60 results on '"Di Stefano, Rosa"'
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52. Parvovirus B19 and ‘cryptogenic’ chronic hepatitis
- Author
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Arista, Serenella, De Grazia, Simona, Di Marco, Vito, Di Stefano, Rosa, and Craxı̀, Antonio
- Published
- 2003
- Full Text
- View/download PDF
53. Schistosomiasis and antiviral treatment of chronic hepatitis C.
- Author
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Di Marco, Vito, Capra, Marcello, Gagliardotto, Francesco, Ferraro, Donatella, and Di Stefano, Rosa
- Published
- 2001
- Full Text
- View/download PDF
54. La ' Littérature ' de Bouvard et Pécuchet d'après les notes sur les ' Grands écrivains '
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Palermo, Rosa Maria, Facoltà di Lettere e Filosofia - Università di Messina - Italia, Università di Messina - Italia, ANR-07-CORP-0009,BOUVARD,Les Dossiers de Bouvard et Pécuchet de Flaubert. Enrichissement, valorisation, documentation d'un corpus multi supports(2007), Palermo Di Stefano, Rosa Maria, and Corpus et outils de la recherche en sciences humaines et sociales - Les Dossiers de Bouvard et Pécuchet de Flaubert. Enrichissement, valorisation, documentation d'un corpus multi supports - - BOUVARD2007 - ANR-07-CORP-0009 - CORP - VALID
- Subjects
[SHS.LITT] Humanities and Social Sciences/Literature ,Flaubert ,édition électronique ,Bouvard et Pécuchet ,[SHS.LITT]Humanities and Social Sciences/Literature ,humanités numériques - Published
- 2012
55. Occult Hbv infection and its reactivation in immunosuppressed patients
- Author
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PIZZILLO, Paola, Pizzillo, ., and DI STEFANO, ROSA
- Subjects
Settore MED/07 - Microbiologia E Microbiologia Clinica ,Occult hbv infection ,immunosuppressed patients - Published
- 2011
56. No detection of occult HBV-DNA in patients with various rheumatic diseases treated with anti-TNF agents: a two-year prospective study.
- Author
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Giardina AR, Ferraro D, Ciccia F, Ferrante A, Di Stefano R, Craxì A, and Triolo G
- Subjects
- Academic Medical Centers, Adult, Antirheumatic Agents adverse effects, Antiviral Agents therapeutic use, Biomarkers blood, Female, Hepatitis B blood, Hepatitis B epidemiology, Hepatitis B prevention & control, Hepatitis B Surface Antigens blood, Hepatitis B virus drug effects, Hepatitis B virus immunology, Humans, Italy epidemiology, Lamivudine therapeutic use, Male, Middle Aged, Polymerase Chain Reaction, Prospective Studies, Rheumatic Diseases diagnosis, Rheumatic Diseases epidemiology, Rheumatic Diseases immunology, Risk Assessment, Risk Factors, Time Factors, Treatment Outcome, Virus Activation, Antirheumatic Agents therapeutic use, DNA, Viral blood, Hepatitis B diagnosis, Hepatitis B virus genetics, Rheumatic Diseases drug therapy, Tumor Necrosis Factor-alpha antagonists & inhibitors
- Abstract
Objectives: The widespread use of tumour necrosis factor (TNF)-targeted therapies in patients with rheumatic, digestive and dermatologic diseases has been associated with reports of reactivation of HBV replication and ensuing hepatitis flares both in asymptomatic HBsAg carriers and in subjects with occult HBV infection. The aim of our work was to investigate in a two-year prospective study the potential for HBV reactivation in patients with inflammatory joint diseases undergoing anti-TNF treatment from a southern Mediterranean area., Methods: Fifty-seven consecutive outpatients attending the Academic Unit of Rheumatology at the University of Palermo (12 with rheumatoid arthritis, 17 with psoriatic arthritis and 28 with ankylosing spondylitis) were enrolled in the study. HBV-DNA was tested by a standard quantitative assay in HBsAg-positive subjects and by an ad hoc highly sensitive PCR in HBsAg-negative patients performed at baseline and then every six months on the anti-TNF agent., Results: Occult HBV-DNA was never detected in the 54 HBsAg negative subjects, regardless of their anti HBs/HBc status. All HBsAg positive patients, who were started on prophylactic lamivudine, remained HBV-DNA undetectable throughout the anti-TNF treatment., Conclusions: Even in an area of previously high HBV endemicity, where occult HBV infection is likely to have a high prevalence, treatment of rheumatological patients with anti-TNF drugs is safe in terms of its potential to reactivate HBV. Prophylaxis with lamivudine is sufficient to prevent reactivation in HBsAg carriers.
