Relevant bibliographies by topics / Hepatitis C chronic/pathology

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Hepatitis C chronic/pathology'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "Hepatitis C chronic/pathology"

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Fiel, M. Isabel. "Pathology of Chronic Hepatitis B and Chronic Hepatitis C." Clinics in Liver Disease 14, no. 4 (2010): 555–75. http://dx.doi.org/10.1016/j.cld.2010.07.001.

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Kage, M., T. Fujisawa, K. Shiraki, et al. "Pathology of chronic hepatitis C in children." Hepatology 26, no. 3 (1997): 771–75. http://dx.doi.org/10.1002/hep.510260333.

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PHULPOTO, JAVED AHMED. "CHRONIC HEPATITIS C-INFECTED PATIENTS;." Professional Medical Journal 20, no. 01 (2012): 068–71. http://dx.doi.org/10.29309/tpmj/2013.20.01.478.

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Background: In our region the sensitivity of serum alanine aminotransferase (ALT) levels in predicting the severity ofhepatitis C virus (HCV) infection is unclear. Objective: To compare histologic scoring of liver pathology in patients with chronic HCVinfection with normal or elevated serum ALT. Study Design: Prospective observational study. Place & Duration of Study: Liver clinic,Ghulam Mohammad Mahar Medical College Hospital, Sukkur, between January 2010 and December 2010. Methods: Liver biopsies wereperformed in patients with HCV infection and either normal (n=40) or elevated (n=76) serum ALT levels, and scored for activity andfibrosis using the modified histological activity index. Results: Patients with normal ALT and elevated ALT had similar demographicfeatures. Median (range) histological activity grade was higher in patients with elevated ALT than in those with normal ALT (6 [1-15] vs. 5[0-11], respectively; p=0.001), as was the fibrosis stage (2 [0-6] vs. 1 [0-6]; p=0.02). Two patients with normal ALT and 4 with elevatedALT had liver cirrhosis. Conclusions: Among patients with chronic HCV infection, liver lesions are milder in those with normal serum ALTlevels than those with abnormal ALT levels. However, some patients with normal ALT too may have advanced liver disease.
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Tsvetkov, V. V., I. I. Tokin, and S. A. Pozdnjakova. "Clinical epidemiology of extrahepatic manifestations of chronic hepatitis C virus infection." Medical Council, no. 21 (January 28, 2020): 248–53. http://dx.doi.org/10.21518/2079-701x-2019-21-248-253.

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Extrahepatic manifestations occur in more than half of patients with chronic hepatitis C virus infection and may be no less dangerous to the health and life of the patient than the isolated pathology of the liver. Chronic hepatitis C virus infection is often accompanied by the formation of neurocognitive disorders, clinically manifested by general weakness, fatigue and the inability to maindoi tain concentration for a long time. Every fifth patient with chronic hepatitis C develops depression. The development of type 2 diabetes among patients with chronic hepatitis C virus infection is observed 1.7 times more often than among non-infected individuals. Mixed cryoglobulinemia is observed in at least 30% of patients, however, the clinical manifestations of this pathology develop only in 4.9% of cases, of which 69–89% of skin lesions, 19–44% of distal sensory and sensorimotor polyneuropathy, 30% of membranoproliferative glomerulonephritis, 28% of joint damage. Among patients with chronic hepatitis C virus infection, higher prevalence than among non-infected individuals is observed, the prevalence rates of such nosologies as lymphoma from cells of the marginal zone are 2.47 times, diffuse large cell B cell lymphoma – 2.24 times, hypothyroidism – 3.1 time. Significantly more rarely encountered extrahepatic manifestations of chronic hepatitis C virus infection are skin lesions that are not associated with the development of cryoglobulinemic vasculitis: acquired late skin porphyria, necrolytic acral erythema and lichen planus. The question of the pathogenetic relationship of chronic hepatitis C virus infection with cardiovascular pathology remains open.
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Stahl, Jurgen. "Yet another cause for granulomatous hepatitis: chronic hepatitis C." Advances in Anatomic Pathology 8, no. 1 (2001): 48–49. http://dx.doi.org/10.1097/00125480-200101000-00010.

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Marinelli, RMA, M. Delle Monache, R. Gerardi, et al. "Liver Pathology in Cytomegalovirus Infection Associated with Hepatitis B Virus." Journal of International Medical Research 21, no. 3 (1993): 154–57. http://dx.doi.org/10.1177/030006059302100306.

