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| 1 | COVID-19 pandemic:Pathophysiology and manifestations from the gastrointestinal tract显示文摘The pandemic of coronavirus disease 2019(COVID-19),caused by a newly identifiedβ-coronavirus(SARS-CoV-2)has emerged as a dire health problem,causing a massive crisis for global health.Primary method of transmission was firstly thought to be animal to human transmission.However,it has been observed that the virus is transmitted from human to human via respiratory droplets.Interestingly,SARS-CoV-2 ribonucleic acid(RNA)has been isolated from patient stools,suggesting a possible gastrointestinal(GI)involvement.Most commonly reported clinical manifestations are fever,fatigue and dry cough.Interestingly,a small percentage of patients experience GI symptoms with the most common being anorexia,diarrhea,nausea and vomiting.The presence of viral RNA in stools is also common and fecal tests can be positive even after negative respiratory samples.The exact incidence of digestive symptoms is a matter of debate.The distribution of Angiotensin converting enzyme type 2 receptors in multiple organs in the body provides a possible explanation for the digestive symptoms’mechanism.Cases with solely GI symptoms have been reported in both adults and children.Viral RNA has also been detected in stool and blood samples,indicating the possibility of liver damage,which has been reported in COVID-19 patients.The presence of chronic liver disease appears to be a risk factor for severe complications and a poorer prognosis,however data from these cases is lacking.The aim of this review is firstly,to briefly update what is known about the origin and the transmission of SARS-CoV-2,but mainly to focus on the manifestations of the GI tract and their pathophysiological background,so that physicians on the one hand,not to underestimate or disregard digestive symptoms due to the small number of patients exhibiting exclusively this symptomatology and on the other,to have SARS-CoV-2 on their mind when the“gastroenteritis”type symptoms predominate. | Michail Galanopoulos Filippos Gkeros Aris Doukatas Grigorios Karianakis Christos Pontas Nikolaos Tsoukalas Nikos Viazis Christos Liatsos Gerassimos J Mantzaris | 2020 | World Journal of Gastroenterology2020，26，31： | 7 |
| 2 | Helicobacter pylori,gastric microbiota and gastric cancer relationship:Unrolling the tangle显示文摘Helicobacter pylori infection(Hp-I)represents a typical microbial agent intervening in the complex mechanisms of gastric homeostasis by disturbing the balance between the host gastric microbiota and mucosa-related factors,leading to inflammatory changes,dysbiosis and eventually gastric cancer.The normal gastric microbiota shows diversity,with Proteobacteria[Helicobacter pylori(H.pylori)belongs to this family],Firmicutes,Actinobacteria,Bacteroides and Fusobacteria being the most abundant phyla.Most studies indicate that H.pylori has inhibitory effects on the colonization of other bacteria,harboring a lower diversity of them in the stomach.When comparing the healthy with the diseased stomach,there is a change in the composition of the gastric microbiome with increasing abundance of H.pylori(where present)in the gastritis stage,while as the gastric carcinogenesis cascade progresses to gastric cancer,the oral and intestinal-type pathogenic microbial strains predominate.Hp-I creates a premalignant environment of atrophy and intestinal metaplasia and the subsequent alteration in gastric microbiota seems to play a crucial role in gastric tumorigenesis itself.Successful H.pylori eradication is suggested to restore gastric microbiota,at least in primary stages.It is more than clear that Hp-I,gastric microbiota and gastric cancer constitute a challenging tangle and the strong interaction between them makes it difficult to unroll.Future studies are considered of crucial importance to test the complex interaction on the modulation of the gastric microbiota by H.pylori as well as on the relationships between the gastric microbiota and gastric carcinogenesis. | Christos Liatsos Apostolis Papaefthymiou Nikolaos Kyriakos Michail Galanopoulos Michael Doulberis Marios Giakoumis Evangelia Petridou Christos Mavrogiannis Theodore Rokkas Jannis Kountouras | 2022 | World Journal of Gastrointestinal Oncology2022，14，5： | 6 |
