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| 1 | Nonalcoholic fatty liver disease: Evolving paradigms显示文摘In the last years new evidence has accumulated on nonalcoholic fatty liver disease(NAFLD)challenging the paradigms that had been holding the scene over the previous 30 years.NAFLD has such an epidemic prevalence as to make it impossible to screen general population looking for NAFLD cases.Conversely,focusing on those cohorts of individuals exposed to the highest risk of NAFLD could be a more rational approach.NAFLD,which can be diagnosed with either non-invasive strategies or through liver biopsy,is a pathogenically complex and clinically heterogeneous disease.The existence of metabolic as opposed to genetic-associated disease,notably including'lean NAFLD'has recently been recognized.Moreover,NAFLD is a systemic condition,featuring metabolic,cardiovascular and(hepatic/extrahepatic)cancer risk.Among the clinico-laboratory features of NAFLD we discuss hyperuricemia,insulin resistance,atherosclerosis,gallstones,psoriasis and selected endocrine derangements.NAFLD is a precursor of type 2 diabetes(T2D)and metabolic syndrome and progressive liver disease develops in T2D patients in whom the course of disease is worsened by NAFLD.Finally,lifestyle changes and drug treatment options to be implemented in the individual patient are also critically discussed.In conclusion,this review emphasizes the new concepts on clinical and pathogenic heterogeneity of NAFLD,a systemic disorder with a multifactorial pathogenesis and protean clinical manifestations.It is highly prevalent in certain cohorts of individuals who are thus potentially amenable to selective screening strategies,intensive follow-up schedules for early identification of liver-related and extrahepatic complications and in whom earlier and more aggressive treatment schedules should be carried out whenever possible. | Amedeo Lonardo Fabio Nascimbeni Mauro Maurantonio Alessandra Marrazzo Luca Rinaldi Luigi Elio Adinolfi | 2017 | World Journal of Gastroenterology2017，23，36： | 33 |
| 2 | Hepatitis B virus burden in developing countries显示文摘Hepatitis B virus(HBV) infection has shown an intermediate or high endemicity level in low-income countries over the last five decades. In recent years, however, the incidence of acute hepatitis B and the prevalence of hepatitis B surface antigen chronic carriers have decreased in several countries because of the HBV universal vaccination programs started in the nineties. Some countries, however, are still unable to implement these programs, particularly in their hyperendemic rural areas. The diffusion of HBV infection is still wide in several low-income countries where the prevention, management and treatment of HBV infection are a heavy burden for the governments and healthcare authorities. Of note, the information on the HBV epidemiology is scanty in numerous eastern European and Latin-American countries. The studies on molecular epidemiology performed in some countries provide an important contribution for a more comprehensive knowledge of HBV epidemiology, and phylogenetic studies provide information on the impact of recent and older migratory flows. | Rosa Zampino Adriana Boemio Caterina Sagnelli Loredana Alessio Luigi Elio Adinolfi Evangelista Sagnelli Nicola Coppola | 2015 | World Journal of Gastroenterology2015，21，42： | 25 |
| 3 | Pathogenesis and significance of hepatitis C virus steatosis:An update on survival strategy of a successful pathogen显示文摘Hepatitis C virus(HCV)is a successful pathogen on the grounds that it exploits its host’s metabolism to build up viral particles;moreover it favours its own survival by inducing chronic disease and the development of specific anatomic changes in the infected organ.Steatosis,therefore,is associated with HCV infection by necessity rather than by chance alone.Approximately6%of HCV patients have steatohepatitis.Interestingly,HCV steatosis occurs in the setting of multiple metabolic abnormalities(hyperuricemia,reversible hypocholesterolemia,insulin resistance,arterial hypertension and expansion of visceral adipose tissue)collectively referred to as'hepatitis C-associated dysmetabolic syndrome'(HCADS).General,nonalcoholic fatty liver disease(NAFLD)-like,mechanisms of steatogenesis(including increased availability of lipogenic substrates and de novo lipogenesis;decreased oxidation of fatty substrates and export of fatty substrates)are