血吸虫病肝硬变伴症状性胆结石患者腹腔镜胆囊切除

目的 探讨血吸虫病肝硬化伴症状性胆结石患者腹腔镜胆囊切除(LC)的效果。方法 回顾性分析4年来我院血吸虫病性肝硬化伴胆囊结石行胆囊切除术265例的临床资料。行LC的74例，与常规开腹手术(OC)组进行对比，比较两组术中出血量、手术时间、住院时间、并发症、术后恢复情况等。结果 手术平均时间LC组为63min，OC组为53min；平均术后住院时间LC组为1．2d，OC组为8．9d；平均手术出血量LC组为15．6ml，OC组为85ml；LC组中转手术6例(8．1％)，无1例发生并发症；OC组术后胆漏1例。结论 血吸虫病性肝硬化胆结石患者只要严格掌握腹腔镜手术适应证，采取正确的手术操作方法，LC是安全可行的。     

槐耳清膏治疗肝癌的实验研究

目的　探讨槐耳清膏对人胎脐静脉内皮细胞的作用 ,以及其对裸鼠皮下接种肝癌细胞形成肝癌的抑制作用及其可能机制。方法　用不同浓度的槐耳清膏作用于人胎脐静脉血管内皮细胞 ,观察其对细胞的增殖能力、迁移能力、附壁能力及血管生成的影响 ,同时观察其对裸鼠皮下接种肝癌细胞形成肝癌过程的影响。结果　槐耳清膏≥ 2mg/ml时可显著降低肿瘤组织的血管内皮细胞增殖能力 ,减少血管形成 ,抑制血管内皮细胞的迁移、黏附 ,从而降低微血管密度。槐耳清膏 ( 3g/kg) MMC( 5 0 0 μg/kg)同时作用于裸鼠的肝癌组织 ,其抑瘤作用最强 ,后依次为MMC组 ,槐耳清膏 ( 3g/kg)组。结论　槐耳清膏对肝癌有抑制作用 ,其可能机制是作用于血管内皮细胞 ,影响血管内皮细胞的增殖能力、迁移能力、附壁能力及血管生成 ,从而抑制肝癌组织的血管生成 ,降低肝癌组织的微血管密度而发挥抑制肝癌生长的作用     

High Prevalence of Helicobacter pylori in Liver Cirrhosis (Relationship with Clinical and Endoscopic Features and the Risk of Peptic Ulcer)

In 153 consecutive patients with cirrhosis weassessed: (1) the prevalence of IgG to Helicobacterpylori and compared it with that found in 1010 blooddonors resident in the same area; and (2) therelationships of IgG to Helicobacter pylori with clinical andendoscopic features and with the risk of peptic ulcer.The IgG to Helicobacter pylori prevalence of cirrhoticswas significantly higher than in blood donors (76.5% vs 41.8%; P < 0.0005) and was notassociated with sex, cirrhosis etiology, Child class,gammaglobulins and hypertensive gastropathy. In bothgroups, the prevalence of IgG to Helicobacter pylori was significantly higher in subjects over 40. Amongpatients with cirrhosis a significantly higherprevalence of Helicobacter pylori was found in patientswith previous hospital admission (P = 0.02) and/or upper gastrointestinal endoscopy (P = 0.01) andpatients with peptic ulcer (P = 0.0004). Multivariateanalysis identified increasing age and male sex as riskfactors for a positive Helicobacter pylori serology and no independent risk factors for pepticulcer. The high prevalence of Helicobacterpylori-positive serology found in the present series isrelated to age and sex and might also be explained byprevious hospital admissions and/or uppergastrointestinal endoscopy. Our results do not confirmthe role of Helicobacter pylori as risk factor forpeptic ulcer in patients with liver cirrhosis.     

