Hepatitis: Loria P

Lonardo A, Adinolfi LE, Petta S, Craxì A, Loria P. · Department of Internal Medicine, University of Modena and Reggio Emilia, Modena, Italy. · Expert Rev Anti Infect Ther. · Pubmed #19344243 No free full text.

Abstract: Type 2 diabetes (T2D) and HCV infection are common conditions involving, respectively, at least 170 and 130 million people worldwide. However, the distribution of such cases does not overlap in the same age groups in different geographic areas. Following pioneering reports of increased prevalence of T2D in HCV-positive cirrhosis, interest concerning the relationship between HCV and T2D has escalated. HCV is able to induce insulin resistance (IR) directly and the role of specific viral genotypes responsible for such effect is disputed. IR has consistently been found to be closely linked to fibrosis in HCV infection, although also typically associated with T2D in prefibrotic stages. HCV infection could be associated with a reduced prevalence of metabolic syndrome owing to virus-associated reduction in BMI (reported in population but not clinical studies) and hypobetaliproteinemia. A three- to ten-fold increased risk of HCV infection was reported among diabetic patients in comparison with different control groups and a meta-analysis showed a 1.8-fold excess risk of T2D among HCV-positive compared with HBV-positive patients. Moreover, HCV positivity is associated with an increased risk of T2D in patients receiving liver or kidney transplantations. T2D and IR are independent predictors of a more rapid progression of liver fibrosis and impaired response to antiviral treatment in chronic hepatitis C. Patients with cirrhosis and T2D have an increased susceptibility to hepatic encephalopathy and hepatocellular carcinoma (HCC). However, the beneficial effects of antiviral treatment on IR and T2D are controversial. Theoretically, glycemic control in chronic hepatitis C, and particularly in cirrhotic patients, could improve the prognosis and the response to antivirals, although the evidence for this is limited. Future studies should elucidate the relationship between insulin signaling, HCV and interferon signaling, entity of cardiovascular risk in patients with HCV infection, the potential role of 'metabolic' strategies added to antiviral treatment schedules, the impact of IR on liver failure, portal hypertension and HCC, particularly in patients managed in a transplant setting.

Argo CK, Loria P, Caldwell SH, Lonardo A. · Department of Medicine, Division of Gastroenterology and Hepatology, University of Virginia, Charlottesville, VA, USA. · Hepatology. · Pubmed #18666246 No free full text.

Abstract: A growing number of chronic liver disease patients, especially those with metabolic syndrome-associated nonalcoholic fatty liver disease or hepatitis C virus-associated dysmetabolic syndrome, will take statins to prevent cardiovascular disease. As a result, clinicians will weigh complex issues raised by the interaction of statins with liver metabolism in these disorders. In this article, we critically review data concerning statins and liver pathophysiology with an emphasis on nonalcoholic fatty liver disease and hepatitis C virus, while also touching on other chronic liver diseases. Basic research interests include statins' mechanism of action and their effects on cholesterol-related cell signaling pathways and angiogenesis. From the clinical standpoint, many chronic liver diseases increase cardiovascular risk and would undeniably benefit from sustained statin use. The false alarms and security accompanying aminotransferase monitoring, however, are disturbing in light of the scarcity of data on statins' long-term effects on liver histology. Although some actions of statins might eventually prove to be particularly useful in nonalcoholic steatohepatitis, hepatitis C virus, or hepatocellular carcinoma, others may prove harmful. The lack of definitive data makes a fully informed decision impossible. Research using histological endpoints is urgently needed to determine the indications and contraindications of this extraordinary class of agents in patients with chronic liver disease.

Lonardo A, Loria P, Carulli N. · Dipartimento Integrato di Medicina, Endocrinologia, Metabolismo e Geriatria, Università degli Studi di Modena e Reggio Emilia, Nuovo Ospedale S. Agostino Estense, Modena, Italy. · Intern Emerg Med. · Pubmed #18274709 No free full text.

