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| 1 | Role of Kupffer cells in the pathogenesis of liver disease显示文摘Kupffer cells, the resident liver macrophages have long been considered as mostly scavenger cells responsible for removing particulate material from the portal circu- lation. However, evidence derived mostly from animal models, indicates that Kupffer cells may be implicated in the pathogenesis of various liver diseases including viral hepatitis, steatohepatitis, alcoholic liver disease, in- trahepatic cholostasis, activation or rejection of the liver during liver transplantation and liver fibrosis. There is accumulating evidence, reviewed in this paper, suggest- ing that Kupffer cells may act both as effector cells in the destruction of hepatocytes by producing harmful soluble mediators as well as antigen presenting cells during viral infections of the liver. Moreover they may represent a significant source of chemoattractant molecules for cy- totoxic CD8 and regulatory T cells. Their role in fibrosis is well established as they are one of the main sources of TGFβ1 production, which leads to the transformation of stellate cells into myofibroblasts. Whether all these variable functions in the liver are mediated by different Kupffer cell subpopulations remains to be evaluated. In this review we propose a model that demonstrates the role of Kupffer cells in the pathogenesis of liver disease. | George Kolios Vassilis Valatas Elias Kouroumalis | 2006 | World Journal of Gastroenterology2006，12，46： | 74 |
| 2 | Patients with primary biliary cirrhosis have increased serum total antioxidant capacity measured with the crocin bleaching assay显示文摘AIM: The balance between oxidants and antioxidants can play an important role in the initiation and development of liver diseases. Recently, we have described a new automated method for the determination of total antioxidant capacity (TAC) in human serum and plasma.METHODS: We measured TAC and corrected TAC (CTAC -abstraction of interactions due to endogenous uric acid,bilirubin and albumin) in 52 patients with chronic liver diseases (41 patients with primary biliary cirrhosis (PBC),10 patients with chronic hepatitis C and 13 patients with viral HCV cirrhosis) as well as in 10 healthy controls. In 23 PBC patients measurement were also done 6 mo after treatment with ursodeoxycholic acid (UDCA). The TAC assay was based on a modification of the crocin bleaching assay. The results were correlated with routine laboratory measurements and the histological stage of PBC.RESULTS: There were no significant differences in TAC between the various groups. However, CTAC was considerably increased in the PBC group compared to controls and cirrhotics. Analysis of these patients according to disease stages showed that this increase was an early phenomenon observed only in stages Ⅰ and Ⅱ compared to controls, cirrhotics and patients with chronic hepatitis C).After 6 mo of treatment with UDCA, levels of CTAC decreased to those similar to that of controls.CONCLUSION: Patients in the early stages of PBC present with high levels of corrected total antioxidant capacity and this maybe related to the pathophysiology of the disease. UDCA treatment restores the levels of CTAC to control levels. | George Notas Niki Miliaraki Marilena Kampa Fillipos Dimoulios Erminia Matrella Adam Hatzidakis Elias Castanas Elias Kouroumalis | 2005 | World Journal of Gastroenterology2005，11，27： | 13 |
