Hepatitis: Rizzetto M

Carosi G, Rizzetto M. · Department of Infectious and Tropical Diseases, University of Brescia, AO Spedali Civili, Brescia, Italy. · Dig Liver Dis. · Pubmed #18499540 No free full text.

Abstract: The changing scenario of hepatitis B virus therapy has encouraged the organisation of a workshop, endorsed by three Italian scientific societies, aimed at defining the current recommendations for hepatitis B virus treatment. Liver histology and stage of disease remain fundamental for treatment decisions; interferon and nucleoside/nucleotide analogues-based therapy represent different strategies for different phases of the hepatitis B virus disease. The recommendations defined: new and lower cut-off of hepatitis B virus-DNA for eligibility to therapy according to disease stage, how to optimise the use of nucleoside/nucleotide analogues and to individualise the monitoring of response and what to do with treatment failures. Specific recommendations have also been given for cirrhosis patients, those immune suppressed and co-infected with HIV and other hepatitis viruses.

Marcellin P, Rizzetto M. · No affiliation provided · Antivir Ther. · Pubmed #18432156 No free full text.

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Rizzetto M. · No affiliation provided · Liver Transpl. · Pubmed #11443580 links to  free full text

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Saracco G, Rizzetto M. · No affiliation provided · Recenti Prog Med. · Pubmed #10608149 No free full text.

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Zeuzem S, Rizzetto M, Ferenci P, Shiffman ML. · JW Goethe University Hospital, Frankfurt, Germany. · Antivir Ther. · Pubmed #19430089 No free full text.

Abstract: Current guidelines recommend a full 24-week regimen for all patients undergoing treatment for genotype 2 or 3 hepatitis C virus (HCV) infection. Recent data from two large randomized studies, one with pegylated interferon-alpha2a plus ribavirin (RBV) and one with pegylated interferon-alpha2b plus RBV assessed treatment duration and on-treatment predictors, such as rapid virological response (RVR; HCV RNA <50 IU/ml at week 4) or sustained virological response rates. Overall, these studies have shown that abbreviated regimens are generally less effective than standard 24-week regimens in genotype 2 or 3 patients because of a higher rate of relapse. However, abbreviated treatment might be offered to selected patients with an RVR provided that they have a low baseline viral load and minimal hepatic fibrosis.

Rizzetto M. · Department of Gastroenterology, University of Turin, Turin, Italy. · Liver Int. · Pubmed #19207978 No free full text.

Abstract: Hepatitis D virus (HDV) infection has considerably diminished in Europe since the 1970-1980s. The prevalence rates of chronic hepatitis D in HBsAg carriers in Italy have declined from 25% at the beginning of the 1980s to 8% in the 1990s. Similar declines in prevalence have been reported in Spain, Taiwan and Turkey. Better public health standards, HBV vaccination and the effect of measures to control the spread of human immunodeficiency virus have brought about a decline in the numbers of HBsAg carriers and therefore a decline in the HBV-dependent HDV. However, HDV has not declined further in Europe in the last decade, as the pool of fresh infections in migrants from HDV-endemic areas is counterbalancing the shrinking cohort of long-standing domestic infections acquired in the epidemic of the 1970-1980s. Hepatitis D remains an important health problem outside Europe, and new foci of infection continue to be identified in developing countries.

Pellicano R, Ménard A, Rizzetto M, Mégraud F. · Department of Gastro-Hepatology, Molinette Hospital, Turin, Italy. · Lancet Infect Dis. · Pubmed #18353266 No free full text.

Abstract: The discovery of Helicobacter hepaticus as a causal agent of hepatitis and hepatocarcinoma in mice has stimulated interest in looking for Helicobacter spp in human liver samples. These bacteria could be a risk factor for the progression of liver disease to cirrhosis and hepatocellular carcinoma, especially among patients chronically infected with hepatitis C virus. We reviewed the studies done on this topic, and, with the exception of one, all studies reported an association between the presence of Helicobacter spp and liver disease. However, these data are weakened by the fact that Helicobacter spp DNA was detected but no bacteria could be grown, and by the difficulties in identifying the Helicobacter spp involved. More studies are therefore needed to confirm whether a causal association exits between the presence of Helicobacter spp in the liver and the development of cirrhosis and hepatocellular carcinoma.

Rizzetto M, Ciancio A. · Gastrohepatology Department, San Giovanni Battista Hospital, University of Turin, Turin, Italy. · Mol Aspects Med. · Pubmed #18067957 No free full text.

