472), whereas it differed significantly between patients with LSM values ��19 kPa and those with LSM values >19 kPa (7/101, 6.9% vs. 12/27, 44.4%; P<0.001; Figure 4). Figure 4 Incidence of LREs according to fibrosis stage and LSM values. Discordance between baseline LSM value and LRE development As shown in Figure 4, discordant Idelalisib FDA results between LSM values and LRE development were identified in 15/27 (55.6%) patients who did not experience LRE development despite baseline LSM values >19 kPa and 7/101 (6.9%) patients who developed LREs despite LSM values ��19 kPa. However, no independent variable that could predict this discordance between LSM value and LRE development was identified. Influence of dynamic LSM changes on LRE development With the exception of 14 patients without follow-up LSMs before LRE development, 114 patients underwent a second LSM before LRE development at a median interval of 13.
1 (range, 3.8�C51.6) months. Of these, LREs developed in 10 (8.8%) patients. To estimate the LRE incidence according to LSM change, we stratified the patients into three groups as follows: baseline and follow-up LSM values ��19 kPa (n=91), baseline LSM >19 kPa and follow-up LSM ��19 kPa (n=11), and any baseline and follow-up LSM values >19 kPa (n=12). The overall incidence of LRE development did not differ among groups (P>0.05). Although we further stratified the study population [LSM value increased by >30% of baseline LSM (n=10), change in LSM values ��30% of baseline LSM (n=70), and LSM decreased by >30% of baseline LSM (n=34)] [26]. no difference in LRE development was identified (P>0.
05). Discussion Advanced liver fibrosis or cirrhosis is significantly related to an increased risk of hepatic decompensation and HCC development, which, in turn, can worsen the prognosis of patients with CLD [27]. At a time when the natural course of chronic viral hepatitis could be observed due to the absence of antiviral agents, the incidence of HCC in highly endemic areas was approximately 1/100 person-years for CHB patients without cirrhosis [28], [29]. Other Asian studies reported that the incidence of HCC in untreated patients with compensated cirrhosis increased to 3�C8/100 person-years [30], [31]. Moreover, the 5-year cumulative incidence of hepatic decompensation was reported as 16�C20% (3.3�C4/100 person-years) [32], [33].
In our study, the incidence of HCC and hepatic Carfilzomib decompensation seemed relatively low (4.7/100 and 2.0/100 person-years, respectively), which can be explained in part by the relative short follow-up period and the inclusion of patients with F3 fibrosis stages. However, effective antiviral agents such as NUCs and interferon (IFN) have emerged and are actively used to prevent or delay disease progression in patients with chronic viral hepatitis [34]�C[36]. Hence, the natural course of chronic viral hepatitis has changed and some recent studies have demonstrated improved prognosis in such patients. George et al.
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