Search

Your search keyword '"Balsano C."' showing total 509 results
Start Over Author "Balsano C."
509 results on '"Balsano C."'

202. Breath tests for the assessment of the orocecal transit time.

Author

SCARPELLINI, E., ABENAVOLI, L., BALSANO, C., GABRIELLI, M., LUZZA, F., and TACK, J.

Abstract

Orocecal transit time (OCTT) is one of the main determinant of the hunger ratings and gastrointestinal sensitivity. While marked- isotopes scintigraphy is the gold standard in its determination in the clinical frame, breath tests are cheap, well-tolerated and non-invasive alternatives. In fact C-13 and C-14 stable isotopes breath tests can be used to assess gastric emptying and OCTT in the clinical and research frames. Moreover, hydrogen (H2) lactulose breath test can be used to assess OCTT in the research frame only due to its laxative action; inulin breath test, devoid of this bias, could be replacing it. However, the main l imitation in the use of breath tests in the OCTT determination is their low reproducibility. [ABSTRACT FROM AUTHOR]

Published
2013

212. Reactive oxygen intermediates mediate angiotensin II-induced c-Jun.c-Fos heterodimer DNA binding activity and proliferative hypertrophic responses in myogenic cells.

Author

Puri, P L, Avantaggiati, M L, Burgio, V L, Chirillo, P, Collepardo, D, Natoli, G, Balsano, C, and Levrero, M

Abstract

Angiotensin II (Ang-II) receptor engagement activates many immediate early response genes in both vascular smooth muscle cells and cardiomyocytes whether a hyperplastic or hypertrophic response is taking place. Although the signaling pathways stimulated by Ang-II in different cell lines have been widely characterized, the correlation between the generation of different second messengers and specific physiological responses remains relatively unexplored. In this study, we report how in both C2C12 quiescent myoblasts and differentiated myotubes Ang-II significantly stimulates AP1-driven transcription and c-Jun.c-Fos heterodimer DNA binding activity. Using a set of different protein kinase inhibitors, we could demonstrate that Ang-II-induced increase in AP1 binding is not mediated by the cAMP-dependent pathway and that both protein kinase C and tyrosine kinases are involved. The observation that in quiescent myoblasts Ang-II increase of AP1 binding and induction of DNA synthesis and, in differentiated myotubes, Ang-II stimulation of protein synthesis are abolished by the cysteine-derivative and glutathione precursor N-acetyl-L-cysteine strongly suggests a role for reactive oxygen intermediates in the intracellular transduction of Ang-II signals for immediate early gene induction, cell proliferation, and hypertrophic responses.

Published
1995

214. Tumor necrosis factor (TNF) receptor 1 signaling downstream of TNF receptor-associated factor 2. Nuclear factor kappaB (NFkappaB)-inducing kinase requirement for activation of activating protein 1 and NFkappaB but not of c-Jun N-terminal kinase/stress-activated protein kinase.

Author

Natoli, G, Costanzo, A, Moretti, F, Fulco, M, Balsano, C, and Levrero, M

Abstract

Like other members of the tumor necrosis factor (TNF) receptor family, p55 TNF receptor 1 (TNF-R1) lacks intrinsic signaling capacity and transduces signals by recruiting associating molecules. The TNF-R1 associated death domain protein interacts with the p55 TNF-R1 cytoplasmic domain and recruits the Fas-associated death domain protein (which directly activates the apoptotic proteases), the protein kinase receptor interacting protein, and TNF receptor-associated factor 2 (TRAF2). TRAF2 has previously been demonstrated to activate both transcription factor nuclear factor kappaB (NFkappaB) and the c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) pathway, which in turn stimulates transcription factor activating protein 1 (AP1) mainly via phosphorylation of the c-Jun component. We have investigated the signaling properties of NFkappaB-inducing kinase (NIK), a TRAF2-associated protein kinase that mediates NFkappaB induction. NIK was found to be unable to activate JNK/SAPK, mitogen-activated protein kinase, or p38 kinase. Moreover, NIK was not required for JNK/SAPK activation by TNF-R1, thus representing the first TNF-R1 complex component to dissect the NFkappaB and the JNK/SAPK pathways. Despite being unable to activate JNK/SAPK and mitogen-activated protein kinase, NIK strongly activated AP1 and was required for TNF-R1-induced AP1 activation. Therefore, NIK links TNF-R1 to a novel, JNK/SAPK-independent, AP1 activation pathway.

Published
1997

216. Recognition of hepatitis B virus envelope proteins by liver-infiltrating T lymphocytes in chronic HBV infection

Author

Barnaba, V., Franco, A., ALFREDO ALBERTI, Balsano, C., Benvenuto, R., and Balsano, F.

Subjects
Adult, Cytotoxicity, Immunologic, Male, Hepatitis B virus, Hepatitis B Surface Antigens, Immunology, Lymphocyte Activation, Clone Cells, Epitopes, Liver, Viral Envelope Proteins, Cell Movement, HLA Antigens, Immunology and Allergy, Humans, Hepatitis, Chronic, T-Lymphocytes, Cytotoxic
Abstract

The Ag specificity and cytotoxic function of human T cell clones, generated from lymphocytes infiltrating the liver of a chronic hepatitis B patient, were studied. Both class I- and class II-restricted T clones specifically proliferated to hepatitis B virus envelope proteins, but not to hepatitis B core Ag. The fine specificity of T cells was studied by using rAg having different composition in relation to HBV-envelope proteins or synthetic peptides of preS regions. The antigenic determinant recognized by T cell clones mapped to the preS2 region based on the response to r(preS1+preS2+S) and to r(preS2+S) and the failure to respond to S or preS1 alone. More precise epitope mapping was based on synthetic preS2 peptides 120-150 or 120-134, which stimulated both class I- and class II-restricted T clones, whereas preS2 153-171 or preS1 1-110 peptides did not; thus, the preS2 120-134 appears to contain both the residues binding to class I molecules and the residues binding to class II molecules. Moreover, strong and specific cytotoxic responses of these clones were observed only when HLA-matched EBV-lines, used as target cells, were previously sensitized with r(preS1+preS2+S) or preS2 peptides, which were shown to stimulate the clones. Thus, a preS2 epitope can represent a target Ag for liver-infiltrating T cells, which could kill the hepatocytes expressing the Ag plus the appropriate MHC molecule.

Published
1989

219. Could monitoring normotensives delay progression to hypertension?

Author

GINO IANNUCCI, Scarpellini, Emidio, Balsano, C., Marino PAROLI, Leone, G., and Maria Fabrizia Giannoni

Subjects
Carotid Artery Diseases, Male, Prehypertension, Carotid Artery, Common, Female, Humans, Arterial Pressure, Blood Pressure Determination, Carotid Intima-Media Thickness, Office Visits, Carotid Artery, Common

221. Office normotensives with a minimal augmentation of intima-media thickness of common carotid arteries: really normotensives?

Author

GINO IANNUCCI, Balsano, C., Marino PAROLI, Scarpellini, Emidio, Leone, G., and Maria Fabrizia Giannoni

Subjects
Adult, Carotid Artery Diseases, Male, Target organ damage, Chi-Square Distribution, genetic structures, Carotid Artery, Common, Office Visits, TOD, Blood Pressure Determination, Blood Pressure Monitoring, Ambulatory, Carotid Intima-Media Thickness, End organ damage, Prehypertension, Cugini's syndrome, Predictive Value of Tests, ABPM, Humans, ABPM-Diagnosable prehypertension, Arterial Pressure, Female, Masked prehypertension, Monitoring prehypertension, Retrospective Studies
Abstract

Blood pressure is an independent predictor of target organ damage (TOD). Recent data from literature suggest that TOD can be present also in pre-hypertensive subjects, diagnosed with pressure monitoring (PM). Aim of this study is to clarify whether an augmentation of the carotid Intima-Media Thickness (cIMT) in office prehypertensives is a TOD associated to monitoring prehypertension (MP).We have analyzed our database of individuals office normotensives showing an increase of cIMT. The ambulatory blood pressure monitoring (ABPM) of these was compared with those of office monitoring normotensives, matched by age and gender, antropometric characteristics, negative for familial hypertension and other risk factors (true normotensives, TN).We have selected 15 presumable prehypetensives (PP) and 8 TN subjects. The ABPM (ambulatory blood pressure monitoring) analysis confirmed that neither the PP nor TN showed systolic (S) and diastolic (D) BP within-day values above their day-night upper reference limits. However the statistical comparison between PP and TN revealed that the first group had a significant elevation of SBP and DBP Daily Mean Level (DML(SBP/DBP): 121 ± 2/81 ± 2 vs 112 ± 2/70 ± 2 mmHg, respectively, p = 0.007 and p = 0.002), confirming the MP diagnosis.These results demonstrate that cIMT increase in PP fulfill the criteria for MP diagnosis, suggesting that MP should be undertaken in all PP with altered cIMT, but larger prospective studies are needed.

