The Doctor says, "it is one of those rare syndromes that happen in 1 in 10 or 20 people where the bile levels are elevated. He says it is called Gilbert's Syndrome."
http://en.wikipedia.org/wiki/Gilbert%27s_syndrome
He advised exercise and diet. That was his best advice. But his diagnosis is I feel wrong. Because the problem with me is not really the bile but the super elevated triglycerides. I asked him why the triglycerides are off the limits and he says that he has no answer to that. Hmmm. He does not know. Diet and exercise were his mantra.
This is the specialist Internal medicine doctor.
There is a fatty liver because of alcohol or hepatitis and a fatty liver without alcohol abbreviated NASH.
Looks like I have to treat myself with herbs. I ordered Kutki herb and I am going to take it for a couple of months and check my triglycerides again.
According to the article in Wikipedia, whose estimates could be dubious, people with NASH have 1 in 5 chances of developing cirrhosis. I do not want to get into those cirrhosis bunch. Lets see.
No more yummy cheese.......
Showing posts with label liver. Show all posts
Showing posts with label liver. Show all posts
Monday, May 10, 2010
Sunday, May 9, 2010
kutki for liver
Kutki
Other Names: Picrorrhiza Kurroa, Katuka, Katki.
This Ayurvedic herb is found in the western Himalayas from Kashmir in India to Sikkim.
Traditional Indian (Ayurvedic) healers have relied on this plant for centuries to treat lung and liver disorders including hepatitis and poor bile production, constipation, digestive upset, and snakebites, among other ailments.
High Quality herb and pure extract of wild crafted herbs from their natural habitat without the use of chemical fertilizers, pesticides or preservatives. Wild Crafted Herbs are more potent and effective than Cultivated Herbs.
Indications (Uses): portal hypertension, ascites, fever, hiccoughs, chronic constipation, renal failure, cirrhotic changes, HIV, rheumatic conditions, CFS, jaundice, hepatitis A (infectious) or B C, cirrhotic changes ,lipomas, gall stones, CFS, cirrhotic changes from alcohol, placque on arteries, gall stones, eczema, peptic ulcer, arteries, rheumatism, immune deficiency, fever, infectioin, pneumonitis, pulmonary congestion, cold, cough, HIV, EBV, chronic hiccough from CHF, renal failure, uremia, chronic constipation from gases, ascites, spleenomegaly, renal failure, hepatomegaly K = dropsy, snakebit, scorpion sting, disease of liver and spleen including jaundice and anemia, constipation due to scanty intestinal secretions, bilious fever as decoction of kutki, neem, licorice, raisins dyspepsia (kutki, vaca, haritaki, citrak with cow's urine in dose of 28ml, scorpion sting, non-specific fever such as with constipation, fever of elephantiasis, infective hepatitis with jaundice, bronchial asthma, hi serum cholesterol and long coagulation times
Contraindications (Cautions): diarrhea, dual hiccoughs, hypoglycemia
Constituents: K = flavonoid, kutkin a glucosida bitter principle actually two glucosides picroside-1 and kutkoside. Petroleum ether extract yielded D-mannitol, kutkiol, kutkisterol, and a ketone identical to apocynin, picrorhizin is its bitter principle, as glucosidovanilloyl glucose was isolated
Active Substances:
Plant Part Used: rhizome
Other Names: Picrorrhiza Kurroa, Katuka, Katki.
This Ayurvedic herb is found in the western Himalayas from Kashmir in India to Sikkim.
As a Dietary Supplement
Kutki helps to maintain healthy bile production and supports healthy liver function. It is safe to use as nutritional support for excessive fat.As per Ayurveda
It balances pitta and kapha (fire and water) in the body. It is used as a mild laxative, hepatoprotective, anti-allergic, anti-inflammatory, analgesic. It helps in cases of skin problems, jaundice and improves eye sight. It is also used to check first stage of liver cancer.Traditional Indian (Ayurvedic) healers have relied on this plant for centuries to treat lung and liver disorders including hepatitis and poor bile production, constipation, digestive upset, and snakebites, among other ailments.
High Quality herb and pure extract of wild crafted herbs from their natural habitat without the use of chemical fertilizers, pesticides or preservatives. Wild Crafted Herbs are more potent and effective than Cultivated Herbs.
Picrorhiza kurroa is a famous herb in the traditional system of medicine i.e. ayurveda and has classically been used to cure disorders of the liver and upper respiratory tract (URT). It also reduce fevers and to resolve dyspepsia, chronic diarrheal condition and bites by scorpion sting. It is a small perennial weed, found in the Himalayan region evolving at heights of 3,000-5,000 meters above sea level. Picrorhiza kurroa or commonly known as kutki has a long, creeping stocks of the roots that is bitter in taste and grows in rock crevices and rocky surfaces and moist, sandy soil. The leaves of the plant are flat, oval, and sharply serrated. The flowers appear in late summers and early rainy seasons. Flowers are white or pale purple in color and borne on a tall spike. It is harvested manually in the early winter season. The active ingredients are achieved from the root and rhizomes. The plant is self-regenerating. Present studies on Picrorhiza kurroa
(kutki) has focused on its hepatoprotective (liver protection), anticholestatic (stablelises cholestrol), antioxidant, and immune-modulating activity. Picrorhiza kurroa improves the gall bladder secretions and helps in digestion and metabolisation of fats. It is very useful in treating fatty liver and also regulates the fat metabolism in liver.
