Lab Findings in Liver Disease
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- Markedly increased bilirubin (up to 40 mg/d) reflects impaired bilirubin excretion.
- Markedly decreased albumin reflects decreased protein synthesis.
- Decreased cholesterol reflects decreased hepatic synthesis of cholesterol
- Serum glutamic-oxaloacetic transaminase (SGOT) (AST [aspartate aminotransferase] and serum glutamic-pyruvic transaminase (SGPT) (ALT [alanine aminotransferase]) - rapid fall from previously elated levels indicates massive loss of liver cells
- Decreased blood urea nitrogen (BUN) reflects decreased protein metabolism
- Increased BUN and creatinine and oliguria reflect oliguric hepatic failure (hepatorenal syndrome)
- Decreased glucose reflects decreased glycogen storage in liver
- Prolonged prothrombin time reflects decreased hepatic synthesis of prothrombin and factors VII, IX and X
- Decreased fibrinogen reflects decreased hepatic synthesis of fibrinogen
- Increased ammonia reflects decreased hepatic urea synthesis.
- Increased pH, decreased PCO2 (respiratory alkalosis) reflects hyperventilation associated with cerebral edema
- Leukocytosis indicates massive liver-cell necrosis.
ALCOHOLIC LIVER DISEASE
- Increased SGOT (AST), SGPT (ALT) - reflect liver-cell necrosis
- Ratio of SGOT-SGPT (AST-ALT) >2 occurs in 70% of patients with alcoholic liver disease. 2
- Increased y-glutamyl transpeptidase (GGT) - this enzyme is a senstive indicator of chronic alcohol consumption
- Increased alkaline phosphatase reflects cholestasis but does not correlate with the severity of alcoholic hepatitis.
- Increased serum bilirubin reflects cholestasis.
- Increased serum immunoglobulins reflect chronic hepatic injury.
- Increased prothrombin time reflects decreased hepatic synthesis of prothrombin and factors VII, IX, X; this indicates severe hepatic injury.
- Macrocytic anemia due to folic acid deficiency, which is the most frequent cause of anemia in alcoholic liver disease.
- Macrocytosis occurs in liver disease, even in the absence of folate deficiency; this is due to excessive lipids in red blood cell (RBC) membranes.
- Microcytic anemia due to iron or pyridoxine deficiency
- Leukocytosis reflects severe hepatic inflammation.
||Central sclerosing hyaline necrosis and alcoholic hepatitis are basically synonyms; here the pattern of necrosis, fibrosis, and Mallory bodies present in zone 3 is quite
evident (Klatskin, x80).
In interpreting serologic tests for hepatitis, remember that all patients with jaundice do not have hepatitis and that all cases of hepatitis are not due to viruses.
- Hepatitis A antigen (HA Ag) is found in the stool 5 days to 6 days before the onset of symptoms or hepatic biochemical abnormalities. The antigen disappears from the stool immediately after the appearance of the antibody (Fig. 4-3).
- Hepatitis a antibody (anti-HAV) appears in the serum soon after onset of the acute illness; its appearance coincides with an increase in serum transaminases (Fig. 4-3). Detection of anti-HAV indicates that the patient has had the infection in the past, will be resistant to subsequent hepatitis a infections, and is no longer infective. The IgM class of anti-HAV appears 1 week to 6 weeks after infection and indicates that HAV infection occurred within the prior 4 weeks to 8 weeks. Anti-HAV IgM is no longer detectable 3 months to 6 months after infection. The IgG class antibody peaks 5 weeks to 10 weeks after infection and indicates that HAV infection occurred more than 8 weeks earlier. The IgG antibody remains elevated indefinitely.
- Hepatitis B Surface Antigen (HBsAg) is the first serologic marker to appear, preceding clinical and laboratory evidence of disease by 1 week to 6 weeks (Fig. 4-5). This persists throughout the clinical illness and usually disappears just before the transminases increase. Persistence for greater than 6 months indicates either development of chronic hepatitis or a benign carrier state . The presence of HBsAg indicates infection with HBV and implies infectivity. The disappearance of HBsAg from the serum does not assure recovery from infection.
