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Page 4 of 8 Yip et al. Hepatoma Res 2020;6:44 I http://dx.doi.org/10.20517/2394-5079.2020.30

misdiagnosing this reactive feature as tumour progression. Focal steatosis may also occur, which is typified
[16]
by decreased attenuation on CT and signal drop on opposed-phase MRI . In rare circumstances, temporary
[16]
biliary dilatation is observed, which tends to resolve after a few months .

LATE IMAGING CHANGES
Months after SBRT, the injured hepatocytes are gradually replaced by fibrosis. CT is not usually sensitive in
[19]
detecting liver fibrosis, although perfusion CT may be more useful for this purpose . This chronic effect can
be better appreciated on MRI with low signal on T1- and T2-weighted images. During the earlier stages of
fibrosis, moderate arterial enhancement is observed, which persists in the delayed phase. As this progresses,
[16]
arterial enhancement diminishes but progressive enhancement in the delayed phase persists .

In most cases, loss of liver volume is observed in the initial 3 months after SBRT. This is followed by
subsequent regeneration and increase in liver volume. However, liver atrophy may also occur in some cases
[16]
with capsular retraction [Figure 3]. In contrast to the early focal steatosis observed, focal sparing of fatty
liver (e.g., in pre-existing fatty liver or post-chemotherapy liver changes) may occur in the months following
[16]
SBRT due to loss of fat in the hepatocytes .

Finally, tumour response after SBRT can be challenging, as described above. Tumour shrinkage may not
happen in the immediate few months after SBRT. Nonetheless, even in the absence of volumetric reduction,
progressive reduction in tumour enhancement is consistent with treatment response. This is typically
[16]
accompanied by a corresponding increase in ADC . An increment in ADC of 20%-25% was found to be an
indicator of SBRT response in a few small retrospective studies [20,21] [Figure 4]. However, the authors did not
use pathological response as the study end-point, and hence are subjected to the same challenges as described
with the use of radiological response criteria as an end-point. Furthermore, there is as yet no standardisation
of DWI acquisition and interpretation, which hinders its use as a standard response evaluation criterion.

ROLE OF POSITRON EMISSION TOMOGRAPHY
18
18 F-Fluorodeoxygluocose positron emission tomography ( F-FDG PET) is not recommended in the
staging of early HCC due to its low sensitivity in detecting low-grade, well-differentiated HCC against
the background liver activity, precluding an accurate primary tumour assessment. Nonetheless, it is more
[22]
sensitive in detecting extrahepatic disease compared to local tumour staging . To our knowledge, there is
no study that evaluated the role of F-FDG PET in treatment response assessment after SBRT for primary
18
18
HCC. However, baseline F-FDG PET maximum SUV value (SUV ) > 3.2 was found to be associated with
max
[23]
higher risk of local failure in a cohort of HCC patients treated with SBRT .
18
18
Other radionuclides being evaluated in HCC include F-Fluorocholine ( F-FCH) that is a biomarker for
11
[24] 18
phosphocholine, which is a major metabolite in cancer cells, and C-acetate . F-FCH is reported to have
[25]
18
a high sensitivity, approaching 90%, in detecting HCC . A decrease of F-FCH SUV > 45% was shown
max
to be associated with longer progression-free survival and improved mRECIST response in patients treated
[26]
with various locoregional therapies, including SBRT for HCC .
The availability of PET/MR imaging is slowly increasing in some parts of the world. This could be a
promising tool in HCC combining the superior MRI soft tissue and primary tumour definition, functional
aspects of MRI such as DWI and the superior sensitivity of PET in extrahepatic staging.
PREDICTION OF LIVER TOXICITIES
Although SBRT is relatively well tolerated in most patients, the risk of radiation-induced liver disease (RILD)
cannot be underestimated in this group of patients who have pre-existing cirrhosis, particularly those with