After a routine health screening, your doctor says you are doing well, except for ALT which stands out as 62 IU/L. ALT is mildly elevated, so the doctor suggests repeating it in three months. But what does that exactly mean, and why should it be a concern?
If you also have a lower level of albumin along with increased levels of bilirubin, then it cannot be ruled as normal. The relatively low ALT value of 62 IU/L will now represent a stressed metabolism of the liver and not just a random fluctuation. This is the fundamental approach to understanding an LFT report - no individual figure should be looked at independently. It is a communication between three separate functional units, and all three should be heard to fully understand what the liver is saying.
Liver function tests do not evaluate one thing. They assess three distinct physiological aspects of the liver. Understanding this is the key to reading any report correctly:
The table below summarises all four injury-related enzymes at a glance:
Reference ranges may vary slightly between laboratories. Always interpret results alongside the laboratory's own reference intervals.
The SGPT/SGOT values provided by the laboratories represent the injury to the hepatocytes of the patient. SGPT is highly selective for the liver and is called alanine aminotransferase (ALT). SGOT is less selective, also indicating myocardial and muscular injury. It is also called aspartate aminotransferase (AST).
The ratio of AST and ALT is called the De Ritis Ratio, which was first defined in 1957. The presence of ALT dominance (less than 1) is indicative of either acute viral hepatitis, MASLD, or drug-induced liver damage. If there is more than two-fold elevation of AST along with high GGT levels, alcoholic liver disease takes precedence as the probable diagnosis. A ratio close to 1 with consistently elevated levels suggests progressive liver fibrosis or cirrhosis.
GGT is the earliest marker of biliary obstruction and a sensitive marker of alcohol abuse and drug intoxication, especially anticonvulsants and statins. Its significance lies in determining the cause of raised ALP, the coexistence of elevated ALP and GGT levels indicates a hepatobiliary problem while isolated elevated ALP with normal GGT suggests a problem with bone rather than liver.
There are several ALP isoenzymes from the liver, bone, placenta, and intestine. There are two common causes of physiological elevations of ALP. One is pregnancy, where ALP level is significantly increased owing to placental ALP production, to reach a mean of 166 IU/L by the third trimester against 96 IU/L in the first. The second is In adolescents, where rapid bone growth drives ALP values that would be alarming in adults. So it is important to always check GGT before attributing a raised ALP to liver disease.
Bilirubin is the pigment which is formed during the breakdown of erythrocytes. LFT Panel distinguishes between two types of bilirubin: direct bilirubin and indirect bilirubin. The importance of this distinction lies in the following: elevated indirect bilirubin is caused by hemolysis or impaired conjugation (Gilbert's syndrome), whereas elevated direct bilirubin suggests structural issues with bile production or excretion. Jaundice becomes clinically visible when total bilirubin exceeds approximately 2.5 mg/dL.
Albumin production is exclusive to the liver. A decrease in albumin concentration, even in the absence of increased or mildly raised SGPT and SGOT, indicates a reduction in the ability of the liver to manufacture protein. This is the important parameter that turns an insignificant enzyme abnormality into a significant medical condition. Total protein measures the combined concentration of albumin and globulins, whereas A:G ratio determines the proportion of the liver produced proteins as compared to globulins, which are products of the immune system. An inverted A:G ratio is an important sign of chronic liver disease and other disorders such as multiple myeloma.
Prothrombin time (PT/INR), although not always part of the LFT panel, is considered the most sensitive test for acute synthetic dysfunction due to the involvement of coagulation factors II, VII, IX, and X, all of which are produced by the liver and have short half-lives.
Epidemiological differences affect this differential as well. A systematic review and meta-analysis in the Journal of Clinical and Experimental Hepatology reported an estimated pooled prevalence of NAFLD/MASLD in Indian adults at 38.6%, implying that fatty liver is statistically more common amongst high-risk individuals. Importantly, India has a significant number of cases with lean MASLD: in a biopsy-based study, 33.7% of lean liver donors had MASLD. A normal BMI cannot preclude fatty liver in an Indian individual presenting with mild elevation of AST.
MASLD aside, the high incidence of tuberculosis in India makes ATT (Anti Tubercular Therapy) one of the main causes of DILI (drug-induced liver injury). Traditional remedies and Ayurvedic drugs also contribute to DILI due to hepatotoxic alkaloids in multiple formulations. However, patients will not volunteer such information unless explicitly asked about their drug intake.
