Hepatitis: Testino G

Testino G, Borro P, Sumberaz A. · Department of Specialist Medicine, San Martino Hospital, Genova, Italy; E-mail: · J Gastrointestin Liver Dis. · Pubmed #19565040 links to  free full text

This publication has no abstract.

Testino G. · Unit of Hepatology and Alcoholic Diseases, Department of Specialistic Medicine, S. Martino Hospital, Genova, Italy. · Hepatogastroenterology. · Pubmed #18613369 No free full text.

Abstract: Alcohol damages every organ and system in the body. The most important effects from a clinical point of view relate to diseases of the circulatory, nervous and hepato-gastrointestinal systems. In the digestive tract the effects range from increased intestinal transit time and gastrophaties, leading to classical early morning nausea and diarrhea, through to significant malabsorption and chronic pancreatitis. In this review the mechanisms of alcoholic damage have been evaluated with particular reference to alcoholic liver disease (ALD). In particular, the natural history, the influence due to host genetic susceptibility and due to cofactors (i.e. hepatitis C virus), the clinical features and the hepatocarcinogenesis mechanisms have been evaluated. Finally, a possible role of abstinence in association with pharmacological therapy in the course of steatohepatitis has also been evaluated.

Testino G. · UOSD Epato-Gastroenterologia, Dipartimento Trapianti di Organo, Azienda Ospedaliera Universitaria Ospedale San Martino, Genova. · Recenti Prog Med. · Pubmed #17547364 No free full text.

Abstract: HCV correlated chronic hepatophaty represents one of the main causes of cirrhosis and, therefore, of orthotopic liver transplantation (OLT). Furthermore, it is known how the post-OLT recurrent chronic hepatitis C represents a main cause for the re-transplantation. Aim of the present review is the analysis of the natural history of HCV cirrhosis and the evaluation of the introduction form in waiting list. It has been examined the management of the main complications due to portal hypertension in patients awaiting OLT with particular reference to the use of TIPS (transjugular intrahepatic porto-systemic stent shunt) and possible antiviral treatment to obtain post-OLT HCV negativization. Finally, the problem of chemoprevention of hepatocellular carcinoma (HCC) has been considered. As a matter of fact, the treatment with Interferon (IFN) has led to undeniable benefits. Nevertheless, its use has not lowered the incidence of HCC. Probably, such an effect will be reached by means of a maintenance treatment with a small weekly dose of Pegylated IFN independently from virological response.

Testino G. · Unità Operativa Dipartimentale Epato-Gastroenterologia, Dipartimento Trapianti di Organo, Azienda Ospedaliera Ospedale San Martino e Cliniche Universitarie Convenzionate, Genova. · Recenti Prog Med. · Pubmed #16496750 No free full text.

Abstract: Steatosis and hepatitis C are two common liver diseases. Epidemiological and experimental data indicate that hepatitis C predisposes to non alcoholic fatty liver disease and the prevalence of coexistent hepatitis C and steatosis is two-three times higher than it would be expected if these were completely independent processes. Two conditions have been defined in course of hepatitis C: the "metabolic fat", characterized by a correlation between steatosis and metabolic alterations and the "viral fat", characterized by a direct action of HCV. Actually, "mixed forms" are often present. Up to today, most of the authors believe that the presence of steatosis accelerates the progression of fibrosis, and therefore the progression to cirrhosis, increases the risk of developing hepatocellular carcinoma, and decreases the antiviral therapy response percentage. The treatment must associate the common antiviral therapy with all the measures fit for facing the metabolic problems, with particular reference to the antioxidant therapy.

Testino G, Icardi G. · No affiliation provided · Hepatogastroenterology. · Pubmed #15966175 No free full text.

This publication has no abstract.

Testino G. · Unità Operativa di Epato-Gastroenterologia, Ospedale San Martino, Genova. · Recenti Prog Med. · Pubmed #12050912 No free full text.

Abstract: The hepatocarcinoma (HCC) represents one of the major causes of morbidity and mortality in course of chronic HCV correlated hepatopathy. Up to today there are no reliable therapies which can delay or avoid the arising of HCC, nonetheless various Authors have noticed a decrease of such incidence in the subjects treated with interferon (IFN). Such encouraging results have not yet found univocal confirmation in course of compensated cirrhosis (Child-Pugh A). In our experience a cohort of 122 patients prospectively followed was analysed retrospectively to asses the effect of IFN therapy (mean follow-up 96 +/- 18.3 months). We conducted a randomized study in compensated cirrhosis with abnormal ALT and HCV-RNA positive serum (post-transfusional infection). Fifty-nine patients (mean age 55.3 +/- 7) received IFN (3 MU three times a week for 12 months) (8 stopped therapy for side effects), 71 did not receive IFN (mean age: 56.8 +/- 8). Baseline characteristics were similar. IFN therapy does not reduce the risk of HCC in compensated cirrhosis. In IFN treated patients it has been noted an improvement in relation with worsening and death/OLT. Moreover, in the non responder group, the number of negative events has been higher than in the sustained responder group and in subjects with relapse. On the contrary, no particular differences have been noticed in relation with the arising of HCC. It can be hypotized that the therapy with IFN does not reduce the risk of HCC in compensated cirrhosis. Such condition represents by itself a risk factor. It can be concluded that the therapy with IFN can be effective in reducing the possibility of clinical-laboratoristic worsening. However, even in case of substained response, the follow-up for the arising of HCC must always be done.

