Diagnosing and staging fatty liver disease
Finding fat in the liver is easy; the real question is how much scarring is there. Today that can be answered in most patients with a blood-test score and a short ultrasound elastography exam in our office — no biopsy. Here is who should be checked, what each test means, and the thresholds at which we bring in a liver specialist.
Key takeaways
- Adults with type 2 diabetes, prediabetes with risk factors, obesity with metabolic risk, or fatty liver on imaging should have a fibrosis risk check.
- Step 1 is FIB-4, calculated from age, AST, ALT and platelets. <1.3 is low risk; anything higher needs a second test.
- Step 2 is shear-wave elastography, which we perform in the office on the Siemens ACUSON Sequoia, together with an ultrasound measurement of liver fat (UDFF). A liver stiffness under 7 kPa is reassuring; 9 kPa or more raises concern for advanced fibrosis.
- Steatosis, MASH, and MASH with mild-to-moderate fibrosis are treated in our practice. Advanced fibrosis or cirrhosis is referred to hepatology; coronary disease and complex lipid disorders to cardiology — while we keep treating the metabolism.
What this means for you
If you have diabetes or a fatty liver, ask for your FIB-4 — it can be calculated from blood work you have probably already had. If it isn't clearly low, an elastography exam in our office tells us whether you need liver-directed treatment, routine monitoring, or a hepatologist.
Who should be checked
The ADA, AACE, AASLD and European guidelines converge on the same high-risk groups for MASLD with fibrosis:
- Type 2 diabetes — all adults (ADA Standards of Care recommend FIB-4 screening even with normal liver enzymes).
- Prediabetes, especially with obesity or other cardiometabolic risk factors.
- Obesity with two or more metabolic risk factors — high blood pressure, high triglycerides or low HDL, elevated glucose.
- Fatty liver seen on any imaging, or persistently elevated ALT or AST.
- First-degree relative with cirrhosis from MASH.
Before attributing liver fat to metabolism, we make sure alcohol use is characterized and that other liver diseases (viral hepatitis, iron overload, autoimmune liver disease, medication effects) are not the explanation.
Step 1: FIB-4 and other blood tests
FIB-4 is a free score calculated from four routine values: (age × AST) ÷ (platelet count × √ALT). It is designed to rule out advanced fibrosis — and it does that well.
| FIB-4 | Risk of advanced fibrosis | Next step |
|---|---|---|
| <1.3 | Low | Treat metabolic risk; repeat FIB-4 in 1–3 years (sooner with diabetes or worsening risk) |
| 1.3–2.67 | Indeterminate | Second-line test: shear-wave elastography (in office) or ELF |
| >2.67 | High | Elastography; referral to hepatology if advanced fibrosis is confirmed |
Two caveats matter. FIB-4 is less reliable under age 35, and it rises with age alone — many experts use a low-risk cutoff of 2.0 in people 65 and older. And a normal ALT does not lower the concern: FIB-4 is useful precisely because liver enzymes miss most fibrosis.
ELF (Enhanced Liver Fibrosis) is a proprietary blood test of three markers of scar turnover. It is a good second-line option when elastography is not available: <7.7 low risk, 7.7–9.8 intermediate, ≥9.8 high risk of advanced fibrosis.
Step 2: Shear-wave elastography in our office
We measure liver stiffness and liver fat ourselves, at the same visit or a short follow-up, with ultrasound shear-wave elastography (SWE) on the Siemens ACUSON Sequoia. The system uses acoustic radiation force impulse (ARFI) technology — Virtual Touch Quantification — to send a focused push pulse into the liver and measure how fast the resulting shear wave travels. Stiffer, more scarred liver carries the wave faster. The exam takes about 10–15 minutes, is painless, and is done after a few hours of fasting.
- Liver stiffness is reported in meters per second (m/s) or kilopascals (kPa); higher means more scar.
- Liver fat is measured in the same exam with ultrasound-derived fat fraction (UDFF), reported as a percentage. It tracks closely with MRI-PDFF, the reference imaging measure of liver fat: a value above about 5% indicates steatosis, and higher values mean more fat. Because it is quick and repeatable, we use it to watch liver fat fall with treatment — often before stiffness changes.
- We see the liver while we measure. Because SWE runs on a full diagnostic ultrasound system, we choose the sampling location under direct imaging, avoid vessels and bile ducts, check measurement quality, and look at the liver's texture, size and surface at the same time.
- We follow you on the same machine. Stiffness values differ between technologies, so repeat measurements on one system are the most reliable way to see whether the liver is improving.
Other tests you may encounter — for example with an outside report — include vibration-controlled transient elastography (VCTE, "FibroScan"), a stand-alone device whose kPa cutoffs are different (roughly 8 and 12 kPa rather than 7 and 9), and MRI-based tests: MR elastography (MRE), the most accurate noninvasive measure of stiffness, and MRI-PDFF for liver fat. We interpret outside results against the device that produced them.