222. Modulation of intracellular signal transduction pathways by the hepatitis B virus transactivator pX

Author

Gioacchino Natoli, Avantaggiati, M. L., Chirillo, P., Marzio, E., Collepardo, D., Falco, M., Balsano, C., and Levrero, M.

Subjects
Transcriptional Activation, Hepatitis B virus, Genes, jun, Transcription, Genetic, Genes, pX, Animals, Humans, Signal Transduction, Transcription Factors
Abstract

The mechanisms by which pX, the transactivator of the hepatitis B virus (HBV), exerts its effects on transcription of viral and cellular genes and affects cell-growth regulation have not yet been fully defined. Previous reports suggested the possibility of a direct interaction of pX, which lacks intrinsic DNA-binding activity, with components of the cellular transcription machinery. More recent investigations support the hypothesis that pX might activate cellular kinases involved in transcriptional regulation and growth control. We characterized the mechanisms of AP-1 transcription factor activation by pX and, in particular, the role of cellular proteins involved in the intracellular signal transduction of growth-factor receptors. The observation that the overexpression of c-fos and c-jun in the cells results in a clear augmentation of the effects of pX on TRE-directed transcription and the induction of the DNA-binding activity of c-jun/c-fos heterodimers by AP1-depleted nuclear extracts from pX-expressing cells strongly supports the involvement of post-translational modifications. In both HeLa and undifferentiated F9 cells, pX was able to increase the activity of exogenous transfected c-jun but not of c-jun mutants bearing mutations in the serine residues located in the amino-terminal transcriptional activation domain. Moreover, by use of Ha-ras and Raf-1 dominant negative mutants, we show that both Ha-ras and Raf-1 are required for pX-induced activation of c-jun transcriptional activity.(ABSTRACT TRUNCATED AT 250 WORDS)

224. Hepatitis B virus and hepatocellular carcinoma: a possible role for the viral transactivators

Author

Massimo Levrero, Balsano C, Ml, Avantaggiati, Natoli G, De Marzio E, and Will H

Subjects
Hepatitis B Antigens, Hepatitis B virus, Carcinoma, Hepatocellular, Liver Neoplasms, Genes, myc, Trans-Activators, Genes, fos, Humans, Viral Regulatory and Accessory Proteins, Hepatitis B
Abstract

Several epidemiological studies have demonstrated a link between chronic B virus infection and primary hepatocellular carcinoma (PHC). HBV DNA sequence integrations into the host cell genome have often been observed in hepatocarcinoma tissues. However, since only in a few cases of PHC the target of HBV-DNA insertion has been identified, alternative mechanisms for HBV-induced hepatocyte transformation have been investigated. Like many other DNA viruses, the hepatitis B virus bears a transactivational potential. Both full length and truncated versions of HBV X protein are able to influence the expression of cellular nuclear protooncogenes c-fos and c-myc. A second transcriptional activator is encoded by the PreS/S region of HBV, but its activity on viral and cellular genes become evident only after dislocations from its downstream sequences. Thus, HBV is able to influence infected cell growth and differentiation using both native proteins, newly generated truncated proteins and virus-cell fusion polypeptides.

229. Breath tests for the assessment of the orocecal transit time

Author

Scarpellini, E., Abenavoli, L., Balsano, C., Gabrielli, M., Francesco Luzza, and Tack, J.

Subjects
Time Factors, Gastrointestinal Diseases, digestive, oral, and skin physiology, Octanoate, Inulin, Reproducibility of Results, OCTT, Lactulose, Breath Tests, Gastric Emptying, Lactose ureyde, Predictive Value of Tests, Animals, Humans, Gases, Gastrointestinal Transit, Biomarkers
Abstract

Orocecal transit time (OCTT) is one of the main determinant of the hunger ratings and gastrointestinal sensitivity. While marked-isotopes scintigraphy is the gold standard in its determination in the clinical frame, breath tests are cheap, well-tolerated and non-invasive alternatives. In fact C-13 and C-14 stable isotopes breath tests can be used to assess gastric emptying and OCTT in the clinical and research frames. Moreover, hydrogen (H2) lactulose breath test can be used to assess OCTT in the research frame only due to its laxative action; inulin breath test, devoid of this bias, could be replacing it. However, the main limitation in the use of breath tests in the OCTT determination is their low reproducibility.

235. Could monitoring normotensives delay progression to hypertension?

Author

Iannucci, G., Scarpellini, E., Balsano, C., Paroli, M., Leone, G., and Giannoni, M. F.

Abstract

A response by G. Iannucci, C. Balsano, M. Paroli, E. Scarpellini, G. Leone and M. F. Giannoni to a letter to the editor about their article "Office Normotensives With a Minimal Augmentation of Intima-Media Thickness of Common Carotid Arteries: Really Normotensives," in the 2013 issue is presented.

Published
2014

240. Inverse correlation between plasma oxysterol and LDL-cholesterol levels in hepatitis C virus-infected patients

Author

Mario Arciello, Giancarlo Labbadia, Clara Balsano, Gino Iannucci, Salvatore Petta, Valerio Leoni, C. Cammà, Antonio Craxì, Arciello, M, Petta, S, Leoni, V, Iannucci, G, Labbadia, G, Cammà, C, Craxì, A, Balsano, C, and Balsano, C.

Subjects
Adult, Male, medicine.medical_specialty, Oxysterol, Hepatitis C virus, Hepacivirus, Isotope dilution, medicine.disease_cause, chronic hepatitis c infection, lipid metabolism, non-alcoholic fatty liver disease, oxidative stress, Non-alcoholic Fatty Liver Disease, Internal medicine, medicine, polycyclic compounds, oxysterol hcv nafld, Humans, oxysterols, sterols, cholesterol, mass spectrometry, metabolomics, Liver X receptor, Ketocholesterols, Hepatology, business.industry, Fatty liver, Gastroenterology, Lipid metabolism, Hepatitis C, Cholesterol, LDL, Middle Aged, medicine.disease, Chronic hepatitis C infection, Hydroxycholesterols, Fatty Liver, Oxidative Stress, Endocrinology, Biochemistry, Multivariate Analysis, Linear Models, lipids (amino acids, peptides, and proteins), Female, business, Oxidative stress
Abstract

Background: Hepatitis C virus infection is characterised by enhanced oxidative stress, which can be measured quantitatively by plasma oxysterol concentration. These molecules may affect lipid metabolism through the activation of Liver X Receptors. Hepatitis C virus exploits host lipid metabolism to facilitate its replication and diffusion. In our study we aimed to evaluate and highlight the potential pathogenetic role of oxysterols, 7-ketocholesterol and 7-β-hydroxycholesterol, in hepatitis C virus-related lipid dysmetabolism. Methods: The study was performed in 42 patients with chronic hepatitis C (93% genotype 1b) and 38 non-alcoholic fatty liver disease patients. Plasma oxysterols 7-ketocholesterol and 7-β-hydroxycholesterol were determined by isotope dilution gas chromatography/mass spectrometry. Results: Gas chromatography/mass spectrometry revealed higher 7-ketocholesterol (71.2 ± 77.3 vs 30.4 ± 14.5; p