- Published
- 2013
57. Liver disease in chelated transfusion-dependent thalassemics: the role of iron overload and chronic hepatitis C.
- Author
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Di Marco V, Capra M, Gagliardotto F, Borsellino Z, Cabibi D, Barbaria F, Ferraro D, Cuccia L, Ruffo GB, Bronte F, Di Stefano R, Almasio PL, and Craxì A
- Subjects
- Adolescent, Adult, Biopsy, Cohort Studies, Female, Hepacivirus genetics, Hepacivirus metabolism, Hepatitis C, Chronic pathology, Humans, Liver pathology, Liver Cirrhosis etiology, Liver Cirrhosis pathology, Liver Cirrhosis virology, Male, Retrospective Studies, Splenectomy, Thalassemia blood, Viral Load, Hepatitis C, Chronic complications, Iron Overload complications, Thalassemia etiology, Transfusion Reaction
- Abstract
Iron overload and hepatitis virus C infection cause liver fibrosis in thalassemics. In a monocentric retrospective analysis of liver disease in a cohort of 191 transfusion-dependent thalassemics, in 126 patients who had undergone liver biopsy (mean age 17.2 years; 58 hepatitis virus C-RNA positive and 68 hepatitis virus C-RNA negative) the liver iron concentration (median 2.4 mg/gr dry liver weight) was closely related to serum ferritin levels (R = 0.58; p<0.0001). Male gender (OR 4.12) and serum hepatitis virus C-RNA positivity (OR 11.04) were independent risk factors for advanced liver fibrosis. The majority of hepatitis virus C-RNA negative patients with low iron load did not develop liver fibrosis, while hepatitis virus C-RNA positive patients infected with genotype 1 or 4 and iron overload more frequently developed advanced fibrosis. Hepatitis virus C infection is the main risk factor for liver fibrosis in transfusion-dependent thalassemics. Adequate chelation therapy usually prevents the development of liver fibrosis in thalassemics free of hepatitis virus C-infection and reduces the risk of developing severe fibrosis in thalassemics with chronic hepatitis C.
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- 2008
- Full Text
- View/download PDF
58. Different doses of consensus interferon plus ribavirin in patients with hepatitis C virus genotype 1 relapsed after interferon monotherapy: a randomized controlled trial.
- Author
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Alaimo G, Di Marco V, Ferraro D, Di Stefano R, Porrovecchio S, D'Angelo F, Calvaruso V, Craxì A, and Almasio PL
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- Adult, Antiviral Agents administration & dosage, Antiviral Agents adverse effects, Dose-Response Relationship, Drug, Drug Administration Schedule, Drug Therapy, Combination, Female, Hepatitis C, Chronic prevention & control, Humans, Interferon Type I administration & dosage, Interferon Type I adverse effects, Interferon-alpha, Male, Middle Aged, Recombinant Proteins, Recurrence, Ribavirin administration & dosage, Ribavirin adverse effects, Treatment Outcome, Viral Load, Antiviral Agents therapeutic use, Hepacivirus genetics, Hepatitis C, Chronic drug therapy, Interferon Type I therapeutic use, Ribavirin therapeutic use
- Abstract
Aim: To assess the efficacy of different schedules of consensus interferon (CIFN) plus ribavirin in retreating chronic hepatitis C patients who relapsed after recombinant interferon (rIFN) monotherapy., Methods: Forty-five patients (34 males and 11 females) with chronic hepatitis due to hepatitis C virus (HCV) genotype 1 who relapsed after a previous course of rIFN monotherapy were randomized to receive 9 mug CIFN three times per week for 52 wk (group A, n = 22) or 18 mug CIFN three times per week for 52 wk (group B, n = 23) in combination with ribavirin 800 to 1200 mg daily for 52 wk (according to body weight). Virological response was evaluated at week 24 (EVR), at the end of treatment (ETR) and at 76 wk (SVR)., Results: By intention-to-treat analysis, subjects in group A had an EVR in 35% of cases, an ETR in 35% and a SVR in 27.3% of cases. Subjects in group B had an EVR in 32% of cases, an ETR in 35% and a SVR in 26.1% of cases. Treatment was stopped because of adverse effects (mostly intolerance) in 15 patients (6 in group A and 9 in group B). IFN dose reduction was needed in 2 patients (1 in group A and 1 in group B). Ribavirin dose was reduced in 2 patients in group A and 1 in group B respectively. Among the 15 subjects who received at least 80% of the intended schedule, the rate of SVR was 80% (6 in group A and 6 in group B)., Conclusion: CIFN in combination with ribavirin when given to HCV genotype 1 relapsers after rIFN monotherapy obtains an unsatisfactory rate of sustained viral clearance independently of dosage of the drug. This may be due to its scarce tolerability.