Fibrosis stages and risk tiers
| Liver stiffness (ARFI shear-wave, kPa) | What it suggests | Who manages |
|---|---|---|
| <7 kPa (≈<1.5 m/s) | No or mild fibrosis (F0–F1) | Our practice — treat the metabolism; re-check in 1–3 years |
| 7–9 kPa (≈1.5–1.7 m/s) | Mild-to-moderate fibrosis (F1–F2) | Our practice — intensify metabolic treatment, liver-directed medication when indicated, and re-measure |
| 9–13 kPa (≈1.7–2.1 m/s) | Possible advanced fibrosis (F3) | Referral to hepatology; we continue metabolic care |
| ≥13 kPa (≈2.1 m/s or more), or low platelets / nodular liver | Probable cirrhosis (F4); above ~17 kPa, possible portal hypertension | Hepatology leads, including liver-cancer and varices surveillance |
The 7–9 kPa tier is where most at-risk MASH (moderate fibrosis, F2) is found — the group for whom liver-directed medication is indicated, and the group we treat in our practice.
These thresholds follow the Society of Radiologists in Ultrasound consensus and AASLD imaging guidance for ARFI-based shear-wave elastography; they are read together with FIB-4, platelets and the ultrasound picture rather than in isolation. Liver biopsy remains the reference standard but is not routinely needed; we reserve it, through hepatology, for cases where results are discordant or another diagnosis is possible.
For cliniciansIdentifying candidates for MASH pharmacotherapy
SWE cutoffs are vendor- and technique-specific. For ARFI-based pSWE/2D-SWE, the SRU "rule of 5" (≤5 kPa normal; 5–9 kPa cACLD unlikely absent other signs; 9–13 kPa suggestive, confirm; >13 kPa highly suggestive of cACLD; >17 kPa suggestive of CSPH) is used alongside fibrosis-stage cutoffs of roughly <7 kPa for F0–F1 and 7–<13 kPa for F2–F3. We obtain the median of 10 valid measurements in the right lobe via an intercostal approach, 1.5–2 cm below the capsule, fasting and in neutral breath-hold, and accept IQR/median ≤30% (kPa). Confounders include recent meals, ALT flares, hepatic congestion and cholestasis. AASLD guidance on resmetirom supports noninvasive identification of noncirrhotic F2–F3 MASH; baseline labs include CMP, CBC with platelets, A1c, lipid panel and TSH, and stiffness and UDFF are tracked on the same system over time. UDFF correlates strongly with MRI-PDFF (ρ ≈0.8 in prospective comparison), and a cutoff of >5% is highly sensitive for steatosis (MRI-PDFF ≥5.5%), with lower specificity.
When we refer to hepatology or cardiology
Steatosis, steatohepatitis, and steatohepatitis with mild-to-moderate fibrosis are metabolic — endocrine — conditions, and we treat them in our practice, including liver-directed medication. When fibrosis becomes advanced, the liver itself becomes the main concern, and that is hepatology's territory. We are explicit about that line — and about when the heart needs a cardiologist — and we refer early rather than late.
| Finding | Who leads |
|---|---|
| Steatosis (MASLD) with no or mild fibrosis (FIB-4 <1.3, or SWE <7 kPa) | Our practice — metabolic treatment and periodic re-staging |
| MASH with mild-to-moderate fibrosis (F1–F2; SWE ~7–9 kPa) | Our practice — including semaglutide or resmetirom when indicated |
| Advanced fibrosis (F3; SWE ≥9 kPa, FIB-4 >2.67, or ELF ≥9.8) | Referred to gastroenterology / hepatology; we continue treating the diabetes, weight, lipids and hormones |
| Cirrhosis or suspected cirrhosis (SWE ≥13 kPa, low platelets, nodular liver, varices) | Hepatology leads — liver-cancer and varices surveillance, transplant evaluation when needed |
| Any sign of decompensation: jaundice, ascites, confusion, GI bleeding | Urgent hepatology (emergency care for bleeding or confusion) |
| A liver mass, or another liver disease suspected | Hepatology |
| Established or suspected coronary artery disease, heart failure or arrhythmia | Cardiology |
| Severe or complex lipid disorders — suspected familial hypercholesterolemia, LDL not at goal on standard therapy, very high triglycerides | Cardiology / lipid specialist |
| Advanced chronic kidney disease | Nephrology |
For cliniciansRunning the pathway in a diabetes clinic
1. Case finding. FIB-4 for every adult with type 2 diabetes, prediabetes with cardiometabolic risk, obesity with two or more risk factors, or steatosis on imaging — at least annually; aminotransferases alone are not a screening tool.