Published
2012

241. The application of artificial intelligence in hepatology: A systematic review

Author

Silvano Junior Santini, Alessio Gerussi, Marco Carbone, Alberto Zanetto, Maurizia Rossana Brunetto, Patrizia Burra, Ferruccio Bonino, Francesco Faita, Anna Alisi, Marcello Persico, Clara Balsano, Pietro Invernizzi, Fabio Piscaglia, Domenico Alvaro, Balsano, C, Alisi, A, Brunetto, M, Invernizzi, P, Burra, P, Piscaglia, F, Alvaro, D, Bonino, F, Carbone, M, Faita, F, Gerussi, A, Persico, M, Santini, S, and Zanetto, A

Subjects
Artificial intelligence, Hepatology, business.industry, Process (engineering), liver diseases, Big data, Intelligent decision support system, Gastroenterology, Deep learning, Bioethics, Transformative learning, Machine learning, Medicine, Humans, business, liver disease, Digital Revolution
Abstract

The integration of human and artificial intelligence (AI) in medicine has only recently begun but it has already become obvious that intelligent systems can dramatically improve the management of liver diseases. Big data made it possible to envisage transformative developments of the use of AI for diagnosing, predicting prognosis and treating liver diseases, but there is still a lot of work to do. If we want to achieve the 21st century digital revolution, there is an urgent need for specific national and international rules, and to adhere to bioethical parameters when collecting data. Avoiding misleading results is essential for the effective use of AI. A crucial question is whether it is possible to sustain, technically and morally, the process of integration between man and machine. We present a systematic review on the applications of AI to hepatology, highlighting the current challenges and crucial issues related to the use of such technologies.

Published
2021

242. Bridging the 'last mile' gap between AI implementation and operation: 'data awareness' that matters

Author

Andrea Campagner, Federico Cabitza, Clara Balsano, Cabitza, F, Campagner, A, and Balsano, C

Subjects
Decision support system, Artificial intelligence, 020205 medical informatics, Computer science, data hygiene, DevOps, last mile, 02 engineering and technology, Review Article, Data governance, 03 medical and health sciences, DevOp, 0302 clinical medicine, 0202 electrical engineering, electronic engineering, information engineering, Mile, Cognitive ergonomics, business.industry, INF/01 - INFORMATICA, Usability, General Medicine, Data science, Automation, 030220 oncology & carcinogenesis, Last mile, business
Abstract

Interest in the application of machine learning (ML) techniques to medicine is growing fast and wide because of their ability to endow decision support systems with so-called artificial intelligence, particularly in those medical disciplines that extensively rely on digital imaging. Nonetheless, achieving a pragmatic and ecological validation of medical AI systems in real-world settings is difficult, even when these systems exhibit very high accuracy in laboratory settings. This difficulty has been called the "last mile of implementation." In this review of the concept, we claim that this metaphorical mile presents two chasms: the hiatus of human trust and the hiatus of machine experience. The former hiatus encompasses all that can hinder the concrete use of AI at the point of care, including availability and usability issues, but also the contradictory phenomena of cognitive ergonomics, such as automation bias (overreliance on technology) and prejudice against the machine (clearly the opposite). The latter hiatus, on the other hand, relates to the production and availability of a sufficient amount of reliable and accurate clinical data that is suitable to be the "experience" with which a machine can be trained. In briefly reviewing the existing literature, we focus on this latter hiatus of the last mile, as it has been largely neglected by both ML developers and doctors. In doing so, we argue that efforts to cross this chasm require data governance practices and a focus on data work, including the practices of data awareness and data hygiene. To address the challenge of bridging the chasms in the last mile of medical AI implementation, we discuss the six main socio-technical challenges that must be overcome in order to build robust bridges and deploy potentially effective AI in real-world clinical settings.

Published
2020

243. Sustained activation of the Raf/MEK/Erk pathway in response to EGF in stable cell lines expressing the Hepatitis C Virus (HCV) core protein.

Author

Giambartolomei, S, Covone, F, Levrero, M, and Balsano, C

Subjects
*HEPATITIS C virus, *CIRRHOSIS of the liver, *LIVER cancer
Abstract

Chronic hepatitis C virus (HCV) infection is a leading cause of liver cirrhosis and hepatocellular carcinoma (HCC) worldwide. The HCV capside core is a multifunctional protein with regulatory functions that affects transcription and cell growth in vitro and in vivo. Here, we show that both HCV genotype 1a and 3 core proteins activate MEK1 and Erk1/2 MAP kinases and that the costitutive expression of the HCV core results in a high basal activity of Raf1 and MAP/kinase/kinase, as determined by endogenous Raf1 in vitro kinase assay and immunodetection of hyperphosphorylated Erk1 and Erk2 even after a serum starvation. Moreover, the activation of both Erk1/2 and the downstream transcription factor Elk-1 in response to the mitogenic stimulus EGF is significantly prolonged. The sustained response to EGF in cells expressing the HCV core occurs despite a normal induction of the MAP phosphatases MKP regulatory feedback and is likely due to the costitutive activation of Raf-1 activity. The ability of HCV core proteins to directly activate the MAP kinase cascade and to prolong its activity in response to mitogenic stimuli may contribute to the neoplastic transformation of HCV infected liver cells. Oncogene (2001) 20, 2606–2610. [ABSTRACT FROM AUTHOR]

Published
2001
Full Text
View/download PDF

244. Prevalence of peripheral artery disease by abnormal ankle-brachial index in atrial fibrillation: implications for risk and therapy