Perasso A, Testino G, Ansaldi F, Venturino V, Icardi GC. · No affiliation provided · Hepatology. · Pubmed #9935339 No free full text.

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Testino G, Sumberaz A, Ancarani AO, Borro P, Ravetti G, Ansaldi F, Andorno E, Gentile R, Icardi G. · Unit of Hepatology and Alcoholic Diseases, S. Martino Hospital, Genova, Italy. · Hepatogastroenterology. · Pubmed #19579629 No free full text.

Abstract: Up to today no work has evaluated yet the importance of parameters such Body Mass Index (BMI), cholesterol, triglycerides (TGC) and hepatic percentage of steatosis in the response to therapy with Pegylated Interferon Alfa-2a and Ribavirin in patients with recurrent hepatitis C (genotype 1). 30 consecutive prospectively followed patients diagnosed with recurrent HCV were considered candidates for antiviral therapy. Qualitative and quantitative detection of HCV-RNA was performed with the Cobas Amplicor Hepatitis C Virus Test, version 2.0 and the Cobas Amplicor HCV Monitor, version 2.0 (Roche Diagnostics, Branchburgh, NJ, U.S.A.). HCV genotyping was performed by sequencing of the 5 untraslated region (5' UTR) (Visible Genetics TruGene Hepatitis Assay, Toronto, Canada). The observed distribution of BMI, cholesterol, TGC and steatosis were confirmed to be normally distributed by the one-sample Kolmogorov-Smirnov Goodness of fit test procedure. Comparison of BMI, cholesterol, TGC and steatosis between non responders (NR), sustained virological responders (SVR) and sustained biochemical responders (SBR) groups were analyzed by ANOVA with a post hoc Bonferroni test and correlation between variables was tested by Pearson test. The multivariate analysis was performed to estimate the chance of response on basis of the above mentioned variables. In patients with abnormal results in at least two out of four considered variables the chance of no-response was 40 times higher than that of SBR and 96 times than that of SVR. We can conclude how the management of dismetabolism, diet and exercise therapy can improve BMI, liver histology and, therefore, the response to PEG-IFN Alfa-2a and Ribavirin.

Grossi S, Sumberaz A, Gosmar M, Mattioli F, Testino G, Martelli A. · Department of Internal Medicine, Clinical Pharmacology and Toxicology Unit, University of Genoa, Genoa, Italy. · Eur J Gastroenterol Hepatol. · Pubmed #18090985 No free full text.

Abstract: BACKGROUND: Both alcohol abuse and hepatitis B or C virus infections are implicated in the development of hepatocellular carcinoma, but it is still controversial whether the pathogenetic mechanism is epigenetic or genotoxic. AIM: Considering that alcohol promotes the generation of reactive oxygen species and both viruses infect peripheral lymphocytes, in this study we investigated the occurrence of DNA fragmentation in peripheral blood lymphocytes from patients with alcoholic cirrhosis and from patients with cirrhosis related to B and C viruses, and analyzed the correlation between the degree of DNA fragmentation and the Child-Pugh score used to assess the degree of hepatic insufficiency. METHODS: The study population consisted of two groups: group I involved 12 patients with alcoholic cirrhosis; group II involved 25 patients with hepatic B virus or hepatic C virus cirrhosis. The control group involved 20 healthy individuals. The degree of DNA fragmentation in peripheral blood lymphocytes was determined with the alkaline Comet assay that provides two indexes of the frequency of DNA single-strand breaks and alkali-labile sites, the tail length and the tail moment. RESULTS: Mean values of both tail length and tail moment were significantly increased (P<0.001) in lymphocytes from 12 patients with alcoholic cirrhosis and in lymphocytes from 25 patients with HBV or HCV cirrhosis, as compared with average tail length and tail moment values of lymphocytes from 20 healthy individuals. A significant positive correlation was found to exist between the degree of DNA fragmentation present in lymphocytes of each of the 37 patients with alcoholic or viral cirrhosis and the corresponding value of the Child-Pugh score. CONCLUSION: The occurrence of DNA fragmentation in peripheral blood lymphocytes reflects a direct genotoxic effect of either alcohol or HBV and HCV and suggests that the same genotoxic effect may operate in the liver and contribute to hepatocarcinogenesis.

