Hepatitis Monthly
Volume:21 Issue: 11, Nov 2021

CD28 expression is correlated with malignancy development in long-term survivors after liver transplantation. Immune cell activation is mediated by the interaction of CD28 with CD4 and CD8.

In this study, we attempted to investigate the expression level and prognostic value of CD28 in hepatocellular carcinoma (HCC).

A total of 54 HCC patients with complete clinical information were examined. The expression level of CD28 in HCC tissues was detected by immunohistochemistry. The correlations of CD28 expression with clinical characteristics, CD4+/CD8+ T-cells, and prognosis in HCC were analyzed. The expression profile of CD28 and survival time of HCC patients were retrieved from the TCGA database, followed by survival analysis.

The positive expression rate of CD28 in HCC tissues was 70.73%. The CD28 expression was significantly higher in the positive expression group (area: 659174.9 ± 670060, IOD: 123348.3 ± 106348.6) than in the negative expression group (area: 8405.7 ± 9983.3, IOD: 1959.6 ± 2117.7) (P < 0.01). The CD4+ and CD8+ cell counts were 526.13 ± 258.17 cells/µL and 383.93 ± 223.39 cells/µL, respectively. The expression level of CD28 was significantly related to the degree of differentiation and the number of CD4+ and CD8+ T-cells (P < 0.05). The survival time of patients was longer in the positive CD28 expression group than in the negative expression group. Based on the CD28 expression profiles of 406 HCC patients retrieved from the TCGA database, patients with high CD28 expression showed a better prognosis than those with low expression (P < 0.05).

CD28 may play a vital role in the occurrence, development, and prognosis of HCC by interacting with CD4+ and CD8+ T-cells. Thus, CD28 could be suggested as the immune checkpoint target for HCC treatment.

In countries with unavailable tenofovir, a combination of lamivudine (LMV) and adefovir (ADV) is recommended for the treatment of LMV-resistant chronic hepatitis B (CHB). Considering that telbivudine (L-dT) was demonstrated to be superior to LMV in previous studies, L-dT and ADV combination therapy is expected to show better antiviral efficacy than the combination of LMV and ADV in patients with LMV-resistant CHB.

This was a prospective randomized multicenter study. The primary endpoint was Hepatitis B Virus (HBV) DNA reduction after 52 weeks of treatment. The secondary endpoints were HBV DNA undetectability, hepatitis B e antigen seroconversion, the incidence of virological and biochemical breakthroughs, and safety during the study period.

A total of 43 LMV-resistant CHB patients were enrolled. Twenty-one were treated with LMV + ADV and 22 with L-dT + ADV. After 52 weeks of antiviral treatment, the HBV DNA reduction showed no significant intergroup difference (-4.54 ± 1.23 log IU/mL in the LMV + ADV group, -4.24 ± 1.46 log IU/mL in the L-dT + ADV group, P = 0.475). There were no significant intergroup differences in HBV DNA undetectability rates, mean HBV DNA level, or hepatitis B e antigen seroconversion rate at 13, 26, 39, and 52 weeks of treatment. In terms of safety, the mean creatine phosphokinase level was significantly higher in the L-dT + ADV group.

In the treatment of LMV-resistant CHB, the combination of L-dT and ADV did not show any clinical benefit compared to the combination of LMV and ADV.

The present study aimed to investigate the relationship of non-alcoholic fatty liver disease (NAFLD) with the severity and extent of coronary stenotic lesions calculated by the Gensini score. In addition, the ability of Fibrosis-4 (FIB4) score to differentiate coronary artery calcification (CAC) and its severity is assessed.

The current retrospective study was performed on a total of 342 patients examined between January and December 2016 in an affiliated hospital of Jiaxing University, Zhejiang, China. The study used liver ultrasonography for the assessment of NAFLD. Furthermore, the FIB4 and Gensini scores were used to predict hepatic fibrosis risk and the severity of coronary stenotic lesions.

The present study revealed that the serum levels of triglycerides, fasting glucose, alanine aminotransferase, and uric acid were significantly higher in patients with NAFLD than in participants without NAFLD (P < 0.001, P < 0.001, P = 0.032, and P = 0.002). Moreover, cases with NAFLD had a higher percentage of diabetes mellitus and hypertension (P < 0.001 and 0.001) than those without NAFLD. It was noted that the level of high-density lipoprotein was lower in patients with NAFLD than in participants without NAFLD (P = 0.006). In addition, we observed that the Gensini score was higher in patients with NAFLD than in participants without NAFLD (P = 0.033). It was found that 27.3%, 25.8%, 45.7%, and 56.3% of the participants had NAFLD in control, single, double, and multi lesion groups, respectively, and the difference was statistically significant (P = 0.008). The number of diseased vessels in patients with severe NAFLD was higher than in the control group (P < 0.001). It was also evident that the number of affected vessels significantly increased (P = 0.010 and P = 0.001) with the stages of NAFLD predicted by the FIB4 and Gensini scores. Furthermore, the Gensini score in patients with moderate and severe NAFLD was higher than in the control group (P = 0.013 and P = 0.019). We also conducted univariate logistic regression analyses to examine the relationship of CAC with FIB4 scores, and it was not significant (P = 0.191).

The present study showed a positive relationship between NAFLD severity and coronary stenotic lesions in the eastern Chinese population. Furthermore, it was found that the higher the degree of FIB4 score, the higher the risk of CAC in patients with NAFLD. Therefore, assessing NAFLD severity using the FIB4 score may be useful for differentiating the patients at a higher risk of CAC. However, further prospective studies are required to establish the link between the FIB4 score and CAC.