shared by all HCV genotypes.However,genotype 3 seemingly amplifies such steatogenic molecular mechanisms reported to occur in NAFLD via more profound changes in microsomal triglyceride transfer protein;peroxisome proliferator-activated receptor alpha;sterol regulatory element-binding proteins and phosphatase and tensin homologue.HCV steatosis has a remarkable clinical impact in as much as it is an acknowledged risk factor for accelerated fibrogenesis;for impaired treatment response to interferon and ribavirin;and development of hepatocellular carcinoma.Recent data,moreover,suggest that HCV-steatosis contributes to premature atherogenesis via both direct and indirect mechanisms.In conclusion,HCV steatosis fulfills all expected requirements necessary to perpetuate the HCV life cycle.A better understanding of the physiology of HCADS will likely result in a more successful handling of disease with improved antiviral success rates. | Amedeo Lonardo Luigi Elio Adinolfi Luciano Restivo Stefano Ballestri Dante Romagnoli Enrica Baldelli Fabio Nascimbeni Paola Loriaca | 2014 | World Journal of Gastroenterology2014，20，23： | 14 |
| 4 | Chronic HCV infection and inflammation:Clinical impact on hepatic and extra-hepatic manifestations显示文摘The liver has a central role in regulating inflammation by its capacity to secrete a number of proteins that control both local and systemic inflammatory responses. Chronic inflammation or an exaggerated inflammatory response can produce detrimental effects on target organs. Chronic hepatitis C virus(HCV) infection causes liver inflammation by complex and not yet well-understood molecular pathways, including direct viral effects and indirect mechanisms involving cytokine pathways,oxidative stress and steatosis induction. An increasing body of evidence recognizes the inflammatory response in chronic hepatitis C as pathogenically linked to the development of both liver-limited injury(fibrosis, cirrhosis and hepatocellular carcinoma) and extrahepatic HCV-related diseases(lymphoproliferative disease,atherosclerosis, cardiovascular and brain disease). Defining the complex mechanisms of HCV-induced inflammation could be crucial to determine the global impact of infection, to estimate progression of the disease, and to explore novel therapeutic approaches to avert HCVrelated diseases. This review focuses on HCV-related clinical conditions as a result of chronic liver and systemic inflammatory states. | Rosa Zampino Aldo Marrone Luciano Restivo Barbara Guerrera Ausilia Sellitto Luca Rinaldi Ciro Romano Luigi E Adinolfi | 2013 | World Journal of Hepatology2013，5，10： | 13 |
| 5 | Chronic hepatitis C virus infection and neurological and psychiatric disorders:An overview显示文摘Hepatitis C virus(HCV)infection is considered a systemic disease because of involvement of other organs and tissues concomitantly with liver disease.Among the extrahepatic manifestations,neuropsychiatric disorders have been reported in up to 50%of chronic HCV infected patients.Both the central and peripheral nervous system may be involved with a wide variety of clinical manifestations.Main HCV-associated neurological conditions include cerebrovascular events,encephalopathy,myelitis,encephalomyelitis,and cognitive impairment,whereas'brain fog',depression,anxiety,and fatigue are at the top of the list of psychiatric disorders.Moreover,HCV infection is known to cause both motor and sensory peripheral neuropathy in the context of mixed cryoglobulinemia,and has also been recently recognized as an independent risk factor for stroke.These extrahepatic manifestations are independent of severity of the underlying chronic liver disease and hepatic encephalopathy.The brain is a suitable site for HCV replication,where the virus may directly exert neurotoxicity;other mechanisms proposed to explain the pathogenesis of neuropsychiatric disorders in chronic HCV infection include derangement of metabolic pathways of infected cells,alterations in neurotransmitter circuits,autoimmune disorders,and cerebral or systemic inflammation.A pathogenic role for HCV is also suggested by improvement of neurological and psychiatric symptoms in patients achieving a sustained virologic response following interferon treatment;however,further ad hoc trials are needed to fully assess the impact of HCV infection and specific antiviral treatments on associated neuropsychiatric disorders. | Luigi Elio Adinolfi Riccardo Nevola Giacomo Lus Luciano Restivo Barbara Guerrera Ciro Romano Rosa Zampino Luca Rinaldi Ausilia Sellitto Mauro Giordano Aldo Marrone | 2015 | World Journal of Gastroenterology2015，21，8： | 6 |