Abstract: Thirty years after its discovery, the hepatitis B virus (HBV) still remains a major global public health problem. Worldwide, two billion subjects have been infected, 300 million have a chronic infection and more than 600,000 die annually of HBV-related liver disease or hepatocellular carcinoma; new infections occur because of the presence of a large reservoir of chronic carriers of the virus. The knowledge of the HBV organization and replication cycle and the availability of sensitive HBV-DNA assays have led to remarkable progress in our understanding of the natural history of chronic hepatitis B infections. Crucial to the prevention of new infections, to the management and the monitoring of HBV carriers and to the choice of best treatment strategy, is the understanding of the natural dynamism of HBV infection and of the virus-host interactions that induce liver damage.

Pellicano R, Fagoonee S, Repici A, Rizzetto M. · Department of Gastro-Hepatology, Molinette Hospital, Turin, Italy. · Panminerva Med. · Pubmed #17625484 No free full text.

Abstract: It is estimated that, in the United States and Europe, 15-30% of people with human immunodeficiency virus (HIV) are coinfected with hepatitis C virus (HCV). Among these patients, approximately 80% are intravenous drug users (IVDU), 71% are hemophiliacs, and around 20% are homosexual/bi-sexual men. HIV infection accelerates the natural history of HCV infection. On the contrary, highly active antiretroviral therapy reduces the rate of mortality due to liver disease by immune restoration. Since having HIV implies being at risk also for HCV as both infections can be acquired in similar ways, all individuals with the former should be screened for the latter. Loss of antibodies against HCV in HIV-seropositive IVDU has been shown. Thus, quantitative tests determining HCV-RNA levels in blood are currently being employed for diagnosis confirmation in case of an obvious ''risk group''. Since HIV can progress more rapidly than HCV, it may be preferable to treat HIV first. The 2007 recommendations from HCV-HIV International Panel indicate current treatment of HCV in coinfected patients with pegylated formulation of interferon at standard doses plus weight based ribavirin. The treatment duration should be evaluated on the basis of HCV genotype. Liver transplantation is a most debated issue when dealing with HCV/HIV coinfected subjects. Mortality among HIV-infected liver transplant recipients is similar to that of age and race-matched HIV-negative controls. The present concise review attempts to highlight on the current clinical situation on HIV/HCV coinfection.

Leone N, Rizzetto M. · U.O.A. Gastroepatologia, Ospedale Molinette, Torino, Italy. · Minerva Med. · Pubmed #16172579 No free full text.

Abstract: Hepatocellular carcinoma (HCC) is common throughout the world. The incidence of HCC is higher in cirrhotic patients and, among these patients, the incidence rate is 3% in Europe. The overall survival rate of HCC ranges between 20 and 30 months, and is influenced by the local stage of the neoplasm and by the liver function. The literature reports several serological, urinary and radiological markers used for the early detection of HCC. Currently, it is highly recommended to periodically screen cirrhotic patients and hepatitis B virus carriers older than 35 by serum alpha-fetoprotein (AFP) and liver ultrasound (US) every 6 months. The concomitant determination of des-g-carboxy prothrombin and AFP allows a 23% increase in sensibility of the diagnosis for HCC avoiding the need for invasive diagnostic procedures.

Pellicano R, Mladenova I, Dimitrova SM, Bruno CM, Sciacca C, Rizzetto M. · Unit of Gastro-Hepatology, Molinette Hospital, Turin, Italy. · Minerva Gastroenterol Dietol. · Pubmed #15719001 No free full text.

Abstract: Since the advent of sensitive diagnostic blood tests for the detection of antibody to hepatitis C virus (HCV) in donors, there has been a large decline in the incidence of transfusion-related hepatitis. Globally, the infection has an estimated prevalence of 3%, with a prevailing 1% in Europe while varying geographically within a North-South gradient, ranging from around 0.5% in Northern countries to 2% in Mediterranean area. The incidence is very difficult to estimate accurately as many patients with acute HCV infection are asymptomatic and, thus, do not present for diagnosis. Data from the US report a fall in the annual occurrence of new cases per year from 230,000 in the late 1980s to approximately 35,000 in the 1990s. Therefore, a reduction in incident cases might eventually lead to lower prevalence of HCV infection. Although the incidence of viral infection may be decreasing, the prevalence of liver disease caused by HCV is on the rise. This is due to the significant lag, often 20 years or longer, between the onset of infection and clinical manifestation of liver disease. HCV can be transmitted by a variety of routes. It is most efficiently passed on by large or repeated percutaneous exposures such as through transfusions, transplantation from an infected donor or intravenous drug use. Transmission may also occur from contacts with infected subjects in the household, through perinatal and parenteral exposures in the health care setting. The risk of sexual transmission of HCV is low. Despite this knowledge, nearly half of infected patients do not have a history suggesting a parenteral route of acquisition. Since a prophylactic vaccine is hitherto not available, prevention becomes extremely important: identification of infected persons and of risk factors associated with acquiring HCV allow to develop strategies for preventing the spread of infection as well as its complications, and for planning appropriate care and support services.