| 3 | Peri-nuclear antibodies correlate with survival in Greek primary biliary cirrhosis patients显示文摘AIM:To investigate possible associations of anti-nuclear envelope antibody(ANEA)with disease severity and survival in Greek primary biliary cirrhosis(PBC)patients.METHODS:Serum samples were collected at diagnosis from 147 PBC patients(85%female),who were followed-up for a median 89.5 mo(range 1-240).ANEA were detected with indirect immunofluorescence on 1% formaldehyde fixed Hep2 cells,and anti-gp210 antibodies were detected using an enzyme linked immunosorbent assay.Findings were correlated with clinical data,histology,and survival.RESULTS:ANEA were detected in 69/147(46.9%) patients and 31/147(21%)were also anti-gp210 positive.The ANEA positive patients were at a more advanced histological stage(Ⅰ-Ⅱ/Ⅲ-Ⅳ56.5%/43.5% vs 74.4%/25.6%,P=0.005)compared to the ANEA negative ones.They had a higher antimitochondrial antibodies(AMA)titer(≤1:160/>1:160 50.7%/49.3%vs 71.8%/28.2%,P=0.001)and a lower survival time(91.7 ±50.7 mo vs 101.8±55 mo,P=0.043).Moreover,they had more advanced fibrosis,portal inflammation,interface hepatitis,and proliferation of bile ductules(P =0.008,P=0.008,P=0.019,and P=0.027,respectively).They also died more frequently of hepatic failure and/or hepatocellular carcinoma(P=0.016).ANEA positive,anti-gp210 positive patients had a difference in stage(Ⅰ-Ⅱ/Ⅲ-Ⅳ54.8%/45.2%vs 74.4%/25.6%,P= 0.006),AMA titer(≤1:160/>1:160 51.6%/48.4%vs 71.8%/28.2%,P=0.009),survival(91.1±52.9 mo vs 101.8±55 mo,P=0.009),and Mayo risk score(5.5 ±1.9 vs 5.04±1.3,P=0.04)compared to the ANEA negative patients.ANEA positive,anti-gp210 negative patients had a difference in AMA titer(≤1:160/>1:160 50%/50%vs 71.8%/28.2%,P=0.002),stage(Ⅰ-Ⅱ/Ⅲ -Ⅳ57.9%/42.1%vs 74.4%/25.6%,P=0.033),fibrosis(P=0.009),portal inflammation(P=0.018),interface hepatitis(P=0.032),and proliferation of bile ductules(P=0.031).Anti-gp210 positive patients had a worse Mayo risk score(5.5±1.9 vs 4.9±1.7,P=0.038)than the anti-gp210 negative ones.CONCLUSION:The presence of ANEA and anti-gp210 identifies a subgroup of PBC patients with advanced disease severity and poor prognosis. | Ourania Sfakianaki Meri Koulentaki Maria Tzardi Elena Tsangaridou Panayotis A Theodoropoulos Elias Castanas Elias A Kouroumalis | 2010 | World Journal of Gastroenterology2010，16，39： | 11 |
| 4 | Pathogenesis of primary biliary cirrhosis: A unifying model显示文摘主要胆汁性肝硬变(PBC ) 是导致小肝内胆汁管并且最后的进步破坏到肝肝硬化和失败的未知病原学的疾病。它被女优势和浆液自身抗体描述到指向 2-oxoacid 脱氢酶建筑群的 E2 部件的 mitochondrial 抗原。尽管他们与疾病致病被联系,没有具体证据到目前为止被介绍了。流行病学的数据显示盒子和可能的环境因素的一个地理聚类在致病被含有。很多个基因因素在决定疾病危险性或前进起一个作用,尽管没有权威的结论到目前为止被得出了。到有免疫力的致病的一个关键因素被认为是有免疫力的忍耐的故障,通过分子的模仿或通过所谓的决定因素,密度当模特儿。在这评论,关于主要胆汁性肝硬变的致病的可得到的数据被描述并且讨论。一个新统一假设基于在主要胆汁性肝硬变(PBC ) 的早 endothelin 生产过剩被介绍并且讨论。 | Elias Kouroumalis George Notas | 2006 | World Journal of Gastroenterology2006，12，15： | 10 |
| 5 | Autophagy in liver diseases显示文摘Autophagy is the liver cell energy recycling system regulating a variety of homeostatic mechanisms.Damaged organelles,lipids and proteins are degraded in the lysosomes and their elements are re-used by the cell.Investigations on autophagy have led to the award of two Nobel Prizes and a health of important reports.In this review we describe the fundamental functions of autophagy in the liver including new data on the regulation of autophagy.Moreover we emphasize the fact that autophagy acts like a two edge sword in many occasions with the most prominent paradigm being its involvement in the initiation and progress of hepatocellular carcinoma.We also focused to the implication of autophagy and its specialized forms of lipophagy and mitophagy in the pathogenesis of various liver diseases.We analyzed autophagy not only in well studied diseases,like alcoholic and nonalcoholic fatty liver and liver fibrosis but also in viral hepatitis,biliary diseases,autoimmune hepatitis and rare diseases including inherited metabolic diseases and also acetaminophene hepatotoxicity.We also stressed the different consequences that activation or impairment of autophagy may have in hepatocytes as opposed to Kupffer cells,sinusoidal endothelial cells or hepatic stellate cells.Finally,we analyzed the limited clinical data compared to the extensive experimental evidence and the possible future therapeutic interventions based on autophagy manipulation. | Elias Kouroumalis Argryro Voumvouraki Aikaterini Augoustaki Dimitrios N Samonakis | 2021 | World Journal of Hepatology2021，13，1： | 7 |