Pharmacological Action: tonic, expectorant, anthelmintic, antiviral, antipyretic, strong purgative, mild diuretic, antispasmodic, hepato and spleenotonic, regulates blood sugar, expectorant, anthelmintic, bhedana, antiviral = also HIV, EBV, purgative provoking pitta remove, anticoagulant, antipyretic, lekhana, diuretic, hepato detoxifier, antipleuritic, antispasmodic = hiccoughs K= kapha pitta hara, pacana, dipana, yakrt utageka, pitta sarka, krmighana, prame hangn, daha prasamk; bitter stomachic, laxative, cathartic in large dose, antiperiodic, cholagogue, mild purgative Indications (Uses): portal hypertension, ascites, fever, hiccoughs, chronic constipation, renal failure, cirrhotic changes, HIV, rheumatic conditions, CFS, jaundice, hepatitis A (infectious) or B C, cirrhotic changes ,lipomas, gall stones, CFS, cirrhotic changes from alcohol, placque on arteries, gall stones, eczema, peptic ulcer, arteries, rheumatism, immune deficiency, fever, infectioin, pneumonitis, pulmonary congestion, cold, cough, HIV, EBV, chronic hiccough from CHF, renal failure, uremia, chronic constipation from gases, ascites, spleenomegaly, renal failure, hepatomegaly K = dropsy, snakebit, scorpion sting, disease of liver and spleen including jaundice and anemia, constipation due to scanty intestinal secretions, bilious fever as decoction of kutki, neem, licorice, raisins dyspepsia (kutki, vaca, haritaki, citrak with cow's urine in dose of 28ml, scorpion sting, non-specific fever such as with constipation, fever of elephantiasis, infective hepatitis with jaundice, bronchial asthma, hi serum cholesterol and long coagulation times
Contraindications (Cautions): diarrhea, dual hiccoughs, hypoglycemia
Constituents: K = flavonoid, kutkin a glucosida bitter principle actually two glucosides picroside-1 and kutkoside. Petroleum ether extract yielded D-mannitol, kutkiol, kutkisterol, and a ketone identical to apocynin, picrorhizin is its bitter principle, as glucosidovanilloyl glucose was isolated
Active Substances:
Plant Part Used: rhizome
Tuesday, May 4, 2010
liver problems
Liver function tests, or LFTs, include tests that are routinely measured in all clinical laboratories. LFTs include bilirubin, a compound formed by the breakdown of hemoglobin; ammonia, a breakdown product of protein that is normally converted into urea by the liver before being excreted by the kidneys; proteins that are made by the liver including total protein, albumin, prothrombin, and fibrinogen; cholesterol and triglycerides, which are made and excreted via the liver; and the enzymes alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), and lactate dehydrogenase (LDH). Other liver function tests include serological tests (to demonstrate antibodies) and DNA tests for hepatitis and other viruses; and tests for antimitochondrial and smooth muscle antibodies, transthyretin (prealbumin), protein electrophoresis, bile acids, alpha-fetoprotein, and a constellation of other enzymes that help differentiate necrotic (characterized by death of tissues) versus obstructive liver disease.
Bilirubin: Drugs that may cause increased blood levels of total bilirubin include anabolic steroids, antibiotics, antimalarials, ascorbic acid, Diabinese, codeine, diuretics, epinephrine, oral contraceptives, and vitamin A.
Ammonia: Muscular exertion can increase ammonia levels, while cigarette smoking produces significant increases within one hour of inhalation. Drugs that may cause increased levels include alcohol, barbiturates, narcotics, and diuretics. Drugs that may decrease levels include antibiotics, levodopa, lactobacillus, and potassium salts.
ALT: Drugs that may increase ALT levels include acetaminophen, ampicillin, codeine, dicumarol, indomethacin, methotrexate, oral contraceptives, tetracyclines, and verapamil. Previous intramuscular injections may cause elevated levels.
GGT: Drugs that may cause increased GGT levels include alcohol, phenytoin, and phenobarbital. Drugs that may cause decreased levels include oral contraceptives.
LDH: Strenuous activity may raise levels of LDH. Alcohol, anesthetics, aspirin, narcotics, procainamide, and fluoride may also raise levels. Ascorbic acid (vitamin C) can lower levels of LDH.