- Antibody to HbsAg (anti-HB ) is the last serological marker to appear . It is not detected until the end of convalescence, serveral weeks after HBsAg disappears. During this "serologic gap" period, neither HBsAg nor anti-HB, is present in the serum. Antibody to HBsAg (anti-HB) must be identified at this stage in order to establish hepatitis infection. The rate of anti-HB appearance may depend on the rapidity of HBsAg clearance. Detectable antibody is present for at least 18 months after its appearance and may persist indefinitely.
- Development of anti-HB, connotes recovery from hepatitis B infection, absence of infectivity and immunity from future HBV infection.
- Hepatitis B Core Antigen (HB Ag) is not found in the serum. This antigen is present in liver cell nuclei at the same time that HBsAg is present in the serum and in liver cell cytoplasm.
- Antibody to HB Ag (anti-HB ) appears in the serum shortly after the appearance of HBsAg. This is the first antibody to appear, filling the "serologic gap" described above. Its presence implies a recent HBV infection. High serum titers correlate well with the continuing presence of viral antigens in the liver. The highest levels of anti-HB are found in the chronic HBsAg carrier state. This can be lifelong but it does not confer immunity as does anti-HB.
- Hepatitis B e Antigen (HB Ag) is found only in serum that is reactive for HBsAg. The biophysical chracteristics and origin of HB Ag remain unknown. It appears in the serum of all patients with acute hepatitis B at about the same time HBsAg appears and before the appearance of any detectable biochemical abnormality. At this time the patient is most infectious. The antigen usually lasts for 2 weeks to 6 weeks and disappears before clearance of HBsAg. Disappearance of HB Ag may be interpreted as probable recovery and clearance of HBsAg. The detection of HB Ag in serum for 10 weeks or more after the onset of illness implies progression of the hepatitis B infection to chronic liver diseae. In some patients with chronic hepatitis, HB Ag eventually disappears from the blood; in others, it persists. The presence of HB Ag indicates that the patient's blood is infectious.
- Antibody to HB Ag (anti-HB ) develops after the detection of anti-HB but before the appearance of anti-HB. It usually appears when HB Ag disappears. The seroconversion from HB Ag to anti-HB, indicates that the infection and the disease are on the wane. In the chronic carrier state, presence of anti-HB, is a favourable sign and indicates decreased infectiousness.
Therefore, the clinical stage may be established only by using the patient's history, physical findings, sequential liver function tests, and sequential serologic tests.
Non-A, Non-B Hepatitis
- At the present time there is no specific serologic test for the non-A, non-B form of hepatitis. This is a diagnosis of exclusion. It should be considered in a patient who develops hepatitis 5 weeks to 10 weeks following blood transfusion and who is negative for anti-HAV, HBsAg, anti-HB and anti-HB.
Other Laboratory Findings
- Markedly increased SGOT (AST) and SGPT (ALT) (from 10 times to 100 times normal) indicates severity of liver cell damage; both enzymes are usually increased to the same degree; a fluctuating course of the transminases is frequently seen in non-A, non-B hepatitis.
- Increased y-glutamyl transpeptidase
- Slightly increased alkaline phosphatase (1-3 times normal) indicates mild cholestasis.
- Slightly increased lactate dehydrogenase (LDH) (1-3 times normal), especially LDH
- Normal sedimentation rate and complete blood count (CBC)
- Severe liver-cell necrosis may result in decreased serum albumin, decreased serum cholesterol, prolonged prothrombin time, and serum bilirubin > 25 mg/dl
- Liver biopsy is used to differentiate among the various stages of hepatitis: protracted acute hepatitis, chronic persistent hepatitis, and chronic active hepatitis.
