ABSTRACT
Primary biliary cholangitis (PBC) is a chronic autoimmune liver disease accompanied by cholestasis, with the histological feature of non-purulent cholangitis. This article briefly describes the advantages and limitations of the traditional pathological staging systems such as Rubin stage, Scheuer stage, and Ludwig stage and the latest Nakanuma stage. Among them, Nakanuma stage refines the histological grading and staging standards to reduce the chance of missed diagnosis due to sampling errors, thus providing more adequate diagnostic and prognostic information for the clinic. A combination of new and traditional staging systems can provide guidance to the diagnosis, treatment, and research of PBC.
ABSTRACT
Portal hypertension (PH) is a common clinical syndrome, and the main risk factor for death is esophageal variceal bleeding. Therefore, the early and accurate diagnosis of PH can reduce the incidence rate of serious complications and mortality rate. Hepatic venous pressure gradient, as a main method for the diagnosis of PH, has certain limitations in clinical application, and thus it is necessary to explore new noninvasive diagnostic techniques. Up to now, ultrasound elastography has become one of the important methods for the noninvasive assessment of PH. This article elaborates on its current application and prospects in the assessment of PH.
ABSTRACT
ObjectiveTo systematically review the clinical of artificial liver support system (ALSS) in the treatment of drug-induced liver failure. MethodsPubMed, Embase, The Cochrane Library, CMB, CNKI, and VIP databases were searched for related randomized controlled trials or randomized controlled trials on ALSS in the treatment of drug-induced liver failure published up to October 2019, and a statistical analysis was performed. Odds ratio (OR) was the effect size for categorical data, and the difference between groups was the effect size for continuous data. The weighted mean difference (WMD) method was used for the pooled analysis of effect size, and 95% confidence interval (CI) was calculated for each effect size. I2 and P values were used to evaluate the heterogeneity of the articles included in the analysis; a fixed effect model was used when I2＜50% and P＞0.1, otherwise a random effects model was used. ResultsA total of 16 articles with 945 patients were included, with 520 patients in the ALSS+routine medical treatment (RMT) group and 425 in the RMT group. The meta-analysis showed that compared with the RMT group, the ALSS+RMT group had a significantly lower mortality rate of drug-induced liver failure (OR=0.27, 95%CI: 0.20-0.36, P＜0.001), significant improvements in albumin (Alb) (MD=1.21, 95%CI: 0.18-2.25, P=0.02) and prothrombin activity (PTA) (MD=11.84, 95%CI: 6.34-17.35, P＜0.001), and a significant reduction in total bilirubin (TBil) (MD=-104.97, 95%CI: -163.63 to -46.30, P＜0.001). Further analysis of Alb, TBil, and PTA after the withdrawal of ALSS showed that ALSS significantly improved Alb (MD=1.74, 95%CI: 1.20-2.27, P＜0.001) and PTA (MD=4.45, 95%CI: 2.80-6.10, P＜0.001) and significantly reduced TBil (MD=-128.41, 95%CI: -217.22 to -39.59, P=0.005). ConclusionCompared with RMT alone, RMT combined with ALSS can significantly improve the main biochemical indicators of patients with drug-induced liver failure and reduce their mortality rate.
ABSTRACT
Progressive familial intrahepatic cholestasis (PFIC) refers to a heterogeneous group of autosomal-recessive disorders. The estimated incidence varies between 1/50,000 and 1/100,000 births. Three types of PFIC have been identified and related to mutations in hepatocellular transport system genes involved in bile formation. PFIC-1, PFIC-2, and PFIC-3 are due to mutations in ATP8B1, ABCB11, and ABCB4 genes involved in bile secretion, respectively. Serum gamma-glutamyl transpeptidase is normal in patients with PFIC-1 and PFIC-2, while it is raised in patients with PFIC3. The main clinical manifestation of PFIC is severe intrahepatic cholestasis. PFIC usually appears in infancy or childhood and rapidly progresses to end-stage liver disease before adulthood. Diagnosis of this disease is based on clinical manifestations, liver function tests, liver ultrasonography, liver histology, and genetic testing. Ursodeoxycholic acid therapy is the initial treatment in all PFIC patients to prevent liver damage. In some PFIC1 and PFIC2 patients, biliary diversion may also relieve pruritus and slow disease progression. However, most PFIC patients are ultimately candidates for liver transplantation.
