Overview
Quick answer
A liver function test panel typically reports ALT, AST and GGT alongside ALP, bilirubin, albumin and total protein. ALT, AST and GGT are enzymes that leak out of liver cells or rise when the liver is working harder to process something; they are damage and workload markers, not a direct measure of what the liver is doing for the body the way albumin and bilirubin are. No fasting is required.
Australian guidance treats ALT above roughly 35 U/L in women or 40 U/L in men as raised, though the exact number on your own report depends on your lab. The most common cause in Australia is MASLD, metabolic dysfunction-associated steatotic liver disease (the renamed NAFLD), which affects an estimated one in three Australian adults, over half of people with type 2 diabetes, obesity or multiple metabolic risk factors, and often produces no symptoms and a normal ALT.
A mildly elevated result is common and usually not an emergency. It is worth taking seriously rather than ignoring, because the more useful comparison is not "abnormal versus normal" but a trend over repeat tests, read alongside the pattern across all three enzymes, your alcohol intake, medications, and metabolic risk factors.
Overview
Key takeaways
ALT and AST sit inside liver cells and leak into blood when those cells are damaged. They measure the rate of cell injury, not liver function in the sense of what the liver produces or clears; albumin and bilirubin are the tests that reflect that synthetic and excretory role.
ALT is more liver-specific than AST. AST is also present in the heart, skeletal muscle, kidney, brain and red blood cells, so an isolated AST rise, especially after exercise, does not automatically mean a liver problem.
GGT rises through two different mechanisms: bile duct obstruction (cholestasis) and enzyme induction, where alcohol or certain medications directly increase the liver's production of GGT as a detoxification response, with no cell damage at all. The two look identical on a report and need the clinical picture to tell apart.
MASLD (metabolic dysfunction-associated steatotic liver disease, formerly NAFLD) affects an estimated one in three Australian adults and is the most common cause of elevated liver enzymes, but in the Australian AusDiab cohort, roughly three-quarters of people with MASLD had a completely normal ALT. A normal result does not rule the condition out.
Common causes of elevated liver enzymes include MASLD, alcohol, viral hepatitis B and C, medications (including some antibiotics, statins, paracetamol overdose, and a growing share of herbal and dietary supplements), autoimmune hepatitis, haemochromatosis, and coeliac disease.
The AST/ALT ratio, also called the De Ritis ratio, is a pattern clue rather than a diagnosis: a ratio below 1 leans toward MASLD or viral hepatitis, and a ratio above 2 leans toward alcohol-related injury, but it is only interpretable when at least one enzyme is actually elevated.
Strenuous exercise, particularly heavy resistance training, can raise ALT and AST for a week or more with no liver damage at all, because both enzymes are also present in skeletal muscle; creatine kinase is the test that tells a muscle-driven rise apart from a liver-driven one.
Liver function tests require no fasting. Medicare funds a standard panel of five or more of these tests together under MBS item 66512 when clinically indicated.
Basics
What are ALT, AST and GGT?
A liver function test is not one test but a panel, and the name is a slight misnomer for half of it. ALT (alanine transaminase), AST (aspartate aminotransferase) and GGT (gamma-glutamyl transferase) are enzymes: proteins that normally do a job inside liver cells, not substances the liver releases on purpose. They only appear in your blood in meaningful amounts when something disrupts the cells that hold them.
ALT: the most liver-specific of the three
ALT sits in the cytosol, the fluid inside liver cells, where it helps metabolise amino acids. It only leaks into blood in meaningful amounts once liver cells are damaged, and it is found in the liver in much higher concentrations than almost anywhere else in the body, which is why a raised ALT points toward the liver more reliably than a raised AST does.
AST: also in the heart, muscle, kidney and blood cells
AST does a similar job to ALT and leaks out the same way when cells are damaged, but it exists in both the cytosol and the mitochondria of liver cells, and it is also present in meaningful amounts in heart muscle, skeletal muscle, kidney, brain, and red blood cells. An AST rise on its own, without ALT, is a weaker liver signal and a stronger cue to consider muscle or another source.
GGT: bile ducts, and a second, separate mechanism
GGT sits on the surface of the cells lining the bile ducts and is involved in glutathione metabolism, part of the body's detoxification machinery. It rises with cholestasis, when bile flow is obstructed and pressure builds in the biliary tree, and separately through enzyme induction: alcohol and certain medications directly increase how much GGT the liver produces, as a metabolic response to processing them, with no cell damage involved at all.