Findings by Stage of Disease
- Increased urine bilirubin
- Increased urine urobilinogen
- Increased SGOT (AST), SGPT (ALT) - level reflects the severity of liver damage; usually precedes jaundice
- Decreased white lood cell (WBC) count with relative lymphocytosis; some atypical lymphocytes
- Normal sedimentation rate
- Retention of indocyanine green (Cardio-Green)
Icteric Period (occurs about 5%-15% as frequently as anicteric hepatitis)
- Increased serum bilirubin (8 mg/dl - 15 mg/d) - rises in 10-14 days, then declines in 2-4 weeks.
- Slightly increased serum alkaline phosphatase reflects mild cholestasis.
- Decreased urine urobilinogen; absent urobilinogen at the peak of diseae.
- Fall in SGOT (AST) and SGPT (ALT) indicates diminishing liver-cell necrosis.
- Increased sedimentation rate
- Increased serum iron reflects release from damaged liver cells.
- Proteinuria might indicate immune-complex damage of the kidney
- Bilirubinuria disappears before bilirubinemia disappears.
- Urine urobilinogen reappears.
- Normal sedimentation rate
- Slight decrease in serum albumin and mild elevation in y-globulin
- Chronic Active Hepatitis
- Increased SGOT (AST) and SGPT (ALT) 5-10 times normal)
- Increased y-globulin (2 times normal) especially IgG
- Increased serum bilirubin (> 4 mg/dl).
- Increased alkaline phosphatase
- Decreased serum albumin
- Presence of smooth-muscle antibody (70% - 90%)
- Persistence of HbsAg anti-HBc HBeAg if the chronic hepatitis is due to HBV (Fig. 4-6)
- Chronic Persistent Hepatitis
- Variable increase in SGOT (AST) and SGPT (ALT) (< 5 times normal)
- Increased serum bilirubin (< 4 mg/d)
- Variable increase in alkaline phosphatase
- Increased y-globulin, slight
- Negative test for smooth-muscle antibody
- Persistence of HBsAg, anti-HBc HBeAg if the chronic hepatitis is due to HBV (Fig. 4-6)
- Liver biopsy is required to establish the stage of chronic liver disease
- Biopsy of the liver shows nodules and fibrous septa.
- Increased nonconjugated bilirubin - impaired bilirubin excretion is a major defect in cirrhosis
- Increased SGOT (AST) and SGPT (ALT) reflect the degree of liver cell necrosis. These are increased to a lesser degree than in hepatitis.
- Increased alkaline phosphatase, 5-nucleotidase, and leucine aminopeptidase reflect cholestasis.
- Slightly increased LDH, especially LDH and LDH.
- Increased y-glutamyl transpeptidase
- Retention of Cardio-Green is a sensitive index of impaired liver function in the absence of jaundice.
- Decreased serum albumin reflects decreased synthesis, contributes to ascites, and indicates advanced liver disease
- Increased ▀ and y-globulins; gamma globulins are polyclonal and reflect chronic inflammation.
- Decreased iron-binding capacity reflects decreased hepatic synthesis of transferrin.
- Increased blood ammonia reflects impaired hepatic detoxification of proteins and occurs in hepatic failure or coma and after surgical anastomosis of the portal vein to the inferior vena cava.
- Decreased serum sodium reflects dilution by increased plasma volume in association with ascites.
- Blood Urea Nitrogen is often decreased with severe liver disease owing to impaired protein metabolism; it may be increased with gastrointestinal (GI) haemorrhage
- Decreased urine volume usually occurs when ascites and edema are present.
- Increased urine bilirubin and urobilinogen reflect impaired bilirubin excretion and impaired hepatic metabolism of urobilinogen.
- Microcytic hypochromic anaemia reflects chronic GI blood loss; this is the most common type of anemia in cirrhosis.
- Normocytic anaemia reflects dilution by increased plasma volume, chronic inflammation, or hypersplenism.
- Macrocytic anaemia, nonmegaloblastic is due to excessive lipid in the RBC membrane; these red cells are more susceptible to haemolysis.
- Macrocytic anaemia, megaloblastic is due to folic acid deficiency.