Some liver function tests are used to determine if the liver has been damaged or its function impaired. Elevations of these markers for liver injury or disease tell the physician that something is wrong with the liver. ALT and bilirubin are the two primary tests used largely for this purpose. Bilirubin is measured by two tests, called total and direct bilirubin. The total bilirubin measures both conjugated and unconjugated bilirubin while direct bilirubin measures only the conjugated bilirubin fraction in the blood. Unconjugated bilirubin is formed in the reticuloendothelial (RE) cells in the spleen that remove old red blood cells from the circulation. The RE cells release the bilirubin into the blood, where it is bound by albumin and transported to the liver. The bilirubin is taken up by liver cells and conjugated to glucuronic acid, which makes the bilirubin water soluble. This form will react directly with a Ehrlich's diazo reagent, hence the name direct bilirubin. While total bilirubin is elevated in various liver diseases, it is also increased in certain (hemolytic) anemias caused by increased red blood cell turnover. Neonatal hyperbilirubinemia is a condition caused by an immature liver than cannot conjugate the bilirubin. The level of total bilirubin in the blood becomes elevated, and must be monitored closely in order to prevent damage to the brain caused by unconjugated bilirubin, which has a high affinity for brain tissue. Bilirubin levels can be decreased by exposing the baby to UV light. Direct bilirubin is formed only by the liver, and therefore, it is specific for hepatic or biliary disease. Its concentration in the blood is very low (0–0.2 mg/dL) and therefore, even slight increases are significant. Highest levels of direct bilirubin are seen in obstructive liver diseases. However, direct bilirubin is not sensitive to all forms of liver disease (e.g., focal intrahepatic obstruction) and is not always elevated in the earliest stages of disease; therefore, ALT is needed to exclude a diagnosis.
ALT is an enzyme that transfers an amino group from the amino acid alanine to a ketoacid acceptor (oxaloacetate). The enzyme was formerly called serum glutamic pyruvic transaminase (SGPT) after the products formed by this reaction. Although ALT is present in other tissues besides liver, its concentration in liver is far greater than any other tissue, and blood levels in nonhepatic conditions rarely produce levels of a magnitude seen in liver disease. The enzyme is very sensitive to necrotic or inflammatory liver injury. Consequently, if ALT or direct bilirubin is increased, then some form of liver disease is likely. If both are normal, then liver disease is unlikely.
These two tests along with others are used to help determine what is wrong. The most useful tests for this purpose are the liver function enzymes and the ratio of direct to total bilirubin. These tests are used to differentiate diseases characterized primarily by hepatocellular damage (necrosis, or cell death) from those characterized by obstructive damage (cholestasis or blockage of bile flow). In hepatocellular damage, the transaminases, ALT and AST, are increased to a greater extent than alkaline phosphatase. This includes viral hepatitis, which gives the greatest increase in transaminases (10–50-fold normal), hepatitis induced by drugs or poisons (toxic hepatitis), alcoholic hepatitis, hypoxic necrosis (a consequence of congestive heart failure), chronic hepatitis, and cirrhosis of the liver. In obstructive liver diseases, the alkaline phosphatase is increased to a greater extent than the transaminases (ALP>ALT). This includes diffuse intrahepatic obstructive disease which may be caused by some drugs or biliary cirrhosis, focal obstruction that may be caused by malignancy, granuloma from chronic inflamation, or stones in the intrahepatic bile ducts, or extrahepatic obstruction such as gall bladder or common bile duct stones, or pancreatic or bile duct cancer. In both diffuse intrahepatic obstruction and extrahepatic obstruction, the direct bilirubin is often greatly elevated because the liver can conjugate the bilirubin, but this direct bilirubin cannot be excreted via the bile. In such cases the ratio of direct to total bilirubin is greater than 0.4.
Aspartate aminotransferase, formerly called serum glutamic oxaloacetic transaminase (SGOT), is not as specific for liver disease as is ALT, which is increased in myocardial infarction, pancreatitis, muscle wasting diseases, and many other conditions. However, differentiation of acute and chronic forms of hepatocellular injury is aided by examining the ratio of ALT to AST, called the DeRitis ratio. In acute hepatitis, Reye's syndrome, and infectious mononucleosis the ALT predominates. However, in alcoholic liver disease, chronic hepatitis, and cirrhosis, the AST predominates.
Alkaline phosphatase is increased in obstructive liver diseases, but it is not specific for the liver. Increases of a similar magnitude (three- to five-fold normal) are commonly seen in bone diseases, late pregnancy, leukemia, and some other malignancies. The enzyme gamma-glutamyl transferase (GGT) is used to help differentiate the source of an elevated ALP. GGT is greatly increased in obstructive jaundice, alcoholic liver disease, and hepatic cancer. When the increase in GGT is two or more times greater than the increase in ALP, the source of the ALP is considered to be from the liver. When the increase in GGT is five or more times the increase in ALP, this points to a diagnosis of alcoholic hepatitis. GGT, but not AST and ALT, is elevated in the first stages of liver inflammation due to alcohol consumption, and GGT is useful as a marker for excessive drinking. GGT has been shown to rise after acute persistent alcohol ingestion and then fall when alcohol is avoided.
