Hepatitis: Pol S

Pol S. · No affiliation provided · Presse Med. · Pubmed #19201152 No free full text.

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Pol S, Marcellin P. · No affiliation provided · Gastroenterol Clin Biol. · Pubmed #18675183 No free full text.

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Cacoub P, Pol S. · No affiliation provided · Rev Med Interne. · Pubmed #15820560 No free full text.

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Pol S. · No affiliation provided · Gastroenterol Clin Biol. · Pubmed #12594370 No free full text.

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Vallet-Pichard A, Fontaine H, Pol S. · Unité d'Hépatologie et U-370, Hôpital Necker, Paris. · Gastroenterol Clin Biol. · Pubmed #12483129 No free full text.

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Albert ML, Decalf J, Pol S. · The Laboratory of Dendritic Cell Biology, Department of Immunology, Institut Pasteur, Paris, France. · J Hepatol. · Pubmed #18929418 No free full text.

Abstract: Chronic hepatitis C is a major public health problem. Despite numerous clinical studies in humans and experimental observations made in chimpanzees, hepatitis C pathogenesis remains poorly understood. Here, we review the clinical features of acute and chronic disease, and discuss the role of the immune system in the pathogenesis of disease. Many are aware of the dual role of T cells: responsibility for clearance of the virus during acute phase; and liver injury during chronic phase. Nonetheless, there is an emerging belief that failure to prime HCV-specific T cells is responsible for the failure to spontaneously clear the virus, and possibly, for the lack of response to pegylated-IFNalpha(2a)/ribavirin therapy. We have focused on the latest suspects, plasmacytoid dendritic cells (pDCs), considered to be the professional type I IFNs producing cells. We review the somewhat contradictory data regarding the functional capacity of pDCs in chronic HCV patients and argue that, while lower in relative concentration as compared to healthy individuals, they are not defective in their ability to initiate an innate inflammatory response. Thus, instead of being the culprit, pDCs may in fact represent a novel therapeutic target in order to improve upon existing therapies for treating HCV patients.

Cacoub P, Sène D, Rosenthal E, Pol S. · Service de Médecine Interne, AP HP, Hôpital La Pitié Salpêtrière, 83, bd de l'Hôpital, 7 5651 Paris cedex 13, France. · Gastroenterol Clin Biol. · Pubmed #18675185 No free full text.

Abstract: Managing chronic hepatitis C in patients coinfected with the human immunodeficiency virus is a significant challenge. Treatment is influenced by a number of viral and host characteristics, including hepatitis C virus genotype, baseline viremia, and adherence to medication. Accelerated progression of liver disease, immunodeficiency, and hepatotoxicity of antiretroviral drugs are additional concerns in coinfected patients. According to the results of 5 randomized clinical trials, 27 %-55 % of coinfected patients who receive therapy with peginterferon alfa plus ribavirin attain sustained virologic response. These studies also confirm the importance of early virologic response as a predictor of treatment outcome and reveal the considerable proportion of patients who experience hematologic tolerability issues. Effective management strategies that encompass patient and viral factors are necessary to improve the long-term outlook for coinfected patients.

Couzigou P, Mathurin P, Serfaty L, Cacoub P, Moussalli J, Pialoux G, Chossegros P, Cattan L, Pol S. · Service d'Hépato-Gastroentérologie, Hôpital du Haut-Lévêque, 1, avenue de Magellan, 33604 Pessac, France. · Gastroenterol Clin Biol. · Pubmed #18675184 No free full text.

Abstract: Patients with chronic hepatitis C have frequently other morbidities, either because they are frequent in the general population (metabolic syndrome) and/or because the route of contamination (chronic alcohol consumption succeeding to drug abuse). These co-morbidities have a harmfull impact on fibrosis progression during the natural history of HCV infection and reduce the efficacy of antiviral treatments. Thus, it is crucial to diagnose early and treat these different diseases which may be combined. They are the metabolic syndrome and/or chronic alcohol consumption resulting in insuline resistance, infection by the human immune deficiency virus or by the hepatitis B virus as well as chronic tobacco use or excessive consumption of cannabis. An optimal is based on a multidisciplinary approach to reduce fibrosis progression and improve the efficiency of antiviral therapies. However, the hepatologist has to come back to a global care, which is mandatory at the individual level as well as for the public health.

Pol S, Marcellin P. · Service d'Hépatologie, Hôpital Cochin, 27, rue du faubourg Saint Jacques, 75014 Paris, France. · Gastroenterol Clin Biol. · Pubmed #18675182 No free full text.

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Pol S, Vallet-Pichard A. · Unité d'hépatologie, Hôpital Cochin, 27, rue du faubourg Saint Jacques, 75014 Paris, France. · Gastroenterol Clin Biol. · Pubmed #18662608 No free full text.