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A retrospective study was carried out in 56 patients to establish the association of cytomegalovirus (CMV) with active or inactive hepatitis B virus (HBV) infection as a possible risk factor in the development of severe liver disease. Patients with positive CMV serology and active or inactive HBV infection had elevated alanine aminotransferase activity and had a relatively high incidence of more severe lesions (chronic hepatitis and active cirrhosis), In the absence of CMV, only one case of cirrhosis was identified compared with seven cases of hepatic fibrosis. By analogy with hepatitis C virus, CMV may bring about activation of the host inflammatory response against hepatocytes following HBV infection, resulting in the development of severe hepatitic disease.
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Nikonorova, Marina A., N. S. Lubskaya, E. V. Volchkova, E. A. Nemilostiva, and O. I. Matros. "VARIANTS OF THYROID GLAND PATHOLOGY IN CHRONIC HEPATITIS C PATIENTS." Epidemiology and Infectious Diseases 22, no. 4 (2017): 172–77. http://dx.doi.org/10.17816/eid40958.

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Introduction. HCV is the cause not only of cirrhosis, hepatocellular carcinoma, but also extrahepatic manifestations. Currently, HCV is considered as an independent risk factor for thyroid pathology. In recent years, the level of pathology of the thyroid gland in the Altai Territory has increased by 16.4 times, which determined the purpose of this study: to study the features of the thyroid status in patients with chronic hepatitis C (CHC) in the Altai Territory. Materials and methods. There was executed a prospective, dynamic clinical, laboratory and instrumental examination of 240 CHC patients (47,5% of men and 52,5% of women aged of from 18 to 50 years), 120 of whom had HCV (49,1% of men and 50,9% of women, aged of from 18 to 50 years, mean age: 41,1±9,91 years) who did not receive antiviral therapy (HTV), the pathology of the thyroid gland in them was established for the first time. The study included the assessment of the level of TSH, total and free T3, T4, antibodies to thyreperoxidase (APPO), ultrasound examination of the thyroid gland. The diagnosis of CHC is based on HCV RNA, anti-HCV (core, NS3-5), blood biochemistry, fibrosis level score according to Metavir (elastometry, PBP). Results of the study. In HCV patients there were revealed autoimmune thyroiditis (AIT) (5%), AIT with hypothyroidism (10%), AIT with latent hypothyroidism (8,3%), latent hypothyroidism (10%), hypothyroidism (16,6%), euthyroidism (49,1%) and thyrotoxicosis in only 1 patient. Variants of thyroid dysfunction were presented in the form of euthyroidism (60%), hypothyroidism (20%), hyperthyroidism (10%) and autoimmune thyroiditis (10%). The relationship between the development of the thyroid dysfunction (TD) and the history of the history of HCV infection has been established. Discussion and conclusions. CHC patients were more likely to have a history of euthyroidism and hypothyroidism. The relationship between TD and the duration of HCV infection can be regarded as its extrahepatic manifestation, and not as comorbid conditions. Thorough examination of the thyroid status it makes possible to identify TD people, which can be reflected in the choice of antiviral therapy and will determine the prognosis of the development of side effects.
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&NA;. "The natural history of chronic hepatitis C." Advances in Anatomic Pathology 4, no. 6 (1997): 380. http://dx.doi.org/10.1097/00125480-199711000-00029.

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Banner, B. F., C. Allan, L. Savas, S. Baker, G. Barnard, and H. L. Bonkovsky. "Inflammatory markers in chronic hepatitis C." Virchows Archiv 431, no. 3 (1997): 181–87. http://dx.doi.org/10.1007/s004280050086.

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Filipovich, O. M., and N. I. Kuznetzov. "Features of chronic hepatitis C course in pregnant women." Kazan medical journal 97, no. 5 (2016): 716–20. http://dx.doi.org/10.17750/kmj2016-716.

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Aim. To study features of the course of chronic hepatitis C virus infection in pregnant women and its effect on pregnancy.Methods. The study included 111 pregnant women: 67 with chronic hepatitis C and 44 healthy women. The mean age was 28 years. The number of pregnancies among examined women ranged from 1 to 8. All pregnant women had no concomitant therapeutic pathology and various addictions (alcohol, nicotine, drugs). The viral load in pregnant women with chronic hepatitis C ranged from 3.18×102 to 2.4×107 IU/mL.Results. Alanine aminotransferase and bilirubin levels in the group of chronic hepatitis C and in healthy pregnant women did not exceed the normal range and were not statistically different from each other. In repeated pregnancies viral load of hepatitis C virus was lower, compared with the first pregnancy: median [25%; 75%] = 5.202 [4.079; 6.364] and 6.658 [5.708; 7.380], respectively (p106 IU/mL). At the same time threatened miscarriage, intrauterine hypoxia and preeclampsia were registered more often.Conclusion. In the first pregnancy the viral load is higher than in repeated pregnancies; pregnancy in women with chronic hepatitis C without concomitant diseases does not cause activation of the inflammatory process in the liver; in pregnant women with chronic hepatitis C, especially at higher viral loads, medical history remarkable for obstetric diseases are more likely detected.
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Dissertations / Theses on the topic "Hepatitis C chronic/pathology"

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Pessôa, Mário Guimarães. ""Hepatite colestática associada ao vírus da hepatite C pós-transplante hepático: estudo virológico, histopatológico e imuno-histoquímico"." Universidade de São Paulo, 2004. http://www.teses.usp.br/teses/disponiveis/5/5144/tde-04042006-090453/.