ABSTRACT
Progressive familial intrahepatic cholestasis (PFIC) refers to a heterogeneous group of autosomal-recessive disorders. The estimated incidence varies between 1/50,000 and 1/100,000 births. Three types of PFIC have been identified and related to mutations in hepatocellular transport system genes involved in bile formation. PFIC-1, PFIC-2, and PFIC-3 are due to mutations in ATP8B1, ABCB11, and ABCB4 genes involved in bile secretion, respectively. Serum gamma-glutamyl transpeptidase is normal in patients with PFIC-1 and PFIC-2, while it is raised in patients with PFIC3. The main clinical manifestation of PFIC is severe intrahepatic cholestasis. PFIC usually appears in infancy or childhood and rapidly progresses to end-stage liver disease before adulthood. Diagnosis of this disease is based on clinical manifestations, liver function tests, liver ultrasonography, liver histology, and genetic testing. Ursodeoxycholic acid therapy is the initial treatment in all PFIC patients to prevent liver damage. In some PFIC1 and PFIC2 patients, biliary diversion may also relieve pruritus and slow disease progression. However, most PFIC patients are ultimately candidates for liver transplantation.
ABSTRACT
Objective To study the adjuvant effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) coding gene on cellular immunity induced by Japanese encephalitis (JE) virus DNA vaccine. Methods GM-CSF coding gene was amplified by nested-reverse transcriptase-polymerase chain reaction (RT-PCR) technique from BALB/c murine spleen cells. Recombinant plasmids pJME/GM-CSF and pGM-CSF were constructed by JE virus (JEV) prM-E protein with GM-CSF coding gene or GM-CSF coding gene only, respectively. The plasmids were transfected into China hamster ovary (CHO) cells by Lipofectamine 2000. The coding protein expressions and distributions were detected by immunofluorescence. The BALB/c mice were vaccinated with indicated immunogens with or without GM-CSF gene. The changes of T lymphocyte subsets in the spleen and levels of intracellular cytokines, such as interferon (IFN)-γ and interleukin (IL)-4 of splenic cells from mice immunized with different immunogens were evaluated by flow cytometry. The cytotoxicity T lymphocyte (CTL) activity was assessed by lactate dehydrogenase (LDH). The data were compared by one-factor analysis of variance and least significant difference. Results The constructed recombinant pGM-CSF and pJME/GM-CSF were confirmed by restrict enzyme digestion and DNA sequencing. The expressions of the above proteins were mainly in the cytoplasm and minor on cell membrane. The percentage of CD4+ T lymphocytes in pJME/GM-CSF vaccinated group was (33.90±0.79)%, which was significantly higher than that of in other groups (t values were 9. 818, 6. 804, 6.594, 10.061, 9.380, and 17.675, all P<0.05). The percentages of CD4+T lymphocytes in pJME +pGM-CSF (0) and pJME+pGM-CSF (-3) vaccinated groups were (29.83±0.61)% and (29.70±0.51)%, respectively, which were both higher than that in pJME+pGM-CSF (+3) vaccinated group of (27.69+0.50)% (t=3.466, t=3.255, both P<0.05). The percentages of CD8+ T cells in pJME/GM-CSF and pJME+pGM-CSF vaccinated groups were both higher than that in empty vector (pcDNA 3.1+) group and JE inactivated vaccine vaccinated group (t values were 3.811, 2.627, 10.537, and 3.811, all P<0.05). The CTL activity in pJME/GM-CSF vaccinated group was (51.48±0.10)%, which was higher than those in other groups (t values were 22.868, 13.823, 5.377, 32.287, 34.632, and 53.795, all P<0.05). The IFN-γ/IL-4 ratios in pJME/GM-CSF, pJME+pGM-CSF (0) and pJME + pGM-CSF (-3) vaccinated groups were (19.13±1.36), (12.32±0.82) and (7.05±0.43), respectively, which were higher than those in other groups (P<0.05). Conclusion GM-CSF coding gene could enhance the cellular immune response induced by Japanese encephalitis DNA vaccine.