Lactate dehydrogenase (LDH) is found in almost all cells in the body. Different forms of the enzyme (isoenzymes) exist in different tissues, especially in heart, liver, red blood cells, brain, kidney, and muscles. LDH is increased in megaloblastic and hemolytic anemias, leukemias and lymphomas, myocardial infarction, infectious mononucleosis, muscle wasting diseases, and both necrotic and obstructive jaundice. While LDH is not specific for any one disorder, the enzyme is elevated (twoto five-fold normal) along with liver function enzymes in both necrotic and obstructive liver diseases. LDH is markedly increased in most cases of liver cancer. An enzyme pattern showing a marked increase in LDH and to a lesser degree ALP with only slightly increased transaminases (AST and ALT) is seen in cancer of the liver (space occupying disease). Such findings should be followed-up with imaging studies and measurement of alpha-fetoprotein and carcinoembryonic antigen, two tumor markers prevalent in hepatic cancers.
Some liver function tests are not sensitive enough to be used for diagnostic purposes, but are elevated in severe or chronic liver diseases. These tests are used primarily to indicate the extent of damage to the liver. Tests falling into this category are ammonia, total protein, albumin, cholesterol, transthyretin, fibrinogen, and the prothrombin time.
Analysis of blood ammonia aids in the diagnosis of severe liver diseases and helps to monitor the course of these diseases. Together with the AST and the ALT, ammonia levels are used to confirm a diagnosis of Reye's syndrome, a rare disorder usually seen in children and associated with infection and aspirin intake. Reye's syndrome is characterized by brain and liver damage following an upper respiratory tract infection, chickenpox, or influenza. Ammonia levels are also helpful in the diagnosis and treatment of hepatic encephalopathy, a serious brain condition caused by the accumulated toxins that result from liver disease and liver failure. Ammonia levels in the blood are normally very low. Ammonia produced by the breakdown of amino acids is converted to urea by the liver. When liver disease becomes severe, failure of the urea cycle results in elevated blood ammonia and decreased urea (or blood urea nitrogen, BUN). Increasing ammonia signals end-stage liver disease and a high risk of hepatic coma.
Albumin is the protein found in the highest concentration in blood, making up over half of the protein mass. Albumin has a half-life in blood of about three weeks and decreased levels are not seen in the early stages of liver disease. A persistently low albumin in liver disease signals reduced synthetic capacity of the liver and is a sign of progressive liver failure. In the acute stages of liver disease, proteins such as transthyretin (prealbumin) with a shorter half-life may be measured to give an indication of the severity of the disease.
Cholesterol is synthesized by the liver, and cholesterol balance is maintained by the liver's ability to remove cholesterol from lipoproteins, and use it to produce bile acids and salts that it excretes into the bile ducts. In obstructive jaundice caused by stones, biliary tract scarring, or cancer, the bile cannot be eliminated and cholesterol and triglycerides may accumulate in the blood as low-density lipoprotein (LDL) cholesterol. In acute necrotic liver diseases triglycerides may be elevated due to hepatic lipase deficiency. In liver failure caused by necrosis, the liver's ability to synthesize cholesterol is reduced and blood levels may be low.
The liver is responsible for production of the vitamin K clotting factors. In obstructive liver diseases a deficiency of vitamin K-derived clotting factors results from failure to absorb vitamin K. In obstructive jaundice, intramuscular injection of vitamin K will correct the prolonged prothrombin time. In severe necrotic disease, the liver cannot synthesize factor I (fibrinogen) or factors II, VII, IX, and X from vitamin K. When attributable to hepatic necrosis, an increase in the prothrombin time by more than two seconds indicates severe liver disease.
Serum protein electrophoresis patterns will be abnormal in both necrotic and obstructive liver diseases. In the acute stages of hepatitis, the albumin will be low and the gamma globulin fraction will be elevated owing to a large increase in the production of antibodies. The alpha-1 globulin and alpha-2 globulin fractions will be elevated owing to production of acute phase proteins as a response to inflamation. In biliary cirrhosis the beta globulin may be elevated owing to an increase in beta lipoprotein. In hepatic cirrhosis the albumin will be greatly decreased, and the pattern will show bridging between the beta and gamma globulins owing to production of IgA. The albumin to globulin ratio (A/G) ratio will fall below one.
The most prevalent liver disease is viral hepatitis. Tests for this condition include a variety of antigen and antibody markers and nucleic acid tests. Acute viral hepatitis is associated initially with 20- to 100-fold increases in transaminases and is followed shortly afterward by jaundice. Such patients should be tested for hepatitis B surface antigen (HbsAg) and IgM antibodies to hepatitis B core antigen (anti-HBc IgM), and anti-hepatitis C virus (anti-HVC) to identify these causes. In addition to hepatitis A-E, viral hepatitis may be caused by Epstein-Barr virus (EBV) and cytomegalovirus (CMV) infections of the liver. Tests for these viruses such as the infectious mononucleosis antibody test, anti-viral capsid antigen test (anti-VCA), and anti-CMV test are useful in diagnosing these infections.