Niro GA, Rosina F, Rizzetto M. · Division of Gastroenterology, Hospital Casa Sollievo Della Sofferenza, IRCCS, San Giovanni Rotondo (FG), Italy. · J Viral Hepat. · Pubmed #15655042 No free full text.

Abstract: Delta virus related chronic hepatitis is difficult to treat. The response to alpha-interferon (IFN), which still represents the only therapy for chronic hepatitis D, varies widely and occurs at different times from the beginning of treatment. The rate of response is proportional to the dose of IFN, with 9 million units (MU) three times a week being more effective than 3 MU thrice weekly. Sustained responses are unusual and are accompanied by the clearance of serum hepatitis B virus surface antigen (HBsAg), seroconversion to anti-HBs and improvement of liver histology. Although disease of a short-standing may respond better to therapy, clear predictors of response are still unidentified. Besides IFN, other therapeutic approaches such as immunosuppressive drugs, acyclovir, ribavirin and thymosin, have been unhelpful. Available evidence does not support the use of deoxynucleotide analogues. Famciclovir has no effect on disease activity and hepatitis D virus (HDV)-RNA levels. Twelve- or 24-month lamivudine treatment does not significantly affect biochemical, virological or histological parameters. Pegylated-IFN could represent a reasonable therapeutic option in the long-term treatment required for chronic hepatitis D. Antisense oligonucleotides and prenylation inhibitors hold promise as therapeutic agents of the future. Liver transplantation provides a valid option for end-stage HDV liver disease; the risk of re-infection is lower for HDV than for HBV under long-term administration of hyperimmune serum against HBsAg. Molecularly tailored drugs capable of interfering with crucial viral replicative processes of HDV appear to be the best prospect in the treatment of hepatitis D.

Astegiano M, Sapone N, Demarchi B, Rossetti S, Bonardi R, Rizzetto M. · Molinette Hospital-SC Gastrohepatology DU, Turin, Italy. · Eur Rev Med Pharmacol Sci. · Pubmed #15209149 No free full text.

Abstract: Because the liver performs multiple functions, no single laboratory test or battery of tests is sufficient to provide a complete estimate of the function of the liver in every clinical situation. A broad array of biochemical tests are used to assess the many functions of the liver and to evaluate patients with suspected or established liver disease. These tests are referred to collectively as "liver function tests" (LFTs). LFTs are used to screen people for the presence of liver disease, suggest the underlying cause, estimate the severity, assess prognosis, and monitor the efficacy of therapy. Abnormal LFTs may be the first indication of sub clinical liver disease and may thereby guide further diagnostic evaluation. After the existence of hepatic dysfunction is recognized, the specific pattern of liver test abnormalities may suggest the category of the underlying liver disease, such hepatitis, biliary obstructions, or infiltrative liver disease. The value of screening healthy, asymptomatic persons for liver disease with the use of LFTs is controversial and may not be cost-effective. If screening is performed a panel of tests (e.g., AST, alkaline phosphatase, bilirubin, albumin) is preferable to using a single test because of superior sensitivity and specificity for liver disease and lower cost than the sum of individually performed tests.

Rizzetto M, Marzano A, Lagget M. · Department of Gastroenterology, University of Turin, Molinette Hospital, Corso Bramante 88, 10125 Turin, Italy. · J Hepatol. · Pubmed #14708698 No free full text.

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Lagget M, Rizzetto M. · Division of Gastroenterology, Ospedale Molinatte, Torino, Italy. · Expert Opin Pharmacother. · Pubmed #14521491 No free full text.