Ansaldi F, Bruzzone B, Testino G, Bassetti M, Gasparini R, Crovari P, Icardi G. · Department of Health Sciences, University of Genoa, Genoa, Italy. · J Viral Hepat. · Pubmed #16364076 No free full text.

Abstract: Reduction of the window period of hepatitis C virus (HCV) infection represents an important goal in the transfusional and diagnostic setting. A prototype assay designed to simultaneously detect circulating HCV antigen and anti-HCV, has been developed. Aim of this study was to evaluate the performance of this new assay in terms of specificity and sensitivity and to compare its efficacy with commercial assays. To evaluate the specificity of the assay, 400 samples from the general population and 100 'difficult' sera, negative for anti-HCV, were tested. To assess sensitivity, the new test was used on 76 PCR-positive and anti-HCV negative sera, seven natural or commercial seroconversion panels that included 17 RNA-positive and anti-HCV negative sera and 31 anti-HCV positive sera, 20 weak anti-HCV positive sera, 80 viraemic and anti-HCV-positive sera from patients infected with different subtypes and 10 sera from patients with HBV-HCV or HIV-HCV co-infections. Of 500 anti-HCV negative samples, 499 (99.8%) were negative with a cut-off index <0.5, while one sample was within the grey zone. Of the 93 HCV-RNA positive and anti-HCV negative sera from patients and panels, 85 (91.4%) resulted positive, and one had the cut-off index in the grey zone. The reduction in the diagnostic window period observed with the new test and HCV-RNA assays were equal, on average, to 24 and 34.4 days respectively. All anti-HCV positive sera were positive. The new assay shows high sensitivity and specificity and could be a useful tool not only in the diagnostic setting, where procedures to reduce the window period, such as antigen or HCV-RNA detection, are not currently recommended, but also in the screening of blood donations, when nucleic acid technologies is not feasible because of costs, organization, emergency and/or logistic difficulties.

Testino G, Ansaldi F, Andorno E, Ravetti GL, Ferro C, De Iaco F, Icardi G, Valente U. · Unit of Hepato-Gastroenterology, S. Martino Hospital, Italy. · Hepatogastroenterology. · Pubmed #12397752 No free full text.

Abstract: BACKGROUND/AIMS: Recent experiences suggest that interferon may significantly decrease the incidence of hepatocellular carcinoma. We conducted a randomized study with interferon versus no therapy in hepatitis C virus Child A cirrhosis with abnormal alanine aminotransferase and HCV-RNA positive serum with the aim to investigate the incidence of hepatocellular carcinoma, worsening of cirrhosis's stage and death or orthotopic liver transplantation. METHODOLOGY: A cohort of 122 patients prospectively followed was analyzed retrospectively to assess the effect of interferon therapy (mean follow-up: 96 +/- 18.3 months). We only chose patients with hepatitis C virus infection who had undergone blood transfusion before 1980. Hepatitis C virus serotype was determined by hepatitis C virus serotyping 1-6 assay (Murex Biothec Limited Temple Hill, Dartford, Kent, UK). HCV-RNA level was determined by bDNA, Chiron Corporation Emeryville, CA. Diagnosis of hepatocellular carcinoma was made on the basis of the appearance of local lesions at periodic ultrasound examination of the liver and confirmed with spiral computed tomography. Fine needle biopsy under sonographic guidance was effected. Fifty-nine patients (mean age: 55.3 +/- 7) received interferon (3MU three times a week for 12 months), 8 stopped therapy for side effects, 71 did not receive interferon (mean age: 56.8 +/- 8). Baseline characteristics were similar. RESULTS: It emerges how interferon does not reduce the risk of hepatocellular carcinoma in compensated cirrhosis. In interferon treated patients an improvement in relation with worsening and death/orthotopic liver transplantation has been noted. CONCLUSIONS: The use of the interferon seems to be scarcely useful when structural alterations of the cirrhotic kind show up, as cirrhosis represents by itself a risk factor for hepatocellular carcinoma. Nevertheless, in relation to the worsening of cirrhosis's stage the interferon therapy can be useful in compensated cirrhosis.

Testino G. · No affiliation provided · J Formos Med Assoc. · Pubmed #19293044 links to  free full text

This publication has no abstract.

Testino G, Sumberaz A. · No affiliation provided · Liver Int. · Pubmed #17311627 No free full text.

This publication has no abstract.

Testino G, Sumberaz A, Ravetti G, Gentile R, Ansaldi F, Icardi G. · No affiliation provided · Dig Liver Dis. · Pubmed #16945599 No free full text.

This publication has no abstract.