Liver disease may be caused by autoimmune mechanisms in which autoantibodies destroy liver cells. Autoimmune necrosis is associated with systemic lupus erythematosus and chronic viral hepatitis usually caused by hepatitis B and hepatitis C virus infections. These conditions give rise to anti-smooth muscle antibodies and anti-nuclear antibodies, and tests for these are useful markers for chronic hepatitis. Antibodies to mitochondrial antigens (antimitochondrial antibodies) are found in the blood of more than 90% of persons with primary biliary cirrhosis, and those with M2 specificity are considered specific for this disease.
AST: High levels may indicate liver cell damage, hepatitis, heart attack, heart failure, or gall stones.
ALP: Elevated levels occur in diseases that impair bile formation (cholestasis). ALP may also be elevated in many other liver disorders, as well as some lung cancers (bronchogenic carcinoma) and Hodgkin's lymphoma. However, elevated ALP levels may also occur in otherwise healthy people, especially among older people.
GGT: Increased levels are diagnostic of hepatitis, cirrhosis, liver tumor or metastasis, as well as injury from drugs toxic to the liver. GGT levels may increase with alcohol ingestion, heart attack, pancreatitis, infectious mononucleosis, and Reye's syndrome.
LDH: Elevated LDH is seen with heart attack, kidney disease, hemolysis, viral hepatitis, infectious mononucleosis, Hodgkin's disease, abdominal and lung cancers, germ cell tumors, progressive muscular dystrophy, and pulmonary embolism. LD is not normally elevated in cirrhosis.
Bilirubin: Increased indirect or total bilirubin levels can indicate various serious anemias, including hemolytic disease of the newborn and transfusion reaction. Increased direct bilirubin levels can be diagnostic of bile duct obstruction, gallstones, cirrhosis, or hepatitis. It is important to note that if total bilirubin levels in the newborn reach or exceed critical levels, exchange transfusion is necessary to avoid kernicterus, a condition that causes brain damage from bilirubin in the brain.
Ammonia: Increased levels are seen in primary liver cell disease, Reye's syndrome, severe heart failure, hemolytic disease of the newborn, and hepatic encephalopathy.
Albumin: Albumin levels are increased due to dehydration. They are decreased due to a decrease in synthesis of the protein which is seen in severe liver failure and in conditions such as burns or renal disease that cause loss of albumin from the blood.
Purpose
Liver function tests done individually do not give the physician very much information, but used in combination with a careful history, physical examination, and imaging studies, they contribute to making an accurate diagnosis of the specific liver disorder. Different tests will show abnormalities in response to liver inflammation; liver injury due to drugs, alcohol, toxins, or viruses; liver malfunction due to blockage of the flow of bile; and liver cancers.Precautions
Blood for LFTs is collected by sticking a needle into a vein. The nurse or phlebotomist performing the procedure must be careful to clean the skin before sticking in the needle.Bilirubin: Drugs that may cause increased blood levels of total bilirubin include anabolic steroids, antibiotics, antimalarials, ascorbic acid, Diabinese, codeine, diuretics, epinephrine, oral contraceptives, and vitamin A.
Ammonia: Muscular exertion can increase ammonia levels, while cigarette smoking produces significant increases within one hour of inhalation. Drugs that may cause increased levels include alcohol, barbiturates, narcotics, and diuretics. Drugs that may decrease levels include antibiotics, levodopa, lactobacillus, and potassium salts.
ALT: Drugs that may increase ALT levels include acetaminophen, ampicillin, codeine, dicumarol, indomethacin, methotrexate, oral contraceptives, tetracyclines, and verapamil. Previous intramuscular injections may cause elevated levels.
GGT: Drugs that may cause increased GGT levels include alcohol, phenytoin, and phenobarbital. Drugs that may cause decreased levels include oral contraceptives.
LDH: Strenuous activity may raise levels of LDH. Alcohol, anesthetics, aspirin, narcotics, procainamide, and fluoride may also raise levels. Ascorbic acid (vitamin C) can lower levels of LDH.