- Published
- 2006
- Full Text
- View/download PDF
59. Hepatitis B virus reactivation and alemtuzumab therapy.
- Author
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Iannitto E, Minardi V, Calvaruso G, Mulè A, Ammatuna E, Di Trapani R, Ferraro D, Abbadessa V, Craxí A, and Di Stefano R
- Subjects
- Alemtuzumab, Antibodies, Monoclonal therapeutic use, Antibodies, Monoclonal, Humanized, Antibodies, Neoplasm therapeutic use, DNA, Viral blood, Female, Hepatitis B chemically induced, Hepatitis B drug therapy, Hepatitis B Surface Antigens blood, Humans, Immunosuppression Therapy adverse effects, Lamivudine therapeutic use, Leukemia, Lymphocytic, Chronic, B-Cell drug therapy, Male, Middle Aged, Reverse Transcriptase Inhibitors therapeutic use, Antibodies, Monoclonal adverse effects, Antibodies, Neoplasm adverse effects, Hepatitis B virus, Leukemia, Lymphocytic, Chronic, B-Cell complications, Virus Activation
- Abstract
Reactivation of hepatitis B virus infection in subjects receiving cytotoxic treatment for heamatological malignancies occurs in 21-53% of chronic HBsAg carriers and in an unknown number of HBsAg negative subjects harbouring occult HBV infection. Immunotherapy with alemtuzumab, a humanized monoclonal antibody against CD52 epitopes on lymphocytes cells produces deep immunosuppression. We describe two subjects with chronic lymphocytic leukaemia and occult HBV infection who developed a virological and biochemical flare of hepatitis B following immunotherapy with alemtuzumab. One of them developed full blown hepatitis with seroreversion from anti-HBs to HBsAg after four weeks of alemtuzumab therapy. Lamivudine (100 mg die) achieved a complete clinical recovery and HBV-DNA clearance from blood within 8 weeks. The second patient (HBsAg and HBV-DNA seronegative, anti-HBs and anti-HBc positive before treatment) was kept under prophylaxis with lamivudine up to three months after alemtuzumab. Two months after withdrawal of lamivudine, clinical and laboratory features of acute hepatitis B developed. Lamivudine therapy was restarted and a prompt recovery was obtained with HBsAg and HBV-DNA clearance.
- Published
- 2005
- Full Text
- View/download PDF
60. HBV-DNA suppression and disease course in HBV cirrhosis patients on long-term lamivudine therapy.
- Author
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Di Marco V, Di Stefano R, Ferraro D, Almasio PL, Bonura C, Giglio M, Parisi P, Cappello M, Alaimo G, and Craxì A
- Subjects
- Adult, Aged, Cohort Studies, DNA, Viral genetics, Drug Administration Schedule, Female, Hepatitis B virology, Hepatitis B virus genetics, Humans, Liver Cirrhosis virology, Male, Middle Aged, Mutation, Virus Replication, Antiviral Agents therapeutic use, DNA, Viral blood, Hepatitis B physiopathology, Lamivudine therapeutic use, Liver Cirrhosis physiopathology
- Abstract
In hepatitis B virus (HBV) cirrhosis patients on long-term lamivudine (LAM), the relationships between HBV suppression, development of viral resistance and disease outcome are unclear. We analysed the dynamic of serum HBV-DNA and its relationship with the clinical course of 59 patients (52 males, mean age 51.4 +/- 8.4 years, 12 HBeAg positive and 47 HBeAg negative, and 57 genotype D and two genotype A) with cirrhosis (45 in Child-Turcotte-Pugh class A) and high levels of serum HBV-DNA (median 14.7 x 10(7) genomes/ml) treated with LAM [median (range): 44 (15-78) months]. A total of 50 patient (84.7%) achieved a virological response (serum HBV-DNA negative by PCR) during the first 6 months of therapy, and nine (13.3%) achieved a reduction in viral load of > 3 log10. Mutations in the YMDD motif of HBV polymerase were documented in 26 patients [median (range) 18: (7-42) months]. At the time of the emergence of mutants, 22 patients had HBV-DNA < 10(5) genomes/ml and normal alanine aminotransferase (ALT) levels. The appearance of virological resistance was followed by an increase of HBV-DNA to > 10(5) genomes/ml and of ALT values in 19 out of 26 patients [median (range): 8 (3-19) months]. Event-free survival was significantly longer (P = 0.001) in patients who maintained virological suppression than in those who did not have a complete virological response or suffered a breakthrough. Patients with advanced cirrhosis were more likely to develop liver failure after the emergence of YMDD mutants. The risk of development of hepatocellular carcinoma in patients with compensated cirrhosis and YMDD mutations was maintained, regardless of HBV-DNA serum levels. Profound and maintained HBV-DNA suppression correlates with a better outcome. Early identification of LAM resistance mutations allows switching to other antivirals before liver decompensation or hepatocellular carcinoma development.
- Published
- 2005
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