone growth in children 2. Osteomalacia 3. rickets 4. Hyperparathyroidism 5. Paget’s 6. Osteosarcoma 7. Osteoblastic metastasis Pregnancy 1. Placental ALP Normal Levels: ALP Males: 25-120 U/L Females: 25-90 U/L Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 23. 23 (viii) Serum GGT High levels also present in diseases of (organs with ducts) - Pancreas - Kidney - Prostate Causes of raised GGT: 1. Alcoholism – a. Marked elevation occurs in acute alcoholic hepatitis b. Also helpful in diagnosing occult alcoholism (with no notable liver damage) 2. Cholestasis – a. Level parallels ALP and 5’ Nucleotidase b. This enzyme is very helpful in combination with above two 3. Recovery from acute hepatitis – a. This is the last enzyme to return to normal following acute hepatitis – decrease in level indicates favourable outcome Normal levels: GGT Males: Females: upto 40U/L upto 25U/L Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 24. 24 (ix) 5’ Nucleotidase a. Is released from liver only b. Used to know whether raised ALP is from liver or other sources Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 25. 25 (x) Dye Excretion test Rationale: a. Some synthetic dyes when introduced in the body are excreted in bile b. Their clearance depends on – hepatic circulation, hepatocyte function, uninterrupted bile flow c. These are sensitive tests for liver function but not used nowadays because of risk of adverse drug reactions d. Most common dyes used include 1. Bromsulphathlein (BSP) 2. Indocyanine green 3. Rose bengal BSP Excretion test: BSP injected IV Taken up by hepatocytes Conjugated to glutathione Excreted in bile Check for dye in blood at 45 min If >50% retained – liver function is abnormal Application: Dubin Johnson syndrome Rotor syndrome @45 min in blood Normal value (>50% excreted in bile) High (<50% excreted in bile) @2 hr in blood Higher than expected (slow excretion after 45 min) Lower than expected (Fast excretion after 45 min) Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 26. 26 *INTERPRETATION OF LIVER FUNCTION TESTS Typical LFT values in: 1. 2. 3. 4. Hepatocellular diseases Hyperbilirubinemia Unconjugated>conjugated Ie indirect>direct Conjugated 20-50% of total AST and ALT - >500 IU/L ALP – raised <3 times Usually no increase in GGT, 5’NT 1. 2. 3. 4. Cholestatic diseases Hyperbilirubinemia Conjugated>unconjugated Ie direct>indirect Conjugated >50% of total AST, ALT- 200-500 IU/L ALP – raised >3 times elevation of GGT and 5’NT Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes
  • 27. 27 *APPROACH TO SUSPECTED HEPATOCELLULAR DISEASE: Suspected hepatocellular disease (Higher indirect Bilirubin, clinically) AST, ALT raised - >300IU/L Acute hepatic injury Acute Viral hepatitis Alcoholic hepatitis AST:ALT>2 Toxic or ischemic injury AST,ALT>3000IU/L Acute hepatitis A Acute Hepatitis B Acute hepatitis C IgM Anti HAV IgM anti HBcAg HBsAg Anti HCV HCV RNA Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes Drug induced
  • 28. 28 *APPROACH TO SUSPECTED CHOLESTATIC DISEASE Suspected cholestatic jaundice (High direct bilirubin, clinically) Raised ALP Evaluate GGT and 5’NT Raised GGT, 5’NT Normal GGT, 5’NT Proves hepatic cause Of raised ALP Non hepatic cause of Raised ALP Abdominal USG/CT Dilatation of bile ducts No dilatation of bile ducts Extrahepatic cause Intrahepatic cause Radiology Radiology a. b. c. d. PSC Ca head of pancreas Stricture Stone in CBD Liver mass Diffuse Liver disease FNAC Biopsy 1’ or 2’ Ca Infilatrative liver dis 1’ biliary cirrhosis Notes on Liver function tests.. By Dr. Ashish Jawarkar Contact: pathologybasics@gmail.com Web: pathologybasics.wix.com/notes

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