Description
The liver is the largest and one of the most important organs in the body. As the body's "chemical factory," it regulates the levels of most of the biomolecules found in the blood, and acts with the kidneys to clear the blood of drugs and toxic substances. The liver metabolizes these products, alters their chemical structure, makes them water soluble, and excretes them in bile. Laboratory tests for total protein, albumin, ammonia, transthyretin, and cholesterol are markers for the synthetic function of the liver. Tests for cholesterol, bilirubin, ALP, and bile salts are measures of the secretory (excretory) function of the liver. The enzymes ALT, AST, GGT, LDH, and tests for viruses are markers for liver injury.Some liver function tests are used to determine if the liver has been damaged or its function impaired. Elevations of these markers for liver injury or disease tell the physician that something is wrong with the liver. ALT and bilirubin are the two primary tests used largely for this purpose. Bilirubin is measured by two tests, called total and direct bilirubin. The total bilirubin measures both conjugated and unconjugated bilirubin while direct bilirubin measures only the conjugated bilirubin fraction in the blood. Unconjugated bilirubin is formed in the reticuloendothelial (RE) cells in the spleen that remove old red blood cells from the circulation. The RE cells release the bilirubin into the blood, where it is bound by albumin and transported to the liver. The bilirubin is taken up by liver cells and conjugated to glucuronic acid, which makes the bilirubin water soluble. This form will react directly with a Ehrlich's diazo reagent, hence the name direct bilirubin. While total bilirubin is elevated in various liver diseases, it is also increased in certain (hemolytic) anemias caused by increased red blood cell turnover. Neonatal hyperbilirubinemia is a condition caused by an immature liver than cannot conjugate the bilirubin. The level of total bilirubin in the blood becomes elevated, and must be monitored closely in order to prevent damage to the brain caused by unconjugated bilirubin, which has a high affinity for brain tissue. Bilirubin levels can be decreased by exposing the baby to UV light. Direct bilirubin is formed only by the liver, and therefore, it is specific for hepatic or biliary disease. Its concentration in the blood is very low (0–0.2 mg/dL) and therefore, even slight increases are significant. Highest levels of direct bilirubin are seen in obstructive liver diseases. However, direct bilirubin is not sensitive to all forms of liver disease (e.g., focal intrahepatic obstruction) and is not always elevated in the earliest stages of disease; therefore, ALT is needed to exclude a diagnosis.
ALT is an enzyme that transfers an amino group from the amino acid alanine to a ketoacid acceptor (oxaloacetate). The enzyme was formerly called serum glutamic pyruvic transaminase (SGPT) after the products formed by this reaction. Although ALT is present in other tissues besides liver, its concentration in liver is far greater than any other tissue, and blood levels in nonhepatic conditions rarely produce levels of a magnitude seen in liver disease. The enzyme is very sensitive to necrotic or inflammatory liver injury. Consequently, if ALT or direct bilirubin is increased, then some form of liver disease is likely. If both are normal, then liver disease is unlikely.
These two tests along with others are used to help determine what is wrong. The most useful tests for this purpose are the liver function enzymes and the ratio of direct to total bilirubin. These tests are used to differentiate diseases characterized primarily by hepatocellular damage (necrosis, or cell death) from those characterized by obstructive damage (cholestasis or blockage of bile flow). In hepatocellular damage, the transaminases, ALT and AST, are increased to a greater extent than alkaline phosphatase. This includes viral hepatitis, which gives the greatest increase in transaminases (10–50-fold normal), hepatitis induced by drugs or poisons (toxic hepatitis), alcoholic hepatitis, hypoxic necrosis (a consequence of congestive heart failure), chronic hepatitis, and cirrhosis of the liver. In obstructive liver diseases, the alkaline phosphatase is increased to a greater extent than the transaminases (ALP>ALT). This includes diffuse intrahepatic obstructive disease which may be caused by some drugs or biliary cirrhosis, focal obstruction that may be caused by malignancy, granuloma from chronic inflamation, or stones in the intrahepatic bile ducts, or extrahepatic obstruction such as gall bladder or common bile duct stones, or pancreatic or bile duct cancer. In both diffuse intrahepatic obstruction and extrahepatic obstruction, the direct bilirubin is often greatly elevated because the liver can conjugate the bilirubin, but this direct bilirubin cannot be excreted via the bile. In such cases the ratio of direct to total bilirubin is greater than 0.4.
Aspartate aminotransferase, formerly called serum glutamic oxaloacetic transaminase (SGOT), is not as specific for liver disease as is ALT, which is increased in myocardial infarction, pancreatitis, muscle wasting diseases, and many other conditions. However, differentiation of acute and chronic forms of hepatocellular injury is aided by examining the ratio of ALT to AST, called the DeRitis ratio. In acute hepatitis, Reye's syndrome, and infectious mononucleosis the ALT predominates. However, in alcoholic liver disease, chronic hepatitis, and cirrhosis, the AST predominates.
Alkaline phosphatase is increased in obstructive liver diseases, but it is not specific for the liver. Increases of a similar magnitude (three- to five-fold normal) are commonly seen in bone diseases, late pregnancy, leukemia, and some other malignancies. The enzyme gamma-glutamyl transferase (GGT) is used to help differentiate the source of an elevated ALP. GGT is greatly increased in obstructive jaundice, alcoholic liver disease, and hepatic cancer. When the increase in GGT is two or more times greater than the increase in ALP, the source of the ALP is considered to be from the liver. When the increase in GGT is five or more times the increase in ALP, this points to a diagnosis of alcoholic hepatitis. GGT, but not AST and ALT, is elevated in the first stages of liver inflammation due to alcohol consumption, and GGT is useful as a marker for excessive drinking. GGT has been shown to rise after acute persistent alcohol ingestion and then fall when alcohol is avoided.