The rest of a standard panel, albumin, bilirubin, and sometimes total protein and globulin, measures something different: what the liver actually produces and clears for the body. That distinction, damage marker versus function marker, is the single most useful thing to carry into reading your own report.
Reading your results
How to read your liver function test report
An Australian pathology report for a liver panel usually lists the same seven or eight fields in a fixed order, each with its own reference interval printed alongside it. Knowing what each one is actually measuring, rather than treating the whole panel as one undifferentiated "liver score", makes the report far easier to read.
ALT (sometimes SGPT)
The most liver-specific enzyme on the panel, and usually the one clinicians weight most heavily for hepatocyte injury. SGPT (serum glutamic-pyruvic transaminase) is the same test under an older name that occasionally still appears on older report templates or overseas results.
AST (sometimes SGOT)
Less liver-specific than ALT because it is also present in heart and skeletal muscle. SGOT (serum glutamic-oxaloacetic transaminase) is the older name for the same test. Read AST alongside ALT and, if muscle is a possibility, creatine kinase (CK), not on its own.
GGT
Sensitive to alcohol and bile duct issues, and to some medications through enzyme induction. Often the first of the three to rise with regular alcohol intake, but not specific on its own, since obesity and metabolic factors also raise it.
ALP (alkaline phosphatase)
Rises with cholestasis alongside GGT, which is why the two are often read together to confirm a bile-flow pattern. ALP is not liver-specific either: it also comes from bone, so it rises normally in growing teenagers and in the third trimester of pregnancy, and can be raised by bone conditions with no liver involvement at all.
Bilirubin (total)
A breakdown product of old red blood cells that the liver processes and excretes into bile. A raised total bilirubin points toward the liver's excretory function rather than cell injury, and a mildly raised result with every other marker normal is the pattern of Gilbert syndrome, covered later in this guide.
Albumin and total protein
Albumin is a protein the liver makes and releases into blood; a low result can reflect reduced synthetic capacity, though it is also affected by inflammation, nutrition and kidney losses, so it is not liver-specific either. Total protein and globulin, sometimes reported with an albumin-to-globulin (A/G) ratio, add further context on the synthetic side of the panel.
If your result sits outside the printed reference interval, check which of these seven or eight fields is actually flagged before assuming the whole panel is abnormal: an isolated ALP rise in a pregnant or growing patient, or an isolated bilirubin rise with everything else normal, tells a very different story from ALT and AST rising together.
Beyond the reference range
Reference range vs a preventative target
The reference interval printed on your report marks where a laboratory's reference population sits, not necessarily where a preventative-health member should aim to be.
A lab reference interval is a population range, not a target
Standard Australian reference intervals for ALT commonly sit up to around 35 to 41 U/L depending on sex and lab, because that range was built to flag clear liver disease in a general population, not to describe optimal metabolic health in someone with no diagnosis.
Hemexa's own preventative band sits tighter, particularly for ALT
Hemexa's own clinical policy treats ALT at or below 25 U/L (both sexes) and AST at or below 25 U/L (men) or 23 U/L (women) as the preventative optimal band, with a watch flag from there up to the reference-interval ceiling reported by Hemexa's own pathology partner, Healius Pathology: ALT 41 U/L (men) or 36 U/L (women), AST 36 U/L (men) or 31 U/L (women). GGT optimal is at or below 30 U/L (men) or 20 U/L (women), watch up to 51 U/L (men) or 36 U/L (women). This is Hemexa's working preventative policy layered on the lab's own reference range, not a separate published medical guideline, and it should be discussed with your clinician rather than treated as a diagnosis.
Why a tighter band is a reasonable preventative choice here
Because ALT and AST are damage markers rather than a diagnostic threshold in themselves, sitting well inside the lab reference range is a more comfortable position than sitting near its ceiling, particularly given how common MASLD with a normal ALT is in the AusDiab data below. A single result inside this tighter band is reassuring; it is not proof nothing is happening, which is the same caveat that applies to a normal result at any threshold.
Trend these three enzymes over successive annual results rather than judging liver health from a single draw, and read them alongside your own alcohol intake, medication list and metabolic risk factors rather than in isolation.
The wider argument, including why a reference interval is not a clinical decision limit and why optimal range is not an RCPA term, is on the reference range vs optimal range guide.
How common
How common are abnormal liver enzymes in Australia?
