## 4 Discussion
These findings were also noted in the validation biopsy group (Figure 2b). In addition, when NAFLD or HCV patients in the biopsy group were stratified by CAP and histology fibrosis scores, significantly lower TE (\(p\) = 0.071-0.030) and FIB4 (\(p\)\(\leq\) 0.002, Table 3a) measurements in the F2-F4 stages were noted in the high CAP group than in the low CAP group. Our findings confirm the findings by [PERSON] et al. [30], which showed that liver stiffness values were lower than expected in NAFLD patients with advanced fibrosis (F3) and severe steatosis (fat cell fraction >33%). Regarding the TE and FIB4 measurements, values in the high CAP patients tended to be lower than those in the low CAP patients (Table 3a). When the cutoff values in the NAFLD and CHC subgroup were evaluated together, the FIB4 cutoff values in moderate fibrosis to cirrhosis (F2 to 4) were 25.1% to 30.7% lower in the high CAP groups than in the low CAP groups (Table 4). Similar findings were observed for the TE cutoff value. The cutoff value for diagnosis of liver cirrhosis was 8.5% lower in the high CAP than the low CAP group. Therefore, liver stiffness measurements should be interpreted with caution for patients with severe steatosis in cases of NAFLD or CHC. ARFI measurement is less influenced by steatosis, and the differences between CAP groups were small (\(-\)2.4% to 1.3%). It is interesting to note that liver steatosis confers minor effects on liver stiffness measurements in patients with CHB (Table 3b). We suspect that this phenomenon is related to the different fibrogenesis rates and fat cell fractions in CHB cases compared to other etiologies. CHB was associated with a relatively lower fat cell fraction in accordance with other previous studies [31; 32]. HBV infection leads to lower levels of triglycerides, which may affect the development of NAFLD [33]. Furthermore, HBV X protein can inhibit the secretion of apolipoprotein B, which is an important component in the formation of very-low-density and low-density lipoproteins [34; 35]. HBV-infected individuals have been shown to have significantly higher serum adiponectin levels compared to healthy individuals [36], and hepatic steatosis is inversely associated with adiponectin level [37]. In addition to the lower hepatic fat cell fraction, [PERSON] et al. [38] reported that in a series of 81 CHB patients who underwent TE, ARFI, and Forms index measurements, inflammation, rather than hepatic steatosis, significantly impacted the level of fibrosis measured by all three modalities. These findings are consistent with the results of this study, possibly indicating that the fibrosis structure differs between CHB and other etiologies. Several characteristics can be mentioned according to the various etiologies of fibrogenesis. Both NAFLD and CHC are associated with slow, progressive inflammation and fibrogenesis [39; 40], and liver cirrhosis developed over several decades after diagnosis. In CHB patients, however, a severe flare-up can rapidly progress to liver cirrhosis within months or years due to bridging hepatic necrosis [41; 42; 43]. In addition, an uneven distribution of inflammation with the presence of relatively non-inflamed zones can be seen in these patients [44]. These manifestations indicate that fibrosis in CHB happens quickly and is less dense than non-HBV fibrosis. Our previous ARFI study proposed that different severities of inflammation may account for the differences observed between CHB and CHC patients [18]. In this study, even with the exclusion of patients with ALT levels >180 IU/L, liver stiffness measurements differed between the low and high CAP patients in the NAFLD and CHC subgroups, but not in the CHB subgroup. A report from [PERSON] et al. revealed that macronodular liver regeneration was more likely to occur in HBsAg positive than in non-HBsAg positive liver cirrhosis (49.0% vs. 37.2%, \(p\) < 0.01) [45], which might be related to the uneven distribution of bridging hepatic necrosis and fibrosis in patients with HBV-related liver cirrhosis.