Lactate dehydrogenase (LDH) is found in almost all cells in the body. Different forms of the enzyme (isoenzymes) exist in different tissues, especially in heart, liver, red blood cells, brain, kidney, and muscles. LDH is increased in megaloblastic and hemolytic anemias, leukemias and lymphomas, myocardial infarction, infectious mononucleosis, muscle wasting diseases, and both necrotic and obstructive jaundice. While LDH is not specific for any one disorder, the enzyme is elevated (twoto five-fold normal) along with liver function enzymes in both necrotic and obstructive liver diseases. LDH is markedly increased in most cases of liver cancer. An enzyme pattern showing a marked increase in LDH and to a lesser degree ALP with only slightly increased transaminases (AST and ALT) is seen in cancer of the liver (space occupying disease). Such findings should be followed-up with imaging studies and measurement of alpha-fetoprotein and carcinoembryonic antigen, two tumor markers prevalent in hepatic cancers.
Some liver function tests are not sensitive enough to be used for diagnostic purposes, but are elevated in severe or chronic liver diseases. These tests are used primarily to indicate the extent of damage to the liver. Tests falling into this category are ammonia, total protein, albumin, cholesterol, transthyretin, fibrinogen, and the prothrombin time.
Analysis of blood ammonia aids in the diagnosis of severe liver diseases and helps to monitor the course of these diseases. Together with the AST and the ALT, ammonia levels are used to confirm a diagnosis of Reye's syndrome, a rare disorder usually seen in children and associated with infection and aspirin intake. Reye's syndrome is characterized by brain and liver damage following an upper respiratory tract infection, chickenpox, or influenza. Ammonia levels are also helpful in the diagnosis and treatment of hepatic encephalopathy, a serious brain condition caused by the accumulated toxins that result from liver disease and liver failure. Ammonia levels in the blood are normally very low. Ammonia produced by the breakdown of amino acids is converted to urea by the liver. When liver disease becomes severe, failure of the urea cycle results in elevated blood ammonia and decreased urea (or blood urea nitrogen, BUN). Increasing ammonia signals end-stage liver disease and a high risk of hepatic coma.
Albumin is the protein found in the highest concentration in blood, making up over half of the protein mass. Albumin has a half-life in blood of about three weeks and decreased levels are not seen in the early stages of liver disease. A persistently low albumin in liver disease signals reduced synthetic capacity of the liver and is a sign of progressive liver failure. In the acute stages of liver disease, proteins such as transthyretin (prealbumin) with a shorter half-life may be measured to give an indication of the severity of the disease.
Cholesterol is synthesized by the liver, and cholesterol balance is maintained by the liver's ability to remove cholesterol from lipoproteins, and use it to produce bile acids and salts that it excretes into the bile ducts. In obstructive jaundice caused by stones, biliary tract scarring, or cancer, the bile cannot be eliminated and cholesterol and triglycerides may accumulate in the blood as low-density lipoprotein (LDL) cholesterol. In acute necrotic liver diseases triglycerides may be elevated due to hepatic lipase deficiency. In liver failure caused by necrosis, the liver's ability to synthesize cholesterol is reduced and blood levels may be low.
The liver is responsible for production of the vitamin K clotting factors. In obstructive liver diseases a deficiency of vitamin K-derived clotting factors results from failure to absorb vitamin K. In obstructive jaundice, intramuscular injection of vitamin K will correct the prolonged prothrombin time. In severe necrotic disease, the liver cannot synthesize factor I (fibrinogen) or factors II, VII, IX, and X from vitamin K. When attributable to hepatic necrosis, an increase in the prothrombin time by more than two seconds indicates severe liver disease.
Serum protein electrophoresis patterns will be abnormal in both necrotic and obstructive liver diseases. In the acute stages of hepatitis, the albumin will be low and the gamma globulin fraction will be elevated owing to a large increase in the production of antibodies. The alpha-1 globulin and alpha-2 globulin fractions will be elevated owing to production of acute phase proteins as a response to inflamation. In biliary cirrhosis the beta globulin may be elevated owing to an increase in beta lipoprotein. In hepatic cirrhosis the albumin will be greatly decreased, and the pattern will show bridging between the beta and gamma globulins owing to production of IgA. The albumin to globulin ratio (A/G) ratio will fall below one.
The most prevalent liver disease is viral hepatitis. Tests for this condition include a variety of antigen and antibody markers and nucleic acid tests. Acute viral hepatitis is associated initially with 20- to 100-fold increases in transaminases and is followed shortly afterward by jaundice. Such patients should be tested for hepatitis B surface antigen (HbsAg) and IgM antibodies to hepatitis B core antigen (anti-HBc IgM), and anti-hepatitis C virus (anti-HVC) to identify these causes. In addition to hepatitis A-E, viral hepatitis may be caused by Epstein-Barr virus (EBV) and cytomegalovirus (CMV) infections of the liver. Tests for these viruses such as the infectious mononucleosis antibody test, anti-viral capsid antigen test (anti-VCA), and anti-CMV test are useful in diagnosing these infections.