MASLD affects an estimated one in three Australian adults
MASLD, metabolic dysfunction-associated steatotic liver disease (renamed from NAFLD in 2023), is described by Australian Prescriber as affecting one in three Australian adults, and more than half of people with type 2 diabetes, obesity, or two or more metabolic risk factors.
Most people with fatty liver disease have a normal ALT
In the AusDiab study of 4,747 Australian adults, 37% had MASLD (then called MAFLD), but only 22% of that group had an elevated ALT, meaning roughly three-quarters had a completely normal result despite having the condition. Elevated ALT overall was found in 13% of the full cohort, rising to 22% among people with diabetes, 18% with obesity, and 17% with metabolic syndrome.
Alcohol-related fatty liver develops quickly at sustained higher intake
Australian Prescriber cites alcohol-related fatty liver disease developing in 90% of people who drink more than 40g of alcohol (four standard drinks) a day over a sustained period, with 8 to 20% of that group going on to develop cirrhosis.
Haemochromatosis, a less obvious cause, is not rare
Hereditary haemochromatosis, caused predominantly by homozygous C282Y mutations in the HFE gene, affects approximately 1 in 200 Australians. Elevated serum ferritin alongside a transferrin saturation over 45% should prompt HFE genotype testing.
Who should test
Who should consider a liver function test?
Metabolic risk factors
- Type 2 diabetes or prediabetes
- Overweight or obesity, particularly with central fat distribution
- High blood pressure, high triglycerides, or metabolic syndrome
- A personal or family history of fatty liver disease
Exposure-based risk factors
- Regular alcohol intake, or a history of higher intake
- Long-term use of medications known to affect the liver, including some statins, anticonvulsants and antibiotics
- Regular use of herbal or dietary supplements, an increasingly recognised cause in Australia
- A history of injecting drug use, or other established hepatitis B or C risk factors
Other reasons to test
- Before starting a medication that carries a liver-monitoring recommendation
- Unexplained fatigue, abdominal discomfort, or itching
- A family history of haemochromatosis, Wilson disease, or autoimmune liver disease
- As part of an annual preventative baseline panel, even with no symptoms
Liver enzymes are frequently included in a general annual blood panel precisely because early MASLD and mild alcohol-related change are so often silent. Your GP can advise whether a specific clinical indication applies to you.
Causes
What causes elevated liver enzymes
Most elevated liver enzyme results in Australia trace back to a small number of recognised causes. None of these is diagnosed from a blood test alone; each needs the wider clinical picture.
MASLD and MASH
MASLD (metabolic dysfunction-associated steatotic liver disease) is fat accumulating in the liver alongside metabolic risk factors such as obesity, type 2 diabetes or high triglycerides. MASH, the inflamed and more serious form, is metabolic dysfunction-associated steatohepatitis. Both are the most common cause of elevated ALT and AST in Australia today, and both can exist with completely normal enzymes.
Alcohol
Alcohol raises GGT earliest and most sensitively, and drives an AST/ALT ratio above 1, sometimes above 2, through mechanisms covered later in this guide. Australian guidance identifies sustained intake above 40g (four standard drinks) a day as the threshold where alcohol-related fatty liver disease becomes common.
Viral hepatitis B and C
Chronic hepatitis B and C can both elevate ALT and AST, sometimes intermittently rather than constantly, which is one reason enzymes can look normal on a given day despite ongoing viral activity. Australia funds hepatitis B and C testing through Medicare when clinically indicated; ask your GP if any personal risk factors apply.
Medications, including a growing supplement problem
Paracetamol overdose is a well-known cause through a specific toxic mechanism (covered below). Antibiotics are the most common non-paracetamol drug cause. A 2021 Medical Journal of Australia study from a Sydney liver transplant centre found that herbal and dietary supplements accounted for a rising share of non-paracetamol drug-induced liver injury admissions, from 15% in 2009-11 to 47% in 2018-20, with a lower 90-day transplant-free survival (59%) than paracetamol-related cases (86%) in that same cohort.
Statins, without needing routine monitoring
Mild transaminase elevation affects a small minority of statin users, usually within the first three months and usually reversible. Current consensus, reflected in Australian Prescriber's guidance that statins are safe for people with MASLD, including compensated cirrhosis, has moved away from routine periodic LFT monitoring for everyone on a statin; testing is now generally reserved for symptoms or a clinically indicated result.
Autoimmune hepatitis and haemochromatosis
Autoimmune hepatitis is an uncommon condition, more common in women, where the immune system attacks liver cells directly. Hereditary haemochromatosis, iron overload from HFE gene mutations, affects roughly 1 in 200 Australians and is usually picked up through ferritin and transferrin saturation rather than the liver panel itself, though it can also raise ALT and AST once iron accumulates in the liver.