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A evolução da recorrência da hepatie C pós-transplante hepático pode ter um curso bastante variável. Raramente a doença pode progredir para uma forma conhecida como hepatite recorrente colestática grave, cuja patogenia ainda não é bem conhecida. Nós estudamos nesse trabalho alguns aspectos virológicos, histológicos e imunohistoquímicos de seis pacientes com essa forma rara de recorrência da doença, tendo como comparação um grupo pareado de seis pacientes transplantados com a forma leve de hepatite C recorrente, e como controle imunocompetente, cinco pacientes não transplantados com hepatite crônica pelo vírus C. Foram avaliados como possíveis fatores preditivos de gravidade da progressão da recorrência: viremia do VHC, evolução de quasispécies, parâmetros histopatológicos, e imunoreatividade para o antígeno core do VHC.
Following liver transplantation (OLT) HCV-related disease severity is highly variable, with a minority of cases progressing to an extremely severe form of cholestatic hepatitis, in which the pathogenesis is not yet understood. We aim to compare virological, histological and immunohistological changes in patients developing mild and severe post-OLT HCV recurrence. Twelve patients with recurrent HCV infection were studied (6 with severe and 6 with mild disease). Five HCV-infected immunocompetent patients were used as controls. We looked at viral load, quasispecies evolution of HCV, several histological parameters and immuno-reactivity of core antigens at three time-points (pre-OLT, early post-OLT and late post-OLT) as predictors of severity of recurrence post-OLT.
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Zaver, Himesh, Momani Laith Al, Kalpit Devani, and Chakradhar M. Reddy. "Ledipasvir/sofosbuvir induced nephrotic syndrome: A challenging case of Hepatitis C management." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/80.

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ABSTRACT: Hepatitis C virus (HCV) is associated with various glomerulopathies and nephrotic syndrome. However nephrotic syndrome following treatment is rare. Ledipasvir/sofosbuvir (L/S) has recently come into favor in treating HCV due to its relatively mild side effects compared to the more traditional interferon therapy. To the best of our knowledge, there are no reported cases of nephrotic syndrome following treatment with L/S. We present a case of nephrotic syndrome suspected secondary to L/S in a patient with chronic kidney disease. Increased vigilance when assessing therapeutic options in HCV patients with renal comorbidities can improve patient outcomes. A 63 year-old male patient presented to the hospital with shortness of breath, and a two-week history of bilateral lower extremity edema. Past medical history was significant for liver cirrhosis secondary to Hepatitis C genotype Ia, hepatocellular carcinoma status post liver transplantation 6 months prior to admission and Stage 3b chronic kidney disease with baseline creatinine (Cr) approximately 1.5 mg/dl. Medications included L/S for HCV and tacrolimus and prednisone for post-transplant treatment. Patient’s vitals were stable and physical exam was remarkable for facial swelling, mainly on the eyelids, decreased breath sounds bilaterally, distended abdomen with a fluid wave, and 2-3+ pitting edema up to the knees on lower extremities bilaterally. Laboratory work-up was remarkable for low albumin of 3.0 g/dl, and total protein of 5.6 g/ dl. Creatinine of 1.8 mg/dl was elevated from patient’s baseline. HCV viral load was undetectable and electrolytes, transaminases and the complete blood count were within normal limits. Subsequently, urine protein to creatinine ratio was measured because of generalized swelling and hypoproteinemia, which was found to be significantly high at 8.80, compared to 0.04 one year prior. 24-hour total urine protein was found to be 2065 mg/day. Renal ultrasonography showed no hydronephrosis and was otherwise unremarkable. Renal biopsy however, revealed changes suggestive of membranoproliferative glomerulonephritis (MPGN] most likely secondary to HCV. No immune complexes, lambda/kappa light chains, or cryogloblin were appreciated. Nephrotoxic agents such as diuretics and corticosteroids were held. Tacrolimus trough was appropriate to dose level and was continued along with L/S. As admission progressed the patient’s creatinine continued to get worse and rose up to 4.3 mg/dl with persistent proteinuria. With tacrolimus trough levels within normal limits and given L/S was the most recently initiated drug, L/S was thought to be the culprit and was thus held. The renal function began to improve gradually, and the patient was discharged in stable condition with close follow up. Follow up one month later found creatinine and renal function return to baseline and proteinuria resolved. Our case shows that Ledipasvir/sofosbuvir may possibly be related to nephrotic syndrome in HCV patients. Although further studies are needed to prove the causality our case seeks to raise clinical suspicion and increase vigilance when assessing therapeutic options in HCV patients with renal comorbidities such as chronic kidney disease.
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Pereira, Haydée Marina do Valle. "Características de pacientes com hepatite C crônica e transaminases normais." Universidade de São Paulo, 2005. http://www.teses.usp.br/teses/disponiveis/5/5134/tde-08102014-103411/.

