المؤلفون: Seminari, E.¹ e.seminari@smatteo.pv.it, Silvestri, A.², Ravasio, V.³, Ludovisi, S.¹, Utili, R.⁴, Petrosillo, N.⁵, Castelli, F.⁶, Bassetti, M.⁷, Barbaro, F.⁸, Grossi, P.⁹, Barzaghi, N.¹⁰, Rizzi, M.³, Minoli, L.¹

المصدر: European Journal of Clinical Microbiology & Infectious Diseases. Feb2016, Vol. 35 Issue 2, p279-284. 6p.

مصطلحات موضوعية: *LIVER failure, *LIVER diseases, *LIVER disease diagnosis, *INPATIENT care, *ENDOCARDIUM diseases, *INFECTIVE endocarditis, *PATIENTS, *GENETICS

مستخلص: Few data have been published regarding the epidemiology and outcome of infective endocarditis (IE) in patients with chronic hepatic disease (CHD). A retrospective analysis of the Studio Endocarditi Italiano (SEI) database was performed to evaluate the epidemiology and outcome of CHD+ patients compared with CHD− patients. The diagnosis of IE was defined in accordance with the modified Duke criteria. Echocardiography, diagnosis, and treatment procedures were in accordance with current clinical practice. Among the 1722 observed episodes of IE, 300 (17.4 %) occurred in CHD+ patients. The cause of CHD mainly consisted of chronic viral infection. Staphylococcus aureus was the most common bacterial species in CHD+ patients; the frequency of other bacterial species ( S. epidermidis, streptococci, and enterococci) were comparable among the two groups. The percentage of patients undergoing surgery for IE was 38.9 in CHD+ patients versus 43.7 in CHD− patients ( p = 0.06). Complications were more common among CHD+ patients (77 % versus 65.3 %, p < 0.001); embolization (43.3 % versus 26.1 %, p < 0.001) and congestive heart failure (42 % versus 34.1 %, p = 0.01) were more frequent among CHD+ patients. Mortality was comparable (12.5 % in CHD− and 15 % in CHD+ patients). At multivariable analysis, factors associated with hospital-associated mortality were having an infection sustained by S. aureus, a prosthetic valve, diabetes and a neoplasia, and CHD. Being an intravenous drug user (IVDU) was a protective factor and was associated with a reduced death risk. CHD is a factor worsening the prognosis in patients with IE, in particular in patients for whom cardiac surgery was required. [ABSTRACT FROM AUTHOR]

المؤلفون: MARRONE, A.¹ (AUTHOR), ZAMPINO, R.¹ (AUTHOR), KARAYANNIS, P.² (AUTHOR), CIRILLO, G.³ (AUTHOR), CESARO, G.¹ (AUTHOR), GUERRERA, B.¹ (AUTHOR), RICCIOTTI, R.¹ (AUTHOR), MIRAGLIA DEL GIUDICE, E.³ (AUTHOR), UTILI, R.⁴ (AUTHOR), ADINOLFI, L. E.¹ (AUTHOR), RUGGIERO, G.¹ (AUTHOR)

المصدر: Alimentary Pharmacology & Therapeutics. Oct2005, Vol. 22 Issue 8, p707-714. 8p. 3 Charts.

مصطلحات موضوعية: *HEPATITIS B virus, *DRUG resistance, *VIRUS inhibitors, *ANTIVIRAL agents, *LIVER diseases, *VIRAL hepatitis, *GENETIC mutation, *THERAPEUTICS

مستخلص: Background : Drug-resistant mutants may emerge in patients with chronic hepatitis B receiving lamivudine therapy. Aim : To evaluate whether different viral mutational patterns may be associated with clinical reactivation during lamivudine treatment in patients with chronic B hepatitis. Methods : Eight anti-hepatitis B e-positive patients with (group A) and 14 patients without clinical exacerbation (five anti-hepatitis B e-positive, group B1; nine hepatitis B e antigen-positive, group B2) during lamivudine treatment were investigated. Results : ‘Polymerase region’: M204V/I variants were found in all group A patients, but in none of group B1 ( P = 0.0007) and in four of nine of group B2 (44%; P = 0.02) patients. The L180M substitution was detected in four of eight (50%) of group A and in none of groups B1 and B2. ‘Core promoter’: the double basic core promoter (A1762T/G1764A) variant was detected in seven of eight (87%) of group A and in one of five (20%; P = 0.03) of group B1 and one of nine (11%; P = 0.002) of group B2 patients. ‘Precore’: the G1896A stop codon mutation was present in seven of eight (87%) of group A and in zero of five ( P = 0.004) of group B1 and one of nine (11%; P = 0.002) of group B2. Conclusions : Different mutational patterns were observed in the lamivudine-treated patients with and without exacerbation. There was an association of the basic core promoter and stop codon mutations with lamivudine resistance in patients with disease exacerbation. [ABSTRACT FROM AUTHOR]

المؤلفون: Marrone, A.¹ aldo.marrone@unina2.it, Zampino, R.¹, Portella, G.², Grimaldi, M.², Mangoni, E. D.¹, Santarpia, L.¹, Ruggiero, G.¹, Utili, R.³

المصدر: Journal of Viral Hepatitis. Mar2005, Vol. 12 Issue 2, p186-191. 6p.

مصطلحات موضوعية: *INTERFERONS, *HEPATITIS B, *ANTINEOPLASTIC agents, *LYMPHOKINES, *GLYCOPROTEINS, *ANTIVIRAL agents, *LIVER diseases

مستخلص: Alpha-interferon (IFN) or lamivudine monotherapy are ineffective in treating chronic HBeAg positive patients with high viral load and low alanine aminotransferase (ALT) levels. We investigated whether priming lamivudine treatment might enhance the antiviral and immunostimulant action of lamivudine/IFN combination in young tolerant patients. Eleven chronic HBeAg positive patients received: 100 mg/day lamivudine for 3 months followed by IFN 5 MU/m2/tiw with lamivudine 100 mg/day for 6 months and then lamivudine alone 100 mg/day for 9 months. Quantitative hepatitis B virus (HBV)-DNA was evaluated during treatment and core-promoter, precore and polymerase HBV mutants were detected by direct sequencing at the end of therapy. Serum HBV-DNA levels dropped during lamivudine monotherapy and in combination with IFN. After IFN withdrawal, viraemia transiently increased to high levels in five of 11 (45%) patients who showed rt M204V/I lamivudine mutant resistant. Two patients cleared HBeAg without anti-HBe seroconversion. One patient presented core-promoter (A1762T/G1764A) and precore stop codon mutations. Hence, three-phase sequential combined lamivudine/IFN treatment reduced HBV-DNA serum level, but did not lead to HBeAg and HBV-DNA clearance in these highly viraemic, normal ALT patients. Lamivudine/IFN combination did not prevent the emergence of YMDD lamivudine resistance. New schedules of antiviral treatments must be evaluated in this population at risk of disease progression. [ABSTRACT FROM AUTHOR]