- WBC is increased with massive hepatic necrosis or GI haemorrhage; it is decreased with hypersplenism or folic-acid deficiency.
- Decreased platelet count reflects hypersplenism; if severe, this suggests disseminated intravascular coagulopathy.
- Prlonged prothrombin time is due to impaired hepatic formation of the vitamin-K dependent clotting factors (prothrombin and factors VII, IX, and X).
- Decreased fibrinogen and factor V reflect impaired hepatic synthesis.
PRIMARY BILIARY CIRRHOSIS
- Marked increase in serum alkaline phosphatase reflects increased synthesis of alkaline phosphatase proximal to the site of intrahepatic obstruction and also indicates impaired excretion of the enzyme.
- Markedly increased conjugated (direct) bilirubin, y-glutamyl transpeptidase, 5-nucleotidase, and serum cholesterol all reflect intrahepatic obstruction and impaired excretion.
- Presence of antimitochondrial antibodies is a chracteristic finding and reflects the immunologic nature of the disorder.
- Increased alpha2 and y-globulins, especially IgM, reflect the immunologic basis of this disorder.
- Slightly decreased albumin occurs early; later it is markedly decreased.
- Increased urine bilirubin and urobilinogen
- Increased urine and hepatic copper reflect impaired hepatic metabolism of copper.
PYOGENIC LIVER ABSCESS
- Marked leukocytosis reflects inflammation.
- Abnormal liver function tests:
- Decreased albumin: increased globulin and alkaline phosphatase
- Bilirubin might be elevated
- Normocytic anaemia, mild to moderate, reflects inflammation.
- Positive aerobic or anaerobic culture of liver abscess
HEPATOMA (HEPATOCELLULAR CARCINOMA)
- Biopsy of the liver is necessary to establish the diagnosis.
- Sudden worsening of laboratory findings in a patient with cirrhosis (see cirrhosis)
- Increased serum alpha1 fetoprotein is a frequent finding.
- Increased serum carcinoembryonic antigen
- Positive HBsAg in a patient with cirrhosis suggests the possibility of hepatoma.
- Blood in ascitic fluid
- Laboratory findings reflecting possible hormonal activity of the tumor, having the effects of insulin, parathormone, erythropoietin, or gonadotropins
METASTATIC CARCINOMA OF THE LIVER
- Biopsy of liver showing tumor is necessary to definitive diagnosis.
- Increased serum alkaline phosphatase occurs in 80% of patients. This reflects liver infiltration by tumor.
- Marked increase in carcinoembryonic antigen
- Increased LDH; isoenzymes do not show specific tissue localization
- Normal serum bilirubin is a common finding.
||Liver with metastatic carcinoma nodules. Note congestiion of liver (red)at periphery of tumor nodules
- Leukocytosis (12,000/Ál - 15,000/Ál) and increased sedimentation rate reflect acute inflammation.
- Increased SGOT (AST), alkaline phosphatase, 5-nucleotidase, and y-glutamyl transpeptidase reflect slight hepatic inflammation and partial biliary obstruction.
- Increased amylase might occur in the absence of clinically evident pancreatitis.
Cholecystitis, Chronic, Gall Bladder
Chronic Cholecystitis 4x
•The surface epithelium has lost its normal delicate papillary appearance(green arrow) with an increase in
fibrous tissue and mild chronic inflammation in the lamina propria
•Rokitansky-Aschoff sinuses are seen in the muscularis(black arrow)
•The degree of chronic inflammation is quite variable and as in this case surprisingly mild
Image Contrib. by: Martin Nadel, M.D. UCHC
Description by: Martin Nadel, M.D. ( 1261-5313)
- Leukocytosis, up to 30,000/Ál indicates inflammation.
- Frequently, positive blood cultures. Escherichia coli is the most frequently encountered organism. Other commonly encountered organisms include klebsiella, Enterobacter, Streptococcus, fecalis, and Bacteroides fragilis.
