Favorable Outcomes of Chinese HCV-Related Cirrhotic Patients with Sustained Virological Response after Pegylated Interferon Plus Ribavirin Treatment.

Few studies have conducted follow-up investigations of the clinical course in HCV-related cirrhotic patients who achieved a sustained virological response (SVR) with pegylated interferon plus ribavirin treatment (PegIFN + RBV). We investigated the clinical course and laboratory data in a prospective cohort study enrolling HCV-related cirrhotic patients who received PegIFN + RBV between August 2008 and July 2013 in China. Complete blood counts, liver function tests, and HCV-RNA were serially examined. Liver-related complications were recorded. To detect hepatocellular carcinoma (HCC), alpha-fetoprotein assays, and ultrasound scans were repeated at 6-month intervals. Twenty-five patients were enrolled, including 8 patients with decompensation events before treatment. Eighteen patients achieved SVR with a mean follow-up period of 25.78 months. During the follow-up period, only one patient exhibited HCV-RNA positivity and no decompensation events were detected, but 4 patients developed HCC after SVR. APRI decreased more in patients with SVR than in patients with non-SVR (median, -1.33 versus 0.86, P < 0.001). The albumin levels and platelet counts significantly increased during the follow-up period after SVR (44.27 ± 4.09 versus 42.63 ± 4.37, P = 0.037 and 173.89 ± 87.36 versus 160.11 ± 77.97, P = 0.047). These data indicated that HCV-related cirrhotic patients with SVR after PegIFN + RBV may have a favorable clinical course and improvements in laboratory data. Moreover, HCC should be monitored.

Prevalence of IL-28B and ITPA genotypes in Chinese Han population infected persistently with hepatitis C virus genotype 6 or HCV-1.

The geographic distribution, demographics, epidemiology, host factors, and clinical characteristics of persistent HCV-6 infection in China need further characterization. This multicenter study enrolled 63 patients with persistent HCV-6 infection and 63 patients with persistent HCV-1 infection as controls. Blood biochemistry, quantitation of HCV RNA levels, and identification of host IL-28B genotypes (rs12979860, rs8099917, and rs12980275) and ITPA genotype (rs1127354) were performed to estimate potential variability in host factors that may affect response to treatment. The mean HCV-6 RNA level (3.8E6 IU/ml) was significantly higher than that in patients infected with HCV-1 (1.7E6 IU/ml; P < 0.001). Patients persistently infected with HCV-6 had a high prevalence of IL-28B rs12979860 CC genotype (92.1%), rs8099917 TT genotype (93.7%), and rs12980275 AA genotype (90.5%). Their prevalence in patients infected with HCV-1 was only modestly lower (82.5%, 84.1%, and 82.5%, respectively; P > 0.05). The inosine triphosphate pyrophosphatase (ITPA) SNP rs1127354 CC genotype was present in 66.7% of patients infected with HCV-6, comparable to that of patients infected with HCV-1 (65.1%; P > 0.05). There were no differences in the liver function, proportion of hepatic cirrhosis patients or patients with increased serum glucose between these two groups. Persistent HCV-6 infection in Chinese Han is found mainly in the southern China. Chinese Han with chronic HCV-1 or HCV-6 infection have IL-28B genotypes, suggesting responsiveness to interferon-based pharmacotherapy. Most patients (67%) possess the ITPA genotype associated with susceptibility to ribavirin-induced hemolysis. The routes of transmission for HCV-6 genotype were more diversified than HCV-1 genotype. The outbreak of HCV-6 infection through blood transfusion progressed faster than HCV-1.

Diethylene glycol poisoning and liver function following accidental diethylene glycol injection.

The aim of the present study was to investigate the hepatotoxic effects of accidental intravenous diethylene glycol (DEG) poisoning in patients with liver disease. Clinical manifestations were recorded and liver function tests were carried out for 64 patients with liver disease who had been accidentally treated intravenously with DEG. Comparisons were made between the poisoned and non-poisoned groups. Of the 64 cases with preexisting liver disease, 15 cases (23.4 %) developed toxic presentations after exposure to DEG. All cases were men. Twelve of the 15 poisoned patients (80 %) died within seven days. The intravenous administration of DEG resulted in only mild liver function impairment. Gender (p = 0.039) and the severity of jaundice prior to DEG administration were risk factors related to the occurrence of toxin-induced renal failure (p < 0.006). The results suggest that DEG may worsen liver damage in patients with preexisting liver disease. However, our study demonstrated only mild, transient alterations in patients' baseline liver functions. Severe liver damage secondary to DEG was only occasionally seen in patients with concomitant renal failure.

[A five-year follow-up of one hundred and thirty-six patients of hepatitis C].