Coeliac disease, a less obvious cause
Undiagnosed coeliac disease raises transaminases in a meaningful minority of newly diagnosed adults and children, with reported rates varying widely across studies (roughly 5 to 40%). The reassuring part is that these elevations typically normalise within about a year of starting a gluten-free diet in people who respond to treatment; a rise that does not settle on a gluten-free diet needs further investigation for a separate liver condition.
Why paracetamol overdose is a special case
At normal doses, paracetamol is safely broken down, with a small fraction converted by liver enzymes into a reactive by-product called NAPQI, which the liver's glutathione stores immediately neutralise. In overdose, the usual breakdown pathways are overwhelmed, far more NAPQI is produced, and it exhausts the available glutathione. Unneutralised NAPQI then binds to proteins inside liver cell mitochondria, disrupting energy production and triggering cell death. This is a dose-dependent, mechanistic injury, different from the mild, idiosyncratic enzyme rises some other medications cause, and it is why paracetamol overdose is a medical emergency rather than a "wait and repeat the test" situation.
Wilson disease, a rare inherited copper accumulation disorder affecting an estimated 1 in 40,000 Australians, is a further, much less common cause worth knowing about if liver disease runs in the family alongside neurological or psychiatric symptoms.
A common, confusing pattern
When GGT rises on its own
GGT rising on its own, with ALT, AST and ALP all normal, is a pattern many people never get an explanation for. It usually means one of a short list of things, none of which is active liver cell damage.
Alcohol, even without heavy daily use
GGT is one of the more alcohol-sensitive markers on the panel, and it can rise through enzyme induction from regular drinking well before ALT or AST move.
Obesity and metabolic factors
GGT correlates with body weight and insulin resistance independent of any diagnosed liver condition, which is part of why it is not specific enough to diagnose fatty liver disease on its own.
Enzyme-inducing medications
Anticonvulsants, including phenytoin and phenobarbital, are well documented to raise GGT two to three times above normal through enzyme induction, with no evidence of actual liver injury on further testing. If you take one of these medications and your GGT is isolated and mildly raised, that is the first thing worth asking your GP about, before further imaging.
An isolated, mild GGT rise with everything else normal is usually followed up by reviewing alcohol intake and medications first, rather than jumping straight to a liver ultrasound.
A pattern clue
The AST/ALT ratio
The AST/ALT ratio, also called the De Ritis ratio after the researcher who first proposed it, is a simple calculation from two numbers already on your report: AST divided by ALT. On its own it is a pattern clue, not a diagnosis.
Below 1: leans toward MASLD or viral hepatitis
MASLD and viral hepatitis typically cause cytosolic hepatocyte injury without the mitochondrial damage alcohol causes, so ALT, which sits mainly in the cytosol, tends to rise more than AST.
Above 2: leans toward alcohol-related injury
Around 90% of people with alcoholic hepatitis have a ratio above 2. Two mechanisms drive it: alcohol's toxic breakdown product accelerates the loss of vitamin B6 (pyridoxal-5-phosphate), which ALT synthesis depends on more heavily than AST does, and alcohol preferentially damages mitochondria, and roughly 80% of liver AST is mitochondrial, so a mitochondria-heavy injury releases disproportionately more AST.
The ratio needs at least one enzyme actually elevated to mean anything
With both ALT and AST sitting comfortably inside the normal range, the ratio between them is not diagnostically useful. Advanced cirrhosis from any cause, not only alcohol, can also push the ratio above 1 to 2, because reduced hepatocyte mass lowers ALT specifically while AST clearance changes with altered blood flow through a scarred liver, so a high ratio in that setting reflects disease severity rather than alcohol specifically.
The ratio is read alongside GGT, the rest of the panel, and your own history, not as a standalone verdict.
Interpretation
Why normal results do not rule out liver disease
A normal ALT and AST is reassuring, but it is not the same as a clean bill of health for the liver, and the reason is built into what these enzymes actually measure.
Enzymes reflect active injury, not accumulated scarring
ALT and AST rise when hepatocytes are actively dying and releasing their contents. Fibrosis, the scar tissue laid down after injury heals, is a separate, accumulated thing. In chronic conditions like hepatitis B, injury can occur in intermittent episodes rather than continuously, so enzymes can look normal on the day of a test even while fibrosis has been building for years; one study of people with chronic hepatitis B and a normal or only minimally elevated ALT found close to half still had significant abnormalities on liver biopsy.
