ABSTRACT
Acute-on-chronic liver failure (ACLF) is a severe syndrome of liver diseases commonly seen in clinical practice and can lead to severe disorders and decompensation of liver synthesis, metabolism, detoxification, and biotransformation, as well as multiple organ failure and an extremely high short-term mortality rate. Infection can induce or aggravate the condition of ACLF and is an independent influencing factor for patient prognosis. This article describes the mechanism and characteristics of ACLF with infection, summarizes the common types and clinical features of infection, reviews the recommended anti-infective regimens, and emphasizes the importance of early prophylactic treatment. ACLF patients with infection tend to have critical conditions, and early diagnosis and empirical anti-infective treatment is the key to successful treatment.
ABSTRACT
Objective@#To clarify the predictive power of PBMCs miR-122, as well as other clinical factors, for response to IFNα therapy in chronic HCV infected patients.@*Methods@#A total of 40 patients chronically infected with HCV genotype 1b were enrolled. All the patients received pegylated interferon alpha (PEG-IFN α) in combination with ribavirin for 48 weeks. To perform the analyses, the patients were compared in terms of achieving sustained virological response (SVR) or not (NSVR) at 24th week after antiviral treatment.@*Results@#SVR rate was 72.5% (29/40) and NSVR rate was 27.5% (11/40). SVR group experienced significantly lower HCV viral load, total bilirubin (TBIL), alpha fetal protein (AFP), fibroscan and laminin (LN) compared with NSVR group before treatment (P<0.05). PBMCs miR-122 expression level was also lower in SVR group than that in SNVR group, although the difference was not statistically significant (P>0.05). and there was no significant change of miR-122 level from baseline to the last available measurement between SVR group and NSVR group. However, no significant association was found between baseline PBMCs miR-122 and HCV viral load, body mass index (BMI), alanine transaminase (ALT), aspartate transaminase (AST), degree of liver fibrosis, respectively.@*Conclusions@#Our result suggest that PBMCs miR-122 level is not an efficient biomarker to predict response to IFN alpha therapy in chronic HCV patients. However, baseline HCV viral load, TBIL, AFP and fibroscan may serve as predictive factors.
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ObjectiveTo explore the differences in clinical characteristics between patients with HBsAg(+) and HBsAg(-)/HBcAb(+) primary hepatic carcinoma (PHC) treated by hepatectomy. MethodsForty-three HBsAg(+) and 18 HBsAg(-)/HBcAb(+) patients who underwent liver resection against PHC from October 2009 to November 2014 in Guangzhou 8th People′s Hospital were selected for the study. The clinical data of the subjects, including sex, age, histological differentiation, intravascular tumor thrombi, and hepatic cirrhosis, were compared, using t test for continuous data, chi-square test for categorical data, and Mann-Whitney U test for non-parametric data. ResultsNo significant differences existed between patients with HBsAg(+) and HBsAg(-)/HBcAb(+) PHC in terms of the age of onset (50.77±12.93 years vs 54.28±9.89 years, t=-1.031, P＞0.05), the incidence of cholangiocarcinoma (2.3% vs 167%, χ2=2.24, P＞0.05), the incidence of hepatic cirrhosis (62.8% vs 44.4%, χ2=1.746, P＞0.05), alpha-fetoprotein level (3638±7869 ng/ml vs 3577±9628 ng/ml, t=0.026, P＞0.05), histological differentiation (Z=-1.085, P＞0.05), and the rate of intravascular tumor thrombi (34.9% vs 22.2%, χ2=0.949, P＞0.05). ConclusionThere are no significant differences in the age of onset and progression of disease between patients with HBsAg(+) and HBsAg(-)/HBcAb(+) PHC treated by hepatectomy. However, given the possibility of occult hepatitis B virus infection, it is necessary to monitor hepatic carcinoma even post HBsAg seroconversion
ABSTRACT
Porcine reproductive and respiratory syndrome virus (PRRSV) has been recognized as one of the most important pathogens of pigs throughout the world. In 2006, more than 10 provinces of China have experienced an epizootic outbreak of pig diseases characterized by high fever, reddened skin and high morbidity and mortality. From June 2006 to April 2007, we have investigated some clinical samples in Hubei province by RT-PCR and cloned several major genes, N, GP5 and NSP2 gene, shown in this study. Phylogenetic analysis of these genes revealed that the highly pathogenic PRRSV variant, ZB, was responsible for 2006 emergent outbreak of pig disease in Hubei province similar with those variants isolated from other provinces in China in 2006, and belongs to the NA-type PRRSV. In the PRRSV variants, the N and GP5 shear about 90% identity with prototypic ATCC VR-2332 and some typical NA-type Chinese isolates, except the 2850bp NSP2 gene (only shares 65% identity with ATCC VR-2332). But they all shear more than and 97% identity with other highly pathogenetic Chinese PRRSV strains. Additionally, there are extensive amino acid (aa) mutations in the GP5 protein and 2 deletions in the Nsp2 protein when compared with the previous isolates. Most of the variants found in 2006 epizootic outbreak of pig diseases in China were the farthest variants from the typical NA-type PRRSV in phylogenetic distance, and these diversities may be responsible for the differences in the pathogenicity observed between these variants and original Chinese PRRSV strains.