Liver disease may be caused by autoimmune mechanisms in which autoantibodies destroy liver cells. Autoimmune necrosis is associated with systemic lupus erythematosus and chronic viral hepatitis usually caused by hepatitis B and hepatitis C virus infections. These conditions give rise to anti-smooth muscle antibodies and anti-nuclear antibodies, and tests for these are useful markers for chronic hepatitis. Antibodies to mitochondrial antigens (antimitochondrial antibodies) are found in the blood of more than 90% of persons with primary biliary cirrhosis, and those with M2 specificity are considered specific for this disease.
Preparation
Patients are asked to fast and to inform clinicians of all drugs, even over-the-counter drugs, that they are taking. Many times liver function tests are done on an emergency basis and fasting and obtaining a medical history are not possible.Aftercare
Patients will have blood drawn into a vacuum tube and may experience some pain and burning at the site of injection. A gauze bandage may be placed over the site to prevent further bleeding. If the person is suffering from severe liver disease, they may lack clotting factors. The nurse or caregiver should be careful to monitor bleeding in these patients after obtaining blood.Normal Results
Reference ranges vary from laboratory to laboratory and also depend upon the method used. However, normal values are generally framed by the ranges shown below. Values for enzymes are based upon measurement at 37°C.- ALT: 5–35 IU/L. (Values for the elderly may be slightly higher, and values also may be higher in men and in African-Americans.)
- AST: 0–35 IU/L.
- ALP: 30–120 IU/LALP is higher in children, older adults and pregnant females.
- GGT: males 2–30 U/L; females 1–24 U/L.
- LDH: 0–4 days old: 290–775 U/L; 4–10 days: 545–2000 U/L; 10 days–24 months: 180–430 U/L; 24 months–12 years: 110–295 U/L; 12–60 years: 100–190 U/L; 60 years: >110–210 U/L.
- Bilirubin: (Adult, elderly, and child) Total bilirubin: 0.1–1.0 mg/dL; indirect bilirubin: 0.2–0.8 mg/dL; direct bilirubin: 0.0–0.3 mg/dL. (Newborn) Total bilirubin: 1–12 mg/dL. Note: critical values for adult: greater than 1.2 mg/dL. Critical values for newborn (requiring immediate treatment): greater than 15 mg/dL.
- Ammonia: 10–70 micrograms per dL (heparinized plasma). Normal values for this test vary widely, depending upon the age of the patient and the type of specimen.
- Albumin: 3.2–5.4 g/L.
Abnormal Results
ALT: Values are significantly increased in cases of hepatitis, and moderately increased in cirrhosis, liver tumor, obstructive jaundice, and severe burns. Values are mildly increased in pancreatitis, heart attack, infectious mononucleosis, and shock. Most useful when compared with ALP levels.AST: High levels may indicate liver cell damage, hepatitis, heart attack, heart failure, or gall stones.
ALP: Elevated levels occur in diseases that impair bile formation (cholestasis). ALP may also be elevated in many other liver disorders, as well as some lung cancers (bronchogenic carcinoma) and Hodgkin's lymphoma. However, elevated ALP levels may also occur in otherwise healthy people, especially among older people.
GGT: Increased levels are diagnostic of hepatitis, cirrhosis, liver tumor or metastasis, as well as injury from drugs toxic to the liver. GGT levels may increase with alcohol ingestion, heart attack, pancreatitis, infectious mononucleosis, and Reye's syndrome.
LDH: Elevated LDH is seen with heart attack, kidney disease, hemolysis, viral hepatitis, infectious mononucleosis, Hodgkin's disease, abdominal and lung cancers, germ cell tumors, progressive muscular dystrophy, and pulmonary embolism. LD is not normally elevated in cirrhosis.
Bilirubin: Increased indirect or total bilirubin levels can indicate various serious anemias, including hemolytic disease of the newborn and transfusion reaction. Increased direct bilirubin levels can be diagnostic of bile duct obstruction, gallstones, cirrhosis, or hepatitis. It is important to note that if total bilirubin levels in the newborn reach or exceed critical levels, exchange transfusion is necessary to avoid kernicterus, a condition that causes brain damage from bilirubin in the brain.
Ammonia: Increased levels are seen in primary liver cell disease, Reye's syndrome, severe heart failure, hemolytic disease of the newborn, and hepatic encephalopathy.
Albumin: Albumin levels are increased due to dehydration. They are decreased due to a decrease in synthesis of the protein which is seen in severe liver failure and in conditions such as burns or renal disease that cause loss of albumin from the blood.
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