Abstract: Parenteral and community-acquired routes of contamination sanguins of hepatitis B virus (HBV) explain its frequency (9 to 20%) in dialysis patients and kidney recipients. In dialysis, HBV infection has few impact on morbidity and mortality; by contrast, in kidney recipients HBV: 1. reduces the allograft survival; 2. the patients survival in association with a frequent and rapid evolution to cirrhosis and hepatocellular carcinoma or rare cholestatic fibrosis. Finally, cirrhosis contra-indicates renal transplantation alone given its poor short-term prognosis and a combined liver-kidney transplantation has to be discussed. Thus, it is necessary to evaluate the liver severity of the liver disease. The treatement of HBV in allograft recipients and dialysis is based on nucleos(t)idic analogues like in the general population with the same advantages and questions. The variations of the immune status either in an HBV-infected patients at the induction or at the reduction of chemotherapies (solid tumors or hemopathies) or allograft transplantation may result in two, potentially severe, events in miror: a reactivation or a spontaneous discontinuation of viral replication (seronconversion). These risks evidence that any HBs Ag carrier exposed to immune suppression has to be diagnosed, evaluated for viral replication and underlying liver disease and has to be treated by a so-called pre-emptive treatment based on analogues.

Pol S, Soriano V. · Liver Unit, Université Paris Descartes, Hôpital Cochin, Paris, France. · Clin Infect Dis. · Pubmed #18513148 No free full text.

Abstract: The management of chronic hepatitis C virus infection in patients coinfected with the human immunodeficiency virus poses a significant challenge. Treatment is influenced by a number of viral and host characteristics, including hepatitis C virus genotype, baseline viremia, and adherence to medication regimen. Accelerated progression of liver disease, immunodeficiency, and hepatotoxicity of antiretroviral drugs are additional concerns in coinfected patients. According to the results of 5 randomized clinical trials, 27%-55% of coinfected patients who received therapy with pegylated interferon-alpha and ribavirin attained a sustained virologic response. These studies also confirm the importance of early virologic response as a predictor of treatment outcome and reveal the considerable proportion of patients who experience hematologic tolerability issues. Effective management strategies that encompass patient and viral factors are necessary to improve the long-term outlook for coinfected patients.

Pol S, Cacoub P, Pialoux G, Benhamou Y, Halfon P, Rosenthal E, Perronne C. · Unité d'Hépatologie, Hôpital Cochin, 27 rue du Faubourg Saint-Jacques, 75014 Paris. · Gastroenterol Clin Biol. · Pubmed #17965629 No free full text.

Abstract: Reciprocal interactions between Human Immunodeficiency Virus (HIV) and Hepatitis C Virus (HCV) are characterized by the absence of clear impact of HCV on HIV; by contrast, HIV markedly modified the natural history of HCV (high viral load, more severe liver disease) at least before the introduction of highly active antiretroviral therapies (HAART). HAART has completely modified the pattern of hepatic events in HIV infection and the liver disease is one of the leading causes of morbidity and mortality nowadays, reflecting several non-exclusive pathogenic processes that include drug-related hepatotoxicities, chronic hepatitis C infection, other liver diseases such as steatosis or non-alcoholic steato-hepatitis (NASH) and other liver diseases that are common in the setting of alcohol or drug abuse. The harmful impact of HIV underlines the need for improving:

Soriano V, Puoti M, Sulkowski M, Cargnel A, Benhamou Y, Peters M, Mauss S, Bräu N, Hatzakis A, Pol S, Rockstroh J. · Department of Infectious Diseases, Hospital Carlos III, Calle Sinesio Delgado 10, 28029 Madrid, Spain. · AIDS. · Pubmed #17502718 No free full text.

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Pol S. · Service d'Hépatologie, Hôpital Cochin, Paris. · Gastroenterol Clin Biol. · Pubmed #17396097 No free full text.

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Pol S, Bourlière M. · Unité d'Hépatologie, Inserm U-567 Hôpital Cochin, Paris, France. · Antivir Ther. · Pubmed #17302365 No free full text.

Abstract: The overarching goal in treating chronic hepatitis C (CHC) is the prevention of serious hepatic complications such as cirrhosis, end-stage liver disease and hepatocellular carcinoma. Successful eradication of the hepatitis C virus has been shown to prevent liver disease progression and even promote regression of fibrosis. The treatment of CHC has improved significantly over the past decade with the introduction of interferons (IFNs), and more recently, pegylated IFNs. Up to two-thirds of all patients treated with a pegylated IFN combined with ribavirin can now achieve viral eradication if treated according to current guidelines. Despite this success rate, limited treatment options currently exist for the growing number of patients who do not respond to this combination, and those who have previously failed treatment with conventional IFN-based regimens. There are numerous host- and viral-related factors that can contribute to these outcomes. In addition, treatment insufficiency, whether due to treatment type, side effects or non-compliance, can result in inadequate antiviral pressure and a reduced likelihood of response. This review explores putative management strategies for patients who have previously failed to achieve a response to IFN-based therapy, and summarises retreatment options that have been, and are currently being evaluated.