| 6 | Chronic hepatitis C virus infection and atherosclerosis: Clinical impact and mechanisms显示文摘Hepatitis C virus(HCV)infection represents a major health issue worldwide due to its burden of chronic liver disease and extrahepatic manifestations including cardiovascular diseases,which are associated with excess mortality.Analysis of published studies supports the view that HCV infection should be considered a risk factor for the development of carotid atherosclerosis,heart failure and stroke.In contrast,findings from studies addressing coronary artery disease and HCV have yielded conflicting results.Therefore,meta-analytic reviews and prospective studies are warranted.The pathogenic mechanisms connecting HCV infection,chronic liver disease,and atherogenesis are not completely understood.However,it has been hypothesized that HCV may promote atherogenesis and its complications through several direct and indirect biological mechanisms involving HCV colonization and replication within arterial walls,liver steatosis and fibrosis,enhanced and imbalanced secretion of inflammatory cytokines,oxidative stress,endotoxemia,mixed cryoglobulinemia,perturbed cellular and humoral immunity,hyperhomocysteinemia,hypo-adiponectinaemia,insulin resistance,type 2 diabetes and other components of the metabolic syndrome.Understanding these complex mechanisms is of fundamental importance for the development of novel therapeutic approaches to prevent and to treat vascular complications in patients with chronic HCV infection.Currently,it seems that HCV clearance by interferon and ribavirin treatment significantly reduces non-liver-related mortality;moreover,interferon-based treatment appears to decrease the risk of ischemic stroke. | Luigi E Adinolfi Rosa Zampino Luciano Restivo Amedeo Lonardo Barbara Guerrera Aldo Marrone Fabio Nascimbeni Anna Florio Paola Loria | 2014 | World Journal of Gastroenterology2014，20，13： | 6 |
| 7 | Predictors of early and late hepatocellular carcinoma recurrence显示文摘Hepatocellular carcinoma(HCC)is the most frequent liver neoplasm,and its incidence rates are constantly increasing.Despite the availability of potentially curative treatments(liver transplantation,surgical resection,thermal ablation),long-term outcomes are affected by a high recurrence rate(up to 70%of cases 5 years after treatment).HCC recurrence within 2 years of treatment is defined as“early”and is generally caused by the occult intrahepatic spread of the primary neoplasm and related to the tumor burden.A recurrence that occurs after 2 years of treatment is defined as“late”and is related to de novo HCC,independent of the primary neoplasm.Early HCC recurrence has a significantly poorer prognosis and outcome than late recurrence.Different pathogenesis corresponds to different predictors of the risk of early or late recurrence.An adequate knowledge of predictive factors and recurrence risk stratification guides the therapeutic strategy and post-treatment surveillance.Patients at high risk of HCC recurrence should be referred to treatments with the lowest recurrence rate and when standardized to combined or adjuvant therapy regimens.This review aimed to expose the recurrence predictors and examine the differences between predictors of early and late recurrence. | Riccardo Nevola Rachele Ruocco Livio Criscuolo Angela Villani Maria Alfano Domenico Beccia Simona Imbriani Ernesto Claar Domenico Cozzolino Ferdinando Carlo Sasso Aldo Marrone Luigi Elio Adinolfi Luca Rinaldi | 2023 | World Journal of Gastroenterology2023，29，8： | 6 |
| 8 | P2X receptors: New players in cancer pain显示文摘Pain is unfortunately a quite common symptom for cancer patients. Normally pain starts as an episodic experience at early cancer phases to become chronic in later stages. In order to improve the quality of life of oncological patients, anti-cancer treatments are often accompanied by analgesic therapies. The P2 X receptor are adenosine triphosphate(ATP) gated ion channels expressed by several cells including neurons, cancer and immune cells. Purinergic signaling through P2 X receptors recently emerged as possible common pathway for cancer onset/growth and pain sensitivity. Indeed, tumor microenvironment is rich in extracellular ATP, which has a role in both tumor