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| 1 | Non-steroidal anti-inflammatory drugs:What is the actual risk of liver damage?显示文摘Non-steroidal anti-inflammatory drugs (NSAIDs) constitute a family of drugs, which taken as a group, represents one of the most frequently prescribed around the world. Thus, not surprisingly NSAIDs, along with antiinfectious agents, list on the top for causes of DrugInduced Liver Injury (DILI). The incidence of liver disease induced by NSAIDs reported in clinical studies is fairly uniform ranging from 0.29/100 000 [95% confidence interval (CI): 0.17-051] to 9/100 000 (95% CI: 6-15). However, compared with these results, a higher risk of liver-related hospitalizations was reported (3-23 per 100 000 patients). NSAIDs exhibit a broad spectrum of liver damage ranging from asymptomatic, transient, hyper-transaminasemia to fulminant hepatic failure. However, under-reporting of asymptomatic, mild cases, as well as of those with transient liver-tests alteration, in conjunction with reports non-compliant with pharmacovigilance criteria to ascertain DILI and flawed epidemiological studies, jeopardize the chance to ascertain the actual risk of NSAIDs hepatotoxicity. Several NSAIDs, namely bromfenac, ibufenac and benoxaprofen, have been withdrawn from the market due to hepatotoxicity; others like nimesulide were never marketed in some countries and withdrawn in others. Indeed, the contro-versy concerning the actual risk of severe liver disease persists within NSAIDs research. The present work intends (1) to provide a critical analysis of the dissimilar results currently available in the literature concerning the epidemiology of NSAIDS hepatotoxicity; and (2) to review the risk of hepatotoxicity for each one of the most commonly employed compounds of the NSAIDs family, based on past and recently published data. | Fernando Bessone | 2010 | World Journal of Gastroenterology2010，16，45： | 16 |
| 2 | Management of hepatitis B reactivation in immunosuppressed patients: An update on current recommendations显示文摘The proportion of hepatitis B virus(HBV) previously exposed patients who receive immunosuppressive treatment is usually very small. However, if these individuals are exposed to potent immunosuppressive compounds, the risk of HBV reactivation(HBVr) increases with the presence of hepatitis B surface antigen(HBsAg) in the serum. Chronic HBsAg carriers have a higher risk than those who have a total IgG anticore as the only marker of resolved/occult HBV disease. The loss of immune control in these patients may results in the reactivation of HBV replication within hepatocytes. Upon reconstitution of the immune system, infected hepatocytes are once again targeted and damaged by immune surveillance in an effort to clear the virus. There are different virological scenarios, and a wide spectrum of associated drugs with specific and stratified risk for the development of HBVr. Some of this agents can trigger a severe degree of hepatocellular damage, including hepatitis, acute liver failure, and even death despite employment of effective antiviral therapies. Currently, HBVr incidence seems to be increasing around the world; a fact mainly related to the incessant appearance of more powerful immunosuppressive drugs launched to the market. Moreover, there is no consensus on the length of prophylactic treatment before the patients are treated with immunosuppressive therapy, and for how long this therapy should be extended once treatment is completed. Therefore, this review article will focus on when to treat, when to monitor, what patients should receive HBV therapy, and what drugs should be selected for each scenario. Lastly, we will update the definition, risk factors, screening, and treatment recommendations based on both current and different HBV management guidelines. | Fernando Bessone Melisa Dirchwolf | 2016 | World Journal of Hepatology2016，8，8： | 10 |
| 3 | Challenge of liver disease in systemic lupus erythematosus:Clues for diagnosis and hints for pathogenesis显示文摘Systemic lupus erythematosus(SLE) encompass a broad spectrum of liver diseases. We propose here to classify them as follows:(1) immunological comorbilities(overlap syndromes);(2) non-immunological comorbilities associated to SLE; and(3) a putative liver damage induced by SLE itself, referred to as 'lupus hepatitis'. In the first group, liver injury can be ascribed to overlapping hepatopathies triggered by autoimmune mechanisms other than SLE occurring with higher incidence in the context of lupus(e.g., autoimmune hepatitis, primary biliary cirrhosis). The second group includes non-autoimmune liver diseases, such as esteatosis, hepatitis C, hypercoagulation state-related liver lesions, hyperplasic parenchymal and vascular lesions, porphyria cutanea tarda, and drug-induced hepatotoxicity. Finally, the data in the literature to support the existence of a hepatic disease produced by SLE itself, or the occurrence of a SLE-associated prone condition that increases susceptibility to acquire other liver diseases, is critically discussed. The pathological mechanisms underlying each of these liver disorders are also reviewed. Despite the high heterogeneity in the literature regarding the prevalence of SLE-associated liver diseases and, in most cases, lack of histopathological evidence or clinical studies large enough to support their existence, it is becoming increasingly apparent that liver is an important target of SLE. Consequently, biochemical liver tests should be routinely carried out in SLE patients to discard liver disorders, particularly in those patients chronically exposed to potentially hepatotoxic drugs. Diagnosing liver disease in SLE patients is always challenging, and the systematization of the current information carried out in this review is expected to be of help both to attain a better understanding of pathogenesis and to build an appropriate work-up for diagnosis. | Ferno Bessone Natalia Poles Marcelo G Roma | 2014 | World Journal of Hepatology2014，6，6： | 7 |
