Transaminases, also known by the acronym GOT (or AST or TGO) and GPT (or ALT or TGP), are essential tools for the diagnosis of liver diseases. These enzymes are part of the hepatogram, a set of laboratory tests to identify alterations in the function of the liver and bile ducts.
In this guide we will explain what each element of the hepatogram means, including GOT (AST), GPT (ALT), alkaline phosphatase, gamma-GT and bilirubins.
What Is the Hepatogram?
We call hepatogram the set of elements measured in the blood that provide indications about the functioning of the liver and bile ducts. Therefore, the hepatogram can also be called liver function test.
The hepatogram consists in the measurement of the following substances:
- AST (aspartate aminotransferase) and ALT (alanine aminotransferase), formerly called GOT (glutamate-pyruvate transaminase) and GPT (glutamate-pyruvate transaminase), respectively.
- Alkaline phosphatase.
- GGT or Gama GT (range glutamyl transpeptidase).
- Bilirubins (direct, indirect and total).
- TPA (activated prothrombin time) or TP (prothrombin time) and INR.
- 5 ‘nucleotidase (5’NTD).
- LDH (lactate dehydrogenase).
In general, in asymptomatic patients without known liver disease, only the first four elements are usually requested. They are screening tests to identify any hidden disease of the liver and / or bile ducts. Already in those who know with liver problems, the dosage of all items is necessary for a better assessment of liver function.
We will then talk in detail about each item.
Obs: GOT, TGO and AST are synonyms, as well as GPT, TGP and ALT. They are different acronyms for the same enzyme. In order not to create confusion, I will use from now on only the initials GOT and GPT, which are still the most used.
Transaminases (Got and Gpt)
The transaminases or aminotransferasas are enzymes present inside the cells of our body, being responsible for the metabolism of some proteins. The two main aminotransferases are GOT (glutamate-pyruvate transaminase) and GPT (glutamate-pyruvate transaminase).
These enzymes are present in several cells of our body and are present in large quantities in hepatocytes (liver cells). The liver is a kind of treatment station, being the organ responsible for the metabolization of all substances present in the blood.
Whenever a cell that contains GOT or GPT suffers an injury, these enzymes “spill” into the blood, increasing its blood concentration. Therefore, it is easy to understand why liver diseases, which cause hepatocyte injury, occur with elevated blood levels of GOT and GPT.
GOT is also present in muscle and heart cells, whereas GPT is found almost only inside liver cells. GPT is, therefore, much more specific for liver diseases than GOT.
A few decades ago, when there were no markers of myocardial infarction, we used GOT as a marker of heart injury in patients with suspected cardiac ischemia. For an obvious reason, in these cases, only the GOT increased, with the GPT remaining at normal levels, since the latter exists only in the liver.
Since the two enzymes are present in similar amounts in the cells of the liver, the diseases of this organ present with elevation of both the GOT and the GPT.
The main diseases that cause elevation of transaminases are:
– Viral hepatitis.
– Hepatic steatosis.
– Alcohol abuse.
– Liver injury due to drugs and medications (drug hepatitis).
– Heart failure.
– Liver ischemia (ischemic hepatitis).
– Liver cancer.
– Muscular diseases.
Rarer diseases that frequently present with liver damage:
– Autoimmune hepatitis.
– Wilson’s disease.
– Deficiency of alpha-1-antitrypsin.
Normal values vary from laboratory to laboratory, however, the upper limit is always around 40 and 50 U / L.
Values up to 3 times greater than the limit are nonspecific and can mean injury to other organs than the liver. Hypothyroidism and muscle injuries are causes of small elevations, mainly of GOT. Lesions restricted to the bile ducts may also present with small increases in transaminases, which are normally associated with high elevations of GGT and alkaline phosphatase (I will explain below).
GOT and GPT above 150 U / L suggest liver disease. Only by the elevated transaminases it is not possible to know the cause of the liver injury, and further investigation is necessary.
GOT and GPT greater than 1000 U / L are usually caused by viral hepatitis, drug hepatitis (more common is paracetamol poisoning) or ischemic hepatitis.
In addition to the absolute value of transaminases, another tip is to compare the relationship between the values of GOT and GPT. Normally, the GOT / GPT = 0.8 ratio, that is, the GPT is usually slightly higher than the GOT. In hepatitis due to alcohol abuse, GOT rises more, becoming at least 2 times higher than GPT (GOT / GPT> 2). In cases of cirrhosis, the values are usually similar (GOT / GPT = 1). Obviously this is only advice. They are given that, isolated, do not establish any diagnosis.
