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ABSTRACT

Title
Peg-Interferon / Telbivudine sequential therapy in e antigen (HBeAg) negative severe chronic hepatitis B.
 
Authors
L. Gallelli1, O. Staltari O2, B. Caroleo2, V.Guadagnino2, G. De Sarro1
 
1Chair of Pharmacology, Department of Experimental and Clinical Medicine, School of Medicine and Surgery, University “Magna Graecia” of Catanzaro, Clinical Pharmacology and Pharmacovigilance Unit, “Mater Domini” University Hospital, Via T. Campanella 115, 88100 Catanzaro, Italy.
 
2Chair of Infective Diseases, Department of Experimental and Clinical Medicine, School of Medicine, University of Catanzaro, Viale Europa – Germaneto, 88100 Catanzaro, Italy.
 
 
Abstract
Peg-Interferon / Telbivudine sequential therapy in e antigen (HBeAg) negative severe chronic hepatitis B. A case report.
 
Introduction
The natural history of chronic HBV infection ranges from a low viremic inactive carrier state to progressive chronic hepatitis, which may evolve to cirrhosis and hepatocellular carcinoma (HCC) (Brunetto et al., 2002; Perz et al., 2006).
The mainstays of pharmacotherapy are immunomodulators, such as interferon alpha and pegylated interferon (Peg-IFN) alpha-2a, and nucleos(t)ide analogues (i.e.: L-nucleosides: lamivudine, telbivudine and emtricitabine; deoxyguanosine analogues: entecavir; acyclic nucleoside phosphonates: adefovir and tenofovir. Adefovir, tenofovir, lamivudine) (Carosi and Rizzetto 2008,2009).
We report the efficacy of sequential Peg-IFN alpha-2a/telbivudine treatment in a patient affected by a severe HBeAg negative chronic infection.
 
Clinical case
63 year-old man, diabetic in insulinic treatment, affected by a histologically documented (Ishak fibrosis score: 6) liver cirrhosis, HBeAg negative, HBV-DNA positive (basal HBV-DNA levels: 2,700,000 IUs / ml by real-time PCR technique), serum alanine aminotransferase (ALT) levels: 140 U/L (n.v. <41U/L); functional class on admission: Child A5 without portal hypertension, anti-HDV and anti-HCV negative.
At the basal screening, all other known possible causes of liver diseases, including autoimmune, tesaurismosic and metabolic origin, were excluded.
On 23rdFebruary 2007, the patient started antiviral therapy with Peg-IFN alpha-2a (180 mcg/weekly subcutaneously) with a satisfactory virologic suppression at week 4. 48 weeks after the beginning of Peg-IFN alpha-2a, blood chemical examinations documented a complete suppression of HBV-DNA levels (<12 IUs/ml) and a normalization in ALT plasma values (38 IU/L); therefore on 6th February 2008 antiviral treatment was stopped.
At the 4th and 8th week after the treatment suspension, we recorded an increase in HBV-DNA plasma levels with normal ALT. On 6th May 2008, an antiviral treatment for HBV reactivation with LdT (600 mgs/day orally) was started with a rapid virologic and biochemical response after 4 weeks. At present, after 124weeks of LdT treatment, blood chemical tests document normal ALT and CPK plasma values; HBV-DNA remains undetectable. Moreover, no adverse drug reaction associated with LdT treatment has been observed.
In conclusion,we report the efficacy of a Peg-IFN alpha-2a/telbivudine sequential treatment in a patient showing a reactivation of HBV replication after a successful treatment course with Peg-IFN alpha-2a monotherapy.
 
Ref
Brunetto et al. J Hepatol 2002; 36: 263-70
Perz JF, et al. J Hepatol 2006; 45(4): 529-38.
Carosi and Rizzetto Dig Liver Dis 2008 Aug: 40 (8): 603-17  
Carosi and Rizzetto Dig Liver Dis 2009 Nov; 41 (11): 839-40)