The pathogenesis of icteric hepatitis is that pathogenic dampness blocks the middle energizer or blood stasis blocks the bile duct,so that the bile is not excreted normally and moves to the skin surface,which makes the skin yellow.Traditior al Chinese medicine (TCM) has unique advantages in the prevention and treatment of icteric hepatitis.This article systematically introduces the etiology and pathogenesis of icteric hepatitis and the TCM syndrome differentiation therapy for icteric hepatitis,in order to provide a reference for the clinical treatment of icteric hepatitis and the improvement in its prognosis.

To explore the changes in blood levels of lipopolysaccharide(LPS), lipopolysaccharide-binding protein(LBP),and soluble CD14 (sCD14), and their clinical significance in patients with severe chronic viral hepatitis B. blood levels of LPS were determined with chromogenic limulus amebocyte lysate assay, and LBP and sCD14 were assayed with ELISA in 24 patients of severe chronic viral hepatitis B. 10 normal subjects and 16 patients with chronic hepatitis B were also enrolled as controls. The results showed that the blood levels of LPS, LBP and sCD14 were significantly higher in patients with the early stage, midterm, late periods of severe chronic viral hepatitis B than in normal subjects and in those with chronic hepatitis B. The blood levels of LPS, LBP and sCD14 were also significantly higher in patients who died of severe chronic viral hepatitis B than in survivors of the same disease. It suggested that when patients with severe chronic viral hepatitis B were complicated by intestinal endotoxemia (IETM), the sensitivity of Kupffer cells to endotoxin was significantly increased, resulting in hepatocyte injury by TNF ?,even in the presence of very low endotoxin concentration .

Objective To investigate expressions of programmed cell death ligand 1 (PD-L1) in hepatic tissues at the different stages of hepatitis B virus ( HBV) infection, and clarify its role in the mechanism of chronic hepatitis B virus infection. Methods The expressions of PD-L1 were detected by immunohistochemistry and computer image quantitative analysis in the hepatic tissues of 65 chronic HBV infected patients and 5 healthy controls. The correlations between PD-L1 expression and inflammatory grading in the hepatic tissues, total bilirubin (TBil), alanine aminotransferase (ALT), aspartate aminotransferase (AST), serum HBV DNA level were analyzed. Results The PD-L1 expressions in hepatic tissues of HBV infection with G0 - G4 inflammatory grades were 3. 07 % ±0.93%, 8.01%±1.49%, 11.60%±2.60%, 18.41%±2.21% and 26. 04% ±3. 41%, respectively,which were all significantly stronger than that in controls (0. 64%±0. 28%). PD-L1 expression was a positively correlated with inflammation grading of hepatitis tissues, TBil, ALT and AST level in serum (r=0. 917, 0. 787, 0. 483, 0. 628; all P<0. 05), and negatively correlated with serum HBV DNA load (r=-0. 620, P<0. 05). Conclusion The upregulated PD-L1 expression may be probably involved in the chronicity of HBV infection.

Objective To explore the variation and clinical significance of growth hormone(GH) and insulin like growth factor-Ⅰ(IGF-Ⅰ) in children with critical disease.Methods One hundred and twenty-two cases were recruited into the study,among which 42 cases were sepsis in paediatric intensive care unit (sepsis group),20 cases had finished the cardiopulmonary bypass surgery without infection (surgery group).Sixty healthy children served as control group.Serum levels of GH and IGF-Ⅰ were deteced with immunochemiluminometric assay.Results The serum levels of GH were (6.71 ± 6.62) ng/ml in sepsis group,(8.86 ±8.06) ng/ml in surgery group,(3.87 ± 3.31) ng/ml in control group.Compared with the control group,the serum levels of GH in sepsis group and surgery group were increased significantly (P ＜ 0.05).There was no significant difference between sepsis group and surgery group.The serum IGF-Ⅰ levels were (63.72 ±54.17) ng/ml in sepsis group,(119.06 ± 102.12) ng/ml in surgery group and(154.22 ± 107.10) ng/ml in control group separately.The serum IGF-Ⅰ level of sepsis group was significantly decreased compared to the other two groups (P ＜ 0.05).There was no significant difference between surgery group and control group (P ＞0.05).In sepsis group,compared with those who died,the GH of the survival showed no significant difference,IGF-Ⅰ was significantly increased.(P ＜ 0.05).Conclusion GH playes a positive effect in patients with critical disease.IGF-Ⅰ decreases greatly in patients with serious infection.It suggests that IGF-Ⅰ could be a sensitive marker for reflecting whether there is serious infection.The sharply decreasing of IGF-Ⅰ may predict a bad outcome.