Author

Violi, Francesco, Daví, Giovanni, Hiatt, William, Lip, Gregory Y. H., Corazza, Gino R., Perticone, Francesco, Proietti, Marco, Pignatelli, Pasquale, Vestri, Anna R., Basili, Stefania, Desideri, ARAPACIS Study Investigators Alessandri Cesare (Dipartimento di Scienze e Biotecnologie Medico-Chirurgiche, G., Sapienza-Università di Roma), Serviddio Gaetano (Department of Medical and Surgical Sciences, University of Foggia), Fascetti Stefano (UOC Medicina Generale, USL 12 Viareggio, Toscana), Serra, Pietro, Palange Paolo(UOC Medicina Interna, I, Dipartimento di Sanità Pubblica, e Malattie Infettive, Greco, Eleonora, Bruno Graziella (Medicina, 3, Department of Medical Sciences, Città della Salute e della Scienza, A. O., University of Turin), Averna, Maurizio, Giammanco Antonina (Dipartimento Biomedico di Medicina Interna, e Specialistica (DIBIMIS), Università di Palermo), Sposito Pietro (Azienda Ospedaliera Ospedali Riuniti Papardo Piemonte, Messina), De Cristofaro Raimondo, De Gennaro Leonardo(Istituto di Medicina Interna, e Geriatria, Centro Emostasi, e Trombosi, Gemelli, Policlinico A., Roma), Loria, Paola, Pellegrini Elisa(Medicina Interna ad Indirizzo Metabolico, – NOCSAE Baggiovara, Department of Internal Medicine, Endocrinology, Metabolism and Geriatrics, Università degli Studi di Modena, e Reggio Emilia), Cominacini, Luciano, Mozzini Chiara (Dipartimento di Medicina, Sezione di Medicina Interna, D, Università di Verona), Sprovieri, Mario, Spagnuolo Vitaliano (UOC Medicina d'Urgenza, e PS, Stabilimento Ospedaliero dell'Annunziata, Cosenza), Cerqua Giannantonio (UOC Medicina Interna per l'Urgenza, S Giovanni Addolorata, Ao, Cerasola Giovanni, Mulé Giuseppe (Università degli Studi di Palermo), Barbagallo, Mario, Lo Sciuto Salvatore, Monteverde Alfredo(UOC di Geriatria, e Lungodegenza, Azienda Ospedaliera Universitaria Policlinico, Aoup, Palermo), Saitta, Antonino, Lo Gullo Alberto (UOC Medicina Interna, Università di Messina), Malatino, Lorenzo, Cilia Chiara (Clinica Medica, Ospedale, Cannizzaro, Università degli Studi di Catania), Licata, Giuseppe, Tuttolomondo, Antonino, Conigliaro Roberta (UOC Medicina Interna, e Cardioangiologia, Dipartimento Biomedico di Medicina Interna, e Specialistica, Università degli Studi di Palermo), Pinto, Antonio, Di Raimondo Domenico (UOC Medicina Vascolare, Dipartimento Biomedico di Medicina Interna e Specialistica, (Di. Bi. M. I. S. )., Signorelli, Santo, Anzaldi Massimiliano (Dipartimento di Medicina Interna, e Patologia, Università degli studi di Catania), De Palma Daniela, Galderisi, Maurizio, Cudemo Giuseppe (Dipartimento di Medicina Clinica, e Sperimentale, AUP Federico II di Napoli), Galletti, Ferruccio, Fazio Valeria(Dipartimento di Medicina Clinica, e Chirurgia, Università di Napoli Federico II), De Luca Nicola, Meccariello Alfonso (Centro Ipertensione, AUO Federico II, Napoli), Caputo, Dario, De Donato Maria Teresa (UO Medicina Interna, Azienda Ospedaliera Universitaria San Giovanni di Dio, e Ruggi D'Aragona, Salerno), Iannuzi, Arcangelo, Bresciani Alessandro (Divisione di Medicina Interna, Cardarelli, Osp. A., Giunta, Riccardo, Cimini Claudia (V Divisione Medicina Interna ed Immunoallergologia, Policlinico, Sun, Utili, Riccardo, Durante Mangoni Emanuele, Agrusta Federica (Medicina Infettivologica, e dei Trapianti, Monaldi, Ao, Sun, Napoli), Adinolfi Luigi, E., Sellitto, Cristiana, Restivo Luciano (Medicina Interna, Seconda Università di Napoli, Ospedale di Marcianise), Bellis, Paolo, Tirelli Paolo (UOC Medicina Interna e di Urgenza, e Pronto Soccorso, del Loreto Nuovo, P. O. S. M., Loreto, Mare), Sacerdoti, David, Pesce Paola (Clinica Medica, 5, Dipartimento di Medicina DIMED, Università degli Studi di Padova), Vanni Dino (UO Medicina Interna Arezzo, Ospedale San Donato, Azienda USL, 8 Arezzo), Iuliano, Luigi, Ciacciarelli, Marco, Pacelli Antonio (Department of Medico-Surgical Sciences and Biotechnology, Vascular Biology, Mass Spectrometry Lab, Sapienza-University of Rome), Palazzuoli Alberto (Sezione Cardiologia, Dipartimento di Medicina Interna, e Malattie Metaboliche, Università di Siena, Ospedale Le Scotte), Cacciafesta, Mauro, Gueli Nicola (UOC di Medicina Geriatrica, e Riabilitazione, Sapienza- Università di Roma, Capeci, William, Tarquinio, Nicola, Pellegrini Francesco (UO Medicina 'SS Benvenuto, e Rocco', Dipartimento di Medicina Interna, Asur, Marche, Area Vasta, n. 2., ex ZT 7), Vincentelli Giovanni Maria (UOS Breve Osservazione, Calibita 'Fatebenefratelli' Isola Tiberina, Ospedale S. G., Ravallese, Ferdinando, Santini Claudio (UOC Medicina Interna, Ospedale, Vannini, Letizia, Claudio, Petramala, Luigi, Zinnamosca Laura (UOD Ipertensione Secondaria, Dipartimento di Medicina Interna, e Specialità Mediche, Cilli, Mirella, Savoriti Claudio (UOC Medicina Interna F, e Malattie Metaboliche Dell'osso-Direttore Minisola Salvatore, Falaschi, Paolo, Martocchia, Antonio, Stefanelli Manuela (UO Geriatria, Andrea, Azienda Ospedaliera S., Facoltà di Medicina, e Psicologia, Marigliano, Vincenzo, Lo Iacono Cristina, Brusco Simona (Centro di Ricerca Interdipartimentale Scienze dell’Invecchiamento, Bertazzoni, Giuliano, Attalla El Halabieh Elias (UOC Medicina d’Urgenza, Dipartimento di Emergenza ed Accettazione, Paradiso, Michele, Lizzi Eugenio Maria, Timmi Stefano (Ospedale San Giovanni Battista, Ordine di Malta, Battisti Paola (Medicina Interna II, Ospedale San Giovanni-Addolorata, Cerci Sabina (UOC Medicina Interna, Ospedali Riuniti Frascati, Marino), Ciavolella Massimo (UOC Cardiologia-UTIC, Ospedale di Frascati, Di Veroli Claudio (Centro dell’Ipertensione Arteriosa e delle Malattie Metaboliche, e Renali, Casa di Cura 'San Domenico', Malci, Francesco, De Ciocchis Anita (UOC di Medicina Interna, Ospedale, ASL Roma, G, Subiaco), Abate, Damiano(Az., Castellino, Pietro, Curto, Irene, Vecchio Claudia (UOC Medicina Interna, Dipartimento di Scienze Mediche, e Pediatriche, Mannarino, Elmo, Pasqualini, Leonella, Fattori Chiara (Medicina Interna, Angiologia, e Malattie da Arteriosclerosi, Università degli Studi di Perugia), Pende, Aldo, Denegri, Andre, Artom Nathan (Clinica di Medicina Interna, 1, Università di Genova, San Martino - IST, IRCCS Az. Osp. Univ., Genova), Ricchio, Roberto, Fimognari Filippo Luca (UOC Geriatria, Azienda Ospedaliera di Cosenza, Alletto, Maurizio, Messina Simona (Unità Operativa di Medicina, Elia, Ospedale S., Caltanissetta), Sesti, Giorgio, Arturi, Franco, Grembiale Alessandro (Università degli Studi, UOC Medicina Interna, Policlinico Universitario 'Mater Domini'), Scarpino Paola Elisa, Carullo Giuseppe (Cattedra di