A "burnt-out" liver can show lower numbers, not higher
As fibrosis advances toward cirrhosis, the total mass of functioning hepatocytes falls. With fewer cells left to leak enzymes, ongoing injury can produce a smaller rise in ALT and AST than the same degree of injury would in a healthier liver, which is a genuinely counterintuitive result worth knowing rather than assuming a falling enzyme level always means improvement.
This is the mechanistic reason liver disease has a reputation for being silent: the marker most people rely on to notice something is wrong is not built to catch every stage of the disease, particularly the slow-building, low-grade kind that MASLD usually is.
Before you test
Exercise, alcohol and other things that can skew a result
A handful of common, temporary factors can shift a liver panel without any underlying liver problem. Knowing them can save an unnecessary round of follow-up testing.
Strenuous exercise, especially resistance training
A study of healthy men found ALT, AST and other muscle-related markers rose significantly after an hour of heavy weightlifting and stayed elevated for at least a week, with no liver injury at all; a separate case report recommended abstaining from strenuous exercise for at least seven days before a liver panel for this reason. Creatine kinase (CK), a muscle-specific enzyme, is the test that distinguishes a muscle-driven rise from a liver-driven one; GGT usually, though not always, stays normal in an exercise-driven rise, which is a further clue.
Recent alcohol intake
Sustained heavier drinking reliably raises GGT and, over time, shifts the AST/ALT ratio; that part of the picture is well established. How much a single drink the evening before a routine test moves the numbers is not well quantified in the available research, so treat any specific claimed effect size with caution. The cautious, practical approach is to avoid alcohol for at least 24 to 48 hours before a test, and to tell your GP or the collecting lab if you have had a recent drink so it can be factored into how the result is read.
Other short-term illness
Acute infections and other transient illness can shift liver enzymes modestly, similar to the way hs-CRP rises with any inflammation. A result taken during a cold, a bout of gastro, or shortly after any acute illness is best repeated once you are well, rather than acted on immediately.
How to order
How Australians get a liver function test
| Approach | Best for | Typical cost | Includes LFTs? |
|---|---|---|---|
| GP-ordered, Medicare-funded | Anyone with a clinical indication: symptoms, risk factors, or monitoring a medication | Bulk-billed or low gap when eligible (MBS item 66512 for a panel of five or more tests from item 66500, schedule fee $17.70) | Yes, the standard panel of ALT, AST, GGT, ALP, bilirubin, albumin and total protein |
| GP-ordered, private (no clinical indication) | Preventative or asymptomatic testing outside MBS criteria | Roughly $25 to $80 standalone, or bundled in comprehensive panels at $80 to $300+ | Yes, as a standalone panel or part of a broader preventative panel |
| Membership platforms (e.g. Hemexa) | Ongoing annual baseline coverage with trend tracking alongside other markers | ~$1,199/year (full membership) | Yes; ALT, AST, GGT, ALP, albumin, bilirubin and more on the annual baseline, among 76–80 signature markers |
No fasting is required for a liver function test. Pathology in Australia requires an authorised request from a registered medical practitioner; a GP can order a standalone panel or include it as part of a broader annual check.
What Medicare funds for a standard liver panel, and when a preventative panel is a private cost, is on the Medicare blood tests guide.
FAQ
Frequently asked questions
- What do ALT, AST and GGT actually measure?
- ALT and AST are enzymes normally inside liver cells; they leak into blood when those cells are damaged, so they measure the rate of injury, not liver function itself. GGT rises with bile duct obstruction and, separately, through enzyme induction, when alcohol or certain medications directly increase the liver's production of it as part of processing them.
- What is a normal liver function test result in Australia?
- Australian guidance treats ALT above roughly 35 U/L in women or 40 U/L in men as raised, with AST and GGT following similar sex-specific patterns. The exact reference interval printed on your own report depends on your lab's analyser and reference population, so use the range on your actual result rather than a number from elsewhere.
- Do I need to fast for a liver function test?
- No. Liver function tests need no special preparation, unlike fasting glucose or a lipid panel. If other tests are being drawn on the same visit, follow whatever preparation those specific tests require.
- Can I have liver damage with a completely normal ALT?
- Yes. In the Australian AusDiab study, roughly three-quarters of people with MASLD (fatty liver disease) had a normal ALT. Enzymes reflect active cell injury, not accumulated scar tissue, and injury in chronic liver conditions can occur in intermittent episodes rather than continuously, so a single normal result does not rule disease out.