Abstract: The virological profile of infection with the hepatitis B virus (HBV) is changing in many parts of the world from the classical hepatitis B e antigen (HBeAg)-positive serological pattern to a HBeAg-negative pattern, linked to the replacement of wild-type HBV by HBV variants with mutations in the core-promoter and in the precore region that prevent the secretion of HBeAg. The wild-type HBV disease is characterised by steady levels of alanine aminotransferase (ALT) and high HBV-DNA levels, responding relatively well to IFN treatment (3 - 5 MU/day or 10 MU every other day for 16 weeks), which induces anti-HBe seroconversion and normalises ALT levels in approximately 30% of the adults, with a minimal risk of relapse. Pegylated-IFN appears to have superior efficacy over conventional IFN-alpha. Mutant-type disease (anti-HBe-positive/HBeAg-negative) is less responsive to IFN given for 6 - 12 months. This has led to the use of novel nucleoside analogues, of which the prototype is lamivudine. The response to lamivudine therapy shares with IFN a rapid decline in ALT accompanied by an improvement in histology; at variance with IFN, in HBeAg-positive chronic hepatitis B (CHB) there is delayed seroconversion to anti-HBe which accumulates over time, the switch to anti-HBs is more rare and in the long-term, the activity of the drug is abolished by the emergence of viral mutations (YMDD-motif mutants) that may rekindle the disease. The combination of IFN plus lamivudine may be more efficacious than IFN or lamivudine monotherapy. Lamivudine therapy needs to be prolonged in HBeAg-negative CHB. Short-term lamivudine-therapy is highly efficacious in preventing HBV reinfection in liver transplants. Recent data suggest that long-term IFN therapy (24 months) may achieve a response in 30% of HBeAg-negative patients. The advent of adefovir, an analogue of adenosine monophosphate, may provide a safer alternative to lamivudine in the control of HBV disease; the drug is well-tolerated and treatment raises drug-resistant mutants in < 2% of the patients over 2 years of therapy. Adefovir provides rescue therapy against YMDD mutants raised by lamivudine therapy.

Saracco G, Olivero A, Ciancio A, Carenzi S, Rizzetto M. · Department of Gastroenterology, Molinette Hospital, Torino, Italy. · Curr Drug Targets Infect Disord. · Pubmed #12570730 No free full text.

Abstract: Combination therapy (Interferon plus ribavirin) is the current therapeutic gold standard for naive Hepatitis C Virus (HCV)-positive patients and with the recent advent of pegylated (PEG) IFN the rate of the sustained virological response (HCV-RNA clearance 6 months after the end of treatment) is about 54%-56% with a therapeutical gain mainly among patients with unfavourable HCV genotype (1a, 1b); in this subset of patients, a 42%-46% sustained response rate is achieved compared with 33%-36% found among genotype 1 patients treated with the standard therapy. Patients who respond to IFN monotherapy but relapse during the follow-up should be re-treated with combination therapy given for at least 6 months at the minimum dose of 3 MU thrice weekly plus ribavirin 1000 mg/daily. Recent data suggest that prolonging the time of treatment (12 months) may induce a significantly higher rate of sustained response among patients with genotype 1. The efficacy of the combination of IFN and ribavirin in retreating patients with chronic hepatitis C not responding to IFN monotherapy is controversial as it ranges between 0% and 40%. Recent data show an overall rate of sustained response of 23% when an aggressive approach is adopted but increasing the dosage and the time of treatment induces a significant therapeutic benefit only in patients with genotype 1. In conclusion, a therapeutic progress for chronic hepatitis C has been achieved during the last 10 years (56% vs 20% of sustained response rate obtained with IFN monotherapy) but several unresolved issues are yet to be addressed.

Rizzetto M, Zanetti AR. · Department of Gastroenterology, University of Torino, Torino, Italy. · J Med Virol. · Pubmed #12116047 No free full text.

Abstract: Hepatitis type B remains an important disease globally. Rapid advances have been made during the last two decades in the understanding of the biology of HBV, the complex interaction between the virus and the host, and the pathology and the clinical aspects of infection. Mass vaccination has been shown to be a safe and highly effective means for the control and prevention of hepatitis B. The presence of a large worldwide reservoir of carriers requires a continuous effort to develop new drugs for the treatment of persistent HBV infection. Efforts to sustain immunization programs and to make vaccines and drugs available to countries with limited resources, are the main challenges to the eradication of hepatitis B in the next few decades.

Rizzetto M, Lagget M. · Dipartimento di Gastroenterologia, Università di Torino, Azienda Ospedaliera S. Giovanni Battista, Torino, Italy. · Forum (Genova). · Pubmed #11948359 No free full text.