| 6 | Systemic treatment for hepatocellular carcinoma:Still unmet expectations显示文摘Many patients with hepatocellular carcinoma(HCC) are diagnosed in an advanced stage, so they cannot be offered the option of curative treatments. The results of systemic chemotherapy are unsatisfactory and this has led to molecular targeted approaches.HCC develops in chronically damaged tissue due to cirrhosis in most patients. Several different cell types and molecules constitute a unique microenvironment in the liver, which has significant implications in tumor development and invasion. This, together with genome instability, contributes to a significant heterogeneity which is further enhanced by the molecular differences of the underlying causes. New classifications based on genetic characteristics of the tissue microenvironment have been proposed and key carcinogenic signaling pathways have been described. Tumor and adjacent tissue profiling seem biologically promising, but have not yet been translated into clinical settings. The encouraging first results with molecular- genetic signatures should be validated and clinically applicable. A more personalized approach to modern management of HCC is urgently needed. | Dimitrios N Samonakis Elias A Kouroumalis | 2017 | World Journal of Hepatology2017，9，2： | 6 |
| 7 | Octreotide induces caspase activation and apoptosis in human hepatoma HepG2 cells显示文摘AIM: To investigate the role of octreotide on cellular proliferation and apoptosis of human hepatoma (HepG2) cells. METHODS: We studied cellular proliferation, apoptosis and the possible internal caspase-mediated apoptosis pathway involved, after treatment of HepG2 carcinoma cells with octreotide in comparison with the apoptosis caused by tumor necrosis factor-α (TNF-α). Activities of caspase-3, caspase-9, caspase-8 and caspase-2 were studied, while apoptosis was investigated through detection of DNA fragmentation and through identification of apoptotic cells with the annexin-V/propidium iodide flow cytometric method. RESULTS: After an initial increase in HepG2 cellular proliferation, a significant inhibition was observed with 10-8 mol/L octreotide, while TNF-α dose-dependently decreased proliferation. Early and late apoptosis was significantly increased with both substances. Octreotide significantly increased caspase-3, caspase-8 and caspase-2 activity. TNF-α signifi cantly increased only caspase-2. Cellular proliferation was decreased after treatment with octreotide or TNF-α alone but, in contrast to TNF-α, octreotide decreased proliferation only at concentrations of 10-8 mol/L, while lower concentrations increased proliferation. CONCLUSION: Our findings are suggestive of caspasemediated signaling pathways of octreotide antitumor activity in HepG2 cells, and indicate that measurements of serum octreotide levels may be important, at least in clinical trials, to verify optimal therapeutic drug concentrations. | Nikos J Tsagarakis Ioannis Drygiannakis Antonis G Batistakis George Kolios Elias A Kouroumalis | 2011 | World Journal of Gastroenterology2011，17，3： | 5 |