Abstract: Although not associated with the metabolic syndrome, HCV is linked with impaired insulin signalling, insulin resistance, hypocholesterolemia and steatosis which represent a distinct HCV-associated dysmetabolic syndrome. Insulin resistance affects the development of diabetes, fibrosis, impaired response to antivirals and perhaps hepatocellular carcinoma risk. HCV infection is associated with hypocholesterolemia and steatosis reversible after sustained virologic response. A "viral", and a "metabolic" steatosis exist as function of viral genotypes. Little is known about the possible role of HCV in further components of the metabolic syndrome such as atherosclerosis, obesity, arterial hypertension, hyperuricemia and thrombotic risk factors.

Lonardo A, Carulli N, Loria P. · University of Modena and Reggio Emilia, Department of Internal Medicine, Metabolism, Endocrinology and Geriatrics, Operating Unit Internal Medicine & Metabolism, Nuovo Ospedale Civile Estense di Baggiovara, Modena 41100, Italy. · Dig Liver Dis. · Pubmed #17611176 No free full text.

Abstract: We used available studies to answer two clinically relevant questions, i.e. whether those with type 2 diabetes should undergo hepatitis C virus screening and whether hepatitis C virus positive individuals should be screened for diabetes. Four reasons argue against the hypothesis of screening diabetics for hepatitis C virus. First, although it induces insulin resistance, hepatitis C virus is not directly diabetogenic. Second, the clinical phenotype of hepatitis C virus-associated type 2 diabetes might be a clue to target the specific diabetic population to be screened. Third, diabetic patients are expected to be poor responders to antivirals and evidence that this might result in recovery from type 2 diabetes is insufficient. Fourth, no econometric data are available in the specific subset of those with type 2 diabetes. Case finding of type 2 diabetes in those with hepatitis C virus infection, in contrast, might be considered in those patients with type 2 diabetes who have cirrhosis, in whom--due to increased prevalence and severity of hepatic encephalopathy--diabetes is associated with increased mortality. Preliminary evidence suggests that the prognosis of cirrhosis might benefit from improved glycemic control and thus from earlier diagnosis of type 2 diabetes. Finally, studies are needed to ascertain the most cost-effective strategy of case-finding type 2 diabetes among those who are hepatitis C virus-infected. In conclusion, available data enabled us to answer the two questions. Hepatitis C virus screening should best be restricted to those (lean) diabetic patients with (advanced) liver disease. Glucose tolerance testing should best be performed in those with hepatitis C virus-related cirrhosis. However, additional studies are needed to support the cost-effectiveness of our conclusions.

Lonardo A, Loria P, Adinolfi LE, Carulli N, Ruggiero G. · Unità Operativa di Medicina Interna e Gastroenterologia, Nuovo Ospedale Civile-Estense di Baggiovara, Modena, Italy. · J Viral Hepat. · Pubmed #16436124 No free full text.

Abstract: The overall prevalence of steatosis in patients with Hepatitis C virus (HCV) chronic infection is 55.5% (range 34.8-81.2%). This is a two to threefold increase compared with the prevalence of steatosis in chronic hepatitides because of other aetiologies and of the figures expected on the grounds of a steatosis-HCV chance association. HCV genotype 3 (HCV-3) has specific epidemiological features; furthermore, as compared with HCV-non-3 genotypes, it is associated with a higher prevalence (74.1%vs 47.9%, P < 0.01) and with more severe grades of steatosis (prevalence of grade 3 steatosis 29.6 vs 5.5 P < 0.01). Host and viral factors play a role, although to a variable extent, in the pathogenesis of HCV-3 and non-3 steatosis. HCV load and body mass index are associated with steatosis in HCV-3 and in HCV-non-3 patients respectively. Serum cholesterol levels and liver steatosis at baseline follow an inverse relationship in HCV infection. As hypocholesterolaemia corrects only in those sustained responders to antiviral treatment both in genotype 3 and in non-3 genotypes, the occurrence of a virally induced, acquired and reversible hypobetalipoproteinaemia seems plausible. Steatosis affects the natural course of HCV infection: it is associated with fibrosis, a possible mediator of increased risk to develop type 2 diabetes, it impairs the response to antiviral treatment in HCV-3 patients and might constitute a risk factor for the development of hepatocellular carcinoma. These observations indicate the need to evaluate the efficacy of combined antiviral and 'metabolic' approaches vs standard antiviral regimes in patients with steatosis and HCV chronic infection.

