Effects of Eradicating Hepatitis C Virus Infection in Patients With Cirrhosis Differ With Stage of Portal Hypertension

Marco, V. Di; Calvaruso, V.; Ferraro, Donatella; Bavetta, Maria Grazia; Cabibbo, Giuseppe; Conte, Elisabetta; Cammà, Calogero; Grimaudo, Stefania; Pipitone, Rosaria Maria; Simone, F.; Peralta, Sergio; Arini, Andrea; Craxı̀, Antonio

doi:10.1053/j.gastro.2016.03.036

Cited by 131 publications

(124 citation statements)

References 42 publications

(50 reference statements)

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“…However, portal hypertension did not resolve in any patient and 20% (4/20) showed an increase in HVPG post-SVR [34]. Di Marco et al, in a single center study of cirrhotics patients with SVR followed for an average of 7.6 years, showed that SVR reduced the risk of de novo varices developing: 2.1% per year in patients with stage 1 cirrhosis with SVR compared to 9.1% of those without SVR (p <0.001) [48]. However, among those with stage 2 cirrhosis, the progression from small to medium/large varices was not significantly decreased, with progression in 10.6% per year in non-SVR patients vs. 5.9% in those with SVR (p = 0.07).…”

Section: Management Of Patient With Svr and Compensated Cirrhosismentioning

confidence: 97%

Management of the patient with SVR

Terrault

Hassanein

2016

Journal of Hepatology

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In the current era of therapy with direct-acting antiviral (DAAs) drugs, achievement of a sustained virological response (SVR) is achievable in ⩾90% of hepatitis C-infected patients. SVR benefits are well-recognized with reductions in rates of liver complications, hepatocellular carcinoma and mortality. Additional benefits include reduced morbidity related to extrahepatic and systemic manifestations of hepatitis C such as renal, dermatologic, and metabolic complications. However, not all patients will derive all of these benefits and monitoring for progression is necessary, especially in those with more advanced fibrosis. To maximize the health benefits of SVR, counseling patients on best means to maintain good liver health and prevent reinfection are also important.

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Section: Management Of Patient With Svr and Compensated Cirrhosismentioning

confidence: 97%

Management of the patient with SVR

Terrault

Hassanein

2016

Journal of Hepatology

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“…However, this is not possible for a significant proportion of patients. Moreover, successful eradication of the underlying disease does not completely eliminate the risk for HCC development, as documented in patients with chronic HCV infection (14, 15). Significant progress has been made in defining the genetic landscape (16) as well as the cellular source of HCC (17).…”

Section: Hepatocellular Carcinomamentioning

confidence: 99%

The Role of Cancer-Associated Fibroblasts and Fibrosis in Liver Cancer

Affò

Schwabe

2017

Annu. Rev. Pathol. Mech. Dis.

451

425

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Liver cancer is the second leading cause of cancer mortality worldwide, causing more than 700,000 deaths annually. Because of the wide landscape of genomic alterations and limited therapeutic success of targeting tumor cells, a recent focus has been on better understanding and possibly targeting the microenvironment in which liver tumors develop. A unique feature of liver cancer is its close association with liver fibrosis. More than 80% of hepatocellular carcinomas (HCCs) develop in fibrotic or cirrhotic livers, suggesting an important role of liver fibrosis in the premalignant environment (PME) of the liver. Cholangiocarcinoma (CCA), in contrast, is characterized by a strong desmoplasia that typically occurs in response to the tumor, suggesting a key role of cancer-associated fibroblasts (CAFs) and fibrosis in its tumor microenvironment (TME). Here, we discuss the functional contributions of myofibroblasts, CAFs, and fibrosis to the development of HCC and CCA in the hepatic PME and TME, focusing on myofibroblast- and extracellular matrix—associated growth factors, fibrosis-associated immunosuppressive pathways, as well as mechanosensitive signaling cascades that are activated by increased tissue stiffness. Better understanding of the role of myofibroblasts in HCC and CCA development and progression may provide the basis to target these cells for tumor prevention or therapy.

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“…With the new interferon-free therapies of HCV infection applying new direct-acting antiviral agents, sustained virological response rates of up to 100% after 12 weeks have been reported in clinical trials irrespective of the genotype and have already been confirmed in real-world settings [23,24,25,26]. Nevertheless, also after an effective HCV infection treatment, HCC still develops in some of these patients, especially in the setting of cirrhosis, although it will occur with less likelihood (HR 0.25 in prospective studies) [27]. It is still not clear, however, how successfully anti-HCV therapy will impact on liver fibrosis in the long term and which parameters are useful to identify patients at risk to develop HCC even after HCV clearance [28,29].…”

Section: Prevention Of Hcv-related Hccmentioning

confidence: 97%

Prevention of Hepatocellular Carcinoma

Schütte

Balbisi

Malfertheiner

2016

Gastrointest Tumors

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The epidemiology of hepatocellular carcinoma (HCC) has significantly changed throughout the past decade and will continue to do so in the future as a consequence of effective primary prevention and treatment of virus-related liver diseases. However, other risk factors for HCC are constantly on the rise, including alcoholic liver disease and nonalcoholic fatty liver disease. The knowledge on these and further risk factors associated with an increased risk of HCC provide the opportunity and chance for the development and implementation of successful preventive strategies to decrease the worldwide burden of HCC. This mini-review gives a short overview on current strategies in primary, secondary, and tertiary prevention of HCC.

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Effects of Eradicating Hepatitis C Virus Infection in Patients With Cirrhosis Differ With Stage of Portal Hypertension

Abstract: In a prospective study of 444 patients with HCV and compensated cirrhosis, HCV eradication reduced risk for liver decompensation, HCC, and death, regardless of whether the patients had EVs.

Cited by 131 publications

References 42 publications

Management of the patient with SVR

Management of the patient with SVR

The Role of Cancer-Associated Fibroblasts and Fibrosis in Liver Cancer

Prevention of Hepatocellular Carcinoma

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