| 8 | Increased ΤGF-β3 in primary biliary cirrhosis: An abnormality related to pathogenesis?显示文摘AIM: To investigate the transforming growth factor-β (TGF-β) isoforms in the peripheral and hepatic venous blood of primary biliary cirrhosis (PBC) patients. METHODS: We examined TGF-β1, TGF-β2 and TGF-β3 (enzyme-linked immunosorbent assay), in 27 stage Ⅳ PBC patients (27 peripheral and 15 hepatic vein sera), 35 early (Ⅰ-Ⅱ) PBC and 60 healthy controls. As disease controls 28 hepatitis C virus (HCV) cirrhosis (28 peripheral and 17 hepatic vein serum), 44 chronic HCV hepatitis and 38 HCV-related hepatocellular carcinomas were included. We also tested liver tissue by immunohistochemistry to identify localization of TGF isoforms. RESULTS: TGF-β1 was significantly decreased in all cirrhotics (PBC Ⅲ-Ⅳ: median 13.4 ng/mL; range, 7.4-26.2, HCV cirrhosis: 11.6 ng/mL; range, 5.0-33.8), compared to controls (30.9 ng/mL; range, 20.9-37.8). TGF-β2 was increased in viral cirrhosis but not in PBC and chronic hepatitis. TGF-β3 (47.2 pg/mL; range, 27.0-79.7 in healthy controls) was increased in early and late PBC (Ⅰ-Ⅱ: 94.3 pg/mL; range, 41.5-358.6; Ⅲ-Ⅳ: 152.8 pg/mL; range, 60.4-361.2; P < 0.001) and decreased in viral cirrhosis (37.4 pg/mL; range, 13.3-84.0; P < 0.05). Hepatic vein TGF-β levels were analogous to those in peripheral blood. Immunohistochemistry identified all isoforms in portal tract lymphocytes, sinusoidal cells and cholangiocytes. TGF-β3 was additionally overexpressed in hepatocytes in PBC patients. CONCLUSION: The serum profile of TGF-β isoforms is different in cirrhotics. Increased TGF-β3 is characteristic of PBC. These findings may be related to the immunological abnormalities of PBC. | Argyro Voumvouraki Mairi Koulentaki Maria Tzardi Ourania Sfakianaki Penelope Manousou George Notas Elias Kouroumalis | 2010 | World Journal of Gastroenterology2010，16，40： | 4 |
| 9 | Clinical outcomes of compensated and decompensated cirrhosis: A long term study显示文摘AIM: To study these characteristics and prognostic patterns in a Greek patient population.METHODS: We analyzed a large cohort of cirrhotic patients referred to the department of Gastroenterology and Hepatology and the outpatient clinics of this tertiary hospital, between 1991 and 2008. We included patients with established cirrhosis, either compensated or decompensated, and further decompensation episodes were registered. A data base was maintained and updated prospectively throughout the study period.We analyzed differences in cirrhosis aetiology, time to and mode of decompensation, hepatocellular carcinoma(HCC) occurrence and ultimately patient survival.RESULTS: Five hundreds and twenty-two patients with median age 67(range, 29-91) years and average follow up 9 years-10 mo(range, 1-206 mo) were studied. Commonest aetiology was hepatitis C virus(HCV, 41%) followed by alcohol(31%). The median survival time in compensated cirrhotics was 115 mo(95%CI: 95-133), whereas in decompensated patients was 55 mo(95%CI: 36-75). HCV patients survived longer while HBV patients had over twice the risk of death of HCV patients. The median time to decompensation was 65 mo(95%CI: 51-79), with alcoholics having the highest risk(RR = 2.1 vs HCV patients). Hepatitis B virus(HBV) patients had the highest risk of HCC, alcoholics the lowest. Leading causes of death: liver failure, hepatorenal syndrome, sepsis and HCC progression. CONCLUSION: Cirrhosis aetiology and decompensation at presentation were predictors of survival. Alcoholics had the highest decompensation risk, HBV cirrhotics the highest risk of HCC and HCV cirrhotics the highest decompensation-free time. | Dimitrios N Samonakis Mairi Koulentaki Constantina Coucoutsi Aikaterini Augoustaki Chryssavgi Baritaki Emmanuel Digenakis Nikolaos Papiamonis Maria Fragaki Erminia Matrella Elias A Kouroumalis Maria Tzardi | 2014 | World Journal of Hepatology2014，6，7： | 4 |