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Hepatite C tem evolução progressiva, persiste na maioria dos pacientes (85%) e leva a uma doença crônica assintomática.A maioria dos pacientes apresenta nível de ALT elevada e aproximadamente 25% normal. Estes geralmente são mulheres e não há associação entre genótipo e severidade da lesão hepática. Histologicamente apresentam lesão mínima e leve fibrose, embora cirrose tenha sido relatado.Visando estimar a prevalência, características demográficas, genotípicas e anatomopatológicas em pacientes com ALT normal, realizamos um estudo de série de 68 casos entre janeiro de 1997 a abril de 2000. A prevalência foi de 13,82%, 45,6% do gênero masculino e 54,4% feminino, média de idade 38 +/- 13 anos. Genótipo 1 em 84,75%, 2 em 6,78% e o 3 em 8,47%. Em 52,9% dos casos biópsia hepática revelou fígado reacional, porém uma importante proporção (29%) dos nossos pacientes com transaminases normais mostrou sinais de fibrose. Estes resultados sugerem a necessidade de revisar os algoritimos da prática de biópsia hepática nessa população
Hepatitis C evolves progressively persisting in the majority of patients (85%) resulting in na asymptomatic chronic disease.Most patients have high ALT levels and approximately 25% normal ALT.The latter are usually female and there is no association between genotype and severity hepatic lesion.Histology shows small lesion and low amount of fibrosis, despite cirrhosis having been reported.Aiming at assessing prevalence, demographic, genotypical and anatomopathological characteristics in patients with normal ALT levels, we studied a series of 68 cases between January 1997 and April 2000.There was a prevalence of 13,82%, 45,6% of which were male and 54,4% female, average age of 38+/-13 years.Genotype 1 in 84,75%, 2 in 6,78% and 3 in 8,47%.In 52,9% of the cases revealed liver reaction, however, an important proportion of patients showed histologic signs of fibrosis (29%).Theses results suggest the need to revisit the algorithm for liver biopsy practice
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Ribeiro, Maria de Fatima Gomes de Sá. ""Fatores prognósticos na evolução da hepatite C"." Universidade de São Paulo, 2005. http://www.teses.usp.br/teses/disponiveis/5/5144/tde-12082005-155039/.