Medicina Interna, UO Malattie Cardiovascolari, Campus Universitario di Germaneto, Università Magna Graecia di Catanzaro), Frugiuele, Pierluigi, Spagnuolo Vitaliano (UOC Medicina Interna, e Reumatologia, Stabilimento Ospedaliero Annunziata, Azienda Ospedaliera Cosenza), Battaglia Giuseppe (UO Lungodegenza, Serra San Bruno, S. O., ASP Vibo Valentia), Vidili, Gianpaolo, Atzori, Sebastiana, Delitala Giuseppe (Clinica Medica, Dipartimento di Medicina Clinica, e Sperimentale, Aou, Sassari), Davì, Giovanni, Angelucci, Ermanno, Sestili Simona (UOC di Clinica Medica, PO Clinicizzato di Chieti), Traisci, Giancarlo, De Feudis Lucrezia (UOC Medicina Interna, 2, PO di Pescara), Di Michele Dario, Fava Alessandra (UOC Medicina Interna, Asl, Teramo), Balsano, Clara, De Ciantis Pierpaolo (Dipartimento di Medicina Interna, e Sanità Pubblica, Università, dell'Aquila), Desideri, Giovambattista, Camerota Antonio (UOC Geriatria, e Lungodegenza Geriatrica, Dipartimento Medico ORM, Avezzano), Po, Migliacci, Rino, Medicina Interna, Porciello Giovanni (S. C., Ospedale della Valdichiana, Cortona, Usl, 8 Arezzo), Mezzetti Matteo (UOC Medicina Interna Ospedale del Casentino-Direttore Dr. Emilio Santoro, AUSL8 Arezzo), Gresele, Paolo, Vedovati, Cristina, Fierro Tiziana (Dipartimento di Medicina Interna, Sezione di Medicina Interna, e Cardiovascolare, Università di Perugia), Puccetti, Luca, Scarpini Francesca (Centro Aterosclerosi, Trombosi, e Coagulopatie, Università degli Studi di Siena, Azienda Ospedaliero-Universitaria Senese), Bertolotti, Marco, Mussi Chiara (UO Geriatria, Università degli Studi di Modena e Reggio Emilia), Dipartimento Integrato di Medicina Endocrinologia Metabolismo e Geriatria., Boddi, Maria, Savino, Andrea, Contri Silvia (Dipartimento di Area Critica Medico- Chirurgica, Università degli Studi di Firenze), Saller, Alois, Fabris Fabrizio (Clinica Medica1, Medicina Interna CLOPD, Departement of Medicine DIMED, University of Padova, Italy), Pesavento, Raffaele, Filippi, Lucia, Vedovetto Valentina (Dipartimento di Scienze Cardiologiche, Toraciche, e Vascolari, Clinica Medica, 2, Azienda Ospedaliera-Università di Padova), Puato Massimo (Clinica Medica IV, Dipartimento di Medicina, Azienda Ospedaliera Universitaria Padova, Padova), Fabris, Fabrizio, Treleani Martina (UOA Medicina, Policlinico, Universitario, Maselli, Monica, Corradin Maria Luisa, Giantin Valter (Clinica Geriatrica, Università di Padova), Semplicini Andrea (Medicina Interna, 1, Giovanni e Paolo, Ospedale SS., Venezia), Minuz, Pietro, Calabria, Stefano, Romano Simone (Sezione di Medicina Interna, C, Università di Verona, Aoui, Verona), Fantin, Francesco, Manica Angela (Dipartimento di Medicina, Sezione di Geriatria, Stockner, Ingrid, Pattis, Peter, Wiedermann), Gutmann Bernhard (Divisione di Medicina Interna-Direttore Prof. J., Ospedale centrale di Bolzano), Catena, Cristiana, Colussi GianLuca (Hypertension Unit and Division of Internal Medicine, Department of Experimental and Clinical Medical Science, University of Udine, Udine, Italy), Annoni, Giorgio, Bruni Adriana Antonella, Castagna Alberto (Clinica Geriatrica, Università degli Studi di Milano- Bicocca, Dipartimento di Scienze della Salute, AO San Gerardo, Monza), Spinelli Diana (Medicina Interna 1a, Dipartimento di Scienze Cliniche, e di Comunità, Fondazione, Irccs, Università di Milano), Corazza Gino Roberto, Miceli, Emanuela, Padula Donatella (Clinica Medica, I, Reparto, 11, IRCCS Policlinico San Matteo di Pavia, Pavia), Schinco, Giuseppina, Spreafico Sibilla (UOC Geriatria, Fondazione IRCCS Cà Granda, Ospedale Maggiore Policlinico), Secchi Beatrice (UOC Medicina Interna, Ospedale, Bassini, Milano), Vanoli, Massimo, Casella Gianluca (SC Medicina Interna, Azienda Ospedaliera della Provincia di Lecco, Ospedale di Merate, Lecco), Serra Maria Grazia (UOC Medicina, Panico', Azienda Ospedaliera 'Cardinale G., Lecce), Longo, Stefania, Antonaci Salvatore (UOC Medicina Interna, Azienda Ospedaliera Policlinico, Bari), Belfiore, Anna, Giuseppe Palasciano, Frualdo Mariella (Clinica Medica 'A. Murri'-Direttore Prof., Ventrella, Francesco, Iamele Luigi (Struttura Complessa di Medicina Interna, Cerignola, Asl, Foggia), Bianco Cesare (UOC Medicina Interna, Tropea), Santovito, Donato, Mezzetti, Andrea, Cipollone Francesco (Centro di Eccellenza Europeo, e di Riferimento Regionale per l'Aterosclerosi, l'Ipertensione Arteriosa, e le Dislipidemie, Università, Chieti), Nicolai, Salvatore, Salvati Filippo (UO Medicina Interna, Ospedale di Ortona, ASL 02 Abruzzo), Rini Giovan Battista, Scozzari Francesca (UOC Medicina Interna ed Ipertensione, Dipartimento Biomedico di Medicina Interna e Specialistica (Di. Bi. M. I., S), Giaccone' di Palermo), Policlinico 'P., Muiesan Maria Lorenza, Salvetti, Massimo, Bazza Abramo (Dipartimento di Scienze Cliniche, e Sperimentali, Università di Brescia, 2° Medicina Generale Spedali Civili, Brescia), Picardi, Antonio, De Vincentis Antonio (UOC Medicina Clinica, Policlinico Universitario Campus Bio-Medico, Cosio, Paolo, Terzolo Massimo (Medicina Interna, 1, Dipartimento di Scienze Cliniche, e Biologiche, AOU San Luigi Gonzaga, Università di Torino), Madaffari, Bruno, Parasporo Bruno (UO Medicina Interna, Azienda Ospedaliera Bianchi Melacrino Morelli, Reggio, Calabria), Fenoglio, Luigi, Bracco, Christian, Melchio Remo (SC Medicina Interna, Croce e Carle, AO S., Cuneo), Gentili, Tamira, Salvi Aldo (Medicina Generale, - Settore Subintensivo, Azienda, Ospedaliero-Universitaria, Ancona), Nitti, Cinzia, Falsetti Lorenzo (Medicina Generale, - Settore Ordinario, Gabrielli, Armando, Paglione Ivano (Clinica Medica, Capucci, Alessandro, Brambatti, Michela, Sparagna Armando (Clinica di Cardiologia, Ospedale, Torrette, Tirotta Daniela (UO Medicina Generale IV, Ospedale, Cervesi, Cattolica), Andreozzi, Paola, Ettorre, Evaristo, Cipriani Elisa (Area Geriatria, DAI Medicina Interna, Sapienza-Università di Roma, Rossi Fanelli Fillippo, Delfino Massimo (UOC Medicina Interna, H, Immunologia, Clinica, Nutrizione, Clinica, Endocrinologia, Glorioso, Nicola, Melis, Giada, Marras, Gianfranca, Matta Michela (Ambulatorio Ipertensione Arteriosa, e Patologie Correlate, Aou, Sassari, Sassari), Sacco Andrea (UOC Medicina Interna, PO Madonna delle Grazie, Matera), Stellitano, Elio, Scordo Anna (UO Medicina, PO 'Tiberio Evoli', Melito Porto Salvo), Russo, Franco, Caruso Assunta Antonietta (UOC Medicina Generale di Rogliano, AO di Cosenza), Porreca, Ettore, Santilli, Francesca, Tana Marco (UO Medicina Interna, e Geriatria, Ospedale Clinicizzato Colle Dell'Ara, D'Annunzio, Università