Loria P, Lonardo A, Carulli N. · Dipartimento di Medicina Interna Università di Modena e Reggio Emilia, Modena, Italy. · Dig Dis. · Pubmed #15920328 No free full text.

Abstract: BACKGROUND: None of the synonyms of nonalcoholic fatty liver disease (NAFLD) include clinical correlates nor do they mention insulin resistance, a recognized determinant of the etiopathogenesis and natural history of NAFLD. METHOD: The literature concerning the pathogenesis and definition of NAFLD is reviewed. RESULTS: The reasons why NAFLD should be renamed are: (a) clinically meaningful hepatic steatosis could be present at less than 5% triglyceride hepatic content; (b) steatosis is usually no longer observed in the most advanced forms of NAFLD ('cryptogenic cirrhosis'); (c) the concurrence of metabolic derangements could be more important than alcohol in the pathogenesis of alcoholic liver disease; (d) a concurrent metabolic etiology might worsen the course of chronic HCV and autoimmune hepatitis; (e) in NAFLD the liver is a target organ of the metabolic syndrome, a systemic subclinical inflammatory state. CONCLUSION: The introduction of a positive criterion also mentioned in its definition would benefit the diagnosis of NAFLD and of steatohepatitis observed in the setting of other liver diseases, help to estimate the risk of its progression and aid the treatment of metabolic (fatty) liver disorders. There is a compelling need for an experts' agreement on a new definition of insulin resistance/metabolic-related liver disease.

Lonardo A, Loria P, Adinolfi LE, Andreana A, Ruggiero G, Carulli N. · UO di Medicina Interna e Gastroenterologia, Ospedale Civile di Modena. · Ann Ital Med Int. · Pubmed #15859390 No free full text.

Abstract: Hepatic steatosis is the hallmark of nonalcoholic fatty liver disease (NAFLD), which is the consequence of multiple metabolic derangements among which insulin resistance plays a pivotal role. Steatosis is, also, a feature of hepatitis C virus (HCV) infection. However, in chronic hepatitis C, the prevalence of steatosis is 2.5-fold more elevated than that expected by a chance concurrence with NAFLD, suggesting that HCV may be implied in the development of steatosis. As observed in NAFLD, in patients infected with HCV genotype 1 steatosis is associated with an increased body mass index. On the other hand, in patients infected with genotype 3 the extent of steatosis strictly correlates with the viral load indicating that steatosis is mainly "virus-related". Regardless of the "metabolic" or "viral" etiology, hepatic steatosis in HCV contributes to the progression of liver fibrosis, to the development of hepatocellular carcinoma and to an impaired response to interferon treatment. Features such as obesity, insulin resistance and type 2 diabetes mellitus are shared by NAFLD and HCV-associated steatosis. In addition, HCV infection, directly or through steatosis, favors the development of type 2 diabetes mellitus. Hyperlipidemia is an independent predictor of the development of NAFLD, but not of HCV-associated steatosis. Arterial hypertension is common in nonalcoholic steatohepatitis patients, and HCV infection has recently been acknowledged as an independent risk factor for atherosclerosis. The role of iron in the progression of both NAFLD and HCV-associated steatosis remains controversial while lipoperoxidation and oxidative stress are pathogenic mechanisms shared by both. Some metabolic risk factors may be shared by both HCV-associated steatosis and NAFLD although the disease progression and pathophysiological background may be different. Preliminary data suggest that the therapeutic options for NAFLD may also be useful to improve HCV-associated steatosis.