Abstract: Therapy with interferon (IFN), an immunomodulant with anti-viral activities, is efficacious only in a minority of chronic hepatitis B (CHB); it is more efficacious in the hepatitis B e antigen (HBeAg)-positive variety sustained by the wild type hepatitis B virus (HBV) than in the HBeAg-negative variety sustained by mutant forms of the virus. Several other therapeutic approaches were attempted in recent years. The most promising is therapy with synthetic nucleosides as anti-virals capable of blocking the replicative activity of the HBV. Lamivudine (LAM) is the first of this class of compounds that has entered clinical use. It is well tolerated and highly effective in inhibiting HBV and abate HBV-related inflammation both in the HBeAg positive and negative variety of CHB. In the HBeAg positive variety it induces sero-conversion to anti-HBe at a rate that linearly increases over the years, reaching 40% at the third year. In the HBeAg-negative variety maintenance of viral repression requires continuative therapy. A major drawback of continued LAM therapy is the risk of the emergence of mutants in the tyrosine-methionine-aspartate-aspartate locus of the polymerase gene. These mutants are no longer responsive to LAM and may rekindle disease; wild type HBV and related disease often return after suspension of therapy. Other anti-viral drugs, the prototype of which is adefovir, are currently under clinical investigation in CHB as monotherapy or complementary therapy to LAM.

Lagget M, Rizzetto M. · Department of Gastroenterology, Azienda Ospedaliera S. Giovanni Battista di Torino, Torino, Italy. · Curr Pharm Des. · Pubmed #11945141 No free full text.

Abstract: Infection with the hepatitis B virus has switched over the last 20 years from the classical HBeAg positive serologic pattern to a HBeAg negative form that is linked, in the Mediterranean basin, with the epidemiologic replacement of the causative wild-type of virus B with mutant variants, whereby mutations in the core-promoter and in the pre-core region prevent the secretion of HBeAg. The wild-type pattern of infection (characterized by relatively high steady level ALT, high HBV-DNA levels and clinically overt liver disease) responds relatively well to Interferon: 3 to 5 mega units daily or 10 mega units every other day for 16 weeks induce anti-HBe seroconversion, normalize the ALT and possibly also eliminate the HBsAg in some 40% of the adults with a minimal (7%) risk of relapse. However, the mutant type infection (anti-HBe positive / HBe Ag negative) is less responsive to Interferon; this has led to the search for novel nucleoside analogues which has currently culminated in the advent of Lamivudine. This competitor of cytidine is 80% bioavailable and devoid of side-effects at the oral dose of 100 mg daily; tolerance continues for therapies up to 3 years. Lamivudine therapy shares with Interferon a rapid decline of ALT accompanied by improvement of histology; at variance with Interferon there is a delayed accumulating seronconversion to anti-HBe and the switch to anti-HBs is rare. Over the long term its activity is abolished by the emergence of specific viral mutations (YMDD mutants) that rekindle the disease. The indications to Lamivudine therapy in HBeAg negative chronic hepatitis B are currently under investigation. Lamivudine is highly efficacious in preventing HBV reinfection in liver transplants.

Rizzetto M. · Department of Gastroenterology, Molinette, University of Torino, Torino, Italy. · J Med Virol. · Pubmed #11857520 No free full text.

Abstract: Hepatitis B e antigen (HBeAg)-negative chronic hepatitis B results from infection with hepatitis B virus mutants unable to produce HBeAg. It accounts for 7-30% of patients with chronic hepatitis B virus (HBV) worldwide, with the highest rates reported for Mediterranean Europe and Asia. Interferon (IFN) is currently the only approved therapy for these patients, but it has an unfavorable tolerance profile and limited efficacy. Studies show that responses to IFN are lower in HBeAg-negative than in HBeAg-positive patients; joint HBV DNA loss/ALT normalization is obtained in 38-59% of HBeAg-negative patients treated for 4-24 months with a high rate of virological relapse (54-87%), at 6-24 months posttreatment. Lamivudine is a nucleoside analogue with potent antiviral properties against HBV. Studies show that response rates in HBeAg-negative and HBeAg-positive patients are equivalent. After 12 months of treatment, 65-96% of HBeAg-negative patients have joint HBV DNA loss/ALT normalization, although 48-74% of patients relapse within 1 year posttreatment. 60% of patients have histological improvement after 12 months of treatment. Lamivudine is well tolerated with a safety profile equivalent to that of placebo. The incidence of YMDD variants increases with extended lamivudine treatment, present in up to 57-64% of patients after 2 years. Their clinical impact is unclear; some studies show breakthrough infection associated with their emergence, whereas other studies show maintained response to lamivudine. Lamivudine has benefits over IFN in its safety and efficacy profile in this patient group. Extended lamivudine treatment beyond 2 years is an option, but further investigation is required to define stopping criteria and the impact of YMDD variants.