Enzymes 1 to 3 times upper limit of normal (ULN): Mild. Usually MASLD, drug related, or recent illness. Recheck in 4 to 8 weeks.
Enzymes 3 to 10 times ULN: Requires further workup. Viral hepatitis should be ruled out, imaging performed, and drug history obtained.
Enzymes More than 10 times ULN: Suggests acute hepatocellular injury and requires prompt investigation.
An important point to note is that patients with liver disease may have completely normal liver enzymes. Compensated cirrhosis may present with normal enzymes.
Jaundice: yellowing of the skin or eyes
Dark (tea-coloured) urine or pale, clay-coloured stools
Severe upper right abdominal pain, particularly after fatty meals
ALT or AST greater than 10 times the upper limit of normal
Liver enzymes rising on serial testing despite stopping the suspected causative drug
Unexplained bruising or prolonged bleeding from minor cuts
Mental confusion or unusual sleepiness in a patient with known liver disease
Any elevated ALP or bilirubin in a pregnant patient with itching or jaundice
Safety Note: Patients with type 2 diabetes, obesity, or metabolic syndrome should have annual LFTs even without symptoms, given silent MASLD prevalence. Patients on long-term ATT, statins, anticonvulsants, or antifungals require periodic monitoring per prescribing guidelines. Pregnant women with elevated ALP should have GGT checked before any hepatobiliary workup is initiated. Anyone using herbal or Ayurvedic preparations alongside conventional medications should inform their treating clinician.
Can I eat before a liver enzyme test?
A light meal generally does not significantly affect ALT, AST, or GGT. A high-fat meal can transiently elevate ALP from intestinal isoenzymes. For a full panel including bilirubin and glucose, 8 to 10 hours of fasting is recommended.
My ALT is slightly above the reference range. Should I be worried?
A single mild elevation warrants attention, not alarm. Rule out heavy exercise, recent alcohol use, or new medications in the preceding 48 hours. If it persists on repeat testing after 4 to 6 weeks, further evaluation for MASLD or viral hepatitis is appropriate.
Why is my GGT high if I do not drink alcohol?
GGT is elevated by MASLD, obesity, diabetes, hypothyroidism, and numerous medications beyond alcohol. An isolated raised GGT in a non-drinker most commonly points to metabolic disease or microsomal enzyme induction.
What does a low albumin on my LFT mean?
Low albumin signals reduced liver synthetic capacity and should never be dismissed as a minor finding. It warrants urgent clinical correlation, particularly if SGPT and SGOT are only mildly elevated, as it may indicate chronic liver disease with significant functional impairment.
Liver function tests measure three distinct pillars: hepatocellular injury, biliary function, and synthetic capacity. No single number tells the full story.
The SGOT:SGPT ratio (De Ritis ratio) distinguishes superficial cell damage from deep mitochondrial injury, separating fatty liver from alcoholic disease.
India's lean MASLD burden and ATT-related drug-induced liver injury make LFT interpretation clinically distinct from Western populations.
Lala, V., Zubair, M., & Minter, D. A. (2023). Liver function tests. In StatPearls. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK482489/
Prabhu, A., et al. (2022). Prevalence of non-alcoholic fatty liver disease in India: A systematic review and meta-analysis. Journal of Clinical and Experimental Hepatology, 12(3), 818-829. https://doi.org/10.1016/j.jceh.2021.11.010
Shaikh, S. M., Varma, A., Kumar, S., Acharya, S., & Patil, R. (2024). Navigating Disease Management: A Comprehensive Review of the De Ritis Ratio in Clinical Medicine. Cureus, 16(7), e64447. https://doi.org/10.7759/cureus.64447
Sharma, S., et al. (2025). MASLD: time to optimise regional research priorities. The Lancet Regional Health Southeast Asia, 33, 100732. https://doi.org/10.1016/j.lansea.2026.100732
Gilboa, D., et al. (2021). Normal distribution of alkaline phosphatase levels during pregnancy. Clinical and Experimental Obstetrics & Gynecology, 48(6). https://doi.org/10.31083/j.ceog4806220
Goyal, M., et al. (2025). Prevalence of MASLD among overweight and obese patients with T2DM. PMC. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12813296/