| 3 | Evaluation of capsule endoscopy in active, mild-to-moderate, overt, obscure GI bleeding <ce:link locator='fx1'/>显示文摘 | Periklis Apostolopoulos Christos Liatsos Ian M. Gralnek Chrissostomos Kalantzis Eleftheria Giannakoulopoulou Georgios Alexandrakis Panagiotis Tsibouris Evagelos Kalafatis Nikolaos Kalantzis | 2007 | Gastrointestinal Endoscopy2007，，6： | 3 |
| 4 | Diagnosis of small-bowel ischemic necrosis by capsule endoscopy显示文摘 | Liatsos C Goulas S Karagiannis S | 2005 | Gastrointest Endosc2005，62，3： | 1 |
| 5 | Unusual onset of varicel- la zoster reactivation with meningoencephalitis, followed by rhabdomy- olysis and renal failure in a young, immunocompetent patient 显示文摘 | Pirounaki M Liatsos G Elefsiniotis I | 2007 | Scand J Infect Dis2007，39，1： | 1 |
| 6 | Relationship of Helicobacter pylori CagA status to gastric cell proliferation and apoptosis显示文摘 | Rokkas T Ladas S Liatsos C | 1999 | Dig Dis Sci1999，44，3： | 1 |
| 7 | Successful recanalization of portal vein thrombosis before liver transplantation using transjugular intrahepatie portosystemic shunt显示文摘 | Liatsos C Vlaehogiannakos J Patch D | 2001 | Liver Transpl2001，7，5： | 1 |
| 8 | Relationship of Helicobacter Pylori CagA status to gastric cell proliferation and apoptosis 显示文摘 | Rokkas T Ladas S Liatsos C | 1999 | Dig Dis Sci1999，44，3： | 1 |
| 9 | Relationship of Helicobacter pylori CagA status to gastric cell proliferation and apoptosis显示文摘 | Rokkas T Ladas S Liatsos C | 1999 | Dig Dis Sci1999，44，3： | 1 |
| 10 | The role of wireless capsule endoscopy in investigating unexplained iron deficiency anemia after negative endoscopic evaluation of the upper and lower gastrointestinal tract显示文摘 | P. Apostolopoulos C. Liatsos I. Gralnek E. Giannakoulopoulou G. Alexandrakis C. Kalantzis P. Gabriel N. Kalantzis | 2006 | Endoscopy2006，，11： | 1 |
| 11 | Safety of extension of a previous endoscopic sphincterotomy: a prospective study显示文摘 | Mawogiannis C Liatsos C Papanikolaou IS | 2003 | Am J Gastroenterol2003，98，1： | 1 |
| 12 | Relationship of helicobacter pylori CagA stutus to gastric cell proliferation and appoptosis显示文摘 | Rokkas T Ladas S Liatsos C | 1999 | Dig Dis Sci1999，44，3： | 1 |
| 13 | Effect of acute ethanol exposure on hepatic stimulator substance(HSS) levels during liver regeneration:protective function of HSS显示文摘 | Liatsos GD Mykoniatis MG Margeli A | 2003 | Dig Dis Sci2003，48，10： | 1 |
| 14 | Case report:mixed cholestatic/hepatocellular liver injury induced by the herbicide quizalofop-p-ethyl显示文摘 | Elefsiniotis I S Liatsos G D Stamelakis D | | 0，，： | 1 |
| 15 | Proliferating cell nuclear antigen (PCNA) immunostaining in helicobacter pylori infection: impact of eradication显示文摘 | Rokkas T Liatsos C Karameris A | 1999 | Pathol Oncol Res1999，5，4： | 1 |
| 16 | Capsule endoscopy image analysis using texture information from various colour models显示文摘 | Vasileios S. Charisis Leontios J. Hadjileontiadis Christos N. Liatsos Christos C. Mavrogiannis George D. Sergiadis | 2011 | Computer Methods and Programs in Biomedicine2011，，1： | 1 |
| 17 | Effect of acute ethanol exposure on hepatic stimulator substance (HSS) levels during liver regeneration (protective function of HSS) 显示文摘 | Liatsos G D Mykoniatis M G Margeli A | 2003 | Dig Dis Sci2003，48，10： | 1 |
| 18 | Unusual onset of varicella zoster reactivation with meningoencephalitis, followed by rhabdomyalysis and renal failure in a young,immunocompetent patient显示文摘 | Pirounaki M Liatsos G Elefsiniotis I | 2007 | Scand J Infect Dis2007，39，1： | 1 |
| 19 | Relationship of Helicobacter pylori CagA(+) status to gastric juice vitamin C levels 显示文摘 | Liatsos C Petridou E Papatheodorou G Karameris A Ladas SD Raptis SA | 1999 | Eur J Clin Invest1999，29，1： | 1 |
| 20 | Needle knife fistulotomy versus needle knife precut papillotomy for thetreatment of common bile duct stones显示文摘 | Mawogiannis C Liatsos C Romanos A | 1999 | Gastrointest Endosc1999，50，3： | 1 |
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