Lonardo A, Bagni A, Tarugi P, Loria P. · Unità Operativa di Medicina Interna e Gastroenterologia, Ospedale Civile di Modena, Università di Modena e Reggio Emilia, Italy. · Eur J Gastroenterol Hepatol. · Pubmed #15371930 No free full text.

Abstract: We report on four cases displaying the wide range of aetiological risk factors (presence or absence of family history of dyslipidaemia and cryptogenic cirrhosis, from subnormal body mass index through morbid obesity, from absent through hepatotoxic alcohol consumption), laboratory test results (from subnormal through elevated uric acid and ferritin values), ultrasonographic changes (from normal findings through 'bright liver' with or without attenuation of ultrasound beam and absence/presence of focal lesions), and histological severity of steatohepatitis (fibrosis appearing to be inversely related to the amount of liver fat but zone 3 accentuation of lesions and ballooning being observed in all cases). Cases illustrate the concepts of overlapping aetiologies of steatohepatitis (hepatitis C, diabetes and lipodystrophy); the relationships between cryptogenic cirrhosis, familial cirrhosis, non-alcoholic fatty liver disease and hepatocellular carcinoma; familial hypobetalipoproteinaemia as an aetiology of steatohepatitis; and alcoholic liver disease in the obese. These issues, which are worthy of future investigation, are reviewed.

Lonardo A, Adinolfi LE, Loria P, Carulli N, Ruggiero G, Day CP. · Division of Internal Medicine and Gastroenterology, Modena City Hospital, Italy. · Gastroenterology. · Pubmed #14762795 No free full text.

Abstract: Nonalcoholic fatty liver disease (NAFLD) and hepatitis C virus (HCV)-related liver disease are common in the general population, but their concurrence is 2- to 3-fold higher than would be expected by chance alone. In patients with chronic HCV infection, steatosis is attributable to a variable combination of the mechanisms considered to play a role in the pathogenesis of NAFLD--insulin resistance in the obese and in the lean subject--along with a direct effect of HCV on hepatic lipid metabolism that leads to triglyceride accumulation through inhibition of export proteins that are required for very low density lipoprotein (VLDL) assembly and secretion. Accumulating evidence suggests that steatosis contributes to the progression of fibrosis in HCV-related disease in a pattern similar to that observed in NAFLD. Potential mechanisms of this effect include the increased sensitivity of steatotic livers to oxidative stress and cytokine-mediated injury. Steatosis-related hepatic insulin resistance may also play a role through the profibrogenic effects of the compensatory hyperinsulinemia and provides a potential explanation for the association between HCV and type 2 diabetes mellitus. Indeed, an appreciation of the importance of fat in HCV has recently led to trials of adjuvant therapy for HCV directed at steatosis-associated disease mechanisms, with encouraging results reported for various modalities, including weight loss and antioxidants. Future therapy should be aimed at exploiting the interactions of HCV with host insulin and lipid metabolism, particularly in nonresponders to standard antiviral schedules.

Lonardo A, Ballestri S, Adinolfi LE, Violi E, Carulli L, Lombardini S, Scaglioni F, Ricchi M, Ruggiero G, Loria P. · Università degli Studi di Modena e Reggio Emilia, Dipartimento di Medicina, Endocrinologia e Geriatria, Modena, Italy. · Can J Gastroenterol. · Pubmed #19373421 No free full text.