2. Clarify the diagnosis. Quantify alcohol (AUDIT-C; consider MetALD or alcohol-associated liver disease above threshold intake), check hepatitis B and C serology, review hepatotoxic or steatogenic medications and iron studies, and look further when the picture does not fit.
3. Second-line test, same visit. FIB-4 ≥1.3 (≥2.0 if 65 or older) → in-office ARFI shear-wave elastography with UDFF.
4. Treat. Everyone: weight-centred lifestyle therapy and optimization of glycemia, blood pressure, lipids, kidney and cardiovascular risk (GLP-1–based therapy, SGLT2 inhibitor and statin as indicated). At-risk MASH (SWE ~7–9 kPa, F2): add semaglutide or resmetirom.
5. Refer. SWE ≥9 kPa, FIB-4 >2.67 confirmed on elastography, discordant results, suspected cirrhosis (SWE ≥13 kPa, low platelets, nodular liver) or another liver disease → hepatology. Established cirrhosis → hepatology-led liver-cancer and varices surveillance.
6. Re-stage. Repeat elastography and UDFF on the same system about 12 months into therapy, and every 1–3 years at low risk.
Questions to ask your doctor
- What is my FIB-4, and has it changed over time?
- Should I have shear-wave elastography — and what were my liver stiffness (kPa or m/s) and liver fat (UDFF %)?
- Do my results put me in the range for liver-directed medication?
- Do I need to see a hepatologist or a cardiologist?
How we grade evidence. Every intervention carries a plain label — from established, guideline-supported care (A) through moderate (B) and mixed or limited (C) to experimental (D) and insufficient (E). An improvement on a liver biopsy or scan is not the same as fewer cirrhosis cases, heart attacks, or deaths, and we say which we mean.
Common questions about liver testing and results.
My FIB-4 is 1.6. Is that bad? Grade A
What the evidence shows
Guideline pathways (AASLD, AACE, ADA, EASL) all use FIB-4 <1.3 to rule out advanced fibrosis and send indeterminate scores for a second test.
In our practice
We perform shear-wave elastography for anyone with FIB-4 ≥1.3 (≥2.0 if 65 or older) and interpret it alongside the full metabolic picture.
Do I need a liver biopsy? Grade A
What the evidence shows
Current AASLD guidance supports noninvasive tests for identifying F2–F3 disease and starting therapy; biopsy is reserved for uncertain or discordant cases.
In our practice
If a biopsy is needed, it is arranged through hepatology.
My elastography showed 10 kPa. What happens now? Grade A
What the evidence shows
Shear-wave stiffness of about 9 kPa or more is suggestive of advanced chronic liver disease and warrants confirmation; liver-related risk climbs steeply at F3.
In our practice
We refer to gastroenterology/hepatology and coordinate treatment so nothing falls between specialties.
References
- American Diabetes Association Professional Practice Committee. 4. Comprehensive medical evaluation and assessment of comorbidities: Standards of Care in Diabetes—2025. Diabetes Care. 2025;48(Suppl 1):S59–S85.
- Cusi K, et al. American Association of Clinical Endocrinology clinical practice guideline for the diagnosis and management of nonalcoholic fatty liver disease in primary care and endocrinology clinical settings. Endocr Pract. 2022;28(5):528–562.
- Rinella ME, et al. AASLD Practice Guidance on the clinical assessment and management of nonalcoholic fatty liver disease. Hepatology. 2023;77(5):1797–1835.
- Kanwal F, et al. Clinical care pathway for the risk stratification and management of patients with nonalcoholic fatty liver disease. Gastroenterology. 2021;161(5):1657–1669.
- EASL–EASD–EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD). J Hepatol. 2024;81(3):492–542.
- Dillman JR, Thapaliya S, Tkach JA, Trout AT. Quantification of hepatic steatosis by ultrasound: prospective comparison with MRI proton density fat fraction as reference standard. AJR Am J Roentgenol. 2022;219(5):784–791.
- Barr RG, et al. Update to the Society of Radiologists in Ultrasound liver elastography consensus statement. Radiology. 2020;296(2):263–274.
- Sterling RK, et al. AASLD practice guideline on imaging-based noninvasive liver disease assessment of hepatic fibrosis and steatosis. Hepatology. 2025;81(2):672–724.
- Chen VL, et al. Resmetirom therapy for metabolic dysfunction-associated steatotic liver disease: October 2024 updates to AASLD Practice Guidance. Hepatology. 2025;81(1):312–320.
- Lomonaco R, et al. Advanced liver fibrosis is common in patients with type 2 diabetes followed in the outpatient setting. Diabetes Care. 2021;44(2):399–406.
Want your liver staged — and a clear plan for what the numbers mean?
FIB-4, in-office shear-wave elastography, and a straight answer about whether you need treatment or a hepatologist.