Fagoonee S, Pellicano R, Rizzetto M, Ponzetto A. · Department of Biology Biochemistry and Genetics, University of Turin, Turin, Italy. · Panminerva Med. · Pubmed #11677423 No free full text.

Abstract: Hepatocellular carcinoma (HCC) is a long-term consequence of chronic liver disease, whose aetiology could result from viral, environmental and hereditary causes. Viral infection, by itself, could only partially explain the pathogenesis of cirrhosis and HCC. A new aetiologic agent capable of inducing chronic active hepatitis and hepatocellular tumours was discovered: it is a bacterium belonging to the genus Helicobacter, and named H. hepaticus. Presence of sequences belonging to the 16S rRNA of Helicobacter species (spp.) has been demonstrated in liver of most patients with cirrhosis and HCC. H. pylori and related bacteria, such as H. hepaticus, produce toxins that kill hepatocyte by a granulating effect on liver cell lines. In vivo, such toxins might reach the liver through the portal tract, thereby causing hepatocellular damage. The recognition of Helicobacter spp. as a possible risk factor for cirrhosis and HCC might have a practical impact on the general population: the treatment of this infection is easy and far less expensive than liver transplantation or any long term treatment for the other risk factors of HCC. Any confirmation of the involvement of Helicobacter in liver disease would eventually come from the success of culturing the bacterium from liver tissues. Future research is needed to clarify the importance of Helicobacter spp. in respect to the other pathogens already known as causative agents of chronic inflammation of the liver and its long term sequelae, namely cirrhosis and HCC.

Rizzetto M. · Div. di Gastroenterologia, Ospedale Molinette, Torino, Italy. · Forum (Genova). · Pubmed #11300125 No free full text.

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Rizzetto M, Marzano A. · Department of Gastroenterology, Cattedra di Gastroenterologia, University of Torino, Azienda Ospedaliera S Giovanni Battista, Torino, Italy. · Liver Transpl. · Pubmed #11084085 links to  free full text

Abstract: Prophylaxis of Recurrent Hepatitis B. 1. Although standard prophylaxis with antibody to hepatitis B surface antigen immunoglobulins (HBIG) is effective, it is difficult to administer and must be administered indefinitely. 2. Preemptive therapy with lamivudine reduces the early risk for recurrence after transplantation, but maintenance with either famciclovir or lamivudine has been ineffective in sustaining remission. 3. The combination of preemptive lamivudine with HBIG prophylaxis may be the most effective treatment to prevent hepatitis B virus reinfection. Treatment of Recurrent Hepatitis B. 1. Interferon-alpha, ganciclovir, and famciclovir have not been helpful. 2. Lamivudine appears promising, but its long-term efficacy is unproven; in immunosuppressed transplant recipients, the rate of emergence of YMDD mutants is high and accelerated, and their emergence is aggravated by consistent liver morbidity.

Leone N, Volpes R, Carrera M, Pellicano R, De Paolis P, Fiorentino M, Fronda GR, Rizzetto M. · Department of Gastroenterology, B Surgery, Molinette Hospital, Turin, Italy. · Panminerva Med. · Pubmed #10965777 No free full text.

Abstract: Hepatocellular carcinoma (HCC) is closely associated with cirrhosis, but it also develops, although much less frequently, in a non-cirrhotic liver. It is suspected that hepatocellular carcinoma has a different etiology when associated and not associated with chronic liver disease. We report two cases of patients with hepatocellular carcinoma that developed in a non-cirrhotic liver. In the first case we describe an incidental liver nodular lesion containing multiple foci of HCC including pseudogland or trabecular formation and areas of sclerosis. The non-cancerous parenchyma of the liver was histologically unremarkable except for mild fatty changes of hepatocytes and minimal dysplasia. The second case describes a combined hepatocellular carcinoma and cholangiocellular carcinoma (CCC) (mixed carcinoma) in a patient who was serologically negative for both hepatitis B and C viruses. The adjacent liver parenchyma showed mild piecemeal necrosis and mild lobular activity compatible with chronic viral hepatitis, but cirrhosis was not established. This case appears to indicate that mixed type carcinoma can develop in a non-cirrhotic liver, with CCC being far more dominant than HCC; such a finding is extremely unusual, based on previously published reports.

Rizzetto M. · Department of Gastroenterology, University of Torino, Italy. · Acta Gastroenterol Belg. · Pubmed #10925472 No free full text.

This publication has no abstract.