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Interleukin 33 (IL-33) is a cytokine belonging to the IL-1 superfamily. Soluble ST2 (sST2) binds to IL-33 and by functioning as trap receptor inhibits signal sending to Th2 via transmembrane ST2. Because Th2-type cytokines play an important role in fibrosis, the aim of this study is to determine whether sST2 can be used as a marker of fibrosis in chronic hepatitis B (CHB) patients or not.The study included 19 healthy controls, 54 patients with CHB, and 14 patients with cirrhosis because of CHB. The aspartate aminotransferase-to-platelet ratio index (APRI) and fibrosis index based on the 4 factors (FIB-4) scores also calculated, and correlations between liver biopsies, sST2 levels, and these scores were analyzed in CHB and cirrhosis patients.The sST2 levels in patients with CHB were significantly higher than those in the control group subjects (median: 1133 pg/mL vs 762.5 pg/mL, respectively [P = 0.035]). In CHB patients, the METAVIR fibrosis score (stages from 0 to 4) showed a moderate correlation with serum sST2 level (r = 0.396, P = 0.004) and a weak correlation with FIB-4 score (r = 0.359, P = 0.008), but no correlation with APRI score (r = 0.253, P = 0.06). The under the curve value of serum sST2 was 0.68, and its prediction of significant fibrosis (METAVIR score ≥2) in values >674 pg/mL had a sensitivity of 91.7% and specificity of 40% (P = 0.009). According to multiple logistic regression analysis, only METAVIR fibrosis stage was found to be an independent predictor of serum sST2 elevation in CHB patients (P = 0.04).The sST2 level can be used for differentiating significant fibrosis from mild fibrosis in CHB patients. However, the efficacy of this marker should be verified by larger studies in the future., Competing Interests: The authors have no funding and conflicts of interest to disclose.

Introduction: In hepatitis B virus (HBV)-related liver cirrhosis, patients with HBV replication show a higher mortality rate than those without. We aimed to investigate the long-term effects of lamivudine on HBV DNA suppression, Child-Pugh score, and survival in patients with hepatitis Be antigen (HBeAg)-negative liver cirrhosis., Methods: Sixty-eight patients (51 male, 17 female) diagnosed with HBV-positive liver cirrhosis, who were monitored by the hepatology and liver transplantation outpatient clinics of our hospital between June 1999 and May 2007, were included in the study. Lamivudine (100 mg/day) was administered orally. Follow-up visits were scheduled monthly during the first 3 months, and every 3 months thereafter. Complete blood count, haemostasis, biochemistry (aspartate aminotransferase [AST], alanine aminotransferase [ALT], amylase, urea, creatinine, total bilirubin, direct bilirubin, total protein, albumin), and alpha-foetoprotein were recorded every 3 months. HBV DNA levels, abdominal ultrasound and the Child-Pugh score were evaluated every 6 months., Results: Sixty-eight patients (mean age, 52.05+/-12.6 years) were monitored for 49.51+/-18.51 months. Basal ALT, HBV DNA levels and Child-Pugh scores were 103.9+/-73.9 IU/ml, 4133+/-121,94 IU/ml, and 7.6+/-2.4, respectively. The ALT normalisation was 59.7% during the first year, 68.2% during the second year and 44.4% during the fifth year. There was a significant decrease in Child-Pugh scores in the first 3 follow-up years when compared with the baseline score (P<0.05). During the treatment, HBV DNA positivity and YMDD mutations were determined in 20 of 68 (29.4%) patients at 46+/-17.9 months. Nine patients (13.2%) developed hepatocellular carcinoma at 44.8+/-21.5 months. Thirteen patients (19.1%) died during the treatment due to liver failure or variceal bleeding., Conclusion: Lamivudine is beneficial in patients with HBeAg-negative liver cirrhosis in terms of improvement in liver function and enhancement of survival and quality of life. An HBV DNA suppressive effect and improvement in Child-Pugh score were seen especially in the first years. It is important to be aware of YMDD mutation early, as addition of new antivirals is necessary to overcome unwanted results of the mutation.