Assessment of Hepatic Functional Reserve in Cirrhotic Patients by Computed Tomography of the Caudate Lobe

In order to investigate whether the size of thecaudate lobe of the cirrhotic liver is related to thehepatic functional reserve, the morphometric analysis ofthe caudate lobe was preformed retrospectively using computed tomography in 106 consecutivepatients of whom 67 had compensated (group 1), and 39uncompensated (group 2) liver cirrhosis. In 51 patients,hepatic measurements were repeated in follow-up. Age- and gender-matched controls were studied.The size of the caudate lobe and the ratio of thecaudate to right lobe were correlated with liverfunction. The caudate lobe was larger in the studypatients than in the controls, and larger in group 1than in group 2 (P < 0.01). The caudate to right loberatios were also greater in the study patientsespecially in group 1 (P < 0.01). In follow-up, the regression coefficient for the caudate to rightlobe ratio was positive in group 1 and negative in group2 (P < 0.05). Even though the caudate lobe ofpatients with uncompensated liver cirrhosis was larger than that of the controls, patients withcompensated liver cirrhosis had a larger caudate lobeand higher caudate to right lobe ratio compared to thepatients with uncompensated liver cirrhosis. The caudate lobe may have played an importantrole in maintaining proper liver function in thesepatients.     

Beer Affects Oxidative Stress due to Ethanol in Rats

The relationship between chronic moderate beerconsumption and oxidative stress was studied in rats.Animals were fed three different isocaloric diets forsix weeks: a beercontaining diet (30% w/w), an ethanol-supplemented diet (1.1 g/100 g, thesame as in the beer diet) and an alcohol-free basaldiet. At the end of the feeding period, rats wereanalyzed for plasma and liver oxidative status. Somelivers were isolated and exposed toischemiareperfusion to assess the additional oxidativestress determined by reperfusion. No significantdifferences in plasma antioxidant status were foundamong the three dietary groups. Lipoproteins from the beer group,however, showed a greater propensity to resist lipidperoxidation. Ischemia caused a decrease in liver energyand antioxidant status in all groups. Nevertheless, ATP was lower in the livers of rats exposed tothe ethanol diet. During reperfusion, lipoperoxidationincreased significantly in all groups. However, liversobtained from ethanoltreated rats showed the higher formation of lipoperoxides. Inconclusion, a moderate consumption of beer in awell-balanced diet did not appear to cause oxidativestress in rats; moreover, probably through its minorcomponents, beer could attenuate the oxidative action ofethanol by itself.     

Expansion Conditions for Early Hepatic Progenitor Cells from Embryonal and Neonatal Rat Livers

Long-term primary cultures were established fromfetal or neonatal livers by using cell suspensionsdepleted of red blood cells and by culturing the cellsin hormonally defined medium containing dimethyl sulfoxide. Two distinct populations of hepaticprogenitor cells were evident in the cultures, based onmorphology, proliferative ability, and liver-specificgene expression. Most colonies consisted of immature hepatic progenitors: small, blastlike cells,weakly expressing alpha-fetoprotein, albumin, and-glutamyltranspeptidase, and showing evidence ofproliferation as measured by bromodeoxyuridineincorporation. At the perimeter of these colonies of immaturecells and forming some colonies by themselves were moremature hepatic progenitor cells: larger cells, withincreased cytoplasmic to nuclear ratios, little proliferation, and strongly expressing albumin,alpha-fetoprotein, and -glutamyltranspeptidase.The latter two proteins were localized to the bilecanalicular membranes of these cells. Glycogen deposits were present in the mature cells from day 14embryos after eight days of culture. Thus, DMSOtreatment of hepatic parenchymal progenitors provides anovel system for studies of liver development.     

Liver Involvement in Obese Children (Ultrasonography and Liver Enzyme Levels at Diagnosis and During Follow-up in an Italian Population)