| 10 | Is there a role for Tc-99m (V) DMSA scintigraphy in ischemic colitis?显示文摘AIM: To evaluate the role of pentavalent Tc-99m dimercaptosuccinic acid [Tc-99m (V) DMSA] in the diagnosis of ischemic colitis. METHODS: Fourteen patients with endoscopically and histologically confirmed ischemic colitis were included in the study. Tc-99m (V) DMSA scintigraphy was performed within 2 d after colonoscopy. Images were considered positive when an area of increased activity was observed in the region of interest and negative when no abnormal tracer uptake was detected. RESULTS: In 3 out of the 14 patients, Tc-99m (V) DMSA images showed moderate activity in the bowel. The scintigraphic results corresponded with the endoscopic findings. In the other 11 patients, no abnormal tracer uptake was detected in the abdomen. CONCLUSION: Besides the limited number of patients, Tc-99m (V) DMSA could not be considered as a useful imaging modality for the evaluation of ischemic colitis. | Maria I Stathaki Ioannis E Koutroubakis Sophia I Koukouraki Elias A Kouroumalis Nikolaos S Karkavitsas | 2008 | World Journal of Gastroenterology2008，14，35： | 4 |
| 11 | Octreotide modulates the effects on fibrosis of TNF-α, TGF-β and PDGF in activated rat hepatic stellate cells显示文摘 | Stefanos Klironomos George Notas Ourania Sfakianaki Foteini Kiagiadaki Costas Xidakis Elias Kouroumalis | 2014 | Regulatory Peptides2014，，： | 2 |
| 12 | Increased serum levels of YKL-40 in patients with inflammatory bowel disease显示文摘 | Ioannis E. Koutroubakis Efthymia Petinaki Philippos Dimoulios Emmanouel Vardas Maria Roussomoustakaki Antonios N. Maniatis Elias A. Kouroumalis | 2003 | International Journal of Colorectal Disease2003，，3： | 2 |
| 13 | Iron as a therapeutic target in chronic liver disease显示文摘It was clearly realized more than 50 years ago that iron deposition in the liver may be a critical factor in the development and progression of liver disease.The recent clarification of ferroptosis as a specific form of regulated hepatocyte death different from apoptosis and the description of ferritinophagy as a specific variation of autophagy prompted detailed investigations on the association of iron and the liver.In this review,we will present a brief discussion of iron absorption and handling by the liver with emphasis on the role of liver macrophages and the significance of the iron regulators hepcidin,transferrin,and ferritin in iron homeostasis.The regulation of ferroptosis by endogenous and exogenous modulators will be examined.Furthermore,the involvement of iron and ferroptosis in various liver diseases including alcoholic and non-alcoholic liver disease,chronic hepatitis B and C,liver fibrosis,and hepatocellular carcinoma(HCC)will be analyzed.Finally,experimental and clinical results following interventions to reduce iron deposition and the promising manipulation of ferroptosis will be presented.Most liver diseases will be benefited by ferroptosis inhibition using exogenous inhibitors with the notable exception of HCC,where induction of ferroptosis is the desired effect.Current evidence mostly stems from in vitro and in vivo experimental studies and the need for well-designed future clinical trials is warranted. | Elias Kouroumalis Ioannis Tsomidis Argyro Voumvouraki | 2023 | World Journal of Gastroenterology2023，29，4： | 2 |