- Can exercise give a false high reading?
- Yes. Strenuous exercise, particularly heavy resistance training, can raise ALT and AST for a week or more because both enzymes are also present in skeletal muscle. Creatine kinase (CK) is the test that distinguishes a muscle-driven rise from a liver-driven one, and some guidance recommends avoiding strenuous exercise for about a week before a liver panel for this reason.
- My GGT is high but ALT and AST are normal. What does that mean?
- Isolated GGT elevation usually reflects alcohol intake, obesity or metabolic factors, or an enzyme-inducing medication such as an anticonvulsant, rather than active liver damage. It is not specific enough to diagnose a liver condition on its own, and is typically followed up by reviewing alcohol intake and medications before further imaging.
- Does drinking alcohol the night before a blood test affect the result?
- GGT is sensitive to alcohol, and sustained heavier drinking reliably raises it, but exactly how much a single drink the evening before affects the number is not well established in the available research. Avoiding alcohol for at least 24 to 48 hours before a test, and telling your GP or the collecting lab if you have had a recent drink, is the sensible practical approach.
- What is the AST/ALT ratio, and what does it tell me?
- It is AST divided by ALT, also called the De Ritis ratio. A ratio below 1 leans toward MASLD or viral hepatitis; a ratio above 2 is seen in around 90% of people with alcoholic hepatitis. It is only meaningful when at least one enzyme is actually elevated, and advanced cirrhosis from any cause can also raise it, so it is a pattern clue rather than a standalone diagnosis.
- What is the difference between a "liver damage" test and a "liver function" test?
- ALT and AST measure enzyme leakage from cell injury, essentially a damage marker. Albumin and bilirubin reflect what the liver actually produces and clears for the body, which is closer to true function. A standard "liver function test" panel reports both kinds together under one name, which is part of why the panel is easy to misread as a single score.
- How much does a liver function test cost in Australia, and does Medicare cover it?
- When clinically indicated, Medicare funds a GP-ordered panel of five or more of these tests under MBS item 66512 (schedule fee $17.70), commonly bulk-billed. Outside a clinical indication, a standalone private panel typically costs around $25 to $80, or is bundled into a broader preventative panel at $80 to $300+. Membership platforms that include it on a comprehensive baseline panel start around AU$1,199 per year.
- Should I worry about a mildly elevated result?
- A mild, isolated elevation is common and rarely an emergency, but it is worth acting on rather than dismissing: mention it to your GP, review recent alcohol, medications and exercise, and repeat the test once any of those temporary factors have settled. A trend across repeat tests, alongside the pattern across all three enzymes, tells you far more than one number in isolation.
How Hemexa fits
How Hemexa can help
A liver panel is easiest to read correctly with the pattern across markers in view, not one number at a time, and with a clear line between what is genuinely a liver signal and what is a lab artefact of something else entirely.
ALT, AST and GGT on the annual baseline, in the Liver Function category
Hemexa includes ALT, AST, GGT, ALP, albumin, total bilirubin, globulin and total protein on the 76–80 marker annual baseline, grouped under Liver Function on the dashboard. These run annually rather than on the six-month retest.
The AST/ALT ratio, calculated automatically
Hemexa calculates the AST/ALT (De Ritis) ratio automatically on every panel, even on a report where the lab has not printed it, using the same optimal-below-1, watch-above-2 pattern described in this guide.
Clinical safety review on a marked result
An ALT or AST above 200 U/L is flagged in Hemexa's clinical safety review for same-day follow-up, rather than left in a PDF for you to interpret alone.
A preventative band tighter than the standard reference interval
Hemexa's dashboard shows your result against both the standard reference interval from Healius Pathology and Hemexa's own tighter preventative optimal band, described earlier in this guide, so a result that is technically 'normal' but climbing toward the reference ceiling is visible rather than hidden inside a single green tick.
Sources
References
Australian Prescriber. Metabolic dysfunction-associated fatty liver disease: an update. View source ↗
Alqahtani, S. A., et al. (2022). A problem of proportions: estimates of metabolic associated fatty liver disease and liver fibrosis in Australian adults in the nationwide 2012 AusDiab Study. Scientific Reports, 12, 1848. View source ↗
Medicare Benefits Schedule, Item 66500. View source ↗
Medicare Benefits Schedule, Item 66512. View source ↗
Healthdirect Australia. Liver function tests. View source ↗