Resting energy expenditure and glucose, protein and fat oxidation in severe chronic virus hepatitis B patients

AIM： To study and determine the resting energy ex- penditure （REE） and oxidation rates of glucose, fat and protein in severe chronic hepatitis B patients. METHODS： A total of 100 patients with liver diseases were categorized into three groups： 16 in the acute hepatitis group, 56 in the severe chronic hepatitis group, and 28 in the cirrhosis group. The REE and the oxidation rates of glucose, fat and protein were as- sessed by indirect heat measurement using the CCM-D nutritive metabolic investigation system. RESULTS： The REE of the severe chronic hepatitis group （20.7 ± 6.1 kcal/d per kg） was significantly lower than that of the acute hepatitis group （P = 0.014）. The respiratory quotient （RQ） of the severe chronic hepatitis group （0.84 ± 0.06） was significantly lower than that of the acute hepatitis and cirrhosis groups （P = 0.001）. The glucose oxidation rate of the severe hepatitis group （39.2%） was significantly lower than that of the acute hepatitis group and the cirrhosis group （P 〈 0.05）, while the fat oxidation rate （39.8%） in the severe hepatitis group was markedly higher than that of the other two groups （P 〈 0.05）. With improve- ment of liver function, the glucose oxidation rate in- creased from 41.7% to 60.1%, while the fat oxidation rate decreased from 26.3% to 7.6%. CONCLUSION： The glucose oxidation rate is signifi-cantly decreased, and a high proportion of energy is provided by fat in severe chronic hepatitis. These re- sults warrant a large clinical trail to assess the optimal nutritive support therapy for patients with severe liver disease.     

Serum neopterin levels in children with hepatitis-B-related chronic liver disease and its relationship to disease severity

AIM： To evaluate serum neopterin levels and their correlations with liver function tests and histological grade in children with hepatitis-B-related chronic liver disease. METHODS： The study population comprised 48 patients with chronic active hepatitis B, 32 patients with hepatitis-B-related active liver cirrhosis and 40 normal controls. Serum neopterin was measured using an enzyme-linked immunosorbent assay. RESULTS： The mean ＋ SD serum neopterin levels were 14.2 ± 5.6 nmol/L in patients with chronic hepatitis, 20.3 ± 7.9 nmol/L in patients with liver cirrhosis and 5.2 ± 1.4 nmol/L in control group. Serum neopterin levels were significantly higher in patients with chronic hepatitis （P = 0.005） and cirrhosis patients （P = 0.008）, than in control subjects. Cirrhotic patients had significantly higher serum neopterin levels than patients with chronic hepatitis （P = 0.004）. There was a positive correlation between serum neopterin levels and alanine aminotransferase levels in patients with chronic hepatitis （r = 0.41, P = 0.004） and cirrhotic patients （r = 0.39, P = 0.005）. Positive correlations were detected between serum neopterin levels and inflammatory score in patients with chronic hepatitis （r = 0.51, P = 0.003） and cirrhotic patients （r = 0.49, P = 0.001）. CONCLUSION： Our results suggest that serum neopterin levels can be considered as a marker of inflammatory activity and severity of disease in children with hepatitis-B-related chronic liver disease.     

Influence of chronic HBV infection on superimposed acute hepatitis E

AIM:To investigate the influence of chronic hepatitis B virus(HBV)infection[based on the status of hepatitis B e antigen(HBeAg),HBV DNA,and cirrhosis]on superimposed acute hepatitis E.METHODS:A total of 294 patients were recruited from the Department of Infectious Diseases of the Third Affiliated Hospital,Sun Yat-sen University,from January 2003 to January 2012.The patients were classified into two groups:an HBV+hepatitis E virus(HEV)group(a group with chronic HBV infection that was superinfected with acute hepatitis E,n=118)and an HEV group(a group with acute hepatitis E,n=176).We retrospectively analyzed and compared the clinical features of the two groups.Statistical analyses were performed using theχ2test or Fisher’s exact test for categorical variables and the Student’s t test forcontinuous variables.A P value<0.05 was considered statistically significant.RESULTS:The peak values of prothrombin time,serum total bilirubin,and Model for End-Stage Liver Disease scores were significantly higher in the HBV+HEV group.More patients in the HBV+HEV group had complications(39.8%vs 16.5%,P=0.000)and developed liver failure(35.6%vs 8.5%,P=0.000).Additionally,the mortality of the HBV+HEV group was significantly higher(20.3%vs 7.4%,P=0.002).Further analysis of the HBV+HEV group showed that there were no significant differences in complication occurrence,liver failure incidence,or mortality between patients with different HBeAg and HBV DNA statuses.However,in patients with underlying cirrhosis,complication occurrence and liver failure incidence significantly increased.In total,12.7%of the patients in the HBV+HEV group received anti-HBV treatment,but this therapy failed to reduce mortality in patients who developed liver failure.CONCLUSION:The presence of underlying cirrhosis in chronic HBV infection results in more severe clinical outcomes with superimposed acute hepatitis E.AntiHBV treatment cannot improve the prognosis of liver failure caused by HBV-HEV superinfection.     

Value of portal hemodynamics and hypersplenism in cirrhosis staging

AIM: To determine the correlation between portal hemodynamics and spleen function among different grades of cirrhosis and verify its significance in cirrhosis staging. METHODS: The portal and splenic vein hemodynamics and spleen size were investigated by ultrasonography in consecutive 38 cirrhotic patients with cirrhosis (Child's grades A to C) and 20 normal controls. The differences were compared in portal vein diameter and flow velocity between patients with and without ascites and between patients with mild and severe esophageal varices. The correlation between peripheral blood cell counts and Child's grades was also determined. RESULTS: The portal flow velocity and volume were significantly lower in patients with Child's C (12.25±1.67 cm/s vs 788.59±234 mm/min, respectively) cirrhosis compared to controls (19.55±3.28 cm/s vs 1254.03±410 mm/min, respectively) and those with Child's A (18.5±3.02 cm/s vs 1358.48±384 mm/min, respectively) and Child's B (16.0±3.89 cm/s vs 1142.23±390 mm/min, respectively) cirrhosis. Patients with ascites had much lower portal flow velocity and volume (13.0±1.72 cm/s vs1078±533 mm/min) than those without ascites (18.6±2.60 cm/s vs1394±354 mm/min). There was no statistical difference between patients with mild and severe esophageal varices. The portal vein diameter was not significantly different among the above groups. There were significant differences in splenic vein diameter, flow velocity and white blood cell count, but not in spleen size, red blood cell and platelet counts among the various grades of cirrhosis. The spleen size was negatively correlated with red blood cell and platelet counts (r= -0.620 and r= -0.8.34, respectively). CONCLUSION: An optimal system that includes parameters representing the portal hemodynamics and spleen function should be proposed for cirrhosis staging.     

Differential hepatic features presenting in Wilson disease-associated cirrhosis and hepatitis B-associated cirrhosis

BACKGROUND Cirrhosis is a chronic late stage liver disease associated with hepatitis viruses,alcoholism, and metabolic disorders, such as Wilson disease(WD). There are no clear markers or clinical features that define cirrhosis originating from these disparate origins. We hypothesized that cirrhosis is not one disease and cirrhosis of different etiology may have differential clinical hepatic features.AIM To delineate the liver features between WD-associated cirrhosis and hepatitis Bassociated cirrhosis in the Chinese population.METHODS In this observational study, we reviewed the medical data of consecutive inpatients who had WD-associated cirrhosis or hepatitis B-associated cirrhosis from January 2010 to August 2018, and excluded patients who had carcinoma,severe heart or pulmonary diseases, or other liver diseases. According to the etiology of cirrhosis, patients were divided into two groups: WD-associated cirrhosis group(60 patients) and hepatitis B-associated cirrhosis group(56 patients). The liver fibrosis degree, liver function indices, and portal hypertension features of these patients were compared between the two groups.RESULTS No inter-group differences were observed in the diagnostic liver fibrosis markers,however, clinical features clearly defined the origin of cirrhosis. WD-associated cirrhosis patients(16-29 years) had lower levels of alanine transaminase,aspartate transaminase, and bilirubin, lower prothrombin time, lower incidence of hepatic encephalopathy, and lower portal vein diameter(P < 0.05), compared to cirrhosis resulting from hepatitis B in older patients(45-62 years). Importantly,they had decreased risks of progression from Child-Pugh grade A to B(odds ratio = 0.046, 95% confidence interval: 0.006-0.387, P = 0.005) and of ascites(odds ratio = 0.08, 95% confidence interval: 0.01-0.48, P = 0.005). Conversely, WDassociated cirrhosis patients had a higher risk of splenomegaly(odds ratio = 4.15,95% confidence interval: 1.38-12.45, P = 0.011).CONCLUSION WD-associated cirrhosis presents a higher risk of splenomegaly associated with leukopenia and thrombocytopenia, although revealing milder liver dysfunction and portal hypertension symptoms, which recommends WD patients to be monitored for associated complications.     

Nutritional status in relation to lifestyle in patients with compensated viral cirrhosis

AIM:To assess the nourishment status and lifestyle of non-hospitalized patients with compensated cirrhosis by using noninvasive methods.METHODS:The subjects for this study consisted of 27 healthy volunteers,59 patients with chronic viral hepatitis,and 74 patients with viral cirrhosis,from urban areas.We assessed the biochemical blood tests,anthropometric parameters,diet,lifestyle and physical activity of the patients.A homeostasis model assessment-insulin resistance(HOMA-IR) value of ≥ 2.5 was considered to indicate insulin resistance.We measured height,weight,waist circumference,arm circumference,triceps skin-fold thickness,and handgrip strength,and calculated body mass index,arm muscle circumference(AMC),and arm muscle area(AMA).We interviewed the subjects about their dietary habits and lifestyle using health assessment computer software.We surveyed daily physical activity using a pedometer.Univariate and multivariate logistic regression modeling were used to identify the relevant factors for insulin resistance.RESULTS:The rate of patients with HOMA-IR ≥ 2.5(which was considered to indicate insulin resistance) was 14(35.9%) in the chronic hepatitis and 17(37.8%) in the cirrhotic patients.AMC(%)(control vs chronic hepatitis,111.9% ± 10.5% vs 104.9% ± 10.7%,P = 0.021;control vs cirrhosis,111.9% ± 10.5% vs 102.7% ± 10.8%,P = 0.001) and AMA(%)(control vs chronic hepatitis,128.2% ± 25.1% vs 112.2% ± 22.9%,P = 0.013;control vs cirrhosis,128.2% ± 25.1% vs 107.5% ± 22.5%,P = 0.001) in patients with chronic hepatitis and liver cirrhosis were significantly lower than in the control subjects.Handgrip strength(%) in the cirrhosis group was significantly lower than in the controls(control vs cirrhosis,92.1% ± 16.2% vs 66.9% ± 17.6%,P 0.001).The results might reflect a decrease in muscle mass.The total nutrition intake and amounts of carbohydrates,protein and fat were not significantly different amongst the groups.Physical activity levels(kcal/d)(control vs cirrhosis,210 ± 113 kcal/d vs 125 ± 74 kcal/d,P = 0.001),number of steps(step/d)(control vs cirrhosis,8070 ±3027 step/d vs 5789 ± 3368 step/d,P = 0.011),and exercise(Ex)(Ex/wk)(control vs cirrhosis,12.4 ± 9.3 Ex/wk vs 7.0 ± 7.7 Ex/wk,P = 0.013) in the cirrhosis group was significantly lower than the control group.The results indicate that the physical activity level of the chronic hepatitis and cirrhosis groups were low.Univariate and multivariate logistic regression modeling suggested that Ex was associated with insulin resistance(odds ratio,6.809;95% CI,1.288-36.001;P = 0.024).The results seem to point towards decreased physical activity being a relevant factor for insulin resistance.CONCLUSION:Non-hospitalized cirrhotic patients may need to maintain an adequate dietary intake and receive lifestyle guidance to increase their physical activity levels.     

Establishing models of portal vein occlusion and evaluating value of multi-slice CT in hepatic VX2 tumor in rabbits

AIM： To establish models of portal vein occlusion of hepatic VX2 tumor in rabbits and to evaluate the value of multi-slice CT.
METHODS： Forty New Zealand rabbits were divided into 4 groups according to digital table： Immediate group （group A; transplantation of tumor immediately after the portal vein occlusion）, 3-wk group （group B; transplantation of tumor at 3 wk after the portal vein occlusion）, negative control group （group C） and positive control group （group D）, 10 rabbits in each group. Hepatic VX2 tumor was transplanted with abdominalembedding innoculation immediately after the portal vein occlusion and at 3 wk after the portal vein occlusion. Meanwhile, they were divided into negative control group （Left external branch of portal vein was occluded by sham-operation, and left exite was embedded and inoculated pseudoly） and positive control group （Transplanted tumor did not suffer from the portal vein occlusion）. All rabbits were scanned with multi-slice CT.
RESULTS： All 40 animals were employed in the final analysis without death. Tumor did not grow in both immediate group and 3-wk group. In 3-wk group, left endite was atrophied and growth of tumor was inhibited. The maximal diameter of tumor was significantly smaller than that in positive control group （2.55±0.46 vs 3.59±0.37 cm, t = 5.57, P 〈 0.001）. Incidences of metastasis in the liver and lung were lower in 3-wk group than those in positive control group （10% vs 400, and 90% vs 100%, respectively）. The expression intensities of the vascular endothelium growth factor （VEGF） in groups A, B, C and D were 0.10±0.06, 0.66±0.21, 0.28±0.09 and 1.48±0.32, respectively. VEGF expression level in the test group A was significantly lower than that in the negative control group C （t = 5.07; P 〈 0.001）.In addition, VEGF expression in the test group B was significantly lower than that in the positive control group D （t = 6.38; P 〈 0.001）. Scanning with multi-slice CT showed that displaying rate of     

Fibrinogen-like protein 2 fibroleukin expression and its correlation with disease progression in murine hepatitis virus type 3-induced fulminant hepatitis and in patients with severe viral hepatitis B

AIM: To evaluate the expression of fibrinogen-like protein 2 (fgl2) and its correlation with disease progression in both mice and patients with severe viral hepatitis. METHODS: Balb/cJ or A/J mice were infected intraperitoneally (ip) with 100 PFU of murine hepatitis virus type 3 (MHV-3), liver and serum were harvested at 24, 48, and 72 h post infection for further use. Liver tissues were obtained from 23 patients with severe acute chronic (AOC) hepatitis B and 13 patients with mild chronic hepatitis B. Fourteen patients with mild chronic hepatitis B with cirrhosis and 4 liver donors served as normal controls. In addition, peripheral blood mononuclear cells (PBMC) were isolated from 30 patients (unpaired) with severe AOC hepatitis B and 10 healthy volunteers as controls. Procoagulant activity representing functional prothrombinase activity in PBMC and white blood cells was also assayed. A polyclonal antibody against fgl2 was used to detect the expression of both mouse and human fgl2 protein in liver samples as well as in PBMC by immunohistochemistry staining in a separate set of studies. Alanine aminotransferase (ALT) and total bilirubin (TBil) in serum were measured to assess the severity of liver injury. RESULTS: Histological changes were found in liver sections 12-24 h post MHV-3 infection in Balb/cJ mice. In association with changes in liver histology, marked elevations in serum ALT and TBil were observed. Mouse fgl2 (mfgl2) protein was detected in the endothelium of intrahepatic veins and hepatic sinusoids within the liver 24 h after MHV-3 infection. Liver tissues from the patients with severe AOC hepatitis B had classical pathological features of acute necroinflammation. Human fgl2 (hfgl2) was detected in 21 of 23 patients (91.30%) with severe AOC hepatitis B, while only 1 of 13 patients (7.69%) with mild chronic hepatitis B and cirrhosis had hfgl2 mRNA or protein expression. Twenty-eight of thirty patients (93.33%) with severe AOC hepatitis B and 1 of 10 with mild chronic hepatitis B had detectable hfgl2 expression in PBMC. No hfgl2 expression was found either in the liver tissue or in the PBMC from normal donors. There was a positive correlation between hfgl2 expression and the severity of the liver disease as indicated by the levels of TBil. PCA significantly increased in PBMC in patients with severe AOC hepatitis B. CONCLUSION: The molecular and cellular results reported here in both mice and patients with severe viral hepatitis suggest that virus-induced hfgl2 prothrombinase/fibroleukin expression and the coagulation activity associated with the encoded fgl2 protein play a pivotal role in initiating severe hepatitis. The measurement of hfgl2/fibroleukin expression in PBMC may serve as a useful marker to monitor the severity of AOC hepatitis B and a target for therapeutic intervention.     

Association between HLA class Ⅱ gene and susceptibility or resistance to chronic hepatitis B

AIM: To investigate the association between the polymorphism of HLA-DRB1, -DQA1 and -DQB1 alleles and viral hepatitis B. METHODS: HLA-DRB1, -DQA1 and -DQB1 alleles in 54 patients with chronic hepatitis B, 30 patients with acute hepatitis B and 106 normal control subjects were analyzed by using the polymerase chain reaction/sequence specific primer (PCR/SSP) technique. RESULTS: The allele frequency of HLA-DRB1*0301 in the chronic hepatitis B group was markedly higher than that in the normal control group (17.31% vs 5.67 %), there was a significant correlation between them (X^2= 12.3068,PC=0.0074, RR=4.15). The allele frequency of HLA-DQAI*0501 in the chronic hepatitis B group was significantly higher than that in the normal control group (25.96 % vs 13.68 %), there was a significant correlation between them (X^2=9.2002, PC=0.0157, RR=2.87). The allele frequency of HLA-DQBI*0301 in the chronic hepatitis B group was notably higher than that in the normal control group (35.58 % vs 18.87 %), there was a significant correlation between them (x^2=15.5938, PC=0.0075, RR=4.07). The allele frequency of HLA-DRB1*1101/1104 in the chronic hepatitis B group was obviously lower than that in the normal control group (0.96 % vs 13.33 %), there was a significant correlation between them (X^2=11.9206, PC=0.0145, RR=18.55). The allele frequency of HLA-DQAI*0301 in the chronic hepatitis B group was remarkably lower than that in the normal control group (14.42 % vs30 %), there was a significant correlation between them (X^2=8.7396, PC=0.0167, RR=0.35). CONCLUSION: HLA-DRBI*0301, HLA-DQAI*0501 and HLA-DQBI*0301 are closely related with susceptibility to chronic hepatitis B, and HLA-DRB1*1101/1104 and HLA-DQAI*0301 are closely related with resistance to chronic hepatitis B. These findings suggest that host HLA class Ⅱ gene is an important factor determining the outcome of HBV infection.     

白细胞介素-17肝内表达与慢性乙型肝炎病毒感染所致肝纤维化的相关性

Objective To explore the relationship between intrahepatic expression of interleukin-17 (IL-17) and liver fibrosis in patients with chronic hepatitis B virus infection. Methods IL-17 expressions in livers with different inflammation activity grades and hepatic fibrosis stages from patients with chronic hepatitis B virus carriers (n= 30), chronic hepatitis B (CHB, n = 55), liver cirrhosis (LC, n=20) were measured by immunohistochemistry. Serum IL-17 and liver fibrosis indices of haluronic acid (HA), laminin (LN), type Ⅲ procollagen (PC Ⅲ ) and type Ⅳ collagen ( Ⅳ C) were determined by enzyme linked immunosorbent assay (ELISA). The differences between groups were compared by Kruskal-Wallis test, and the Mann-Whitney test, and the correlation analysis was done by Spearman test. Results Intrahepatic IL-17 expression in LC group was significantly higher than CHB group (x2 =25. 3982, P=0. 004), and that in CHB group was higher than chronic hepatitis B virus carriers group (x2 = 11. 5056, P= 0. 001). The inflammation activity grade and hepatic fibrosis stage were both positively correlated with IL-17 expression (r= 0.718, 0. 693, respectively; both P＜0.01). IL-17 mainly located in portal area and the expression was positively correlated with serum levels of HA, LN, PCⅢ and ⅣC (r=0. 793, 0. 834, 0. 722, 0. 883, respectively; all P＜0.01).Conclusion Intrahepatic IL-17 expression is closely correlated with liver inflammation activity grade and hepatic fibrosis stage.     

Diagnostic value of Doppler assessment of the hepatic and portal vessels and ultrasound of the spleen in liver disease

OBJECTIVES: To investigate the clinical utility and the intra-observer and inter-observer variability of Doppler ultrasound assessment of the hepatic and portal vessels along with measurement of spleen size in the diagnosis of chronic liver disease and cirrhosis. METHODS AND MATERIALS: Ultrasound measurements of portal vein diameter (PVD), portal vein velocity (PVV), hepatic arterial resistance index (HARI), hepatic vein profile (HVP), and spleen size were obtained in 49 controls and 45 patients with liver disease (23 with primary biliary cirrhosis, 22 with hepatitis C) by two experienced observers, who each performed three blinded measurements of each variable. Control values were derived from normal hospital workers. Percutaneous liver biopsies in 41 of the patients showed cirrhosis (14 patients), moderate/severe fibrosis (13 patients), and early disease (14 patients). RESULTS: Seventy-one percent of cirrhotic patients had splenomegaly (> 13.6 cm). The spleen size was significantly larger in cirrhotics (16.0 cm) than in non-cirrhotics (13.0 cm, P < 0.009) and healthy controls (10.7 cm, P < 0.00005), and was the only independent predictor of cirrhosis, with a threshold of 15 cm predicting cirrhosis with a specificity of 98%, positive predictive value of 93%, sensitivity of 57% and negative predictive value of 80%. HVP was abnormal in 76.9% of cirrhotics, 57.7% of non-cirrhotics and 2.1% of controls (P < 0.04). However, the mean PVV, PVD and HARI were no different between controls and patients or between cirrhotic and non-cirrhotic liver disease. There was significant inter-observer variability for PVV, but intra-observer and inter-observer variability was acceptable for the other measurements. CONCLUSIONS: Splenomegaly size and abnormal HVP are useful predictors of chronic liver disease and cirrhosis, and both can be measured reliably and reproducibly. However, Doppler measurements of PVV, PVD and HARI are not useful in distinguishing patients with chronic liver disease from normal controls.     

Physical hemodynamic interaction between portal venous and hepatic arterial blood flow in humans.

OBJECTIVE: The hepatic arterial end-diastolic velocity (HAEDV) is normally equal to portal vein peak velocity (PVPV). However, there is no report of quantitative measurement that HAEDV was equal to PVPV. We investigated the interaction in PVPV and HAEDV in both chronic and acute hepatic hemodynamic changes. METHODS: One hundred and nineteen patients (54 with cirrhosis, 23 with chronic hepatitis, and 42 with no diffuse liver disorder) were enrolled. We investigated the differences in PVPV and HAEDV among the patients with and without liver disorder. In addition, we measured the intraindividual changes in HAEDV when PVPV was mechanically changed by percutaneous isolated hepatic perfusion in six patients and by percutaneous transhepatic portal embolization (PTPE) in six more. RESULTS: HAEDV was nearly equal to PVPV not only in patients with both normal and hepatitis but also in those with cirrhosis (PVPV-HAEDV = 3.0 +/- 5.2, 2.2 +/- 5.4, 2.3 +/- 6.5 cm/s, respectively). In the intraindividual study, both PVPV and HAEDV decreased during hepatic mechanical perfusion and HAEDV was equal to PVPV (8.2 +/- 2.8, 10.5 +/- 1.5 cm/s, respectively). After PTPE, PVPV was increased and hepatic arterial peak systolic velocity was reciprocally decreased. However, HAEDV was nearly equal to PVPV 7 days after PTPE (PVPV-HAEDV = 5.9 +/- 5.1 cm/s). CONCLUSIONS: Since arterial end-diastolic velocity depends on the downstream vascular resistance, lower HAEDV in patients with cirrhosis was considered to reflect a high outflow resistance. If there is no collateral pathway, we consider that HAEDV may actually reflect sinusoidal resistance to the same degree as PVPV.     

Simultaneous Doppler measurement of portal venous peak velocity,hepatic arterial peak velocity,and splenic arterial pulsatility index for assessment of hepatic circulation

BACKGROUND/AIMS: Quantitative Doppler assessment of hepatic circulation is widely performed in patients with cirrhosis. Since few studies have attempted to evaluate the various parameters simultaneously, we sought to examine the applicability and possible advantages of such simultaneous measurement for assessment of hepatic function. METHODOLOGY: In 64 patients (21 with cirrhosis, 17 with chronic hepatitis, and 26 with no liver disorder) we prospectively performed Doppler measurement of right portal venous peak velocity (PVPV), right hepatic arterial peak systolic velocity (HAPSV) and splenic arterial pulsatility index (SAPI) and calculated a novel parameter, the hepatic circulatory index (HCI). The HCI was calculated using the formula: HCI (cm2/s2) = PVPV (cm/s) x HAPSV (cm/s)/SAPI. RESULTS: Not every Doppler parameter was useful in itself for quantitative assessment of liver function. On the other hand, hepatic circulatory index was significantly higher in controls (1275.1 +/- 297.5) than in patients with hepatitis (931.7 +/- 270.5, P = 0.0003), or cirrhosis (586.4 +/- 264.9, P < 0.0001) and was highly correlated with the plasma clearance rate of indocyanine green (KICG; r = 0.848, P < 0.0001). CONCLUSIONS: Hepatic circulatory index was correlated with KICG, which reflects hepatic circulation. The hepatic circulatory index is a novel parameter of hepatic circulation that can be measured easily at bedside, accurately reflecting hepatic circulatory status.     

Measurement of Intrahepatic Pressure as an Index of Hepatic Sinusoidal Pressure

Intrahepatic pressure was measured in 148 patients with liver disease (32 outpatients, 116 inpatients) and 13 controls with almost normal liver histology (inpatients), with a 23-gauge needle (inner diameter 0.38 mm). Intrahepatic pressure was significantly elevated in the group order of chronic active hepatitis without bridging necrosis (n = 17, 9.2 +/- 3.0 mm Hg), chronic active hepatitis with bridging necrosis (n = 24, 12.3 +/- 5.7), and posthepatitic liver cirrhosis (n = 65, 18.8 +/- 4.2), compared with controls (n = 13, 6.8 +/- 2.7), whereas it was not elevated in the group of idiopathic portal hypertension (n = 9, 7.8 +/- 2.5 mm Hg), acute hepatitis (n = 10, 8.4 +/- 2.6 mm Hg), and chronic persistent hepatitis (n = 23, 7.9 +/- 2.7 mm Hg), compared with controls. As complications, four patients had abdominal discomfort continuing for more than a day; however, patients were allowed to walk after they had rested on their beds for 30 min. In 37 patients (27 with cirrhosis, seven idiopathic portal hypertension, and three others), portal vein and/or hepatic vein catheterization was performed during the same procedure of intrahepatic pressure measurement. Intrahepatic pressure showed significant correlations with corrected wedged hepatic vein pressure (r = 0.91), portohepatic gradient (r = 0.69), wedged hepatic vein pressure (r = 0.79), and portal vein pressure (r = 0.68). Slopes were 0.97, 0.83, 0.66, and 0.65, respectively. In conclusion, intrahepatic pressure reflects hepatic sinusoidal pressure (corrected wedged hepatic vein pressure), and intrahepatic pressure starts to elevate at the stage of chronic active hepatitis.     

Comparison between portal vein pressure and wedged hepatic vein pressure in hepatitis B-related cirrhosis

Portal vein pressure and wedged hepatic vein pressure were measured simultaneously in 21 patients with hepatitis B-related cirrhosis of the liver and were compared to pressure measured in six patients with idiopathic portal hypertension. No significant difference in the portal venous pressure gradient was found between patients with cirrhosis and those with idiopathic portal hypertension (17.3 +/- 4.3 mmHg (mean +/- S.D.) vs. 19.7 +/- 3.1 mmHg, P greater than 0.05). However, the difference between the portal and the hepatic venous pressure gradient was significantly smaller in patients with cirrhosis than in idiopathic portal hypertension patients (1.3 +/- 1.7 vs. 10.8 +/- 2.1 mmHg, P less than 0.001). An excellent correlation was found between portal vein pressure and wedged hepatic vein pressure in hepatitis B-related cirrhosis (r = 0.94, P less than 0.001). There was no linear relationship between the portal venous pressure gradient and varix size or bleeding episodes. We concluded that a close agreement existed between portal vein pressure and wedged hepatic vein pressure in hepatitis B-related liver cirrhosis. Therefore, measurement of wedged hepatic vein pressure reliably reflects portal vein pressure in these patients.     

乙肝肝硬化患者门静脉宽度与门静脉血栓形成的关系

背景门静脉血栓(portal vein thrombosis,PVT)的早期诊断仍是临床上一个难题,急需要发现可早期预测诊断的无创指标.目的探讨门静脉宽度与PVT形成之间的关系.方法收集418例乙肝肝硬化患者.根据是否发生PVT分为PVT组(n=66)和非PVT组(n=352)组.比较两组患者的一般资料差异,使用多因素Logistic回顾分析影响PVT发生的危险因素.通过受试者工作特征(receiver operating characteristic,ROC)曲线评估不同危险因素预测PVT的效能.结果与非PVT组患者相比,PVT组患者的Child-Pugh评分更高、Child-Pugh A级比例更低、血小板水平更高、D-二聚体水平更高、门静脉宽度更宽、门静脉血流更慢,上述差异均存在统计学意义(P<0.05).Logistic回归显示门静脉宽度(OR=3.941,P=0.001)、门静脉血流(OR=0.841,P=0.007)、血小板水平(OR=1.024,P=0.008)和D-二聚体水平(OR=2.383,P=0.000)是肝硬化患者发生PVT的独立危险因素.门静脉宽度诊断PVT的ROC曲线下面积最大为0.874,最佳诊断值为>12.5 mm,此时的预测敏感性和特异性分别为78%和82%.结论门静脉直径增加是肝硬化患者PVT发生的危险因素,对PVT诊断具有一定价值.     

恩替卡韦联合复方甘草酸苷治疗代偿期活动性乙型肝炎肝硬化患者的临床研究

目的观察ETv分散片联合复方甘草酸苷治疗代偿期活动性乙型肝炎肝硬化患者的临床疗效并探讨其作用机制,为进一步提高代偿期活动性乙型肝炎肝硬化临床疗效提供依据。方法将60例代偿期活动性乙型肝炎肝硬化患者随机分为研究组和对照组,对照组应用ETV分散片0．5mg／次,1次,d,晨起空腹口服。治疗组在对照组基础上联合复方甘草酸苷片75mg／次,37次／d,口服。两组患者疗程均为48周。比较两组患者治疗前后肝功能、血清肝纤维化指标、肝硬度指标、血清病毒学（HBVDNA、HBeAg及抗．HBe）指标,运用彩色多普勒超声检查比较肝脏、脾脏和门静脉内径变化。结果两组患者治疗48周肝功能指标（ALT、AST、ALB、TBil）、血清肝纤维化指标（HA、LN、PCIII、IV．C）和肝硬度指标比较差异均有显著统计学意义（P均=0．000）;两组患者治疗前后血清HBVDNA水平比较差异均有显著统计学意义（P均=O．000）,但组间比较差异均无统计学意义（P=0．490、0．630）。对照组治疗48周发生HBeAg低于检测下限的比率为30．8％、血清学转换率23．1％;治疗组治疗48周发生HBeAg低于检测下限的比率为50．0％、血清学转换率为35．7％。两组患者HBeAg低于检测下限的比率和血清学转换率比较,差异均有统计学意义（P=0．029、0．040）。两组患者治疗前后门静脉内径、脾脏长径、脾脏厚度、脾静脉宽度比较差异均无统计学意义（P=0．830、0．350、0．870、0．490）。结论ETv联合复方甘草酸苷对代偿期乙型肝炎肝硬化患者治疗有协同作用,其作用机制可能与抗-HBV、抗肝纤维化、改善肝功能、免疫调节等有关。     

超声波检查对肝脏纤维化分期的诊断价值

目的 了解超声波检查对早期肝硬化的诊断价值及其与肝纤维化程度的相关性。方法２６３例慢性乙型病毒性肝炎患者经皮肝脏穿刺活检术行病理组织学检查，同时行空腹肝脏Ｂ型超声波检查肝硬化声像、门静脉主干和脾静脉宽度及脾脏肿大，检查结果经 ｔ检验、ｘ２检验确定统计学意义。结果 ２６３例患者中 ６０例为早期肝硬化，超声波检查对早期肝硬化的诊断灵敏度 ５２．５％，特异度 ８８．３％，误诊率 １１．７０％，漏诊率 ４７．５％，约登指数 ０．５０８；肝纤维化Ｓ１、Ｓ２、Ｓ３、Ｓ４期的门静脉主干宽度分别为（１０．９３± １．２５）ｍｍ、（１１．３５±１．０６）ｍｍ、（１１．２９± １．５２）ｍｍ及（１１．４８±１．２５）ｍｍ，其中以与Ｓ１比较差异有显著意义（Ｐ＜０．０５）；脾静脉宽度分别（６．５１８±２．０３３）ｍｍ、（７．１９０±１．５６９）ｍｍ、（７．４４４±１．８０５）ｍｍ及（８．４０６±２．２２７）ｍｍ，其中 Ｓ４与 Ｓ２比较差异有显著意义（Ｐ＜０．０５）；脾脏肿大发生率随肝纤维化程度加重而增加。结论 超声波检查对早期肝硬化的诊断敏感度亟待提高，不足以作为早期肝硬化的常用诊断方法；门静脉主干、脾静脉宽度及脾脏肿大发生率与肝纤维化程度呈正     

CT血管三维重建鉴别布加综合征与乙型肝炎肝硬化价值分析*

目的 研究CT血管三维重建对鉴别布加综合征(BCS)与乙型肝炎肝硬化的临床价值。方法 2017年3月～2020年3月我院诊治的BCS患者28例,乙型肝炎肝硬化患者46例,接受CT血管三维重建检查,记录两组CT三维重建检查影像学特点。采用Logistic多因素回归分析探讨各征象对诊断BCS的价值,并建立回归方程。采用受试者工作特征曲线(ROC)分析回归方程诊断BCS的应用价值。结果 BCS组肝内静脉侧支开放发生率为82.1%,显著高于肝硬化组的15.2%(P<0.05),奇静脉与腰升静脉交通发生率为46.4%,显著高于肝硬化组的10.9%(P<0.05),下腔静脉和肝静脉充盈缺损为85.7%和92.9%,显著高于肝硬化组的10.9%和8.7%(P<0.05);腹膜后静脉丛曲张为35.7%,显著高于肝硬化组的10.9%(P<0.05),尾状叶增大为64.3%,显著高于肝硬化组的6.5%(P<0.05),地图状/雪花样强化为82.1%,显著高于肝硬化组的6.5%(P<0.05),门脉期不均匀强化为85.7%,显著高于肝硬化组的13.0%(P<0.05);Logistic多因素分析显示肝内静脉侧支开放(95%CI=1.035～3.332,P=0.038)、奇静脉与腰升静脉交通(95%CI=1.203～2.296,P=0.002)、下腔静脉充盈缺损(95%CI=1.694～4.893,P=0.000)、肝静脉充盈缺损(95%CI=1.695～3.156,P=0.000)、尾状叶增大(95%CI=1.012～1.901,P=0.042)和门脉期不均匀强化(95%CI=1.234～2.916,P=0.004)是诊断BCS的独立指标;ROC分析结果显示我们建立的回归方程诊断BCS的AUC为0.888(95%CI=0.812～0.965,P=0.000),显著高于其他各征象诊断。结论 CT血管三维重建检查有助于鉴别BCS与乙型肝炎肝硬化,综合CT三维重建征象建立预测模型有助于对BCS患者的早期筛查和诊断。