development and pain sensation. The study of the different mechanisms by which P2 X receptors favor cancer progression and relative pain, represents an interesting challenge to design integrated therapeutic strategies for oncological patients. This review summarizes recent findings linking P2 X receptors and ATP to cancer growth, progression and related pain. Special attention has been paid to the role of P2X2, P2X3, P2X4 and P2X7 in the genesisof cancer pain and to the function of P2X7 in tumor growth and metastasis. Therapeutic implications of the administration of different P2 X receptor blockers to alleviate cancer-associated pain sensations contemporarily reducing tumor progression are also discussed. | Alessia Franceschini Elena Adinolfi | 2014 | World Journal of Biological Chemistry2014，5，4： | 5 |
| 9 | Clinical features and natural history of cryptogenic cirrhosis compared to hepatitis C virus-related cirrhosis显示文摘AIM To characterize natural history of cryptogenic cirrhosis(CC) and compare its clinical features and outcomes to those of hepatitis C virus(HCV)-related cirrhosis.METHODS A prospective cohort of 102 consecutive patients at their first diagnosis of CC were enrolled in this study. The clinical data and outcomes were compared to an ageand Child-pugh class-matched cohort of 110 patients with HCV-related cirrhosis. Diagnosis of cirrhosis was based on compatible clinical and laboratory parameters, ultrasound/endoscopic parameters and, whenever possible, on histological grounds and transient elastography. All cases of cirrhosis without a definite etiology were enrolled in the CC group. The parameters assessed were:(1) severity of liver disease at the time of first diagnosis;(2) liver decompensation during follow-up;(3) hepatocellular carcinoma(HCC);(4) orthotopic liver transplantation; and(5) death. The independent associated factors were evaluated by multiple logistic regression analysis, and survival and its determinants by the Kaplan-Meier model, log-rank test and Cox regression.RESULTS At the first observation, median age was 66 and 65 years and male gender was 36% and 58% for CC and HCV cirrhosis, respectively. CC showed Child-pugh class A/B/C of 47%/31%/22%, respectively. Compared to HCV cirrhosis, CC exhibited a significantly higher prevalence of metabolic syndrome(12% vs 54%, respectively), overweight/obesity, high BMI, impaired glucose tolerance, high blood pressure, dyslipidemia, hyperuricemia, cardiovascular diseases, extrahepatic cancer, and gallstones. Over a median period of 42 mo of follow-up, liver decompensation, HCC development and death for CC and HCV-related cirrhosis were 60.8%, and 54.4%, 16.7% and 17.2%, 39.2% and 30%, respectively. The median survival was 60 mo for CC. Independent predictors of death were age and Childpugh class at diagnosis. CC showed an approximately twofold higher incidence of HCC in Child-pugh class A.CONCLUSION Undiagnosed nonalcoholic fatty liver disease has an etiologic role in CC that is associated with a poor prognosis, early HCC development, high risk of cardiovascular disease and extrahepatic cancer. | Luca Rinaldi Fabio Nascimbeni Mauro Giordano Chiara Masetti Barbara Guerrera Annalisa Amelia Maria Chiara Fascione Stefano Ballestri Dante Romagnoli Rosa Zampino Riccardo Nevola Enrica Baldelli Natalina Iuliano Valerio Rosato Amedeo Lonardo Luigi Elio Adinolfi | 2017 | World Journal of Gastroenterology2017，23，8： | 5 |
| 10 | Steatosis accelerates the progression of liver damage of chronic hepatitis C patients and correlates with specific HCV genotype and visceral obesity显示文摘 | Luigi E. Adinolfi Michele Gambardella Augusto Andreana Marie-fran?oise Tripodi Riccardo Utili Giuseppe Ruggiero | 2001 | Hepatology2001，，6： | 4 |
| 11 | Abdominal fat interacts with PNPLA 3 I148M, but not with the APOC 3 variant in the pathogenesis of liver steatosis in chronic hepatitis C显示文摘 | R. Zampino N. Coppola G. Cirillo A. Boemio M. Pisaturo A. Marrone M. Macera E. Sagnelli L. Perrone L. E. Adinolfi E. Miraglia del Giudice | 2013 | J Viral Hepat2013，，8： | 3 |
| 12 | Chronic HCV infection is a risk of atherosclerosis. Role of HCV and HCV-related steatosis显示文摘 | Luigi E. Adinolfi Luciano Restivo Rosa Zampino Barbara Guerrera Amedeo Lonardo Laura Ruggiero Francesco Riello Paola Loria Anna Florio | 2012 | Atherosclerosis2012，，2： | 3 |