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O consumo alcoólico pode levar à deterioração da lesão hepática em pacientes com hepatite C. A progressão da doença na hepatite C crônica depende de vários outros fatores relacionados com o hospedeiro, vírus e o meio ambiente embora os mecanismos patogênicos ainda não sejam bem conhecidos. OBJETIVOS: avaliar os dados demográficos, epidemiológicos, clínicos e bioquímicos dos pacientes com hepatite C crônica em relação ao consumo alcoólico e relacionar as variáveis clínicas, epidemiológicas e bioquímicas em relação às alterações histopatológicas ausente e leve em comparação às intensas. MÉTODOS: Nós estudamos os dados demográficos, clínico-epidemiológicos e laboratoriais comparando-os às alterações histopatológicas em 120 doadores voluntários de sangue com hepatite C, divididos em três grupos de acordo com a ingestão alcoólica: (i) grupo abstêmio: n=41; (ii) grupo consumo alcoólico leve: n=36; (iii) grupo consumo alcoólico acentuado: n=43. Os parâmetros histopatológicos como alterações estruturais ou fibrose, atividade periportal e lobular e infiltrado portal foram graduados de 0 a 4 e divididas em leve (0/1/2) e intensa (3/4). RESULTADOS: Quase 70% dos pacientes eram homens e a maior proporção deles (83,5%) era de alcoolistas (leve e acentuado).Por outro lado, as mulheres eram habitualmente abstêmias (58,5%). Transfusão, como fator de risco para hepatite C foi mais freqüente em abstêmios (p=0,056) enquanto que o uso de drogas predominou no grupo de consumo alcoólico acentuado (p < 0,001). Com relação aos grupos, não foram observadas diferenças quando analisados o tempo de ingestão alcoólica, abstinência alcoólica, cirurgia e outros modos de contaminação, níveis séricos de alanina aminotransferase, aspartato aminotransferase, gama-glutamiltransferase, graus de fibrose, atividade lobular e infiltrado portal.Atividade periportal leve foi relevante nos grupos abstêmios e consumo alcoólico leve enquanto a atividade periportal intensa foi maior no consumo alcoólico acentuado (p=0,033). Quando comparamos os diferentes parâmetros histopatológicos, a idade mais avançada foi associada de modo significativo com fibrose (p=0,004), atividade periportal (p=0,001) e infiltrado portal intensos (p=0,001). Valores mais altos de índice de massa corpórea correlacionaram significativamente (p=0,013) com fibrose intensa enquanto maior tempo de ingestão alcoólica foi relacionado com atividade periportal intensa (p=0,001). Níveis de alanina aminotransferase foram maiores significativamente com intensas fibrose (p < 0,001), atividade periportal (p=0,031) e atividade lobular (p=0,013), enquanto níveis elevados de aspartato aminotransferase correlacionaram com fibrose (p < 0,001), atividade periportal (p < 0,001), atividade lobular (p=0,001) e infiltrado portal intensos (p < 0,018). Valores de gama-glutamiltransferase foram significativamente maiores com intensas fibrose (p=0,012), atividade periportal (p=0,013 e atividade lobular (p=0,003) e níveis mais altos de imunoglobulina G correlacionaram com intensas fibrose (p=0,040) e atividade lobular (p=0,048). A contagem de plaquetas foi significativamente menor quando comparada com intensas fibrose (p < 0,001) e atividade periportal (p=0,049). Análise de regressão logística identificou aspartato aminotransferase e contagem de plaquetas como fatores preditivos independentes de intensa fibrose. CONCLUSÕES: Nosso estudo mostrou correlação entre consumo de álcool e atividade periportal mas não com fibrose que está relacionada com idade, índice de massa corpórea, alanina aminotransferase, aspartato aminotransferase, gama-glutamiltransferase e menor contagem de plaquetas. Níveis de aspartato aminotransferase e contagem de plaquetas foram os melhores fatores preditivos de fibrose intensa
INTRODUCTION: The interaction of hepatitis C with alcohol consumption is thought to be a deleterious one. Progression of liver disease in chronic hepatits C depends on several other factors related to the host, virus and the enviroment but, these factors are not well understood yet. AIMS:To analyze demographic, epidemiological, biochemical and histopathological data of patients with hepatitis C according to heavy, light or no alcohol consumption.To assess the behavior of clinical, epidemiological and biochemical variables in relation to absent or mild histopathological alterations in contrast to severe alterations. METHODS: We have studied the demographic, epidemiological and laboratory data and then compared them to the histopathological alterations in 120 volunteer blood donors with hepatitis C virus divided into three groups according to alcohol intake: abstainers: n=41, light drinkers: n=36 and heavy drinkers: n=43. Liver histopathology alterations, namely architectural staging, periportal and lobular inflammation as well as portal inflammatory infiltrate were graded from 0 to 4 and afterwards divided into light (0 to 2) and severe (3 to 4). RESULTS: Almost 70% (83/120) of the patients were men and a high proportion of men (83.5 %) were drinkers (light and heavy). Women, on the other hand were more likely to be abstainers: 58.5% of them did not drink. Transfusion as risk factor for HCV was more frequent in abstainers (p= 0.056) whereas drug addiction predominated in heavy drinkers (p < 0.001). Regarding these groups no differences were found when duration of alcohol intake, abstinence of alcohol, surgery, other contamination factors, ALT, AST, GGT, degree of fibrosis, lobular inflammation and portal infiltrate were consider.Regarding three groups, mild periportal inflammation was significantly related with abstainers and light drinkers groups whereas severe periportal inflammation was more predominant in heavy drinkers (p=0.033). When we compared mild with severe histopathological alterations older age was significantly associated with severe fibrosis (p=0.004), periportal inflammation (p=0.001) and portal inflammatory infiltrate (p=0.001). Higher BMI values correlated significantly (p=0.013) with severe fibrosis whereas higher duration of alcohol intake was related to severe periportal inflammation (p=0.001). ALT level was significantly higher in severe fibrosis (p < 0.001), periportal inflammation (p=0.031) and lobular inflammation (p=0.013), whereas higher levels of AST correlated with severe fibrosis (p < 0.001), periportal inflammation (p < 0.001), lobular inflammation (p=0.001) and portal inflammatory infiltrate (p=0.018) . GGT values were significantly higher in severe fibrosis (p=0.012), periportal inflammation(p=0.013) and lobular activity (p=0.003) and higher levels of IgG correlated with fibrosis (p=0.040) and lobular inflammation (p=0.048). In the end, platelets were significantly lower (p < 0.001) in severe fibrosis and periportal inflammation (p=0.049). Logistic regression analysis identified AST and platelet count as independent predictors of severe fibrosis.CONCLUSIONS: Our study has shown a correlation between alcohol consumption and periportal inflammation, but not with fibrosis, which is correlated with age, high enzymes levels and low platelet count. AST and platelet count were the best predictors of severe fibrosis
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Trepo, Eric. "Role of genetic factors in the progression of fibrosis in alcoholic liver disease and chronic hepatitis C." Doctoral thesis, Universite Libre de Bruxelles, 2012. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209659.