Pol S, Mallet VO. · Université Paris Descartes; APHP, Hôpital Cochin, Hépatologie; INSERM U. 567, Institut Cochin; Paris, France. · Discov Med. · Pubmed #17234140 No free full text.

Abstract: Hepatitis C virus (HCV) infects about 2% of the world population or approximately 123 million people. The disease causes a significant level of morbidity and mortality among those afflicted. The combination of interferon and ribavirin is effective in many patients. However, the right treatment doses and duration, among other attributes, have a large impact on the treatment outcome.

Pol S, Michel ML. · Unité d'Hépatologie, Liver Unit, Hôpital Cochin, Université Paris V-René Descartes and Inserm U-567, 27 Rue du Faubourg Saitn Antoine, 75014 Paris, France. · Expert Rev Vaccines. · Pubmed #17181443 No free full text.

Abstract: Despite effective prophylactic vaccines against hepatitis B virus existing for over 20 years, more than 2.5 billion people worldwide have been exposed to the disease and approximately 370 million people are chronically infected with it. Chronic infection in more than two thirds of infected patients results in chronic liver disease, which may lead to cirrhosis, exposure to noncarcinomatous complications and hepatocellular carcinoma. Currently available therapies fail to allow complete control of viral replication in most patients. Viral persistence has been associated with a defect in the development of hepatitis B virus-specific cellular immunity. Immunomodulatory strategies to boost or to broaden the weak virus-specific T-cell response have been proposed to bypass the chronic hepatitis B infection, including hepatitis B virus envelope- and nucleocapsid-based vaccines, and new formulations for recombinant and DNA-based vaccines, which are currently being evaluated in clinical trials.

Pol S. · Unité d'Hépatologie et INSERM U-370, Hôpital Necker, 149, rue de Sèvres, 75015 Paris, France. · Gastroenterol Clin Biol. · Pubmed #17075494 No free full text.

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Pol S, Mallet VO. · Hôpital Necker, APHP, Unité d'Hépatologie, 149 rue de Sèvres, 75015 Paris Cedex 15, France. · Expert Opin Biol Ther. · Pubmed #16918259 No free full text.

Abstract: The estimated prevalence of hepatitis C virus (HCV) infection is 2%, representing 123 million infected individuals worldwide. HCV infection burdens public health in relation to hepatic (cirrhosis and its complications in 20% of patients) and extrahepatic (vasculitis) complications, and lessens quality of life. Major progress has been made in the last two decades for the diagnosis and treatment of HCV, including more appropriate screening strategies for HCV infection (improved sensitivity of serological and virological tests); a better evaluation of the impact of chronic HCV infection on the liver (semi-quantitative scoring systems of necro-inflammation and fibrosis on liver biopsy, non-invasive evaluation of fibrosis with biochemical markers and elastometry); and improved therapeutic regimens. This progress provides a better definition of who to treat (clinical impact or significant fibrosis); how to treat; tailoring therapies for doses and durations of the pegylated interferon plus ribavirin combination according to virological (mainly genotype and early viral kinetics, but also baseline viral load) and hosts factors (fibrosis, immune status, weight); and how to monitor efficacy and tolerance of therapy. The progress has now resulted in a 50% rate of complete HCV eradication, ranging 45 - 90% according to the genotype and especially in those patients with early viral response. New therapies, specifically HCV protease or polymerase inhibitors, in combination with pegylated interferon, or more potent and less toxic new formulations of interferons or ribavirin, will increase these encouraging results in the future.

Pol S. · Unité d'hépatologie et Inserm U-370, Hôpital Necker, Paris. · Presse Med. · Pubmed #16493335 No free full text.