G., Chieti-Pescara), Ferri, Claudio, Grassi, Davide, Di Giosia Paolo (Divisione di Medicina Interna Universitaria, - Ospedale San Salvatore, Dipartimento, Mesva, Università, Dell'Aquila, L'Aquila), Portincasa Piero (Clinica Medica 'Murri', Dipartimento di Scienze Mediche, e Oncologia Umana, Università degli Studi di Bari), Muscianisi Giuseppe (ASP Reggio Calabria, Saline Joniche), Giordani, Sara, Stanghellini Vincenzo (Dipartimento di Scienze Mediche, e Chirurgiche, Università degli Studi di Bologna), Sabbà, Carlo, Suppressa Patrizia (UOC Geriatria e Centro di assistenza, e ricerca sovraziendale per le malattie rare, Mancuso, Giuseppe, Bartone, Mosè, Calipari Daniela (UOC Medicina Interna, Presidio, Ospedaliero, ASP di Catanzaro), Arcidiacono, Giuseppe, Bellanuova Ignazio (UOC Cardiologia, e UTIC, Catania), Ferraro, Maria, Scalzo, Antonio, Marigliano Giampietro (ASP Cosenza), Cozzolino, Domenico, Lampitella, Antonio, Acri Vera (Dipartimento di Internistica Clinica, e Sperimentale, Galasso, Domenico, Mazzei, Francesca, Galasso Salvatore (RSA Madonna di Porto Gimigliano, Catanzaro), Buratti Alberto (Azienda Ospedaliera della Provincia di Pavia, UO Medicina Interna, Ospedale, Civile, Casorate, Primo, Porta, Massimo, Brizzi Maria Felice (SC Medicina Interna 1U, Azienda, Ospedaliera, Torino), Fattorini, Annalisa, Sampietro, Francesca, D’Angelo Armando (Coagulation Service and Thrombosis Research Unit, IRCCS Ospedale San Raffaele, Pala, Marco, Fabbian, Fabio, Manfredini Roberto (UOC Clinica Medica, Anna, Azienda Ospedaliera-Universitaria S., Ferrara), Moroni, Carlo, Valente, Lucia, Lopreiato Francesco (Laboratorio di Ecocardiografia-Cardiologia Preventiva, DAI Cuore, e Grossi Vasi, Parente Fernando (UOC Medicina Interna, Granata Massimo (Immunologia Clinica, A, Moia, Marco, Braham Simon (Fondazione IRCCS Ca'Granda, Ospedale Maggiore Policlinico, Rossi, Marco, Pesce Margherita (Dipartimento di Medicina Clinica, e Sperimentale, Università di Pisa), Gentile, Adelina, Catozzo Vania (UO Medicina, Ldp, Loreto, Ferranti, Edoardo, Soldini, Maurizio, Di Napoli Mariarosaria, Baciarello Giacinto (UOC Cardiologia Preventiva, e Riabilitativa, Rancan, Elena, Ageno, Walter, Guasti Luigina (Dipartimento di Medicina Clinica, e Sperimentale, Università, Dell'Insubria, Varese), Ciccaglioni, Antonio, Negri, Silvia, Polselli Marco (Centro Elettro-Stimolazione Cardiaca, Prisco Domenico (SOD Patologia Medica, Aou, Careggi, Firenze), Pignataro Francesca Serena, Pastori, Daniele, Ferro, Domenico, Loffredo, Lorenzo, Cangemi, Roberto, Perri, Ludovica, Polimeni, Licia, Catasca, Elisa, Raparelli, Valeria, Napoleone, Laura, Schillizzi, Marianna, Vicario, Tommasa, Russo, Roberta, Gentile Maria Cristina, Saliola, Mirella, Del Ben Maria, Angelico Francesco (I Clinica Medica, Sapienza-Università di, Roma)., Violi F, Daví G, Hiatt W, Lip GY, Corazza GR, Perticone F, Proietti M, Pignatelli P, Vestri AR, Basili S, ARAPACIS Study Investigators: […, Alessandri C, Serviddio G, Fascetti S, Serra P, Palange P, Greco E, Bruno G, Averna M, Giammanco A, Sposito P, De Cristofaro R, De Gennaro L, Loria P, Pellegrini E, Cominacini L, Mozzini C, Spovieri M, Spagnuolo V, Cerqua G, Cerasola G, Mulé G, Barbagallo M, Lo Sciuto S, Monteverde A, Saitta A, Lo Gullo A, Malatino L, Cilia C, Licata G, Tuttolomondo A, Conigliaro R, Pinto A, Di Raimondo D, Signorelli S, Anzaldi M, De Palma D, Galderisi M, Cudemo G, Galletti F, Fazio V, De Luca N, Meccariello A, Caputo D, De Donato MT, Iannuzi A, Bresciani A, Giunta R, Cimini C, Utili R, Durante M, Emanuele AF, Adinolfi LE, Cristiana S, Restivo L, Bellis P, Tirelli P, Sacerdoti D, Pesce P, Vanni D, Iuliano L, Palazzuoli A, Cacciafesta M, Gueli N, Capeci W, Tarquino N, Pellegrini F, Vincentelli GM, Ravallese F, Santini C, Letizia C, Petramala L, Zinnamosca L, Cilli M, Savoriti C, Falaschi P, Martocchia A, Stefanelli M, Marigliano V, Lo Iacono C, Brusco S, Bertazzoni G, El Halabieh Elias A, Paradiso M, Lizzi EM, Stefano T, Paola B, Cerci S, Ciavolella M, Di Veroli C, Malci F, De Ciocchis A, Abate D, Castellino P, Curto I, Vecchio C, Mannarino E, Pasqualini L, Fattori C, Pende A, Denegri A, Nathan A, Ricchio R, Fimognari FL, Alletto M, Messina S, Sesti G, Arturi F, Gembiale A, Scarpino PE, Carullo G, Pierluigi F, Battaglia G, Vadili G, Atzori S, Delitala G, Davì G, Angelucci E, Simona S, Giancarlo T, De Feudis L, Di Michele D, Fava A, Balsano C, De Ciantis P, Giovambattista D, Camerota A, Migliacci R, Porciello G, Mezzetti M, Gresele P, Vedovati C, Fierro T, Puccetti L, Scarpini F, Bertolotti M, Mussi C, Boddi M, Savino A, Contri S, Saller A, Fabris F, Pesavento R, Filippi L, Vedovetto V, Puato M, Treleani M, Maselli M, Corradin ML, Giantin V, Semplicini A, Minuz P, Calabria S, Romano S, Fantin F, Manica A, Stockner I, Pattis P, Guttman B, Catena C, Colussi GL, Annoni G, Bruni AA, Castagna A, Miceli E, Padula D, Schinco G, Spreafico S, Secchi B, Vanoli M, Casella G, Serra MG, Longo S, Antonaci S, Belfiore A, Frualdo M, Francesco V, Iamele L, Bianco C, Santovito D, Mezzetti A, Cipollone F, Nicolai S, Salvati F, Battista RG, Scozzari F, Muiesan ML, Salvetti M, Bazza A, Picardi A, De Vincentis A, Cosio P, Terzolo M, Fenoglio L, Bracco C, Melchio R, Gentili T, Salvi A, Nitti C, Falsetti L, Gabrielli A, Paglione I, Capucci A, Brambatti M, Sparagna A, Tirotta D, Andreozzi P, Ettorrre E, Cipriani E, Fanelli Fillippo R, Delfino M, Glorioso N, Melis G, Marras G, Matta M, Sacco A, Stellitano E, Scordo A, Russo F, Caruso Assunta A, Porreca E, Santilli F, Tana M, Ferri C, Grassi D, Di Giosia P, Portincasa P, Muscianisi G, Giordani S, Stanghellini V, Sabbà C, Supressa P, Mancuso G, Bartone M, Calipari D, Arcidiacono G, Bellanuova I, Ferraro M, Scalzo A, Marigliano G, Cozzolina D, Lampitella A, Acri V, Galasso D, Mazzei F, Galasso S, Buratti A, Porto M, Brizzi MF, Fattorini A, Sampietro F, D'Angelo A, Pala M, Fabbian F, Manfredini R, Moroni C, Valente L, Lopreiato F, Parente F, Granata M, Moia M, Braham S, Rossi M, Pesce M, Gentile A, Catozzzo V, Ferranti E, Soldini M, Di Napoli M, Baciarello G, Rancan E, Ageno W, Guasti L, Ciccaglioni A, Negri S, Polselli M, Prisco D, Pignataro FS, Pastori D, Ferro D, Loffredo L, Cangemi R, Perri L, Polimeni L, Catasca E, Raparelli V, Napoleone L, Schillizzi M, Vicario T, Russo R, Gentile MC, Saliola M, Del Ben M, Angelico F, Farcomeni A, Di Tanna G, Davi' G, Traisci G, Montebianco Abenavoli L, Grembiale A, Di Minno G, Durante ME, Pattoneri P, Boari B, Fabio G, Perego F, Bianchi Paola I, Angeli A, Colombo BM, Giannelli G, Vidili G, Torres D, Hijazl D, Gatta A, Mannucci Mannuccio P, Licata G., and …]

