Liver function tests


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.


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.


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.


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.


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.


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.

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.

Patient education

Health-care providers should inform the patient of any abnormal results and explain how these values reflect the status of their liver disease. It is important to guide the patient in ways to stop behaviors such as taking drugs or drinking alcohol, if these are the causes of the illness.



Burtis, Carl A. and Edward R. Ashwood. Tietz Textbook of Clinical Chemistry. Philadelphia: W. B. Saunders, 1999.

Cahill, Matthew. Handbook of Diagnostic Tests. 2nd ed. Springhouse, PA: Springhouse Corporation, 1999.

Henry, J. B. Clinical Diagnosis and Management by Laboratory Methods. 20th ed. Philadelphia: W. B. Saunders, 2001.

Wallach, Jacques. Interpretation of Diagnostic Tests. 7th ed. Philadelphia: Lippincott Williams & Wilkins, 2000.


Jensen, J. E. Liver Function Tests. [cited April 4, 2003]. .

National Institutes of Health. [cited April 4, 2003]. .

Worman, Howard J. Common Laboratory Tests in Liver Disease. [cited April 4, 2003]. .

Jane E. Phillips, Ph.D.
Mark A. Best, M.D.

User Contributions:

Leti Contreras
Thank you for this article it really help me understand liver funtion test.
someone with liver cancer and high ammonia levels, but has no
symptoms of hepatic encephalopathy?
I am looking for some information on ALT and AST enzymes. I was scheduled for major back surgery tomorrow but it was canceled due to high enzymes in my blood test. In 1990 I was told I had Hep c. In 1997 a Doctor suggested a liver biopsy. The liver biopsy was clear, perfect infact. I have never been told I had Hep C by anyone before and then the red cross told me it showed up in my giving blood. I now need to know what could cause high ALT or AST other than than Hep C virus. I have never been sick a day in my life. In fact my medical history is near nothing. I do not ever get sick or catch the common flu's other people do. Do you have any info for me? I would appreciate it. By the way I am 53 years old.
The best article uptothe points I have read till date.
I had a high ast on two separate blood test and high normal results alt and direct bilirubin. Should I have further testing done?
Hi. I recently had blood work done for my physical, and found that my Liver Function test were MILDY elevated. I am 46 years old. My ALT was 73, and my AST was 50. I am going back in 2 weeks to be retested. Should I be concerned? What my be some of the diagnosis of these levels. I was told that all other levels were fine.
Thank you very much.
what would cause high ammonia levels when liver function tests are normal? Albumin is slightly low.
Patient is taking Nexavar,Dilantin and Phenobarbitol
I just had my annual physical at Kaiser and they called me to come back and give more blood because my ALT was 50 and last year was 30. Ever since I was in my 20's I have been told it seems my liver test were "elevated" but I never knew the scores back then. I have no known health problems but for the last year and a half I have had MAJOR dental work and pain and relied heavily on Motrin. This dental work has been non-stop as he has pretty much gone around my whole mouth accept the smile. Permannet bridges on all back teeth upper and lower, two root canals which required removing a permanent bridge and then replacing again. Some gum cutting or laser type work. A lot of stress and pain trying to adapt to all the new realignment of these bridges etc. Motrin was used daily for weeks. I actually finally was able to stop using the Motrin two months ago because my dental pain is over. I don't drink or smoke or take anything else. Why is my liver ALT 50? I feel ok. Is this SERIOUS or do other people have this problem? Also I had Hep B vaccine in 2000 so I don't think I have that and I don't think I have any Hepatitis because I don't feel sick or yellow or anything. Also the dentist gave me antibiotics over the past year at different times. I have had Cipro recently, Erthromyacin, Penicillian. The only vitamins I take is B complex suggested by my dentist, calcium and Acidophilus on and off if I take antibiotics.
this is the perfect article i've been looking for about liver function tests. it's got everything from definition to management. thanks!
Liver funtion tests are those tests which act as markers of the hepatic synthetic activity to estimate the level of funtioning hepatocytes.Additional markers of hepatic activity are albumin and prothrombin time.
Dear Author,
Thankyou for this write up. It has been very helpful to me regarding how different levels of the various reference ranges may show what could be the underlying cause or 'point us in the right direction to various problems/diseases' and what to look for when levels are not in the normal range. It also gave me a much better understanding of the entire test and the results and also the functions the liver provides. I found this one of the easier articles to read for a layman such as myself.....some of them can be truly inconprehensible unless you have some medical background/knowlege regarding terminology and overall fuction of the organs.
I would like to extend a big thankyou to you and will go on to source the books that you read to compile this write up.....hopefully it will be as easy and as useful as your work has been.
Warmest regards
karinda xx
Hi, my husband has been on a liver transplant list for 6.5 yrs now and suffers from recurrent hepatic encephalopathy. He was recently hospitalized for PSE with Hypokalemia and ofcourse Cirrhosis. We were told by one of the "fellows" that with a meld of 14 we shouldn't even be listed and that "HE" hepatic encephalopathy is very manageable and not life threatening. My husband has become so debilitated by this "HE" that he can no longer drive, and most days can't use the remote for tv. Every 3 mnth appt with hepatologist we are desperate for help and I hear we can fix this, but in reality it becomes more and more difficult. His k+ was 2.8 and after 2 days of Iv K+ we were dc'd with a k+3.5. We are both depressed and feel betrayed, my husband cried and said he feels he has been lied to for the past 6.5 yrs. He is about maxed out on most druds for "HE", xifaxin, lactulose, sodium benzonate, carnitine, zinc, and they just gave the ok to use neomycin again in addition to every thing else. So far his kidney function "bun" is perfect and tends to keep him low on meld score. My question: if the liver can't break down the ammonia that is responsible for "HE" into urea would the bun ever be elevated in re: to meld scoring? Please advise, Connie
Hey Connie,

