Liver fibrosis — LSM (kPa)
Liver stiffness is highly correlated with fibrosis stage across major aetiologies, including chronic hepatitis B and C, alcoholic liver disease, and non-alcoholic fatty liver disease (NAFLD).
Physical principle
Vibration-controlled transient elastography for quantitative assessment of hepatic fibrosis and steatosis
iLivTouch Mini800 applies controlled transient elastography (TE) — the same scientific principle as the HISKY FibroTouch platform — to measure liver stiffness (LSM, kPa) and the ultrasound attenuation parameter (UAP). Together these biomarkers support non-invasive staging of fibrosis and fatty change, enabling earlier intervention in chronic liver disease.

The interrogated volume is a cylinder approximately 10 mm in diameter and 40 mm in length.
A controlled low-frequency shear wave is generated at the body surface and propagates through hepatic parenchyma. High-frequency ultrasound tracks that wave. Because shear-wave speed increases with tissue stiffness, a scientifically derived liver stiffness measurement (LSM, expressed in kilopascals) can be obtained and used to assess the degree of fibrosis. Concurrently, the system records energy loss of the ultrasound beam during propagation, yielding the ultrasound attenuation parameter (UAP) as a quantitative index of hepatic steatosis.
The speed of shear waves depends on the stiffness of the tissues they are travelling through.
Transient elastography for tissue-stiffness measurement is widely cited by major hepatology societies:
Liver stiffness is highly correlated with fibrosis stage across major aetiologies, including chronic hepatitis B and C, alcoholic liver disease, and non-alcoholic fatty liver disease (NAFLD).
UAP stratifies steatosis as normal, mild, moderate, or severe, providing an objective complement to conventional B-mode ultrasound, which often misses fat fractions below about 30%.
An optional ultrasound imaging probe on Mini800 assists probe placement and morphological context while LSM and UAP remain the quantitative core of the examination.
Clinical rationale
“Anyone who can stop or delay liver fibrosis would be able to cure most chronic liver diseases.”
Dr Hans Popper, founder of hepatology
The liver is the metabolic centre of the body and contains no pain-sensing nerves, so substantial injury may remain clinically silent. Fibrosis is the shared histopathological sequence through which diverse chronic liver diseases progress toward cirrhosis, hepatocellular carcinoma, and liver failure. Early- and mid-stage fibrosis is widely regarded as reversible; timely diagnosis and treatment can interrupt that trajectory.
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Early and intermediate fibrosis is clinically acknowledged to be reversible.
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Early diagnosis and treatment can prevent progression to cirrhosis, liver cancer, and liver failure.
Histology remains the reference standard, yet each established method has constraints that motivate a rapid, quantitative, non-invasive alternative.
No blood collection. Suitable for longitudinal follow-up of fibrosis and steatosis and for evaluating treatment response.
Fibrosis (LSM) and steatosis (UAP) are obtained in one sitting, with results stored for intra-patient comparison over time.
A complete examination typically takes only a few minutes, with stiffness and attenuation reported immediately.
The ~10 × 40 mm cylindrical volume is ≥100× a biopsy core and shows high consistency with histological results.
Quantitative TE supports both case-finding in at-risk populations and serial monitoring in established liver disease.
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