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La maladie alcoolique du foie (MAF) et l’hépatite C chronique (HCC) sont les causes les plus fréquentes de cirrhose, carcinome hépatocellulaire (CHC) et transplantation hépatique dans les pays industrialisés. La fibrose hépatique est le stigmate lésionnel de la progression de la maladie vers la cirrhose comme dans toutes les hépatopathies chroniques. Certains facteurs de risque cliniques environnementaux ont été identifiés. Toutefois, ils n’expliquent pas l’extrême variabilité individuelle de la progression de la fibrose. L’influence ethnique à développer une maladie plus sévère ainsi que les études de concordance des jumeaux mono- et di-zygotiques sur la prévalence de la cirrhose alcoolique ont suggéré l’existence de facteurs génétiques associés. Les nombreuses études de gènes candidats réalisées n’ont identifié que très peu de variants associés de manière reproductible. Pour l’HCC par exemple, le score de risque de cirrhose ou « CRS » a montré sa capacité à prédire une fibrose avancée dans diverses cohortes caucasiennes. Récemment, une étude d’association pangénomique (GWAS) dans la stéatohépatopathie non-alcoolique (NAFLD) a mis en évidence un singleton (single nucleotide polymorphism [SNP]) particulier (rs738409 C>G) dans le gène PNPLA3. Ce dernier s’est révélé être, dans diverses études, le SNP ayant l’impact le plus robuste et le plus reproductible dans cette maladie. Par ailleurs, ce même variant a également été significativement associé à la cirrhose alcoolique chez les hispaniques.

Les travaux réalisés dans le cadre de cette thèse ont permis de montrer que :

1) Le CRS avait la capacité de prédire la progression de la fibrose chez des patients caucasiens ayant une HCC dans 2 cohortes européennes indépendantes.

2) Par ailleurs, dans la MAF, nous avons répliqué chez des patients caucasiens l’association entre le SNP rs738409 dans le gène PNPLA3 et la cirrhose. Nous avons également montré pour la première fois, que l’expression de PNPLA3 était significativement diminuée chez les patients avec une fibrose plus avancée. De plus, nous avons observé dans 2 cohortes européennes que rs738409 était également associé à la prévalence du CHC.

3) Enfin, nous avons également mis en évidence l’impact de ce même SNP sur la stéatose hépatique et la fibrose dans l’HCC sans toutefois qu’il influence la réponse à la thérapie antivirale dans 3 cohortes caucasiennes indépendantes.

Ainsi de manière remarquable, un même SNP (rs738409) apparait associé à des lésions hépatiques sévères dans les trois pathologies hépatiques chroniques les plus fréquentes (la MAF, l’HCC et la NAFLD). Ceci suggère des voies pathogéniques communes de la fibrogénèse hépatique. Par ailleurs, ces travaux soulignent indirectement que les GWAS ont la capacité d’ouvrir de nouvelles voies physiopathologiques et d’identifier de nouveaux variants, gènes ou région génétiques capables de constituer de nouveaux biomarqueurs et cibles thérapeutiques dans l’HCC et la MAF.
Doctorat en Sciences médicales
info:eu-repo/semantics/nonPublished

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Deltenre, Pierre. "Hépatite C: contribution à l'évaluation de l'histoire naturelle et à la prise en charge thérapeutique de l'hépatite chronique." Doctoral thesis, Universite Libre de Bruxelles, 2012. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209708.

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L’hétérogénéité de l’histoire naturelle de l’hépatite C est expliquée par l’existence de facteurs environnementaux ou liés au malade qui influencent l’évolution de la maladie. L’obtention d’une réponse virologique soutenue est l’objectif principal de la prise en charge thérapeutique car c’est la seule façon de réduire l’incidence de la cirrhose et la mortalité liée au virus de l’hépatite C. Pour être efficaces, les stratégies thérapeutiques doivent être élaborées à deux niveaux. A l’échelle individuelle, elles doivent optimaliser les chances de réponse virologique tout en limitant l’exposition aux effets secondaires. A l’échelle d’une population, la meilleure stratégie est celle qui aura l’impact le plus important sur l’incidence de la cirrhose et sur la mortalité liées au virus de l’hépatite C.

Les travaux réalisés dans le cadre de cette thèse ont permis d’identifier des critères virologiques autorisant l’arrêt d’un traitement inefficace dès le terme de la 4ème semaine chez les malades présentant des transaminases normales et chez les malades non répondeurs à un premier traitement, de quantifier la perte de chance de réponse virologique lorsque la durée du traitement est limitée à 24 semaines chez les malades infectés par un génotype 1, d’évaluer la place de l’amantadine dans l’arsenal thérapeutique, de quantifier l’impact d’une insulino-résistance sur le taux de réponse virologique, de contribuer à l’élaboration d’une stratégie thérapeutique permettant une meilleure tolérance hématologique chez les malades hémodialysés et de quantifier l’impact des polymorphismes de l’interleukine 28B sur le taux réponse virologique des malades infectés par un génotype 2 ou 3. Nos travaux ont également permis de mesurer l’impact d’une consommation excessive d’alcool sur la morbi-mortalité liée au virus de l’hépatite C à l’échelle d’une population et de quantifier l’impact des mesures thérapeutiques actuelles et de stratégies thérapeutiques alternatives sur cette morbi-mortalité.