Our aim was to evaluate incidence and riskfactors of liver involvement in obese Italian childrenas assessed by both ultrasonographic and biochemicalparameters. In seventy-five consecutive obese children (age 9.5 ± 2.9 years, males/females41/34), serum levels of enzymes and ultrasonography ofthe liver were evaluated. Tests were repeated one,three, and six months after starting a moderatehypocaloric diet and an exercise program. Three obese childrenwho were found to have chronic viral hepatitis wereexcluded from the study. Thirty-eight of 72 (53%) obesechildren had an ultrasonographic image of bright liver consistent with liver steatosis. Thelatter was severe in nine children, moderate in 16, andmild in 13. Eighteen obese children (25%) had elevatedtransaminase levels. Bright liver andhypertransaminasemia were not due to any of the most common causesof liver disease. Both were rapidly responsive to lossof weight, confirming that liver involvement wassecondary to obesity and that steatosis orsteatohepatitis rather than fibrosis were involved. Obesityduration not more than three years (odds ratio = 4.77),a higher degree of obesity (odds ratio = 2.09), andhypertransaminasemia (odds ratio = 2.15) appeared asimportant predictive factors of liver involvement atultrasonography. Incidence of liver involvement assessedby means of ultrasonography is significantly higher thanthat revealed by measurement of serum liver enzymes. A short duration of obesity emerged as apotentially new risk factor of liver involvement in thepediatric obese population and needs to be confirmed infuture studies.     

Hepatitis G Virus Infection Among Liver Graft Recipients: Anatomoclinical Correlations

Hepatitis G virus (HGV) causes persistent infection in man, but its disease association is controversial. We studied the HGV disease association in 25 liver transplantation (LT) recipients without evidence of hepatitis B and C infection. HGV RNA was tested by semiquantitative RT-PCR in serial serum samples and its presence was correlated with the biochemical and histological evidence of liver damage. The overall prevalence of HGV infection in this population was 9/25 (36%), one patient being HGV RNA positive since before LT, while the other eight apparently acquired de novo infections after LT. In five cases, appearance of HGV was followed by biochemical and histological evidence of liver damage: the liver biopsy showed acute rejection in two cases, acute cholangitis in two, and acute hepatitis in one. At the end of follow-up, histological evidence of chronic hepatitis was found in one HGV-positive patient but also in three HGV-negative patients, whereas the only patient with acute hepatitis at the time HGV RNA was first detected in serum developed an intralobular gigantocellular granuloma. In conclusion, HGV infection after LT may be seldom associated with acute and chronic liver damage, but comparable histological features can be observed also among HGV-negative controls.     

Sclerostin Expression in Bile Ducts of Patients With Chronic Cholestasis May Influence the Bone Disease in Primary Biliary Cirrhosis

Sclerostin is involved in the regulation of osteoblastogenesis and little is known about its role in the development of bone disease in primary biliary cirrhosis (PBC), characterized by low bone formation. Therefore, we have assessed the circulating levels and the liver expression of sclerostin in this cholestatic disease. Serum sclerostin levels were measured in 79 women with PBC (mean age 60.6 ± 1.2 years) and in 80 control women. Lumbar and femoral bone mineral density (BMD), as well as parameters of mineral metabolism and bone remodeling, were measured. Moreover, sclerostin gene (SOST) expression in the liver was assessed by real‐time PCR in samples of liver tissue taken by biopsy in 11 PBC patients and in 5 normal liver specimens. Presence and distribution of sclerostin was evaluated in liver slices from 11 patients by immunohistochemistry. The severity of histologic lesions was assessed semiquantitatively in the same liver samples. PBC patients had higher sclerostin levels than controls (75.6 ± 3.9 versus 31.7 ± 1.6 pmol/L, p < 0.001). Serum sclerostin correlated inversely with markers of bone formation and resorption. Sclerostin mRNA in the liver was overexpressed compared with control samples (2.7‐fold versus healthy liver). Sclerostin was detected by immunohistochemistry in 7 of the 11 liver samples, mainly located in the bile ducts. Liver sclerostin was associated with the severity of cholangitis (p = 0.02) and indirectly with the degree of lobular inflammation (p = 0.03). Sclerostin mRNA expression was higher in samples that tested positive by immunohistochemistry and particularly in those with lobular granuloma (p = 0.02). The increased expression of sclerostin in the liver and the association with histologic cholangitis may explain the high serum levels of this protein in patients with PBC, thus suggesting that sclerostin may influence the decreased bone formation in this cholestatic disease. © 2016 American Society for Bone and Mineral Research.