Abstract: BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) and chronic hepatitis C feature steatosis and insulin resistance (IR), conditions associated with the metabolic syndrome (MS). OBJECTIVES: To assess the prevalence of MS and determinants of IR in patients with NAFLD and chronic hepatitis C. METHODS: Ninety-three consecutive patients with NAFLD, 97 with chronic hepatitis C virus (HCV) genotypes 1 and 2, and 182 'healthy' controls without steatosis were enrolled in the present study. The prevalence of MS was assessed by modified Adult Treatment Panel III criteria and IR by the homeostasis model assessment of insulin resistance (HOMA-IR). IR was defined as the 75th percentile of the HOMA-IR of control subjects. RESULTS: While the prevalence of IR was similar in NAFLD and HCV-infected subjects (70.0% and 78.7%, respectively), the prevalence of MS was significantly higher in NAFLD patients than in HCV-infected patients (27.9% versus 4.1%) and in controls (5.6%). With multivariate analysis, IR was predicted by body mass index (OR 1.263; 95% CI 1.078 to 1.480) and triglyceridemia (OR 1.011; 95% CI 1.002 to 1.020) in NAFLD and by sex (OR for female sex 0.297; 95% CI 0.094 to 0.940) and fibrosis stage (OR 2.751; 95% CI 1.417 to 5.340) in chronic hepatitis C. CONCLUSIONS: IR is independently associated with body mass index and triglyceridemia in NAFLD, sex and fibrosis in chronic HCV infection, and has a higher prevalence in NAFLD and chronic hepatitis C than in controls. However, the frequency of MS in HCVinfected patients, similar to that of controls, is significantly lower than that seen in NAFLD patients. The current diagnostic criteria of MS are more likely to 'capture' patients with NAFLD than with chronic hepatitis C, although both groups are insulin resistant.

Guaraldi G, Squillace N, Stentarelli C, Orlando G, D'Amico R, Ligabue G, Fiocchi F, Zona S, Loria P, Esposito R, Palella F. · University of Modena and Reggio Emilia School of Medicine, Modena, Italy. · Clin Infect Dis. · Pubmed #18532884 No free full text.

Abstract: BACKGROUND: The prevalence and predictors of nonalcoholic fatty liver disease (NAFLD) in human immunodeficiency virus (HIV)-infected highly active antiretroviral therapy-experienced patients and the association of NAFLD with risk of cardiovascular disease and subclinical atherosclerosis are unknown. METHODS: We performed a cross-sectional observational study. NAFLD was defined by liver-spleen attenuation values of <1.1 on computed tomography in persons who had neither evidence of chronic viral hepatitis nor a significant history of alcohol consumption. RESULTS: We enrolled 225 patients; 163 (72.4%) were men. Mean (+/-SD) HIV infection duration was 145 +/- 60 months, and mean (+/-SD) body mass index (calculated as weight in kilograms divided by the square of height in meters) was 23.75 +/- 3.59. NAFLD was diagnosed in 83 patients (36.9% of the total cohort). The following variables were significantly associated with NAFLD in univariate analyses: sex, waist circumference, body mass index, cumulative exposure to nucleoside reverse-transcriptase inhibitors, visceral adipose tissue, homeostasis model assessment of insulin resistance index, serum alanine and aspartate aminotransferase levels, and ratios of total serum cholesterol to high-density lipoprotein cholesterol. Coronary artery calcium scores and a diagnosis of diabetes were not associated with NAFLD. In multivariable logistic regression analyses, factors associated (P<0.001) with NAFLD were higher serum alanine to aspartate ratio (odds ratio, 4.59; 95% confidence interval, 2.09-10.08), male sex (odds ratio, 2.49; 95% confidence interval, 1.07-5.81), greater waist circumference (odds ratio, 1.07; 95% confidence interval, 1.03-1.11), and longer nucleoside reverse-transcriptase inhibitor exposure (odds ratio, 1.12 per year of exposure; 95% confidence interval, 1.03-1.22). CONCLUSIONS: NAFLD is common among HIV-infected persons who have the traditional risk factors for NAFLD (elevations in serum alanine level, male sex, and increased waist circumference) apparent. Exposure to nucleoside reverse-transcriptase inhibitors was an independent risk factor for NAFLD, with an 11% increase in the odds ratio for each year of use.