Au cours de la prochaine décennie, le traitement de l’hépatite chronique C sera articulé autour des molécules antivirales spécifiques agissant directement contre le virus de l’hépatite C. De nouvelles stratégies thérapeutiques intégrant la cinétique virale et les marqueurs génétiques prédictifs de la réponse virologique soutenue devront être élaborées afin d’offrir les meilleures chances d’éradication virologique au plus grand nombre de malades.
Doctorat en sciences médicales
info:eu-repo/semantics/nonPublished

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Savage, Anne Kay. "The pathology of hepatitis C virus infection." Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362544.

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Lim, Teegan Reina. "Metabolic effects of hypoxia and chronic hepatitis C." Thesis, University of Birmingham, 2018. http://etheses.bham.ac.uk//id/eprint/8535/.

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Hypoxia has been linked to the pathogenesis of hepatic steatosis in murine and human models. There is an abundance of data suggesting that HIFs play a central role in regulating hepatic lipid metabolism. This study suggested that hypoxia-induced hepatic lipid accumulation is through de novo lipogenesis and free fatty acid uptake, and is dependent on hypoxia inducible factors la and 2a. On the contrary, hepatitis C infection reduced de novo lipogenesis and free fatty acid uptake in both normoxic and hypoxic conditions in vitro, and this inhibition is viral strain-dependent. In the clinical setting, chronic hepatitis C {CHC) and non-alcoholic fatty liver diseases {NAFLD) are associated with hepatic steatosis and insulin resistance. Using an integrative physiological approach that measures lipid and carbohydrate flux in vivo we demonstrated that patients with CHC had modest increase in insulin resistance and that the relative contribution of tissue specific insulin sensitivity in patients with CHC and NASH varied. Furthermore, curing HCV infection improved hepatic and subcutaneous adipose tissue insulin resistance. The improvement in hepatic and adipose tissue insulin resistance was more pronounced in patients infected with genotype 3 HCV, whilst the improvement in skeletal muscle insulin resistance was more evident in genotype 1 infection, demonstrating a genotype-specific effect in the metabolic perturbation in CHC. Further studies are required to confirm that genotype specific effect of HCV on insulin resistance and its link with NASH.
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Christie, John Michael Landale. "Viral persistence in hepatitis C virus infection." Thesis, University of Southampton, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268465.

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HAYASHI, HISAO, TOSHIKUNI TAKlKAWA, KATSUMI KATO, et al. "BIOCHEMICAL IMPROVEMENT OF CHRONIC HEPATITIS C AFTER GASTROINTESTINAL BLEEDING." Nagoya University School of Medicine, 1994. http://hdl.handle.net/2237/16077.

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Books on the topic "Hepatitis C chronic/pathology"

1

Ozaras, Resat, and Dominique Salmon-Ceron, eds. Viral Hepatitis: Chronic Hepatitis C. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-03757-4.

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Shiffman, Mitchell L., ed. Chronic Hepatitis C Virus. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-1192-5.

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National Digestive Diseases Information Clearinghouse (U.S.). Chronic hepatitis C: Current disease management. National Digestive Diseases Information Clearinghouse, 2006.

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Dammacco, Franco. HCV Infection and Cryoglobulinemia. Springer-Verlag Italia, 2012.

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Shih, Chiaho. Chronic hepatitis B and C: Basic science to clinical applications. World Scientific, 2012.

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Foster, Graham. Management of Chronic Viral Hepatitis. Taylor & Francis Group Plc, 2004.

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D, Goldin R., ed. Management of chronic viral hepatitis. Martin Dunitz, 2002.

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San Francisco (Calif). Dept. of Public Health. Communicable Disease Control Unit. Chronic hepatitis B and hepatitis C infection surveillance report: 2009, San Francisco, California. San Francisco Department of Public Health, 2010.

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San Francisco (Calif). Dept. of Public Health. Communicable Disease Control Unit. Chronic hepatitis B and hepatitis C infection surveillance report: 2010, San Francisco, California. San Francisco Department of Public Health, 2012.

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Takahashi Memorial Forum (1995 Tokyo, Japan). Interferon therapy on chronic hepatitic C: Proceedings of the "Takahashi Memorial Forum", held in Tokyo, Japan on 25 November 1995. Edited by Takahashi Tadao 1908-, Yamanaka Masami, Okabe Kazuhiko, and Toda Gotaro. Elsevier, 1996.

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Book chapters on the topic "Hepatitis C chronic/pathology"

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Wight, D. G. D. "Chronic Hepatitis." In Atlas of Liver Pathology. Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-2212-2_7.

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Trabut, Jean Baptiste. "Chronic Hepatitis C." In Encyclopedia of Quality of Life and Well-Being Research. Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-007-0753-5_365.

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Athwal, Varinder, and Martin Prince. "Chronic Hepatitis C." In In Clinical Practice. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-43126-0_11.

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Cohen, Stanley Martin. "Chronic Hepatitis C." In Liver Disease. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-98506-0_7.