| 13 | Metabolic alterations and chronic hepatitis C: treatment strategies显示文摘 | Luigi E Adinolfi Luciano Restivo Rosa Zampino Amedeo Lonardo Paola Loria | 2011 | Expert Opinion on Pharmacotherapy2011，，14： | 3 |
| 14 | TM 6 SF 2 E167K variant is associated with severe steatosis in chronic hepatitis C, regardless of PNPLA 3 polymorphism显示文摘 | Nicola Coppola Zampino Rosa Grazia Cirillo Maria Stanzione Margherita Macera Adriana Boemio Anna Grandone Mariantonietta Pisaturo Aldo Marrone Luigi E. Adinolfi Evangelista Sagnelli Emanuele Miraglia del Giudice | 2015 | Liver Int2015，，8： | 3 |
| 15 | Chronic hepatitis C,atherosclerosis and cardiovascular disease: What impact of direct-acting antiviral treatments?显示文摘Hepatitis C virus (HCV) infection is associated with extrahepatic manifestations, among these there is an increased risk of atherosclerosis and cardiovascular disease as well as an increased cardiovascular mortality. Several direct and indirect HCV pro-atherogenic mechanisms have been proposed. HCV lives and replicates within carotid plaques, promoting a local environment of pro-atherogenic factors. In addition, it causes conditions such as insulin resistance, diabetes, hepatic steatosis, cryoglobulinemia and endotoxinemia that are associated with the development of atherosclerosis and cardiovascular disease. Therapeutic regimens based on direct-acting antiviral agents (DAA) are currently available with high efficacy in HCV clearance and improvement of liver disease, but does HCV eradication also improve atherosclerosis and the risk of cardiovascular disease? Recently, a multi-center study has shown that elimination of HCV improves carotid atherosclerosis. Two studies have shown that DAA treatments significantly reduce the risk of cardiovascular events. Several studies have assessed the impact of HCV clearance on pro-atherosclerosis metabolic conditions showing improvement in cardiovascular risk biomarkers, disappearance or improvement of insulin resistance, reduction of risk of developing diabetes and improvement of glycemic control. There are also evidences that HCV clearance promotes the recovery of cytokines and inflammatory markers associated with atherosclerosis and the disappearance of cryoglobulinemia. Available data show that clearance of HCV by DAAs is associated with an improvement in atherosclerosis and metabolic and immunological conditions that promote the development of cardiovascular disease. However, the data are not sufficient to allow definitive conclusions and further studies will be needed to definitively clarify the impact of HCV clearance on atherosclerosis and cardiovascular disease. | Luigi Elio Adinolfi Luca Rinaldi Riccardo Nevola | 2018 | World Journal of Gastroenterology2018，24，41： | 3 |
| 16 | Role of interleukin 28-B in the spontaneous and treatment-related clearance of HCV infection in patients with chronic HBV/HCV dual infection显示文摘 | N. Coppola A. Marrone M. Pisaturo M. Starace G. Signoriello I. Gentile L. E. Adinolfi E. Sagnelli R. Zampino | 2014 | European Journal of Clinical Microbiology & Infectious Diseases2014，，4： | 3 |
| 17 | Abdominal fat interacts with PNPLA 3 I148M, but not with the APOC 3 variant in the pathogenesis of liver steatosis in chronic hepatitis C显示文摘 | R. Zampino N. Coppola G. Cirillo A. Boemio M. Pisaturo A. Marrone M. Macera E. Sagnelli L. Perrone L. E. Adinolfi E. Miraglia del Giudice | 2013 | J Viral Hepat2013，，8： | 3 |
| 18 | Chronic HCV infection is a risk of atherosclerosis. Role of HCV and HCV-related steatosis显示文摘 | Luigi E. Adinolfi Luciano Restivo Rosa Zampino Barbara Guerrera Amedeo Lonardo Laura Ruggiero Francesco Riello Paola Loria Anna Florio | 2012 | Atherosclerosis2012，，2： | 2 |
| 19 | Association Between a Polymorphism in Cannabinoid Receptor 2 and Severe Necroinflammation in Patients With Chronic Hepatitis C显示文摘 | Nicola Coppola Rosa Zampino Giulia Bellini Margherita Macera Aldo Marrone Mariantonietta Pisaturo Adriana Boemio Bruno Nobili Giuseppe Pasquale Sabatino Maione Luigi Elio Adinolfi Laura Perrone Evangelista Sagnelli Emanuele Miraglia Del Giudice Francesca | 2013 | Clinical Gastroenterology and Hepatology2013，，： | 2 |
| 20 | Practice guidelines for the diagnosis and management of nonalcoholic fatty liver disease显示文摘 | P. Loria L.E. Adinolfi S. Bellentani E. Bugianesi A. Grieco S. Fargion A. Gasbarrini C. Loguercio A. Lonardo G. Marchesini F. Marra M. Persico D. Prati G. Svegliati- Baroni | 2010 | Digestive and Liver Disease2010，，4： | 2 |
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