My father is having liver problems. I am not a doctor but I feel that your husband is very sensitive to the ammonia(and other)levels. There is not much literature on this issue. I say that you must be very strict on the diet. Avoid foods that cause high ammonia levels,, animal proteins.., . Live on greens. Again,, I'm not a doctor,, but they don't seem to have a clue either. Good luck. Work on that diet, it has to be a function of something going into his body. Keep a diary of food eaten vs. effect on mind.
hi,i hope someone can help me,i feel dreadful.i have been diagnosed with an overactive thyriod,however my alt is at 151 and ast 164.i am suffering from severe vomiting,dark thick urine as well as all the symptoms of an overactive thyriod including a pulse that averages 140 beats a minute.i have had an ultrasound scan on my liver which showed a dilation of liver duct,pancreas and gallbladder ducts.i am now awaiting a ct scan.does anybody have any idea if these are connected to my thyriod or if i have a few things wrong.i also suffer from R.A and have been diagnosed with this for the last 2 years.i am awaiting an autoimmune hep test.could someone please give me any ideas as the doctors i have seen so far say the dont know what is wrong,this obviously is no good to me as a diagnosis.many thanks cher
how long does it take to normalise blood levels ggt after alcohol
Hello i m nazia now a days i am 32 week pregnent i m check my sgot is 90.67 and sgpt is 141 and alkaline phosphatase is 1123 is to high what happan now i am very disturb pls tell me but can i do
my s.bilirubin total is 1.0 mg/dl is it normal value or critical?
Hi my 18month old daughter is being hospitalized for high liver enzymes. Her first blood test was done 4 days ago and these were her levels: ast-1660. Alt-2153 and bilirubin was 2.4. Her levels have slightly come down but not alot and her bilirubin has now increased to 4.2. They cannot find answers and i was just wondering if u had any ideas? As u can imagine im very worried and looking for answers. Thank you.
Hi, my husband has had blood tests during a general check up which told our gp that his liver count is 450 when it should be 50, we've been told that his liver is producing 3000 times moreiran in a day than it needs,and blood tests detected Hep A which really floored us, because never in his life has he had contact with anything or person to have this show up,
is there a clear answer in english as to the possible cause of this detection because 1 gp could only conclude that it was from a vacination during childhood because we've never travelled abroard and live a fairly subdued life style, he has had a gene test for what is commonly called fatty liver which came up clear,
he's asking me to find out as much as I possibly can in relation to the causes because there were no symptoms, as well as foods to help his health because he thinks he'll starve to death with the list that he has to avoid at all costs,
his doctor is very clearly concerned and organizing more tests for a few weeks time
thank you
Hi, I had many blood tests done to see if I had Lupus. I have Raynard's syndrome. Well The rheumatology dr. told me nothing was wrong on her end and to go see my regular Dr. So I will on Thursday. Is it something to worry about of My blood urea nitrogen is a 4 and supposed to be a 6-27? Also my creatinine level is 0.38 supposed to be 0.50 to 1.20. Then my Albumin is 2.5 and supposed to be 3.4 to 5.0 Also my globulin level is high at 5.1 and supposed to be 2.4-4.0 my Albumin/globulin together is low at 0.5 supposed to be 1.0-1.8 finally my bilirubin is high 1.6 supposed to be 0.2-1.0 Can you please tell me if these are all something to worry about or not? Thank you
hi,,, ive drunk heavily for the past 15yrs, im now 36yr,,, my alt test was 100 yesterday,, ive stopped!! drinking! how long should i wait before i go check again?? thank you!!!
my recent liver score in the AST was 40. the score on my ALT was 78.
i am a 67 old male who has been drinking for a long time. am i in immediate danger of Cirrhosis of my liver? what can i do besides stop drinking to improve my liver health?.
I am 25 years old.For the past 6 months onwords i was suffering with Typhoid fever and jaundice.i was checked the total bilirubin test in the diagnostic center.That time i had 1.8 mg/dl.I was using anti biotic tablets and liv-52 tablets daily from 2 months.still i am using Liv 52 tabs 2 tablets 3 times daily.But yesterday i checked my total bilirubin test it is showing : Total bilirubin 1.8 mg/dl,direct bilirubin 0.8 mgs/dl,direct bilirubin 1.0mgs/dl.Please help me out wheather i have Jaundice or not and my liver functionality is correct or not.Thanks in advance.
Dear Sir,

