SGOT and SGPT Test in Hyderabad, India

Principle behind interpreting levels of SGPT and SGOT

The aminotransferases (both ALT and AST) plays a responsible role in both gluconeogenesis and protein metabolism. Both these mechanisms are necessary for body maintenance. ALT and AST necessarily ease up the redistribution of nitrogen between oxoacids and corresponding amino acids. The AST demonstrates a reduction in the activity levels starting from heart, liver, skeletal muscle, kidney, pancreas, spleen and ending with the lungs.

Although there are similarities in the relative tissue concentration and distribution of ALT and AST, there are considerable differences. While highest activity of ALT is found in the liver, its decreasing concentrations are seen in kidney, myocardium, skeletal muscle, pancreas, spleen, and lungs. Although ALT concentration in the hepatic cell cytoplasm can be comparable to AST; the mitochondrial ALT is not found. In all other tissues, ALT activity is significantly less than AST.

There are various hepatic and non-hepatic factors which can increase the levels of SGPT and SGOT. Upon encountering such factors, the doctors may perform a combination of a history and clinical examination along with liver test abnormalities interpretation to identify the type and aetiology of various liver diseases, allowing for a targeted investigation approach. A few of the common factors which can increase the levels of SGPT and SGOT (liver function test) are:

• Alcohol 
• Medication
• Viral hepatitis
• Autoimmune hepatitis
• Non-alcoholic fatty liver disease (NAFLD)
• Haemochromatosis
• Wilson’s disease 
• α1-Antitrypsin deficiency

Alcohol:  The general physician may look into the patient’s history to make a diagnosis. 

• Nevertheless, gamma glutamyl transferase (GGTP) may be prescribed and if its level is twice than the normal with an AST/ALT ratio being ≥2:1, it is highly suggestive of alcohol abuse. 
• However, it must be understood that gamma glutamyl transferase (GGTP) is not specific to alcohol and the general physician may hesitate to be used as an isolated test. 
• Notably, AST levels which are more than eight times the normal range and ALT levels which are greater than five times than the normal range are exceptionally rare in alcoholic liver disease. 
• Conversely, ALT may depict normal values even in severe alcoholic liver disease. 
• Typically, aminotransferase levels are <300 U/L in alcohol-induced liver injury unless other insults such as viral or drug-induced liver injury are superimposed on alcoholic liver disease.

Medication:  Various drugs can raise liver enzymes, commonly nonsteroidal anti-inflammatory drugs, antibiotics, statins, antiepileptics and antituberculosis drugs. 

• The doctor may initiate a specific inquiry about herbal remedies, alternative medications and substance abuse if any. 
• Sometimes with medication there might be rise in liver enzymes, if that is the case, then hepatologist may suggest stopping the use of drug to see if the enzymes levels go back to normal.
• In the case of an essential drug which is necessary for the patient, a risk–benefit assessment may be performed. 
• A liver biopsy can assess both the confirmation and severity of a drug-induced reaction

Viral hepatitis:  Hepatitis B and C are common causes and hepatitis serology and the hepatologist may consider the other diagnostic laboratory features in turn.

• Screening for hepatitis B infection is done by HBsAg testing, and A positive HBsAg could represent an acute/chronic infection. 
• Around 2–8 weeks before biochemical evidence of jaundice or liver damage, the HBsAg becomes positive. 
• Anti-HBc is the first antibody to be detected after acute infection, initially as IgM, which is detected before clinical symptoms of elevated ALT is lost after about 6 months, while IgG type develops after 6–8 weeks of infection and persists lifelong. 
• IgM anti-HBc can also reappear during flare of chronic hepatitis. If it is positive and acute infection is suspected clinically, HBsAg and anti-HBs can be obtained after 6 months.

Autoimmune hepatitis:  An unresolving inflammation of the liver of unknown cause, autoimmune hepatitis is associated with interface hepatitis on histological examination, hypergammaglobulinemia and autoantibodies. 

• On serum protein electrophoresis, around ≥80% of patients demonstrate hypergammaglobulinemia. 
• Polyclonal immunoglobulins could be more than twice normal.
• Appropriate tests which the hepatologist would include immunoglobulins, antinuclear antibodies, antibodies to smooth muscle, anti-liver–kidney microsomal antibodies etc. 
• The hepatologist may not routinely prescribe the use of all three tests. Nevertheless, liver biopsy could be prescribed useful.

Non-alcoholic fatty liver disease (NAFLD):  NAFLD is the most common cause of chronic liver disease now. NAFLD can vary from simple steatosis (fat buildup) without inflammation to non-alcoholic steatohepatitis (NASH) with active inflammation and hepatocytes injury, which can progress to cirrhosis and eventually hepatocellular carcinoma. 

• NAFLD is usually asymptomatic but has mild increase in ALT or a detection of fatty liver on ultrasound on evaluation for other diseases.
• It is usually suspected in individuals with raised body mass index, type 2 diabetes mellitus and hyperlipidaemia consuming less than three units (in males) and two units (in females) of alcohol per day. 
• NAFLD is probably the most common cause of mild aminotransferase elevation. The AST to ALT ratio is usually less than 1:1. Total bilirubin and albumin are usually normal. 
• The hepatologist may search for leucopenia and thrombocytopenia as they could raise concerns for the existence of cirrhosis and occult portal hypertension. 
• Ultrasonography may also be prescribed which may confirm fatty infiltration. 
• Liver biopsy may be prescribed as it is currently the most reliable way to find the differenences between simple steatosis from NASH. 
• However, since it is impractical to biopsy everyone with fatty liver, the hepatologist prescribes biopsy only for those with pre-test probability of NASH (based on the presence of metabolic syndrome or elevated non-invasive markers) or in those where a confounding cause of deranged liver function must be ruled out.
• Steatosis follows a benign course, whereas NASH may progress to cirrhosis, though liver failure is uncommon. 

Haemochromatosis:  A common autosomal-recessive condition with characterized by an increased iron absorption in the intestine followed by excessive deposition of iron in the liver, pancreas and other organs. 

• If the patient is suffering from symptomatic haemochromatosis, the doctor may look for cutaneous hyperpigmentation, diabetes mellitus and chronic liver disease, etc.
• In such cases, raised serum ferritin could be due to underlying haemochromatosis. transferrin saturation is a much reliable test which works by measuring serum iron and total iron binding capacity. 
• Although the discovery of the haemochromatosis gene in 1996 has revolutionised the diagnosis of haemochromatosis, and the availability of genetic testing became widespread, it usually is not recommended for people younger than 18 years of age. 
• Liver biopsy is necessary to confirm the iron overload to assess hepatic iron index. Liver biopsy is not necessary in patients suffering from hereditary haemochromatosis.

Wilson’s disease:  This congenital disorder characterised by biliary copper excretion is detected commonly between the 5–25 years. 

• The hepatologist may prescribe serum ceruloplasmin - the usual screening test which is reduced in approximately 85% of cases. 
• In case of a normal ceruloplasmin and absence of Kayser–Fleischer rings, the hepatologist may opt for a 24 hrs urinary copper excretion.
• Liver biopsy can confirm the diagnosis if hepatic copper concentrations are >250 μg/g dry liver weight.

α1-Antitrypsin deficiency:   An uncommon cause of chronic liver disease in adults. 

• Low levels of α-antitrypsin may be detected by direct measurement of serum levels or by the lack of a rise in α-globulin bands on serum protein electrophoresis.