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Table of Content
31 August 2016, Volume 21 Issue 8
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Original Articles
Logistic regression analysis of prognostic factors in 91 patients with hepatic myelopathy
YU Si-miao, ZHANG Ning, DU Ning, WANG Li-fu, SUN Yong-qiang, JING Jing, ZHOU Chao, ZHANG Fan, WANG Rui-lin, ZHU Yun
2016, 21(8): 617-619.
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Objective
To investigate the prognostic factors for patients with hepatic myelopathy (HM) and its risk factors.
Methods
In this retrospective cohort study, clinical data of 91 cases with HM admitted in our hospital from January 2006 to April 2015 was collected. The patients were divided into improved group (
n
=12) and deteriorated group (
n
=79). The correlation between prognosis and clinical features, which including age, sex, duration of liver disease, Child-Pugh score, drinking alcohol hobby, history of splenectomy, history of transjugular intrahepatic portosystemic shunt, complications of liver cirrhosis, comorbidies, laboratory indicators and so on, were analyzed by univariate analysis and further investigated by logistic regression analysis.
Results
Univariate analysis revealed that prothrombin activity (PTA), cholinesterase (CHE) and Child-Pugh score were important factors affecting the prognosis (
P
<0.05). Compared with the improvement group, the deterioration group showed lower levels of PTA and CHE, higher Child-Pugh score (
P
<0.05). Furthermore, logistic regression analysis indicated that low level of CHE and high Child-Pugh score had statistically significant correlation with poor prognosis of HM patients (
P
<0.05), with odds ratio as 0.243 and 32.825 respectively.
Conclusion
CHE and Child-Pugh score are independent risk factors for prognosis of HM patients. For those patients, low level of CHE and high rank of Child-Pugh class predicts poor prognosis.
The clinical value of MELD and SOFA scoring system in predicting short-term prognosis to acute-on-chronic liver failure patients
XIE Ying, WU Zhi-qin, HANG Xiao-feng, ZHANG Rui-qi, XU Wen-sheng
2016, 21(8): 620-622.
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Objective
To investigate the clinical value of the model for end-stage liver disease (MELD) and the sequential organ failure assessment (SOFA) scoring systems in predicting short-term prognosis of patients with acute-on-chronic liver failure (ACLF).
Methods
Seven-eight ACLF patients were divided into survival group and death group according to their 3-month living conditions. MELD and SOFA score were calculated among those patients. Receiver operating characteristic curve (ROC) was applied to evaluate the predictive value, and differences between two models were analyzed by K-M survival curve.
Results
MELD and SOFA scoring systems could well predict the mortality of ACLF patients in 3 months with C-statistics of 0.826 and 0.825, respectively, which showed no significant differences (
Z=0.0148, P
=0.988). Compared with patients with SOFA score ≥ 7 points and MELD score ≥ 23.9 points, patients with SOFA score < 7 points and MELD score < 23.9 points had significantly higher survival rate, respectively (
χ
2
=17.66 and 28.33, both
P
=0.000).
Conclusion
Efficiencies of MELD and SOFA scoring systems shows no significant difference in predicting the short-term prognosis of ACLF patients.
Clinical analysis of 2510 patients with abnormal liver function test of unknown etiology
SUN Yan-hua, LIN Zhi-mei, XIANG Xiao-gang, CAI Wei
2016, 21(8): 623-625.
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Objective
To investigate the etiology and clinical characteristics of patients with abnormal liver function, and to assess the spectrum of liver dysfunctions at present.
Methods
Data of in-patients diagnosed of abnormal liver function from January 2010 to May 2015 in our department was retrospectively analyzed.
Results
Among 2510 cases with abnormal liver function during the past 5 years, certain causes could only be found in 925 cases (36.85%) involving 19 kinds of diseases. Furthermore, viral hepatitis (17.65%, 443/2510), drug-induced liver injury (7.81%, 196/2510), biliary hepatitis (3.75%, 94/2510) and autoimmune liver diseases (3.23%, 81/2510) ranked the top 4 in those with clear diagnosis.
Conclusion
More than half cases (63.15%) with abnormal liver function were very difficult to be exactly diagnosed. In addition, drug-induced liver injury, biliary hepatitis and autoimmune liver disease could not be ignored besides viral hepatitis.
Evaluation of CT perfusion imaging and the relative value analysis in differential diagnosis between hepatocellular carcinoma and hepatic focal nodular hyperplasia
HUANG Yu-feng, CHEN Jian-xin, ZHANG Tong-hua, GU Jia
2016, 21(8): 626-629.
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Objective
To investigate computed tomography (CT) perfusion imaging of hepatocellular carcinoma (HCC) and hepatic focal nodular hyperplasia (FNH), and its role in differential diagnosis.