Subjects
Adult, Male, Risk, therapy, atrial fibrillation, cardiovascular disease, peripheral vascular disease, Aged, Atrial Fibrillation, Female, Humans, Internal Medicine, Italy, Middle Aged, Peripheral Arterial Disease, Prevalence, Registries, Societies, Medical, Ankle Brachial Index, ATRIAL FIBRILLATION, Cardiology and Cardiovascular Medicine, Medical, RISK FACTORS, cardiovascular diseases, Societies
Abstract

To the Editor: Nonvalvular atrial fibrillation (NVAF) is the most common sustained arrhythmia encountered in clinical practice and is associated with a 5-fold increased risk for stroke (1). Moreover, patients with NVAF often suffer from atherosclerotic complications such as acute myocardial infarction (AMI) (2). Peripheral artery disease (PAD) is an established marker of systemic atherosclerosis but its prevalence in NVAF is still unclear. We reasoned that inclusion of ankle-brachial index (ABI), which is an established tool for diagnosis of PAD (3), in the CHA2DS2-VASc (4) score would better define the prevalence of vascular disease. To address this issue, the Italian Society of Internal Medicine (SIMI) established an Italian registry documenting ABI in NVAF patients. The Atrial Fibrillation Registry for the ARAPACIS (Ankle-brachial Index Prevalence Assessment: Collaborative Italian Study) study is an independent research project involving all Regional Councils of SIMI. The first objective of the study was to estimate the prevalence of ABI ≤0.90 in NVAF patients. Consecutive patients with NVAF referred to internal medicine wards were eligible for the enrollment. Enrollment started in October 2010 and continued until October 30, 2012. Patients were enrolled if they were 18 years or older and had a diagnosis of NVAF, recording during the qualifying admission/consultation or in the preceding 12 months, and if it was possible to obtain the ABI measurement. Exclusion criteria included the following: acquired or congenital valvular AF, active cancer, disease with life expectancy 0.90 (93% vs. 82%; p < 0.0001). Logistic regression analysis demonstrated that ABI ≤0.90 was significantly associated with a smoking habit (odds ratio [OR]: 1.99; 95% confidence interval [CI]: 1.48 to 2.66; p < 0.0001), diabetes (OR: 1.93; 95% CI: 1.51 to 2.46; p < 0.0001), age class 65 to 74 years (OR: 2.05; 95% CI: 1.40 to 3.07; p < 0.0001), age class ≥75 years (OR: 3.12; 95% CI: 2.16 to 4.61; p < 0.0001), and history of previous transient ischemic attack/stroke (OR: 1.64; 95% CI: 1.20 to 2.24; p = 0.002). Vascular disease, as assessed by the history elements of CHA2DS2VASc score, was recorded in 17.3% of patients; inclusion of ABI ≤0.90 in the definition of vascular disease yielded a total prevalence of 33%. A higher prevalence of vascular disease was detected if ABI ≤0.90 was included in the CHA2DS2VASc score (Fig. 1). CHA2DS2VASc including ABI ≤0.90 was more associated with previous stroke (43%; OR: 1.85; 95% CI: 1.41 to 2.44; p < 0.0001) compared to CHA2DS2VASc with ABI 0.91 to 1.39 (23%; OR: 1.52; 95% CI: 1.10 to 2.11; p = 0.0117). To the best of our knowledge, there is no large-scale study that specifically examined the prevalence of ABI ≤0.90 in NVAF. In our population, 21% had ABI ≤0.90 indicating that NVAF is often associated with systemic atherosclerosis. The CHADS2 has been recently refined with the CHA2DS2-VASc score, which includes vascular disease as documented by a history of AMI, symptomatic PAD, or detection of atherosclerotic plaque in the aortic arch (4). Comparison of vascular prevalence as assessed by CHA2DS2-VASc score and/or ABI ≤0.90 is of interest to define the potentially positive impact of measuring ABI in the management of NVAF patients. Inclusion of ABI ≤0.90 in the definition of vascular disease greatly increased the prevalence of vascular disease, which increased from 17.3% (based on history alone) to 33% (based on ABI) in the entire population. If ABI ≤0.90 was encompassed in the definition of vascular disease of CHA2DS2-VASc score the prevalence of vascular disease increased in every risk class. Inclusion of ABI ≤0.90 in the CHA2DS2-VASc score allowed us to better define the risk profile of NVAF patients with an up-grading of the risk score in each CHA2DS2-VASc score category. This may have important therapeutic implications if the new score could be tested prospectively, as a higher number of NVAF patients would potentially be candidates for an anticoagulant treatment by measuring ABI. A prospective study is, therefore, necessary to validate the risk score of this new definition of vascular disease. In conclusion, this study provides the first evidence that one-fifth of NVAF patients had an ABI ≤0.90, indicating that it may represent a simple and cheap method to better define the prevalence of vascular disease in NVAF.

Published
2013

245. Ketoprofen, peginterferon-alpha2a and ribavirin for genotype 1 chronic hepatitis C: a phase II study

Author

S. Anticoli, Carmela Cursaro, Maddalena Salerno, Marzia Margotti, Annagiulia Gramenzi, Giuliano Furlini, Silvia Galli, Mauro Bernardi, Clara Balsano, Elisabetta Loggi, A. Spaziani, Pietro Andreone, Gramenzi A, Cursaro C, Margotti M, Balsano C, Spaziani A, Anticoli S, Loggi E, Salerno M, Galli S, Furlini G, Bernardi M, and Andreone P.

Subjects
Male, Ketoprofen, LIVER, viruses, Pilot Projects, Pharmacology, Polyethylene Glycols, law.invention, chemistry.chemical_compound, law, Interferon, CLINICAL PHARMACOLOGY, 2',5'-Oligoadenylate Synthetase, Medicine, Clinical pharmacology, Anti-Inflammatory Agents, Non-Steroidal, Gastroenterology, virus diseases, General Medicine, Hepatitis C, Middle Aged, Recombinant Proteins, STAT1 Transcription Factor, Treatment Outcome, Drug Therapy, Combination, Female, Viral hepatitis, Signal Transduction, medicine.drug, Adult, NON-STEROIDAL ANTIINFLAMMATORY, Adolescent, Genotype, Brief Article, Combination therapy, VIRAL HEPATITIS, Interferon alpha-2, CHRONIC HEPATITIS C, Antiviral Agents, Young Adult, Ribavirin, Humans, Aged, business.industry, Interferon-alpha, Hepatitis C, Chronic, biochemical phenomena, metabolism, and nutrition, medicine.disease, digestive system diseases, stomatognathic diseases, chemistry, Pharmacodynamics, business
Abstract

To evaluate the safety of adding ketoprofen to pegylated-interferon (PEG-IFN) with or without ribavirin and the effect on viral kinetics, STAT1 activity and expression of 2'-5'-oligoadenylate synthetase (2'-5'OAS) in genotype 1 chronic hepatitis C in a phase II study.Forty-five patients were studied: fifteen were randomized to PEG-IFN plus ribavirin (PR), 16 to PEG-IFN plus ketoprofen and 14 to PR and ketoprofen. The molecular study of IFN-dependent signal transduction was conducted in 9 patients from each group.The combination of ketoprofen and PEG-IFN with or without ribavirin was safe and well tolerated. An early activation of STAT1 was observed in ketoprofen-treated patients, but this activation was less sustained over time. Conversely, ketoprofen plus PEG-IFN and ribavirin induced an early and sustained increase of 2'-5'OAS transcription starting 24 h after the first dose until the 36th wk. These data are consistent with the clinical results, showing a better sustained virological response and a lower relapse rate in patients receiving ketoprofen plus PEG-IFN and ribavirin.The addition of ketoprofen to the standard therapy of chronic hepatitis C should be explored in larger randomized clinical studies.

Published
2009

246. Differential regulation of E2F1 apoptotic target genes in response to DNA damage

Author

Laura Belloni, Alessandra Ianari, Natalia Pediconi, Antonio Porcellini, Edoardo Alesse, Massimo Levrero, Isabella Screpanti, Rita Gallo, Letizia Cimino, Alberto Gulino, Clara Balsano, Antonio Costanzo, Pediconi, N, Ianari, A, Costanzo, A, Belloni, L, Gallo, R, Cimino, L, Porcellini, Antonio, Screpanti, L, Balsano, C, Alesse, E, Gulino, A, and Levrero, M.