Objective To investigate the relationship between clinical presentation and pathological characteristics in HBeAg negative chronic hepatitis B(CHB) patients with steatosis, and to find out the predictors of hepatic inflammation and fibrosis. Methods HgeAg negative CHB patients with (n=56) or without (n=60) steatosis confirmed clinically and pathologically were enrolled in the study. All patients were examined for fasting blood glucose(FBG), fasting insulin (FINS), triglyceride (TG), cholesterol (TC), alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyhransferase (GGT), alkaline phosphatase (ALP) albumin (Alb), globulin(Glb), homeostatic model assessment of insulin resistance (HOMA-IR), HBV-DNA and body mass index(BMI). The association of above parameters with hepatic inflammation, fibrosis and fatty deposition were analyzed statistically. Results It was demonstrated that BMI, FBG, FINS, TG, TC, GGT, ALP , Glb and HOMA-IR were significantly higher in HBeAg negative CHB patients with steatosis than those without steatosis (P<0.05). Whereas the levels of HBV-DNA, Alb, ALT and AST were significantly lower in HBeAg negative CHB patients with steatosis compared with those without steatosis (P<0.05). The hepatic inflammation and fibrosis were aggravated in patients with steatosis. It was implicated that BMI,FBG, FINS, TG, TC, GGT and HOMA-IR(all P values 0.05) were significant predictors for hepatic steatosis, while ALT, AST, Glb and HBV-DNA(all P values <0.05) were significant predictors for hepatic inflammation. And the predictors for hepatic fibrosis were ALT, AST, Alb, Glb and HBV-DNA(all P values <0.05). Conclusions Hepatic steatosis is common in HBeAg negative CHB patients which is positively associated with parameters including BMI, FBG, FINS, TG, TC, GGT, ALP and HOMA-IR. Besides steatosis, the hepatic inflammation and fibrosis are also aggravated in these patients.

Adult ; Autonomic Nervous System Diseases ; etiology ; physiopathology ; Biopsy ; adverse effects ; Hepatitis B, Chronic ; pathology ; physiopathology ; Humans ; Liver ; pathology ; physiopathology ; Male ; Vagus Nerve ; physiopathology ; Vasomotor System ; physiopathology

Objective To investigate the expressions of insulin receptor substrate-1 (IRS-1) and insulin receptor sub-strate-2 (IRS-2) in adipocytes during catch-up growth in neonatal rats with intrauterine growth restriction (IUGR) and their correlations with the insulin resistance. Methods Sprague-Dawley rats (clean grade) were randomly divided into control group and food-restricted group after fertilization. Food-restricted group were received about 30%of food amount consumed in control group every day through the whole pregnant period to establish IUGR animal model, and were fed increased amount of breast-milk from postnatal day 1 to 21 to establish the period of catch-up growth in IUGR animal model (IUGR-CG). Fasting serum glu-cose, insulin and triglyceride were measured in blood from heart ventricles of 4-week old SD rats and insulin resistance index was calculated. Pre-adipocytes and mature adipocytes were obtained from SD rats at different age (1-week, 3-week, 5-week and 7-week old) and the former were induced to differentiate toward mature adipocytes. The levels of IRS-1, IRS-2 in the two kinds of mature adipocytes were detected by Real-Time PCR and Western blot. Results The expression levels of IRS-1, IRS-2 mRNA in mature adipocytes of IUGR-CG rats were signiifcantly lower than those of IUGR rats at 5-weeks and 7-weeks old (P<0.05) while the ex-pression levels of IRS-1, IRS-2 mRNA in differentiated adipocytes of IUGR-CG rats were signiifcantly lower than those of IUGR rats at 5-weeks old (P<0.05). The expression levels of IRS-1, IRS-2 protein in two kinds of adipocytes (mature and differentiated adipocytes) of IUGR-CG rats were signiifcantly lower than those of IUGR rats from postpartum week 1 through 7 (P<0.05). Conclusions IRS-1 and IRS-2 expression levels are downregulated in adipocytes during catch-up growth of IUGR rats, which may be closely related with insulin resistance.

Objective To explore the clinical characteristics of chronic hepatitis B patients with metabolic syndrome (MS).Methods A total of 127 patients with untreated chronic hepatitis B infection were recruited.The patients were divided into two groups according to the diagnosis of MS,with 45 in MS group and 82 in non-MS group.Age,gender,body mass index (BMI),waist-to-hip ratio (WHR),fasting blood glucose (FBG),triglyceride (TG),total cholesterol (TC),aspartate aminotransferase (AST),alanine aminotransferase (ALT),hepatitis B e antigen (HBeAg),hepatitis B virus deoxyribonucleic acid (HBV DNA) were compared between groups.Liver biopsy was performed in 94 patients,including 31 in MS group and 63 in non-MS group,to compare the histological characteristics of liver between two groups.A chi-square test and t test were used for the data analysis.Results BMI,WHR,TG,TC,and FBG results of patients in MS group and nonMS group were (28.88±3.00) kg/m2,0.93±0.03,(2.77±0.17) mmol/L,(6.51±0.95) mmol/L,(6.67±0.45) mmol/L,and (24.64± 2.21) kg/m2,0.91±0.04,(1.50±0.65) mmol/L,(4.38±0.71) mmol/L,(4.91±0.92) mmol/L,respectively.Patients in MS group had higher BMI,WHR,FBG,TG and TC compared with those in non-MS group (t=9.109,3.245,2.642,3.762 and 2.586,respectively; all P＜0.05).No statistical significant differences were found in age,ALT or AST between two groups (t=2.224,0.703 and 0.141,respectively; all P＞0.05).Neither any statistical difference was found in gender,the positive rate of HBeAg and HBV DNA between two groups (x2 =1.662,0.037 and 0.944,respectively; all P＞0.05).In inflammation activity comparison,the result of liver biopsy showed that 48.39 ％ (15/31) were classified as G0-G1 and 51.61％(16/31) as G2-G4 in MS group,and those in non MS group were 49.21％(31/63) and 50.79％(32/63),respectively.No statistical significance was reached (x2 =0.006,P＞0.05).In fibrosis stage comparison,patients in MS group classifies as S0-S1 and S2-S4 were 32.26％ (10/31) and 67.74％(21/31),respectively,and those in non-MS group were 60.32％ (38/63)and 39.68％ (25/63),respectively.The liver fibrosis in MS group was significantly more severe than that in non-MS group (x2 =6.546,P＜0.05).Conclusions The CHB patients with MS have higher BMI,WHR,FBG,TG and TC.The presence of MS may promote the progress of liver fibrosis in CHB patients.