Carulli L, Lonardo A, Lombardini S, Marchesini G, Loria P. · No affiliation provided · Hepatology. · Pubmed #16799969 No free full text.

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Lonardo A, Lombardini S, Scaglioni F, Carulli L, Ricchi M, Ganazzi D, Adinolfi LE, Ruggiero G, Carulli N, Loria P. · Unità Operativa di Medicina Interna e Gastroenterologia, Nuovo Ospedale Civile-Estense, Via Giardini, Baggiovara, Modena 41100, Italy. · J Hepatol. · Pubmed #16168516 No free full text.

Abstract: BACKGROUND/AIMS: To ascertain whether the etiology of hepatic steatosis modulates insulin resistance (IR) and to determine the predictors of IR. METHODS: We studied IR through HOMA IR in 146 subjects, 99 of whom had ultrasonographic and/or histologic steatosis. Twenty-two had familial heterozygous hypobetalipoproteinemia (FHBL), 48 had non-alcoholic fatty liver disease (NAFLD), 34 HCV infection (17 with HCV1b, 17 with HCV3a) and 42 were healthy controls without steatosis. RESULTS: Steatosis was present in 77.3% of FHBL and, by enrolment criteria, in all NAFLD and HCV cases. Overall HOMA-IR correlated with BMI and GGT (P<0.01). FHBL and healthy groups had similar HOMA-IR and GGT values, whereas higher levels were observed in HCV and NAFLD. HCV3a and FHBL patients were hypolipidemic. HOMA-IR was similar in FHBL patients and controls and lower than in HCV and NAFLD. FHBL patients had a high extent of steatosis, similar to that observed in HCV3a, but lower grading and staging than NAFLD and HCV. At multivariate analysis, steatosis and GGT predicted HOMA-IR. CONCLUSIONS: Data suggest that not all hepatic fat associates with IR. FHBL patients, for some aspects, resemble HCV3a infection, possibly suggesting a shared steatogenic mechanism. Among steatotic patients serum GGT levels is the independent predictor of IR.

Loria P, Lonardo A, Leonardi F, Fontana C, Carulli L, Verrone AM, Borsatti A, Bertolotti M, Cassani F, Bagni A, Muratori P, Ganazzi D, Bianchi FB, Carulli N. · Dipartimento di Medicina Interna-Medicina III, Università degli Studi di Modena e Reggio Emilia, Policlinico, Via del Pozzo 71, 41100 Modena, MO, Italy. · Dig Dis Sci. · Pubmed #14705824 No free full text.

Abstract: Eighty-four consecutive subjects with nonalcoholic fatty liver disease (NAFLD) were tested for non-organ-specific autoantibodies (NOSA) by indirect immunoflorescence. Indices of insulin resistance and biochemical and anthropometric parameters were assessed. The overall prevalence of anti-nuclear-antibodies (ANA), smooth muscle antibodies (SMA) and anti-mitochondrial-antibodies (AMA) was 35.7% (30/84), 18 subjects (21.4%) being positive for ANA, 4 (4.7%) for SMA, 6 for ANA and SMA, and 2 for AMA. NOSA-positive subjects were older (P < 0.01) and mostly females (63.3%). No significant difference was found in the age-corrected parameters studied, except for copper and ceruloplasmin, which was more elevated in NOSA-positive patients. The subset of high titer (>1:100) ANA-positive patients had significantly (P < 0.05) greater insulin resistance than ANA-negative patients. In contrast, SMA-positive patients had higher gammaglobulin and significantly lower insulin resistance as compared to high-titer ANA-positive patients. In 3 NOSA-positive but not in NOSA-negative patients, liver biopsy disclosed features of overlapping NASH with autoimmune hepatitis, partially responding to diet combined with steroid treatment. In conclusion, NOSA positivity in NAFLD is more prevalent than in the general population. High-titre ANA but not SMA positivity is associated with insulin resistance.

