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Cheng et al. Advances in liver fibrosis

to assess transplant-free survival of the patients with regression was also supported by data from Chinese
primary sclerosing cholangitis, [95] HCV/HIV co-infected and Korean cohorts established that metabolic
women [96] and the prognosis if patients with different syndrome is a risk factor of advanced liver fibrosis and
chronic liver diseases. [70] cirrhosis independent of viral factors in CHB. [107,108]
New-onset metabolic syndrome and some of its
HCC components (namely central obesity and low high-
There is good evidence show the strong predictive and density lipoprotein cholesterol) were found associated
even diagnostic role of the non-invasive tests for HCC. with liver fibrosis progression, independent of change
ARFI is used for differentiating benign and malignant in viral load and ALT level. [109] Therefore controlling
liver tumors by the assessment of virtual touch tissue metabolic factors in CHB patients already have good
imaging (VTI) and virtual touch tissue quantification viral suppression with antiviral treatment would be
(VTQ), as VTI appears to be stiffer and VTQ is higher important, not only to enhance liver fibrosis regression
in malignant lesion than its benign counterpart. [97] For and hepatic events, but also to minimize cardiovascular
MRE, the measurement of loss modulus in liver tumor death. [110]
can help differentiating the benign lesions from the
malignant ones, with the former having a lower value. [98] Indirect evidence of antiviral treatment reversing liver
Non-invasive test is also an important part of some fibrosis also came from two studies using serial LSM
HCC risk score. For example, LSM-HCC score, which results to assess the change in liver fibrosis in large
is optimized from CU-HCC score with LSM, further cohorts of asymptomatic CHB patients revealed low
increases the negative predictive value to close to 100% incidence rate of liver fibrosis progression, defined
for HCC prediction in 3 to 5 years in CHB patients. [99] as an increase in LSM by 30% or more. [111,112] It was
Both FibroTest and LSM results can help predict the because patients who had active disease, as evidenced
occurrence of HCC in patients with viral hepatitis. [100] by raised ALT and high HBV DNA, had been started on
Patients with ELF higher than 10.4 is known to have antiviral treatment.
higher risk of liver-related events, in which HCC is at
the top of the list. [101] Non-invasive tests can also play CHC
some part in prognosis of HCC. For example, in HCC Data from last century illustrated the conventional
patients receiving partial hepatectomy or transarterial interferon regresses liver fibrosis in CHC patients
chemoembolization, LSM and APRI is an independent with sustained virologic response (SVR). [113] Similar
prognostic factor. [90,91,102] findings have been reported in sustained responders to
pegylated interferon. [114,115] Regression of liver fibrosis,
TREATMENT OF LIVER FIBROSIS which occurred in 82% of patients, was sustained at 5
Treatment for underlying diseases years after SVR; more impressively recovery of normal
or nearly normal liver architecture is possible.
[103]
With very potent antiviral agents, patients with chronic
viral hepatitis often have liver fibrosis and even Now it is the era of direct-acting antiviral (DAA) agents
cirrhosis regressed after sustained viral suppression in treating CHC patients, which leads to an SVR close to
or viral clearance. [103,104] 100%. [116] Studies evaluating liver fibrosis regression in
DAA-treated CHC patients often adopted non-invasive
CHB assessments like transient elastography. A small study
There is ample evidence to support the fact that of 54 DAA-treated patients with baseline cirrhosis
effective antiviral treatment reverses liver fibrosis in revealed more pronounced reduction in LSM happened
majority of CHB patients. [104,105] Cumulative entecavir between baseline to end-of-treatment visit, but less
therapy for 3 to 7 years regressed liver fibrosis in obvious in the post-treatment period. Hence the authors
88% of 57 CHB patients, including all 10 patients with concluded that decreased LSM was likely accounted by
advanced fibrosis or cirrhosis. [105] This observation the reduced necroinflammation and probably to a less
was further confirmed by a larger cohort of 348 extent to regression of cirrhosis. [117] Another study of
patients who tenofovir disoproxil fumarate, in which larger sample size already made use of serum makers
176 (51%) had regression of fibrosis at week 240. [104] on top of LSM revealed that FIB-4 and APRI improved
More importantly, most (71%) patients with cirrhosis to the same extent of LSM after SVR. [118] Yet whether
at baseline had regression of cirrhosis. Data from the this indicated a true regression of fibrosis or merely
same trial revealed that body mass index at baseline resolution of chronic liver inflammation remained to be
was the single negative predictor of liver fibrosis determined. [118]
regression. [106]
NAFLD
Importance of metabolic factors on liver fibrosis Similar to chronic viral hepatitis, controlling underlying
Hepatoma Research ¦ Volume 3 ¦ August 08, 2017 161