Objective To explore the influencing factors of hepatic steatosis in patients with chronic hepatitis B (CHB),and to provide a theoretical basis of hepatic steatosis prevention and control.Methods A total of 291 hospitalized CHB patients in affiliated Southeast Hospital of Xiamen University were enrolled and divided into two groups:132 CHB patients with hepatic steatosis as the case group and 159 CHB patients without hepatic steatosis as the control group.Conducted a case control study and compared the two groups in terms of body mass index (BMI),waist-to-hip ratio (WHR),fasting blood glucose (FBG),triglyceride (TG),total cholesterol (TC),aspartate aminotransferase (AST),gamma-glutamyl transpeptidase (γ-GT),hepatitis B e antigen (HBeAg),hepatitis B virus DNA (HBV DNA) by descriptive analysis and inferential statistics to analyze the association of these factors with hepatic steatosis in CHB patients.The histological characteristics of the liver were observed.The date analysis used rank sum test and t test.Results FBG,TG,TC,γ-GT,AST of the case group and the control group were (5.11±0.62) mmol/L,(1.81±0.89) mmol/L,(5.29±1.05) mmol/L,(65.04±53.89) U/L,(65.60±71.52) U/L and (4.94±1.89) mmol/L,(1.21±0.79) mmol/L,(4.25±1.58) mmol/L,(146.48±200.39) U/L,(165.35±180.57) U/L,respectively.The case group had significantly higher FBG,TG and TC than the control group (Z=3.607,4.039 and 4.197,respectively,all P＜0.01),while the control group had significantly higher γ-GT and AST (Z=2.672 and 3.020,respectively,both P＜0.01).BMI of the two groups were (26.89±2.78) kg/m2 and (21.17±2.96) kg/m2,respectively,higher in the case group (t=9.711,P＜0.01).WHR in male patients of two groups were 0.93±0.05 and 0.87 ± 0.06,respectively,higher in male patients of the case group (t=4.469,P＜0.01).Positive rate of HBeAg,HBV DNA between the case group and the control group hadn't significantly difference (x2 =0.334,2.960; both P＞0.05).The case group had more severe degree of hepatic steatosis than the control group (Z=-16.145,P＜0.01),while the inflammatory activity and fibrosis were more advanced in the control group (Z=-12.639,P＜0.01; Z=-11.242,P＜0.01,respectively).Conclusions BMI,WHR,FBG,TG and TC appear to be the influencing factors of CHB with hepatic steatosis.The hepatic steatosis in CHB patients is mainly caused by the changes of anthropometric indexes and metabolic factors rather than the effect of HBV.If effective measures are taken,hepatic steatosis in CHB patients can be effectively prevented.

Objective To investigate the impact of reduced glutathione(GSH) on the prolifera- tion,oxidative stress and transforming growth factor?1(TGF-?1) expression of human hepatocytes and hepatic stellate cells(HSCs)(LX-2 cell line).Methods Human hepatocytes and HSCs were incubated with various concentrations of GSH(0.5—50 mmol/L or 0.5—10 mmol/L).The effects of GSH on the proliferation of hepatocytes and HSCs were studied by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphennyhera- zolium bromide colorimetric assay.Human hepatocytes and HSCs were co-cultured with GSH and ferric nitrilotriacetic acid,superoxide dismutase (SOD) activity and malondialdehyde (MDA) contents were detected.HSCs were incubated with high(5.0 mmol/L),media(2.5 mmol/L) and low (0.5 mmol/L) concentrations of GSH,the expressions of TGF-?1 mRNA and protein were detected by ELISA and real- time PCR.Results In concentration ranged from 2.5 to 10 mmol/L,the GSH could promote the pro- liferation of hepatocytes but no HSCs,significantly increased the activity of SOD and decrease the con- tents of MDA in hepatocytes and HSCs,and inhibited the expression of TGF-?1 in HSCs.Conclusions GSH can not only promote the proliferation of hepatocytes,but also protect hepatocytes and HSCs from oxidative stress,and inhibit the secretion of TGF-?1 in HSCs.GSH may play a role in hepatocellular protection,antioxidation and anti-fibrosis.