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Arends, Joop E., Maria Cristina Leoni, and Dominique Salmon-Ceron. "Acute Hepatitis C." In Viral Hepatitis: Chronic Hepatitis C. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-03757-4_11.

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Sun, Jiaren, Gaurav Chaturvedi, and Steven A. Weinman. "Viral Hepatitis C." In Molecular Pathology Library. Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-7107-4_38.

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Dieterich, Douglas, Marie-Louise Vachon, and Damaris Carriero. "Hepatitis C in Special Populations." In Chronic Viral Hepatitis. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-565-7_4.

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Forns, Xavier, and Jose M. Sánchez-Tapias. "Chronic viral hepatitis C." In Textbook of Clinical Gastroenterology and Hepatology. Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118321386.ch81.

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Ozaras, Resat, and Hakan Leblebicioglu. "Global Epidemiology of Chronic Hepatitis C Virus Infection." In Viral Hepatitis: Chronic Hepatitis C. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-03757-4_1.

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Karaca, Çetin. "Extrahepatic Manifestations of Hepatitis C Virus Infection." In Viral Hepatitis: Chronic Hepatitis C. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-03757-4_10.

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Conference papers on the topic "Hepatitis C chronic/pathology"

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Prasetia Nurwidda, Arvi Dian, Poernomo Boedi Setiawan, Iswan Abbas Nusi, et al. "Thrombocytopenia in Chronic Hepatitis C." In Surabaya International Physiology Seminar. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007340404460452.

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Kchir, H., D. KAFFEL, H. Dabbebi, et al. "AB1049 Rheumatological manifestations during chronic hepatitis c." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5886.

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Nevkhoroshev, Yevhen, and Deonis Tkemaladze. "AUTOIMMUNE THYROIDITIS IN PATIENTS WITH CHRONIC HEPATITIS C." In TENDANCES SCIENTIFIQUES DE LA RECHERCHE FONDAMENTALE ET APPLIQUÉE, chair Lilia Bobro. European Scientific Platform, 2020. http://dx.doi.org/10.36074/30.10.2020.v2.07.

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"Secrum microRNA-122 with HCC in chronic hepatitis C." In 2018 International Conference on Medicine, Biology, Materials and Manufacturing. Francis Academic Press, 2018. http://dx.doi.org/10.25236/icmbmm.2018.63.

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hela, KCHIR, Ons Gharbi, Dhilel Issaoui, et al. "AB0529 SICCA SYNDROME DURING CHRONIC HEPATITIS C: PREVALENCE AND CHARACTERISTICS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.7584.

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Schlevogt, B., K. Böker, S. Mauss, et al. "Weight gain after interferon-free clearance of chronic hepatitis C – Results from the German Hepatitis C-Registry (DHC-R)." In Viszeralmedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1695343.

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"3.0T 1H MRS in Assessing the Steatosis in Chronic Hepatitis C Patients." In 2018 International Conference on Medicine, Biology, Materials and Manufacturing. Francis Academic Press, 2018. http://dx.doi.org/10.25236/icmbmm.2018.64.

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Ruiz Gómez, A., L. Menéndez Naranjo, M. Sáez Garrido, et al. "5PSQ-033 Glecaprevir/pibrentasvir use in chronic hepatitis C: effectiveness and safety." In 25th EAHP Congress, 25th–27th March 2020, Gothenburg, Sweden. British Medical Journal Publishing Group, 2020. http://dx.doi.org/10.1136/ejhpharm-2020-eahpconf.350.

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Ionescu, R. A., L. M. Pana, V. M. Pompilian, et al. "SAT0668 Articular involvement in chronic hepatitis c infection – a preliminary ultrasound study." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.7464.

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Ma, Ling, YongSheng Yang, Xin Ge, YiDan Wan, and Xin Sang. "Prediction of disease progression of chronic hepatitis C based on XGBoost algorithm." In 2020 International Conference on Robots & Intelligent System (ICRIS). IEEE, 2020. http://dx.doi.org/10.1109/icris52159.2020.00151.

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Reports on the topic "Hepatitis C chronic/pathology"

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Kancheva, Lyudmila, Petar Nikolov, Tsvetelina Velikova, Ivan Valkov, Rossen Nikolov, and Lyudmila Mateva. Soluble CD14 is Associated with Disease Activity and Severity in Chronic Viral Hepatitis C and B. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, 2018. http://dx.doi.org/10.7546/crabs.2018.06.17.

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Evon, Donna, Jipcy Amador, Paul Stewart, et al. Changes in Health for Patients Who Complete Treatment for Chronic Hepatitis C Virus -- The PROP up TARGET Study. Patient-Centered Outcomes Research Institute® (PCORI), 2020. http://dx.doi.org/10.25302/06.2020.cer.140820660.

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Xu, Yan, Yuyang Zhao, Yong Wang, et al. Concurrent hepatic steatosis increases the risk of hepatocellular carcinoma in patients with chronic hepatitis B or C virus infection: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2020. http://dx.doi.org/10.37766/inplasy2020.7.0099.

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