Muratori P, Muratori L, Gershwin ME, Czaja AJ, Pappas G, MacCariello S, Granito A, Cassani F, Loria P, Lenzi M, Bianchi FB. · Department of Internal Medicine, Cardioangiology, Hepatology, Alma Mater Studiorum - University of Bologna, Bologna, Italy. · Clin Exp Immunol. · Pubmed #14678277 links to  free full text

Abstract: Anti-mitochondrial antibody (AMA) is considered the serological hallmark of primary biliary cirrhosis (PBC), but may be missing in a proportion of these patients. We assessed sensitivity and specificity of the currently available techniques for AMA detection in a large series of PBC patients and controls, and analysed their clinical and immunological features according to the AMA status. By indirect immunofluorescence on rat tissue sections and HEp-2 cells, Western immunoblot with bovine submitochondrial particles, and two ELISAs with AMA-specific recombinant proteins, we evaluated the presence of AMA in 127 PBC patients, 166 patients with type 1 autoimmune hepatitis and 100 with non alcoholic fatty liver disease. In PBC patients Western immunoblot detects AMA significantly more often than indirect immunofluorescence on HEp-2 cells (85%versus 72%, P = 0.02) or rodent tissue sections (71%, P = 0.01); both ELISAs are only slightly less sensitive than Western immunoblot (81% and 78%). Ten patients with non alcoholic fatty liver disease were AMA-positive by indirect immunofluorescence, but none recognized AMA-specific epitopes in Western immunoblot or in ELISAs. Twelve patients with type 1 autoimmune hepatitis were AMA-positive by indirect immunofluorescence, but only 6 (3.6%) reacted by Western immunoblot and ELISAs. Western immunoblot or ELISA should be regarded as first-line assay for the detection of AMA. Up to 15% of PBC patients are consistently AMA-negative, yet they share the same clinical, biochemical and histological features of AMA-positive PBC. Detection of AMA in type 1 autoimmune hepatitis might identify a subset of patients at risk of developing a hepatitic/cholestatic syndrome.

Cermelli C, Concari M, Pietrosemoli P, Meacci M, Sabbatini AM, Divincenzo A, Carubbi F, Loria P, Bagni A, Carulli N, Portolani M. · Department of Hygiene, Microbiology and Biostatistics, University of Modena, Italy. · J Clin Virol. · Pubmed #10548125 No free full text.

Abstract: BACKGROUND AND AIMS: Herpesviruses infect the liver and cause minor hepatitis. Our aim is to verify the presence of herpesviruses in the liver from hepatitis C patients and the possible influence of these viruses in the liver disease. METHODS: We searched for herpesvirus DNA in liver biopsies from patients with hepatitis C and from a control group without hepatitis by means of nested polymerase chain reaction. Serological investigations were carried out as well. RESULTS: Thirty-four liver specimens from hepatitis C patients were examined, 12 of which (35.3%) were positive for at least one herpesvirus DNA, whereas among the 19 control specimens only two were positive (10.5%; P = 0.049). Liver biopsies from seven patients, three with acute hepatitis of unknown origin, three with non-alcoholic steatohepatitis and one with autoimmune hepatitis were also investigated and three positive samples were found. CONCLUSIONS: The prevalence of herpesvirus DNA was found higher in patients with hepatitis C than in individuals without hepatitis. The influence of herpesviruses on the clinical course of hepatitis C is considered.

Lonardo A, Loria P. · No affiliation provided · Hepatology. · Pubmed #18756483 No free full text.

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Lonardo A, Loria P, Bertolotti M, Carulli N. · No affiliation provided · Hepatology. · Pubmed #17187410 No free full text.

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Loria P, Carulli N, Lonardo A. · No affiliation provided · Am J Gastroenterol. · Pubmed #15842599 No free full text.

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Lonardo A, Loria P. · No affiliation provided · Dig Liver Dis. · Pubmed #11926561 No free full text.

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