It is important to note that it is perfectly possible to have a chronic liver disease and possess normal transaminases. This is very common in people with chronic hepatitis C, for example. Therefore, the absence of alterations in the GOT and GPT does not rule out liver diseases.
LDH is an enzyme present in various tissues of the body. In cases of liver damage, their values also increase. She, however, is much less specific to the liver than GOT and GPT. But it is always more a fact to take into account.
Alkaline Phosphatase (Fa) and Gt Range (Ggt)
While transaminases are used to evaluate lesions of liver cells, alkaline phosphatase and Gama GT are enzymes that rise when there is injury to the bile ducts.
Note in the illustration below. The liver produces bile, which is drained by the bile ducts. The biliary tree is born inside the liver and its ramifications end up joining, forming a common bile duct, already outside the liver, called common bile duct.
GGT and alkaline phosphatase are enzymes present in bile duct cells and, analogous to GOT and GPT, the damage of these cells causes the elevation of their enzymes in the blood.
However, GGT and FA are not as specific for bile ducts as GOT and, mainly, GPT are for the liver. Alkaline phosphatase can be found in large quantities in several other organs, mainly in the bones, placenta and intestines. The GT Range is also found in the heart, in the pancreas and in the liver itself.
In general, suggesting lesions of the bile duct is the concomitant elevation of both enzymes. The main pathologies that occur with joint elevation of GGT and alkaline phosphatase are:
– Obstruction of the bile ducts.
– Primary biliary cirrhosis.
– Cholangitis (infection of the biliary tract).
– Cancer of the biliary tract.
– Use of some medications (corticoids, barbiturates and phenytoin).
The abuse of alcoholic beverages usually causes a higher elevation of GGT than alkaline phosphatase. One patient with elevation of GPT smaller than GOT and a GGT higher than alkaline phosphatase, probably has a liver disease caused by alcohol.
Liver diseases that cause injury to the intrahepatic bile ducts can present with elevation of the GOT, GPT and also of GGT and FA. Similarly, obstructions of the biliary tract that occur with liver injury can also occur with elevation of the 4 enzymes.
The 5 ‘nucleotidase (5’NTD) is another enzyme present in the bile ducts, similar to GGT. Its increase has the same meaning.
The bilirubins are remnants of the destruction of old and defective red blood cells by the spleen. The bilirubin produced in the spleen is transported by the blood to the liver, where it is processed and eliminated in the bile. Bile is played in the intestine, participates in digestion, and is subsequently eliminated in the feces (hence the brown color of them).
The bilirubin in the spleen is called indirect bilirubin, whereas the bilirubin in the liver is direct bilirubin.
In blood tests we were able to measure the two types of bilirubin. In line with the type that is presented increased, we can have an idea of the cause.
If, for example, we have any disease that increases the destruction of red blood cells (hemolysis), we will have an increase in indirect bilirubin in the blood. Similarly, if our liver is sick and does not work well, the transformation of indirect bilirubin into direct is impaired, causing accumulation of the former.
Some people have genetic alterations and are unable to conjugate indirect bilirubin directly. The most common alteration is Gilbert’s syndrome that is present in up to 7% of the population. Frequently, this syndrome is discovered by chance when the hepatogram is requested.
On the other hand, we have cases in which bilirubin is transformed into direct, but the liver can not eliminate it, causing it to accumulate in the blood. This can occur in cases of obstruction of the common bile duct, either by stone or by neoplasms. In cases of acute hepatitis, edema of the intrahepatic bile ducts and difficulty of the liver cells in excreting direct bilirubin can occur.
The total bilirubin is the sum of the direct with the indirect. Since its blood value is greater than 2 mg / dl, the patient usually presents with jaundice, the clinical manifestation of bilirubin deposition in the skin (yellow skin).
When jaundice occurs by direct bilirubin increase, this means that it can not reach the intestines. It is common for faeces to remain very clear, almost white, due to the lack of excretion of their pigment.
Once the diagnosis of liver injury is established, it is possible to have an idea of the degree of liver failure. The two main tests for this purpose are albumin and TAP (TP).
Albumin is a protein produced in the liver and the fall in blood values may indicate poor liver function.
Similarly, the liver also participates in the production of vitamin K that is involved in the blood clotting process. People with hepatic failure have greater difficulty in coagulating the blood, which can be verified with the dosage of the TAP (TP) or the INR.