OBJECTIVE: To investigate the clinical outcome and effect of interferon treatment on patients with chronic hepatitis C. METHODS: 136 cases of patients with chronic hepatitis C were followed up by methods of retrospective survey combined with prospective study. SPSS16. 0 was used to perform chi-square test and multiple logistic regression. RESULTS: 136 cases of patients were infected with HCV virus mainly through blood and blood products transfusion. They were diagnosed mainly between 2000 and 2005. 98 cases of them had anti-viral treatment with interferon and ribavirin, while the rest did not; 12 new cases developed HCV-related cirrhosis or liver carcinoma in five years, which accounted for 8.8% of the total. Among 76 cases once treated with interferon, 46 cases (60.5%) relapsed in five years. For patients with age < 40, the rates of cirrhosis and liver cancer were 0, and patients with age ≥ 40 but < 60 years, the rates of cirrhosis and liver cancer were 12.5% (7/56 cases), while for those ≥ 60 years old the rates were 35.7% (10/28 cases). The difference was significant ( B = 0.111, Wald = 4.324, P = 0.038) as analysed by logistic regression. The rates of cirrhosis and liver cancer were zero for those with normal or within twice the upper normal AST limit in five years, 43.5% (10/23 cases) for those with AST ranging from 2 to 4 fold the upper normal limit, and 58.3% (7/12 cases) for those with AST higher than four times the upper normal limit. The difference was also significant ( B = 2.184, Wald = 5.443, P = 0.02) by logistic regression analysis. The rate of relapse was 29.7% (11/37 cases) for those using pegylated interferon and 89.7% (35/39 cases) for those using interferon. The difference was significant ( Result of logistic regression showed-B = -2.077, Wald = 4.352, P = 0.037). The rate of relapse was 100% (15/15 cases) for those with treatment less than 24 weeks, 76.2% (16/21 cases) for those with treatment more than 24 weeks but less than 48 weeks, and 37.5% (14/40 cases) for those with treatment more than 48 weeks. The difference was significant (Result of logistic regression showed-B = -1.632, Wald = 6.651, P = 0.01). 42 cases of the relapsed (91.3%) were administrated with interferon once again with ideal effect. CONCLUSION: Hepatitis C virus infection increases the risk of liver cirrhosis and liver cancer. Interferon combined with ribavirin therapy could effectively control the virus and improve outcomes. We can reduce the incidence of relapse by choosing the treatment of pegylated interferon instead of interferon and by completing the full treatment.

[The effects of diethylene glycol on liver function].

OBJECTIVE: To investigate the hepatotoxic effects of accidental intravenous diethylene glycol (DEG.) poisoning in patients with liver disease. METHODS: Clinical data and liver function results were obtained from 64 patients with liver diseases who had been accidentally treated with diethyl glycol-contaminated agent and 45 cases with hepatorenal failure. The hepatotoxic effects of diethylene glycol DEG on the patients with liver diseases were assessed by multivariable logistical regression analysis. RESULTS: Of the 64 cases with liver diseases, 15 cases (23.4%) developed toxic presentations following the accidental administration of DEG. All affected cases were male. Twelve of the 15 poisoned patients (80%), died within 7 days of exposure to DEG. The most common clinical manifestations included kidney damage, renal failure, metabolic acidosis, and nerve system disturbances. The intravenous administration of DEG resulted in only mild liver function impairment. In terms of risk factors, both gender (r = 4.266, P less than 0.05) and the severity of jaundice prior to DEG administration were related to the occurrence of toxin-induced renal failure (r = 7.640, P less than 0.01). CONCLUSIONS: DEG may worsen liver damage in patients with liver diseases.

Expression of SOCS-1 in the liver tissues of chronic hepatitis B and its clinical significance.

AIM: To study the expression of suppressor of cytokine signaling-1 (SOCS-1) in the liver tissues of chronic hepatitis B (CHB) and the clinical significance of this expression. METHODS: The expression of SOCS-1 in liver tissues of 45 cases of CHB was investigated by immunohistochemical staining, and its correlations with inflammation grades and fibrosis stage were analyzed by SPSS statistics software. RESULTS: The result showed SOCS-1 expressing could be observed in the liver tissue of CHB. The expression of SOCS-1 was mainly distributed near the portal area in the liver tissue of mild inflammation CHB group, and was diffusely distributed in the liver tissue of moderate and severe inflammation groups. SOCS-1 positive stains mainly appear in the hepatocytes, only a few of liver interstitial cells were involved. Inside the hepatocyte, SOCS-1 positive stains are mainly distributed in the plasma. Some of the staining was observed on the membrane. The inclusion bodies in the plasma of hepatocytes were observed occasionally. There were both obvious correlations between the expression of SOCS-1 and the inflammatory grade, and that between the expression of SOCS-1 and the fibrosis stage. CONCLUSION: The distribution of SOCS-1 in the liver tissue of CHB is variable. This expression was correlated with the inflammation grade and fibrosis stage.