| 4 | Influence of alloying elements and microstructure on aluminium sacrificial anode performance: case of Al–Zn显示文摘 | D.R. Salinas S.G. García J.B. Bessone | 1999 | Journal of Applied Electrochemistry1999，，9： | 3 |
| 5 | Long-Term Treatment With Entecavir Induces Reversal of Advanced Fibrosis or Cirrhosis in Patients With Chronic Hepatitis B显示文摘 | Eugene R. Schiff Samuel S. Lee You–Chen Chao Seung Kew Yoon Fernando Bessone Shun–Sheng Wu Wieslaw Kryczka Yoav Lurie Adrian Gadano George Kitis Suzanne Beebe Dong Xu Hong Tang Uchenna Iloeje | 2011 | Clinical Gastroenterology and Hepatology2011，，3： | 3 |
| 6 | Hepatotoxicity Induced by Biological Agents: Clinical Features and Current Controversies显示文摘Novel biological agents including cytokines and recombinant fusion proteins are increasingly prescribed for cancer,rheumatologic,autoimmune,and inflammatory diseases,and are currently being evaluated in hepatocellular carcinoma(HCC).They are classified by their mechanism of action and include tumor necrosis factor-alpha(TNF-α)antagonists,T cell mediated antitumor inhibitors,interleukin receptor antagonists,and immune checkpoint inhibitors(ICIs).Some ICIs cause frequent hepatotoxicity with a variable clinical,biochemical,and serological presentation,especially in patients receiving another immunomodulatory agent.Half of the cases of liver damage induced by biological agents spontaneously regress after drug withdrawal,but the others require steroid therapy.Unfortunately,there are no widely accepted recommendation for the use of corticosteroids in these patients,even though international cancer societies have their own guidelines.Differentiating drug-induced autoimmune hepatitis(DIAIH)from classic AIH is challenging for pathologists,but liver biopsy is valuable,particularly in cases with unclear clinical presentation.Interesting,novel histological patterns have been described in liver damage induced by these agents(i.e.,endothelitis,ring granuloma and secundary sclerosing cholangitis associated with lymphocytic infiltration of cytotoxic CD8+T cells).Here,we describe the clinical and biochemical characteristics of patients with hepatotoxicity induced by TNF-αantagonists and ICIs.Controversial issues involved in the administration of corticosteroid therapy,and hepatitis B virus(HBV)reactivation induced by immunosuppressive therapy are also discussed. | Nelia Hernandez Fernando Bessone | 2022 | Journal of Clinical and Translational Hepatology2022，10，3： | 2 |
| 7 | Electrochemical behaviour of Al-In alloys in chloride solutions显示文摘 | S. B. Saidman S. G. Garcia J. B. Bessone | 1995 | Journal of Applied Electrochemistry1995，，3： | 2 |
| 8 | Parameter estimation for random amplitude chirp signals显示文摘 | BESSON O GHOGHO M SWAMI A | 1999 | IEEE Trans on Signal Processing1999，47，12： | 2 |
| 9 | A mechanism for transition-metal nanoparticle self-assembly显示文摘 | Besson C Finney E E Finke R G | 2005 | J Am Chem Soc2005，127，22： | 1 |
| 10 | Knowledge-aided covariance matrix estimation and adaptive detection in compound-Gaussian noise显示文摘 | Bandiera F Besson O and Ricci G | 2010 | IEEE Transactions on Signal Processing2010，58，10： | 1 |
| 11 | Direction finding in the presence of an intermittent interference显示文摘 | Besson O Stoica P Kaniya Y | 2002 | IEEE Trans on SP2002，50，7： | 1 |
| 12 | PTEN/MMAC1 mutations in signal transduction and tumorigenesis显示文摘 | BESSON A ROBBINS SM YONG VW | 1999 | Eur J Biochem1999，263，： | 1 |
| 13 | Structure de la bacillomycine L, antibiotique de Bacillus subtilis显示文摘 | Besson F Peypoux F Michel G | 1977 | Europ Biochem1977，77，： | 1 |
| 14 | Cholesterol-lowering effects of guar gum:changes in bile acid pools and intestinal reabsorption显示文摘 | Moriceau S Besson C Levrat MA | 2000 | Lipids2000，35，： | 1 |
| 15 | A pathway in quiesceni cells that controls P27^kip1 stability, subcellular localization, and tumor suppression 显示文摘 | Besson A Gurian-West M Chen X | 2006 | Genes & Dev2006，20，： | 1 |
| 16 | Association of dopamine and opioid receptor genetic polymorphisms with response to methadone maintenance treatment显示文摘 | Crettol S Besson J Croquette - Krokar M | 2008 | Prog Neuropsychopharmacol Biol Psychiatry2008，32，： | 1 |
| 17 | Detection in the presence of surprise or under- hulled interference显示文摘 | Besson O | 2007 | IEEE Signal Processing Letters2007，14，5： | 1 |
| 18 | p27Kip1and p21Cip1 collaborate in the regulation of transcription by recruiting cyclin-Cdkcomplexes on the promoters of target genes显示文摘 | Orlando S Gallastegui E Besson A | 2015 | Nucleic Acids Res2015，43，14： | 1 |
| 19 | Involvement of p21 (Waf1/Cip1) in protein kinase C alpha-induced cell cycle progression显示文摘 | Yong VW | 2000 | Mol Cell Biol2000，20，： | 1 |
| 20 | Characterisation of iturin A in antibiotics from various strains of Bacillus subtilis显示文摘 | Besson F Peypoux F Michel G | 1976 | J Antibiot1976，29，10： | 1 |
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