Subjects
Messenger, Apoptosis, Cell Cycle Proteins, Histones, Genes, Reporter, Tumor Cells, Cultured, E2F1, Tumor Protein p73, Genes, Tumor Suppressor, Promoter Regions, Genetic, Etoposide, Settore MED/35 - Malattie Cutanee e Veneree, Cultured, Nuclear Proteins, E2F1 Transcription Factor, Acetylation, Chromatin, Cell biology, Tumor Cells, DNA-Binding Proteins, biological phenomena, cell phenomena, and immunity, E2F Transcription Factors, Tumor Suppressor, Transcriptional Activation, endocrine system, DNA damage, Biology, Promoter Regions, Genetic, DNA Damage, Humans, Doxorubicin, Tumor Suppressor Proteins, Fibroblasts, Gene Deletion, RNA, Messenger, Transcription Factors, Gene Expression Regulation, E2F, Transcription factor, Reporter, Cell Biology, Genes, Cancer research, RNA, Chromatin immunoprecipitation
Abstract

E2F1, a member of the E2F family of transcription factors, in addition to its established proliferative effect, has also been implicated in the induction of apoptosis through p53-dependent and p53-independent pathways. Several genes involved in the activation or execution of the apoptotic programme have recently been shown to be upregulated at the transcriptional level by E2F1 overexpression, including the genes encoding INK4a/ARF, Apaf-1, caspase 7 and p73 (refs 3-5). E2F1 is stabilized in response to DNA damage but it has not been established how this translates into the activation of specific subsets of E2F target genes. Here, we applied a chromatin immunoprecipitation approach to show that, in response to DNA damage, E2F1 is directed from cell cycle progression to apoptotic E2F target genes. We identify p73 as an important E2F1 apoptotic target gene in DNA damage response and we show that acetylation is required for E2F1 recruitment on the P1p73 promoter and for its transcriptional activation.

Published
2003

247. Occult hepatitis B virus infection

Author

Massimo Levrero, Giovanni Squadrito, Claudio Tiribelli, Mario U. Mondelli, Antonio Craxì, Teresa Pollicino, Fabio Farinati, Clara Balsano, Giovanni Raimondo, Raimondo, G, Balsano, C, Craxi, A, Farinati, F, Levrero, M, Mondelli, M, Pollicino, T, Squadrito, G, and Tiribelli, Claudio

Subjects
Male, ACUTE VIRAL-HEPATITIS, POSTTRANSFUSION HEPATITIS, HBV SURFACE-ANTIGEN, Comorbidity, HBV genome, HBsAg-negative, liver DNA, liver disease, medicine.disease_cause, Severity of Illness Index, SEROLOGICAL MARKERS, TRANSPLANT RECIPIENTS, HEPATITIS C VIRUS, HEPATOCELLULAR-CARCINOMA, CHRONIC LIVER-DISEASE, POLYMERASE CHAIN-REACTION, occult hepatitis B virus infection, Liver disease, Chronic/diagnosis* Hepatitis B, Differential Disease Progression Female Hepatitis B Surface Antigens/analysis* Hepatitis B, hbsag-negative, hbv genome, liver disease, liver dna, Incidence, Hepatocellular/diagnosis Carcinoma, Liver Neoplasms, Gastroenterology, Hepatitis C, Hepatitis B, Prognosis, Chronic/epidemiology* Humans Incidence Liver Neoplasms/diagnosis Liver Neoplasms/epidemiology* Male Prognosis Risk Assessment Severity of Illness Index, Carcinoma, Hepatocellular/diagnosis Carcinoma, Hepatocellular/epidemiology* Comorbidity DNA, Viral/analysis Diagnosis, Differential Disease Progression Female Hepatitis B Surface Antigens/analysis* Hepatitis B, Chronic/diagnosis* Hepatitis B, Chronic/epidemiology* Humans Incidence Liver Neoplasms/diagnosis Liver Neoplasms/epidemiology* Male Prognosis Risk Assessment Severity of Illness Index, Hepatocellular carcinoma, Disease Progression, Female, Carcinoma, Hepatocellular, Risk Assessment, Diagnosis, Differential, Hepatitis B, Chronic, Viral/analysis Diagnosis, medicine, Humans, Risk factor, Hepatitis B virus, Hepatitis B Surface Antigens, Hepatology, business.industry, Carcinoma, medicine.disease, Occult, Virology, Hepatocellular/epidemiology* Comorbidity DNA, Viral replication, Immunology, DNA, Viral, business
Abstract

Many studies have shown that hepatitis B virus infection may also occur in hepatitis B surface antigen-negative patients. This occult infection has been identified both in patients with cryptogenic liver disease and in patients with hepatitis C virus-related chronic hepatitis, and much evidence suggests that it may be a risk factor of hepatocellular carcinoma development. However several aspects of this occult infection remain unclear such as its prevalence and the factor(s) involved in the lack of circulating hepatitis B surface antigen. Moreover, it is uncertain whether the occult hepatitis B virus infection may contribute to chronic liver damage, considering that it is usually associated with a suppressed viral replication. Evidence and hypotheses concerning this fascinating field of bio-medical research are reviewed.

Published
2000

248. Fas/Apo1 mutations and autoimmune lymphoproliferative syndrome in a patient with type 2 autoimmune hepatitis

Author

Gioacchino Natoli, Daniele Accapezzato, Angelo Ianni, C. Balsano, R. Nisini, Lina Pensati, Angela Vegnente, Raffaele Iorio, Cristiana Almerighi, Massimo Levrero, Antonio Costanzo, Pietro Vajro, Pensati, L, Costanzo, A, Ianni, A, Accapezzato, D, Iorio, Raffaele, Natoli, G, Nisini, R, Almerighi, C, Balsano, C, Vajro, P, Vegnente, A, and Gastroenterology, LEVRERO M. FASAPO MUTATIONS AND AUTOIMMUNE LYMPHOPROLIFERATIVE SYNDROME IN A. PATIENT WITH TYPE AUTOIMMUNE H. E. P. A. T. I. T. I. S.

Subjects
Male, pediatrics, CD3, Hepatosplenomegaly, Apoptosis, Autoimmune hepatitis, medicine.disease_cause, Autoimmunity, Autoimmune Diseases, Hepatitis, Liver disease, Liver Function Tests, T-Lymphocyte Subsets, medicine, Humans, Point Mutation, Fas/Apo1 mutations, fas Receptor, Alleles, Autoantibodies, autoimmune lymphoproliferative syndrome, type 2 autoimmune hepatitis, Hepatology, biology, Gastroenterology, Syndrome, Fas receptor, medicine.disease, Lymphoproliferative Disorders, Immunoglobulin A, Pedigree, Immunoglobulin M, Autoimmune lymphoproliferative syndrome, Child, Preschool, Immunoglobulin G, Immunology, Splenomegaly, biology.protein, Female, medicine.symptom, Hepatomegaly
Abstract

Inherited mutations of the Fas/Apo1/CD95 gene, a cell-surface receptor involved in cell death signaling and in the control of self-reactivity, characterize the recently identified autoimmune lymphoproliferative syndromes. A patient with type 2 autoimmune hepatitis with the immunologic and genetic features of autoimmune lymphoproliferative syndrome is described. The clinical picture was dominated by liver disease with hepatosplenomegaly and positivity for anti-liver-kidney microsome 1 and anti-liver-cytosol 1 antibodies. A marked increase in CD3+CD4-CD8-T lymphocytes and inherited mutations in Fas alleles that led to the expression of a soluble form of the protein were also found. Fas-mediated apoptosis was deficient in the patient as it was in her mother and her sister, who carried the same allele 2 mutation. This observation links type 2 autoimmune hepatitis, an organ-specific disease, with a genetically determined defect in peripheral tolerance control.

Published
1997

Catalog

Books, media, physical & digital resources
See catalog results