I am 45 years old,My LFT result is AST is 30 and ALT is 75 my Total Bilirubin is 1.7 and Direct Bilirubin is 2.5 Albumin 5.2 globulin 3.4 A/G ratio 1.5 : 1 Protein 8.6 rest of all are normal and Contrast CT scan findings cirrhosis of liver can u please tell me about my liver disease stages and further useful treatment to avoid complications in future.
Medical student
Thank you.

Made everything about LFT clear.

Medical student.
T. Marks
I am a 60 year old male. My ALT level just came back with a reading of 56. On my blood test the year before my ALT level was 38. My AST, Albumin & bilirubin have All reached the upper level but still within range. They have all increased since a year ago. I am taking Percocet, morphine, Zocor & testosterone shots. Have just started the testosterone shots, morphine in the past 4 months. I am trying to figure out what might cause this elevation & can it be brought back down. I am also 30lbs over weight. Are these levels serious? Thank you for your help on this.
i have hep c my empzemes are 134 should i be concerned that considered to be serious.thank you can you please give me a answer
Kishor chauhan
Dear Sir,

I am 33 years old,My LFT result is AST is 49and ALT is 91 my Total Bilirubin is 0.8 and Direct Bilirubin is 0.3 Albumin 4.4Globulin 2.2 A/G ratio 2.0 Protein 6.6 GGT 124 rest of all are norml can u please tell me about my liver disease stages and further useful treatment to avoid complications in future.
64 yo female 13 years post liver transplant. ALT 25 AST 22 and all other CMP results well within normal. 5 years post kidney removal due to renal cell carcinoma. Kidney functions within one point of normal. However, my ammonia is 71. Why is it high?
Last month my ALT was 40 and AST was 35. My ALT went to 295 and AST to 91. My ultrasound was clear. I drink maybe once a month and tested negative all forms of hepatitis and lime disease. I have polycythemia and chronic osteomyelitis as a kid. I'm 36 now and feel like I aged 15 years over night. I used to run 9-30 miles a day. Now I can't. My joints ache, bone pains, chest pains and abdominal pains.
sir my sgot AST 39 iu/l and sgpt ALT 54iu/l. i was warried is this problam and how reduced this problam
I brought my friend 53 yo female. to her pcp whom she hasnt seen for several yrs. at which time was told she had an enlarged liver due to alcohol)She has been drinking heavily for over 20 yrs. She presented with severe wt loss, trouble walking due to muscle weakness and balance, obviously "jaundice" yellow skin,dark yellow where it should be "white part of her eyes"
severe bloating in abdominal region, pain in back "Kidney area!! Not eating or drinking sufficient amts of anything, wt of 99.6lbs.Shouldnt she have been hospitalized
matt revels
alt alt levels above 480 each Its my mom shes 63 dr said hep b chronic maybe more and to go home what should i do for her
Tacha Dumuje
I recently had blood work done for my physical, and found that my Liver Function test were MILDY elevated. I am 31 years old. My ALT was 80, and my AST was 50. I am going back in 2 weeks to be retested. Should I be concerned? What my be some of the diagnosis of these levels. I was told that all other levels were fine.
This is the best article upon to the point this article really help to understand the lvr functions
This is the best article on LFT. Now I have full knowledge about Liver and take care of it. Thanks to the author.

Comment about this article, ask questions, or add new information about this topic: