AIM The hepatic content of collagens (type I, Ⅲ and Ⅶ) and laminin (LN) in rat model of experimentalliver fibrosis was observed to find out their roles in the pathogenesis of liver fibrosis.METHODS The experimental rat model was established by immunological injury induced by injectinghuman albumin. Histopathological and immunohistochemical methods were used to measure the hepaticcontent of collagens and laminin in the fibrotic rat livers.RESULTS The hepatic contents of collagens (type I, Ⅲ, Ⅶ) and LN in the fibrotic rat livers weresignificantly increased as compared with those in the control group, and they were found to be mainlylocalized in the portal space, central veins and fibrous septa. Electron microscopic study showed that pro-collagens were present around the “activated” hepatic stellate cells (HSC) and the hepatocytes atrophied.CONCLUSION Pathological deposition of collagens (type Ⅰ, Ⅲ and Ⅶ ) and laminin was the fundamentallesion of liver fibrosis. HSC may be the major cellular source of collagens (type Ⅰ, Ⅲ and Ⅶ) and laminin inthe liver tissue.

AIM To observe the regulating effect of decoction shugan bushen (SGBS) on testosterone (Te) andadrenocortiotropin (ACTH).METHODS Fifty wistar male rats divided into four groups randomly, that is, normal group, hepaticfibrosis group, and two Chinese herb medicine treatment groups. The model of toxic hepatic fibrosis wasinduced by 0.5% dimethylnitrosamine (DMN). The decoction SGBS is composed of such herbs as bupleurumRoot. Dodder Seed, curcuma rood indianmulberry etc. According to the different doses of the drugs, ratsare divided into two groups in the treatment groups. The Chinese herb medicine treatment begins in a weekafter the second celiac injection of DMN, lastiong 8 weeks. The rats of normal group and hepatic fibrosisgroup are fed with distilled water once a day. After 11 weeks of Chinese herb medicine treatment, the Teand ACTH were tested insera of rats, and the livers were dissected for the pathology examination.RESULTS The results of pathology examination in rat livers of each group show that the hepatocytes of thenormal group have normal array, no degeneration and fibrosis. Those in the pathology group have obviousdegenerative necrosis and hepatic fibrosis, and in some cases show the evidence of cirrosis. The results intreatment groups are essentially similar to those of normal group. Variance analysis of least significantdifference (LSD) method is employed to compare the hormone level between groups. The serum levels of Teand ACTH in the normal group are 75.30±45.25 ng/dl and 141.02±68.70 ng/L. The levels in hepaticfibrosis group are obviously lower than those of normal group, as 19.77±16.92 ng/dl and 92.85±27.24ng/L, respectivite and with statistically different (P < 0.01 ). But that levels in the two treatment groups arerespectively 63.29±26.09 ng/dl 135.48±36.89 ng/L and 59.77±4.64 ng/dl, 130.8±17.35 ng/L, whichare obviously higher than those of pathology group and approximale to those of normal group (P>0.05).Two different doses make no obvious difference between the treatment groups (P>0.05).CONCLUSION SGBS can correct the hormone disturbance and shows the effect of anti-hepatic fibrosis.

AIM To assess the relationship between HBV X-gene, X-gene product and Fas/ FasL which mediatehepatocellular apoptosis in patients with hepatocellular carcinoma.METHODS Tissue from 34 patients with hepatocellular carcinoma was tested for the expression of HBxAg.Quantitative ELISA assay was used to detect sFas; and sFasL and PCR were used to detect the HBV X-genein sera from 30 patients with hepatocellular carcinoma, 32 patients with liver cirrhosis and 20 normalcontrols.RESULTS The positive expression of HBxAg, Fas and FasL in carcinoma tissue was 97.06%, 85.29% and100%, respectively. The positive signal was mainly presented in the plasma, and all of these three positivestaining may appear in the same area. Redit analysis showed that there was no significant difference amongthese three positive staining (P >0.05). The mean levels of sFas in sera from hepatocellular carcinoma, livercirrhosis and normal controls were 722.97±321.12, 801.90±419.94 and 224.07±148.23, respectively,showing that sFas levels in patients with hepatocellular carcinoma and liver cirrhosis were significantlyelevated than that in normal controls (P < 0.0l). The mean levels of sFasL in sera from hepatocellularcarcinoma, liver cirrhosis and normal controls were 152.27±7.99, 162.97±12.40 and 154.99 ± 6.96,showing that sFasL level in patients with liver cirrhosis was significantly higher than that in patients withhepatocellular carcinoma and normal controls (P< 0.01). HBV X-gene was found to be positive in sera of30% patients with hepatocellular carcinoma; HBV X-gene was found to be positive in sera of 43.75% ofpatients with liver cirrhosis. There was no significant difference in sFas/sFasL level between HBV X-genepositive patients and HBV X-gene negative patients (P >0.05).CONCLUSION The expression of HBxAg and Fas/FasL in the tissue of hepatocellular carcinoma seemed tobe almost the same, but relation between cause and effect is unclear. The detection of sFas and sFasL inpatient sera may reflect the state of apoptosis mediated by Fas/FasL system. Our data showed that HBV X-gene expression in sera seemed to have no relation to sFas/sFasL level; however, these data also suggestedthat some patients with negative HBsAg in sera might have integrated HBV X-gene in liver tissues, andtherefore X-gene is detectable in those patient sera.

AIM To study the relationship between nitric oxide (NO), nitric oxide synthase (NOS) and humanhepatocellular carcinoma (HCC).METHODS Plsama NO2-/NO3- was measured by Griess reaction in 122 patients with chronic hepatitis(CH) and compensated liver cirrhosis (LC), among which 62 patients were complicated with HCC(CH = 28, LC = 34), and the rest 60 patients were not (CH = 29, LC = 31). Thirty healthy persons served asnormal controls (NC). There were no prominent differences among the groups in sex, age and the ratio ofCH to LC. The expression of inducible nitric oxide synthase (iNOS) in HCC (n = 40), CH (n = 30) and LC(n = 30) samples obtained from liver biopsy or operation was compared with that in normal liver tissues byusing immunohistochemistry. Ten normal liver tissue samples obtained from liver operation served as normalcontrols. The samples were fixed in formalin and embeded in paraffin. Anti-iNOS antibody (Santacruzcompany) was served as antibody-Ⅰ in immunohistochemical assay of iNOS in tissue.RESULTS Plasma NO2-/NO3- level in normal was 11.5 μmol/L±4.2μmol/L. The plasma level ofNO2 /NO3- in CH (58.6±17.4 μmol/L) and LC (38.7±10.6μmol/L) accompanied with HCC wasnotably higher than in those patients without HCC (CH: 24.8±9.4 μmol/L; LC: 22.3±8.7μmol/L,t=2.901, 2.756, P<0.01). Plasma NO2-/NO3- level in HCC accompanied with CH was significantlyhigher than in those accompanied with LC ( t = 2.216, P<0.05). Positive rate of iNOS in HCC, CH and LCwas 95%, 93% and 57% respectively. iNOS was not expressed in normal liver tissues. The expression level ofiNOS in HCC (χ2=17.4, P<0.001) and CH (χ2=11.64, P<0.025) was much higher than in LC.CONCLUSION Plasma NO2 / NO3- level significantly increased in patients with HCC and theimmunohistochemical staining of iNOS was positive. This suggests that the liver secrets NO in the higherlevel may participate in the carcinogenesis and progression of HCC.

AIM To investigate the expression of endothelial NO synthase (eNOS), inducible NO synthase (iNOS)protein and eNOS mRNA gene in the splanchnic organs of liver cirrhosis and portal hypertensive rats.METHODS In control and CCl4-induced liver cirrhotic rats, the expression of eNOS and iNOS proteins wasdetected by immunohistochemical method, and eNOS mRNA was detected by in situ hybridization.RESULTS The expression of eNOS protein and eNOS mRNA increased in most organs of the cirrhotic rats,including bronchial and alveolar epithelial cells, renal tubular epithelial cells and mesenchyma, endothelialand adventitial cells of aorta and superior mesenteric artery, whereas no significant increase of iNOS proteinwas found. In the hepatic tissue, NOS protein and eNOS mRNA were present in mesenchymal cells and vesseladventitial cells, no difference was observed in the expression between control and cirrhotic rats.CONCLUSION The expression of NOS varied in region. In splanchnic organs and vasculars there was anincreased expression of eNOS which induced aplanchnic vasodilation and increased the inflow of portal vein,while in the liver tissue and blood vessel showed no increased expression, which may be associated withincreased intrahepatic vascular resistance.

AIM To study the changes of IL-6,IL-2, sIL-2R and TNF ir patients with hepatocellular carcinoma(HCC)and their clinical significance.METHODS IL-6, IL-2, sIL-2R and TNF were detected by avidin-biotin-system ELISA, double-sandwichELISA respectively in 60 patients with HCC and 36 patients with liver cirrhosis (LC) and 66 healthy persons.RESULTS The levels of IL-6, sIL-2R and TNF increased, but IL-2 level was lower in patients with HCCthan that in normal controls (NC) (t test, t=8.21, 4.71, 3.87, 2.13, P<0.01 or 0.05). IL-6 level in HCCwas 10 fold higher than NC, and also much higher than LC. IL-6 level was higher in later stage than that inearlier stage. There was a positive correlation between IL-6 and sIL-2R, TNF, while no positive correlationwas found between IL-2 and IL-6, sIL-2R in HCC.CONCLUSION The remarkably higher level of IL-6 is helpful for the early diagnosis of HCC.

AIM To probe into the effect of abnormal protection on coronary artery disease (CAD) in patients withliver cirrhosis (LC).METHODS Fifty-two cases of LC associated with diabetes mellitus (DM) and 63 cases of simple DM werecompared prospectively. Blood biochemistry, blood viscosity and ECG were examined carefully every threemonths, and the three-year morbidities CAD in both groups were monitored dynamically.RESULTS There were significant decreases in blood biochemistry and viscosity in LC group as comparedwith those in control (P<0.05 or 0.01), and there was a more significant decrease in ST-T abnormality ratein LC group than in the simple DM group (P<0.05). As a result, the three-year morbidity of CAD in LCgroup was 64% lower than in the control 1group.CONCLUSION There is truly an abnormal protection against CAD in patients with LC.

Hepatocellular carcinoma (HCC) is one of the most common malignancies in China. To date, surgery is still the best solution to it. However, metastatic recurrences after curative hepatic resections are very common. Tang et al have reported that recurrence rate within 5 years of curative hepatic resection is 61.5% [1]. As curative hepatic resection has a high tendency for metastatic recurrence, therapeutic interventions such as transarterial embolization and antiangiogenesis have been tried to further improve prognosis of HCC patients. Therefore, establishing a dependable, sensitive, easy, and economical method to predict metastatic recurrence following curative hepatic resection is of clinical urgency.

肝硬化肝性脑病诊疗指南

The Chinese Society of Hepatology developed the current guidelines on the management of hepatic encephalopathy (HE) in cirrhosis based on the published evidences and panelists'' consensus. The guidelines provided recommendations for the diagnosis and management of hepatic encephalopathy including minimal hepatic encephalopathy (MHE) and overt hepatic encephalopathy (OHE) emphasizing the importance on screening MHE in patients with end-stage liver diseases. The guidelines emphasized that early identification and prompt treatment are essential to improve the prognosis of HE. The principles of treatment mainly consist of eliminating precipitating factors, treating hyperammonemia to improve acute neuropsychiatric abnormalities rapidly, primary and secondary prophylaxis.

外周血单个核细胞移植相比粒细胞集落刺激因子单纯动员治疗乙型肝炎相关性失代偿肝硬化的临床对照研究

近年研究发现,干细胞生物治疗可促进肝脏再生,因此备受关注.在动物体内,骨髓来源的干细胞可参与损伤肝脏的恢复,促进肝细胞的再生.

Objective To investigate the differences of clinical and biochemical characteristics between patients with liver cirrhosis induced by HBV infection combined with and without mild alcohol intake. Methods Data of patients with liver cirrhosis who were hospitalized in the First Hospital Afifliated to Xinjiang Medical University were retrospectively analyzed. Patients were divided into three groups: patients with liver cirrhosis induced by HBV infection and combined with mild alcohol intake, patients with HBV-related cirrhosis, and patients with alcohol-related cirrhosis. Biochemical detections including liver function, fasting lipid proifles, lipoprotein, kidney function, glucose, uric acid and regular blood tests were carried out and results were compared among three groups. Data were analyzed through STATA software and co-variant analysis. Results Total of 2 350 patients with liver cirrhosis were included, 732 patients had cirrhosis induced by HBV infection combined with mild alcohol intake, 1 316 patients had HBV-related liver cirrhosis, 302 patients had alcohol-related cirrhosis. The highest mean level of white cell count, mean corpuscular volume,γ-glutamyltranspeptidase and uric acid were observed in HBV infection combined with mild alcohol intake group. Multivariate regression analysis revealed that HBV infection, excessive alcohol intake, male and age were risk factors for hepatocellular carcinoma (HCC) in patients with liver cirrhosis. Conclusions HBV infection combined with mild alcoholic-related liver cirrhosis group showed the highest oxidative stress compared with alcoholic liver cirrhosis group, which suggested that mild alcohol intake may increase the incidence of liver cirrhosis in HBV infected patients and may not increase the incidence of HCC.

肝硬化肝移植术后贫血的病因及防治

贫血是肝移植术后常见的并发症之一,解放军第四五八医院2004年3月至2005年11月共完成的26例肝移植,受体为肝炎后肝硬化14例,14例中10例术后早期出现贫血,5例术后1个月后复诊时仍存在贫血.

循证医学时代对门静脉高压症外科治疗的思考

人类在同疾病的斗争中,对于任何一种疾病的认识都要经历从不了解到了解,从知之不多到知之较多,进而有了全面深入的认识.伴随着对疾病认识的不断深入,其治疗方法也都会经历从束手无策到探索多种治疗方法,进而确立一种疗效肯定的治疗方法.

肝硬化门静脉高压症高血流动力学的发生机制与治疗

肝硬化门静脉高压症(PHT)的发病机制至今尚未完全明了.1900年Preble在研究肝硬化合并上消化道出血死亡的病人中发现,80%以上出血为食管静脉曲张破裂所致,推论有门静脉回流障碍所致的侧支循环形成.1928年,McIndoe研究发现肝硬化时肝内门静脉分支减少,受再生结节压迫变细.

重视酒精性肝病的诊断与治疗

酒精性肝硬化（alcoholic liver cirrhosis, ALC）已经成为我国终末期肝病的第二大病因，但过量饮酒所造成的酒精性肝病（alcoholic liver disease, ALD）并未得到广泛关注。在发展为ALC之前，及时限酒或戒酒，配合适当的抗炎保肝治疗，ALD是可以恢复的。

Objective To investigate early changes in systemic and splanchnic hemodynamics after orthotopic liver transplantation (OLT) in normal and cirrhotic rats.Methods Male Sprague-Dawley rats were divided into 4 groups:normal controls (NL,n=10),intrahepatic portal hypertension (IHPH, n=10) induced by injection of CCl4, normal rats with OLT (NL-OLT,n=9) and IHPH rats with OLT (IHPH-OLT,n=16). IHPH-OLT rots were divided into 2 subgroups: 3 days (Group A,n=9) and 7 days (Group B, n=7) after OLT. OLT was pedormed in rats using cuffs for the anastomosis of the suprahepatic inferior vena cava,infrahepatic vena cava and portal vein. Two weeks after production of IHPH rots, 7 days after NL-OLT rats, 3 days and 7 days after IHPH-OLT rats, radicective microspheres were used in a hemodynamic study.Results There were no significant differences in hemodynamic changes between NL-OLT and NL rets,except mean arterial blood pressure (MAP).The characteristies of systemic and splanchnic hyperdynamic circulatory slate,including increased cardiac output and splanchnic blood flow, decreased mean acterial blood pressure, total peripheral vascular resistance and splanchnic vascular resistance were ibserved in IHPH, IHPH-OLT A, and IHPH-OLT B rats,The magnitude of hyperhemodynamics was in the order of IHPH＞IHPH-OLT A＞IHPH-OLT B rats.Moreover, the derangement of splanchnic hyperhemodynamice was more significant than that of systemic hyperhemodynamics.Conclusioos The present study demonstrates that the persistence of early systemic and splanchnic hyperkinetic circulation after OLT may be the consequence of factors which maintain hyperhemodynamics in liver cirrhosis, where portal hypertension is not completely eliminated. Hyperhemodynamics is not induced by OLT per se.

Objective To study whether liver cirrhosis associated with Helicopacter pylori (H. pylori)infection will induce increased serum ammonia and whether the peripheral serum ammonia reflects the level of portal vein serum ammonia.Methods Blood was taken from the portal vein and the cubital vein in cirrhotic patients with and without H.pylori infection and non-cirrhotic patients (splenic rupiure) with and without H. pylori infection, and the serum ammonia was measured.Results The mean levels of serum ammonia in the group of cirrhotic patients with H. pylori infection were 167.82±8.97 μmol/L (pertal vein) and 142.2±13.35 μmol/L (cubital vein). They were increased significantly as compared with cirrhotic patients without H.pyiori infection(47.68±12.03 μmol/L portal vein and 37.23±7.04 μmol/L cubital vein),and also compared with the groups of splenic rupture patients with and without H. pylori infection (P＜0.0t).There was no significant difference between the serum ammonia level of the cubital vein and pertal vein(P＞0.05).Conclusions H.pylori intection can induce an increase in serum ammonia in patients with liver dysfunction,and the peripheral serum ammonia measurement may replace the portal vein serum ammania as a monitoring method. Eradication of H.pylori in cirrhotic patients may prevent hepatic encephalopathy(HE).

肝硬化急性肾损伤及肝肾综合征的诊治路径

?肝肾综合征（HRS）是指在未发生肾脏病变的严重肝病患者中发生的肾功能衰竭［1］。HRS是一种功能性而非器质性的肾功能失调，一般认为其肾脏的组织学检查结果正常；但2012年美国肝脏病学会（AASLD）成人肝硬化腹水诊疗指南指出，HRS存在一定的组织学损伤，即球管反流［2］。为了使严重肝病患者发生肾损伤时能够得到及时的救治，2015年?国际腹水俱乐部（ICA）制定了肝硬化急性肾损伤（AKI）诊断与管理共识［3］，简称ICA-AKI。现整理出ICA-AKI和AASLD成人肝硬化腹水诊疗指南中HRS的临床诊治路径，并结合国内外进展进行综述。

非酒精性脂肪性肝病发病机制的研究进展

非酒精性脂肪性肝病(nonalcoholic fattyliver disease,NAFLD)是遗传-环境-代谢应激相关因素所致的以肝细胞脂肪变性为主的临床病理综合征,包括单纯性脂肪肝(nonalcoholic fatty liver,NAFL)、脂肪性肝炎(nonalcohlic steatohepatitis,NASH)、脂肪性肝硬化(fatty liver cirrhosis,FLC)三种类型,是仅次于病毒性肝炎的第二位常见肝病,是二十一世纪肝病领域面临的新挑战.

影响肝硬化患者健康教育效果的因素分析及对策

肝硬化是一种或多种病因长期或反复作用于肝脏而造成的进行性弥散性肝损害.临床上以肝功能损害和门静脉高压为主要表现,晚期常出现消化道出血、肝性脑病、腹水、继发性感染等严重并发症.