| 14 | Presence of disease specific autoantibodies against liver sinusoidal cells in primary biliary cirrhosis显示文摘AIM: To investigate the presence of autoantibodies directed against liver sinusoidal cells in primary biliary cirrhosis(PBC).METHODS: Liver biopsies from 21 PBC patients were studied and compared with 12 liver biopsies from disease controls [3 patients with hepatitis B(HBV) virus,3 patients with hepatitis C virus(HCV), 3 patients with non-alcoholic steatohepatitis and 3 patients with acute alcoholic hepatitis(AAH)]. As healthy controls, we used tissue specimens adjacent to metastatic liver adenocarcinoma. Normal serum was taken from staff members of the unit. The determination of the cell type targetedby autoantibodies present in the patients sera was performed by indirect immunofluorescence(IIF) analysis using paraffin-embedded liver sections as a substrate.Sera from homologous or heterologous PBC patients or sera from the disease control group were used as primary antibodies. The presence of autoantibodies was identified using confocal microscopy.RESULTS: In total, 18/21(85.7%) PBC patients exhibited positive staining in the sinusoidal cells, 10/21(47.6%) in lymphocytes, 8/21(38%) in cholangiocytes and 7/21(33.3%) in hepatocytes, when homologous serum and fluorescein isothiocyanate-conjugated immunoglobulin type G(IgG) secondary antibody were used. PBC sections incubated with heterologous PBC serum showed reduced staining(20% for sinusoidal cells, 20% for lymphocytes, 20% for cholangiocytes and 13.3% for hepatocytes). When IgM immunoglobulin, instead of IgG, was used as secondary antibody,positive staining was observed in 75% of lymphocytes,62.5% of cholangiocytes, 37.5% of hepatocytes and50% of the sinusoidal cells with a much stronger staining intensity. No staining was observed when either normal or PBC sera were used as a primary antibody on liver sections from the disease control group. When PBC sera were incubated with healthy control sections,weak positive staining of cholangiocytes was observed in 3/21(14.3%) PBC serum samples. Steatohepatitis serum on PBC sections gave a positive staining of some hepatocytes and lymphocytes but no staining on viral hepatitis sections. Incubation with HBV sera stained some hepatocytes, cholangiocytes and intra-sinusoidal or portal lymphocytes of PBC, HBV and AAH patients but not HCV patients.CONCLUSION: In this study, for the first time in diseased liver tissue, we have demonstrated that a large proportion of PBC patients have disease specific autoantibodies against liver sinusoidal cells. | Ourania Sfakianaki Maria Tzardi Argyro Voumvouraki Aikaterini Afgoustaki Meri Koulentaki Elias Kouroumalis | 2013 | World Journal of Hepatology2013，5，10： | 2 |
| 15 | Mean platelet volume: a useful marker of inflammatory bowel disease activity显示文摘 | Andreas N Kapsoritakis Michael I Koukourakis Aekaterini Sfiridaki Spiros P Potamianos Maria G Kosmadaki Ioannis E Koutroubakis Elias A Kouroumalis | 2001 | The American Journal of Gastroenterology2001，，3： | 2 |
| 16 | Ileal Malignant Melanoma Causing Intussusception: Report of a Case显示文摘 | Konstantinos Karmiris Maria Roussomoustakaki Maria Tzardi John Romanos John Grammatikakis Manolis Papadakis Maria Polychronaki Elias A. Kouroumalis | 2007 | Surgery Today2007，，6： | 2 |
| 17 | Somatostatin for acute severe bleeding from portal hypertensive gastropathy显示文摘 | Kouroumalis EA Koutroubakis IE Manousos ON | 1998 | Eur J Gastroenterol Hepatol1998，10，： | 1 |
| 18 | Geoepidemiology and space–time analysis of Primary biliary cirrhosis in Crete, Greece显示文摘 | M Koulentaki A Mantaka D Sifaki‐Pistolla E Thalassinos N Tzanakis E Kouroumalis | 2014 | Liver Int2014，，7： | 1 |
| 19 | Treatment of hepatocellular carcinoma with octreotide: a radomised controlled study显示文摘 | Kouroumalis E Skoridilis P Thermos K | 1998 | CUT1998，42，3： | 1 |
| 20 | Octreotide for cancer of the liver and biliary tree显示文摘 | Kouroumalis EA | 2001 | Chemotherapy2001，47，2： | 1 |
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