Abstract: Hepatitis B virus (HBV) is transmitted by parenteral, sexual and perinatal routes. While fulminant hepatitis may occur in 1% of cases of symptomatic acute hepatitis, the principal problem of HBV infection is that it may become chronic, classically defined by carriage of HB surface antigens (HBsAg) for more than 6 months. This occurs in only 0.5 to 3% of immunocompetent adults but more frequently in children (up to 90%) and in immune-compromised patients (30 to 100%). The course of chronic HBV infection is characterized by variations in viral replication with spontaneous reactivation or discontinuation, and potential exacerbations observed clinically or by laboratory testing. The pathogenesis of HBV infection is mainly immune-mediated, resulting from host-virus interactions but also from the complexity of the virus itself (integration, mutation, occult replication). These factors explain the variety of presentations of chronic HBV infection, which range from immune tolerance to inactive carriage of HBsAg, passing through a stage of immune clearance, where chronic active hepatitis which may lead to cirrhosis (yearly incidence of 1.3 to 5.9%). Cirrhosis may be complicated by portal hypertension, liver failure, or hepatocellular carcinoma, which together explain 80% of the morbidity and mortality associated with HBV. The 5-year survival rate for HBV-related cirrhosis ranges from 52 to 82%. Immunosuppression, hepatitis D virus superinfection, and chronic alcohol consumption are the principal factors that modify this natural history. Chronic HBV infection is a major public health problem, particularly in developing countries, and it requires that efforts to make HBV vaccination universal be intensified.

Vallet-Pichard A, Pol S. · Inserm U-370 et Unité d'Hépatologie, Hôpital Necker; Faculté Paris V, 149 Rue de Sèvres, 75015 Paris, France. · J Hepatol. · Pubmed #16343684 No free full text.

Abstract: Co-infection by the hepatitis C virus (HCV) is observed in up to 30% of HIV-infected individuals. In studies conducted in the 'pre-HAART era', the late consequences of HCV-related chronic liver disease were overshadowed by extra-hepatic causes of deaths, related to severe immune deficiency, and the impact of HCV infection on mortality of HIV-infected patients was low. While the development of HAART has resulted in a significant decrease in morbidity and mortality amongst HIV-infected patients, this clear benefit allowed the expression of liver-related complications associated with HCV chronic infection. The impact of HCV on HIV remains debated but HIV infection significantly modifies the natural history of HCV infection. HIV infection increases levels of HCV viraemia by 2- to 8-fold, resulting in a significant decrease in spontaneous recovery of acute hepatitis. HIV co-infection also worsens the histological course of HCV infection by increasing and accelerating the risk of cirrhosis or leading to rare but lethal fibrosing cholestatic hepatitis. Liver disease is now one of the leading causes of morbidity and mortality in co-infected patients, even if HAART and especially protease inhibitors, may decrease the severity of the liver disease and the liver-related mortality. Several non-exclusive pathogenic processes explain the increasing rate of liver complications associated with HCV-related liver disease.

Pol S. · hôpital Necker, 75743 Paris Cedex 15. · Rev Prat. · Pubmed #15913111 No free full text.

Abstract: The transmission of the hepatitis B virus (HBV) is parenteral, sexual and perinatal. If a fulminant hepatitis may occur in 1% of cases of symptomatic acute hepatitis, the main problem of HBV infection is its chronicity, as defined by HBs antigen carriage for more than 6 months. It occurs in only 0.5 to 3% of immunocompetent adults but more frequently in children (up to 90%) or in immunocompromised patients (30 to 100%). Evolution of HBV chronic infection is characterized by variations of viral replication with spontaneous reactivations or discontinuations with potential clinical and biochemical exacerbations. Pathogeny of HBV infection is mainly immune-mediated, resulting from the host-virus interactions but also from the complexity of HBV (integration, mutation, occult replication), explaining the polymorphism of chronic HBV infection; it includes immune tolerance, inactive carriage of HBs antigen but also immune elimination with chronic active hepatitis which may lead to cirrhosis (yearly incidence of 1.3 to 5.9%). Cirrhosis may result in complications of portal hypertension and liver failure or hepatocellular carcinoma which explain 80% of morbidity and mortality of HBV: the 5-year survival of HBV-related cirrhosis ranges from 52 to 82%. Immunosuppression, delta virus superinfection or chronic alcohol consumption are the main factors which modify the natural history of HBV infection. HBV chronic infection is a problem of public health, particularly in developing countries, evidencing the need for universal HBV vaccination.

Pol S. · Unité d'Hépatologie et Inserm U-370, Hôpital Necker, Paris, France. · Gastroenterol Clin Biol. · Pubmed #15864199 No free full text.

This publication has no abstract.

Vallet-Pichard A, Pol S. · Unité d'Hépatologie et Inserm U-370, Hôpital Necker, 149 Rue de S èvres, 75015 Paris, France. · J Hepatol. · Pubmed #15246224 No free full text.

This publication has no abstract.

Lebray P, Vallet-Pichard A, Michel ML, Fontaine H, Sobesky R, Bréchot C, Pol S. · Service d'Hépatologie, Hôpital Necker Enfants Malades, 75730 Paris Cédex 15, France. · J Hepatol. · Pubmed #14708695 No free full text.

This publication has no abstract.