Methods
24 HCC patients and 17 FNH patients in our hospital from March 2015 to November 2015 were enrolled. CT routine scan and liver perfusion scan were carried out in all those patients. Comparison of CT perfusion values, including hepatic arterial perfusion, portal perfusion, hepatic perfusion, hepatic arterial perfusion index, between HCC and FNH group, as well as carcinoma, peri-carcinoma and distant liver in HCC, and lesions and distant liver in FNH group, respectively.
Results
Comparing with FNH group, HCC group showed lower hepatic arterial perfusion and hepatic arterial perfusion index, but higher portal venous perfusion, which were statistically significant differences. Among cases with HCC, carcinoma tissue showed higher hepatic artery perfusion and hepatic arterial perfusion index than peri-carcinoma and distant liver, but lower portal perfusion, which were statistically significant differences. Similarly, focal tissue in FNH group showed higher hepatic arterial perfusion lesion, hepatic arterial perfusion index and lower portal venous perfusion than distant liver tissue with statistically significant differences. However, the total liver perfusion in all comparisons had no statistically significant differences.
Conclusion
CT perfusion imaging and relative value analysis might play important roles in differential diagnosis between HCC and FNH.
Expression of IL-22 in hepatic steatosis intervened by blueberry probiotic serum
ZHU Juan-juan, CHENG Ming-liang
2016, 21(8): 630-635.
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Objective
To investigate mechanism of blueberry probiotic in treating nonalcoholic fatty liver disease (NAFLD) via affecting expression of interlukin-22 (IL-22).
Methods
Serum from rats treated with saline, and low, medium and high dose of blueberry probiotic by gavage were collected, respectively. Cell steatosis model was constructed by stimulating normal liver cell line L-02 with free fatty acid (FFA). Serum from different dose blueberry probiotic treated rats were added into cell culture medium as 10% concentration for the L-02 steatosis model, respectively. Intracellular lipid deposition was observed by oil red O staining and level of triglyceride (TG) was quantitatively determined. Gene expression of IL-22 was detected by reverse transcription polymerase chain reaction (RT-PCR) and protein expression of IL-22 was detected by western blot and immunofluorescence.
Results
After 24-hour FFA stimulation in L-02 cell with serum, a pile of lipid deposition could be observed and TG level was significantly increased (
P
=0.000), while mRNA and protein levels of IL-22 were decreased (
P
=0.000). In blueberry probiotic serum groups, TG levels and lipid depositions were negatively correlated with the dose of blueberry probiotic. In high-dose blueberry probiotic serum group, expression of IL-22 was significantly enhanced comparing with the other groups (
P
=0.000). However, there was no significant difference in expression of IL-22 between the low- and medium-dose serum groups (
P
>0.05).
Conclusion
Blueberry probiotic might play a role in treatment of NAFLD by enhancing the expression of IL-22.
TLR protects liver against acetaminophen-induced Hepatotoxicitin via activating the Nrf2 antioxidant signaling pathway
GU Jia-yi, YU Feng-rong
2016, 21(8): 636-640.
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Objective
To investigate the protective effect of Lipopolysaccharide (LPS) and toll-like receptors (TLRs) on acetaminophen (APAP)-induced liver injury and its potential mechanism.
Methods
Forty male mice were randomly divided into 4 groups. Mice in control group were intraperitneally (i.p.) injected with saline, in LPS group were i.p. given with 10 μg/kg LPS, and in APAP group were i.p. administrated with APAP (300 mg/kg). LPS+APAP group were i.p. pretreated with LPS (10 μg/kg) 16 h before APAP (300 mg/kg) injection. Serum and liver tissue among 4 groups were collected for further analysis. Liver injury was assessed by detection of serum ALT and AST levels and HE staining of liver tissue. The oxidative stress was evaluated by measuring hepatic glutathione (GSH) and malondialdehyde (MDA) levels, and Dihydroethidium (DHE) staining. Expression of Nrf2, Gclc and HO-1 were measured by western blot and real time-polymerase chain reaction.
Results
Compared with APAP groups, LPS+APAP group showed lower serum levels of ALT (518.3±142.3 vs. 4542±498.4 U/L,
P
<0.05) and AST (643.3±105.6 vs. 5432.1±569.2 U/L,
P
<0.05), milder liver tissue damage, lower MDA levels (78.0±14.5 vs.141.7±26.4 mmol/mg tissue,
P
<0.05) and higher GSH levels (6.2±1.7 vs. 3.5±1.0 μmol/g tissue,
P
<0.05), which revealed that APAP-induced liver injury and oxidative stress response were significantly attenuated by LPS pretreatment. Moreover, LPS pretreatment could enhance the expression of Nrf2 and other antioxidant genes significantly.
Conclusion
LPS plays an important role in protection against APAP-induced hepatotoxicity in mice via activating antioxidant signaling pathway of Nrf2, which might become a new strategy for APAP-induced liver injury therapy.