- Increased serum bilirubin, 5-nucleotidase, alkaline phosphatase, y-glutamyl transpeptidase, leucine aminopeptidase, SGOT (AST), and SGPT (ALT) reflect partial biliary obstruction.
MAJOR BILE-DUCT OBSTRUCTION
- Increased serum conjugated (direct) bilirubin
- Increased urine bilirubin
- Decreased or absent urine urobilinogen
- Increased serum 5-nucleotidase, leucine aminopeptidase, and alkaline phosphatase reflect bile-duct obstruction.
- Increased y-glutamyl transpeptidase shows a faster and greater rise than does alkaline phosphatase or leucine aminopeptidase.
- Prolonged prothrombin time is the result of impaired intestinal absorption of vitamin K and impaired hepatic synthesis of prothrombin and factors VII, IX, and X.
- Increased amylase reflects possible accompanying pancreatitis.
- Increased serum cholesterol and triglycerides
- Increased alpha2 and ▀-globulins correspond to increased serum lipids.
- Leukocytosis (10,000/Ál - 15,000/Ál )
Stones in Bile Duct
- Increased serum amylase begins after 3-6 hr, peaks at 20-30 hr, persists for 48-72 hr; some patients with severe disease may have normal values; no correlation exists between the severity of pancreatitis and the degree of serum amylase elevation. Amylase passes from the inflamed pancreas directly into the bloodstream or into the peritoneal cavity.
- Increased serum lipase peaks at 72-96 hr and persists up to 14 days after serum amylase has returned to normal.
- Increased urine amylase occurs 6-10 hr after serum amylase elevation; urine levels are higher and of longer duration than serum levels. This is believed to be due to a reversible renal tubular defect, which results in decreased amylase reabsorption.
- Increased amylase-creatinine clearance ratio; amylase clearance by the kidneys is accelerated in acute pancreatitis; this also occurs in nonpancreatic diseases, such as diabetic ketoacidosis and extensive burns
- Decreased serum calcium occurs in severe acute pancreatitis; this is the result of calcium binding to fatty acids in fat, which undergoes from pancreatic enzyme action.
- Leukocytosis (10,000/Ál - 20,000/Ál )
- Increased hematocrit reflects hemoconcentration.
- Increased blood glucose, transient-probably due to decreased release of insulin, increased release of glucagon, and increased output of glucorticoids and catecholamines
- Hypertriglyceridemia, usually in association with alcoholism
- Increased erythrocyte sedimentation rate reflects acute inflammation.
- Pleural or ascitic fluid with increased amylase and albumin; presence of blood in ascitic fluid occurs in haemorrhagic pancreatitis
- Poorer prognosis exists when three or more of the following are present: ---
- Initial WBC > 16,000/ Ál
- Initial blood glucose > 200 mg/dl
- Decreased serum calcium < 8 mg/dl
- Fall in hematocrit > 10%
- Rise in BUN > 5 mg/dl
- Arterial PO2 < 60 mm Hg
- Metabolic acidosis with base deficit > 4 mEq/l
- Initial serum LDH > 350 IU/l
- Initial serum SGOT > 250 IU/l
Fat necrosis secondary to acute pancreatitis
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- Abnormal secretin test - after intravenous administration of secretin, decreased volumes of amylase and bicarbonate are secreted into the duodenum
- Abnormal Lundh test - following a fat meal, decreased trypsin is secreted into the duodenum
- Increased stool neutral fat (unsplit fats); increased total fat in 72-hour stool sample when the patient has been on a 100-g fat diet daily for three days
- Increased stool nitrogen reflects impaired protein digestion.
- Impaired protein digestion - demonstrated by undigested muscle fibers in the stool.
- Increased serum bilirubin and alkaline phosphatase reflect obstruction of the intrapancreatic portion of the common bile duct.
- Impaired oral glucose tolerance - diabetic curve may be seen in far-advanced disease
- Increased ascitic fluid amylase reflects leakage from the injured pancreas.
- Laboratory findings of maldigestion
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