Dendritic cells (DCs) play a crucial role in controlling viral infections. Little is known about the changes in frequencies of the DC subsets in patients with chronic hepatitis C (CHC), particularly in the era of interferon-free regimens. We aimed to evaluate the impact of sofosbuvir/daclatasvir on the frequency of different peripheral DC subsets, the expression of the inhibitory CD200R and its ligand CD200 on DC, and their relation to the treatment outcome. A total of 1000 patients with CHC were enrolled and treated with a fixed oral dose of 400 mg of sofosbuvir and 60 mg of daclatasvir for 12 weeks. A total of 940 patients achieved sustained virologic response (SVR), and only 60 patients were non-responders (NRs). The frequencies of the peripheral plasmacytoid (pDC) and myeloid (mDCs) subsets and their surface expressions of CD200R and CD200 molecules were analyzed using flow cytometry. This analysis included 60 non-responders (NR group), 60 randomly selected sustained virologic responders (SVR group) at baseline, and at the end of treatment, and 60 healthy controls. HCV infection was associated with a down-regulation in the frequency of mDC, compared to healthy controls. In addition, mDC in HCV-infected patients showed lower levels of CD200R. However, neither the pDC frequency nor their CD200R expression was significantly altered. Interestingly, by the end of therapy, the frequencies of circulating mDCs and CD200R⁺mDC increased significantly in the SVR group and were even comparable to healthy controls. The levels of these cells were not normalized in the NR group. Percentages of mDCs and CD200R⁺mDC subsets showed good prognostic accuracy for predicting virologic response to therapy. Our results showed that HCV infection was associated with modulation of the mDC frequency and their surface expression of CD200R. Successful daclatasvir and sofosbuvir combined therapy was associated with the normalization of the percentages of mDC and CD200R⁺mDC.

Background A glycoprotein with a molecular weight of 25 kDa is known as neutrophil gelatinaseassociated lipocalin (NGAL). It is often detected in tiny amounts in many human organs. Aim of the research: To identify the profile of circulating NGAL in liver disease patients with different morbidities and also evaluate the potential for NGAL as a prognostic indicator for early identification of AKI in these individuals. Patients & methods: This cross-sectional research was performed on 230 cases with different liver diseases, selected from the inpatient and outpatient clinics in the hepatology and gastroenterology departments of the multicentric They were divided into four groups: Group A: nonalcoholic fatty liver disease patients (NAFLD), Group B: nonalcoholic steatohepatitis patients (NASH); Group C: compensated liver disease patients; and Group D: decompensated liver disease. Results There was a significant variance between different liver disease groups concerning NGAL. Thus, NGAL was significantly higher among NASH patients than compensated liver disease cases and decompensated liver disease cases among NAFLD patients. A significant positive association was noted among NGAL with creatinine and SGPT. Nevertheless, there was a significant negative association between NGAL and eGFR among NAFLD patients. NGAL yields a significant level at a cutoff level of >128 ng/ml in predicting renal impairment among decompensated liver disease cases, with a sensitivity of 96% and a specificity of 100%. Conclusion NGAL is a useful prognostic marker for early identification of acute kidney injuries in individuals with liver disease.