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Review
. 2016 Dec 7;22(45):9880-9897.
doi: 10.3748/wjg.v22.i45.9880.

Hepatic steatosis and fibrosis: Non-invasive assessment

Rustam N Karanjia  1 , Mary M E Crossey  1 , I Jane Cox  1 , Haddy K S Fye  1 , Ramou Njie  1 , Robert D Goldin  1 , Simon D Taylor-Robinson  1
Affiliations
Review

Hepatic steatosis and fibrosis: Non-invasive assessment

Rustam N Karanjia et al. World J Gastroenterol. .

Abstract

Chronic liver disease is a major cause of morbidity and mortality worldwide and usually develops over many years, as a result of chronic inflammation and scarring, resulting in end-stage liver disease and its complications. The progression of disease is characterised by ongoing inflammation and consequent fibrosis, although hepatic steatosis is increasingly being recognised as an important pathological feature of disease, rather than being simply an innocent bystander. However, the current gold standard method of quantifying and staging liver disease, histological analysis by liver biopsy, has several limitations and can have associated morbidity and even mortality. Therefore, there is a clear need for safe and non-invasive assessment modalities to determine hepatic steatosis, inflammation and fibrosis. This review covers key mechanisms and the importance of fibrosis and steatosis in the progression of liver disease. We address non-invasive imaging and blood biomarker assessments that can be used as an alternative to information gained on liver biopsy.

Keywords: Blood biomarker; Fibrosis; Hepatic steatosis; Non-invasive assessment; Ultrasound.

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Conflict of interest statement

Conflict-of-interest statement: The authors declare no relevant or potential conflicts of interest.

Figures

Figure 1
Figure 1
Histology of normal liver, fibrosis and cirrhosis. A: Representative histological images (using Sirius red staining), normal liver; B: Mild to moderate fibrosis with portal tract expansion (METAVIR F = 2, Ishak stage 3); C: Moderate “bridging” fibrosis (METAVIR F = 3, Ishak stage 4); D: Cirrhosis (METAVIR F = 4, Ishak 5 or 6).
Figure 2
Figure 2
Summary of metabolic mechanisms leading to hepatic steatosis. Reproduced from Dowman et al[155] with permission from Oxford University Press.
Figure 3
Figure 3
Hepatic vascular transit times in normal patients and patients with cirrhosis. Time intensity curves from the hepatic vein show earlier arrival of contrast in the cirrhotic liver[83].
Figure 4
Figure 4
31P magnetic resonance spectroscopy of patients with increasing severity of liver disease vs controls. PME/PDE ratios obtained from in vivo hepatic 31P MRS correlating with severity of liver disease in patients with hepatitis C[116]. MRS: Magnetic resonance spectroscopy; PME: Phosphomonoester; PDE: Phosphodiester.
Figure 5
Figure 5
Diagnostic algorithm and patient flow chart of the non-invasive biomarker and transient elastography pathway[123]. ALT: Alanine aminotransferase; AST: Aspartate aminotransferase; GP: General practitioner; TE: Transient elastography.
Figure 6
Figure 6
Transverse MR images of cirrhotic liver in vivo[128]. A: SPIO-enhanced two-dimensional spoiled gradient echo (SPGR) image with echotime of 2.65 ms; B: Double-enhanced SPGR image at the same level, showing hyperintense reticulations and hypointense nodules (arrows), thought to represent fibrous septal bands surrounding regenerative nodules.
See this image and copyright information in PMC

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