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Interferon-α-induced retinopathy in chronic hepatitis C treatment: summary, considerations, and recommendations.
Rentiya, ZS, Wells, M, Bae, J, Chen, KJ, Chao, AN, Turgeon, N, Shah, SM, Hanout, M
Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie. 2019;(3):447-452
Abstract
Interferons are cytokines that regulate the host's response to viral infection, particularly in the setting of the immunologic response to the hepatitis C virus (HCV). While the virus has the ability to evade the host's innate and specific immunity, exogenous interferon-α with combined ribavirin, treatments have been found to achieve a significant sustained viral response in subgroups of patients with chronic HCV. One of the major side effects of interferon-α is an ocular retinopathy characterized by flame-shaped hemorrhages and cotton wool spots visualized on funduscopic examination. There have been documented cases of more severe side effects including optic nerve and retinal artery damage; however, these instances are the minority. We sought to investigate the literature surrounding interferon-induced retinopathy, clinically correlate our findings with two recent cases, and provide recommendations for practitioners who continue to manage chronic HCV patients using interferon-α with combined ribavirin treatments.
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2.
CD8+ T cells of chronic HCV-infected patients express multiple negative immune checkpoints following stimulation with HCV peptides.
Barathan, M, Mohamed, R, Vadivelu, J, Chang, LY, Vignesh, R, Krishnan, J, Sigamani, P, Saeidi, A, Ram, MR, Velu, V, et al
Cellular immunology. 2017;:1-9
Abstract
Hepatitis C virus (HCV)-specific CD4+ and CD8+ T cells are key to successful viral clearance in HCV disease. Accumulation of exhausted HCV-specific T cells during chronic infection results in considerable loss of protective functional immune responses. The role of T-cell exhaustion in chronic HCV disease remains poorly understood. Here, we studied the frequency of HCV peptide-stimulated T cells expressing negative immune checkpoints (PD-1, CTLA-4, TRAIL, TIM-3 and BTLA) by flow cytometry, and measured the levels of Th1/Th2/Th17 cytokines secreted by T cells by a commercial Multi-Analyte ELISArray™ following in vitro stimulation of T cells using HCV peptides and phytohemagglutinin (PHA). HCV peptide-stimulated CD4+ and CD8+ T cells of chronic HCV (CHC) patients showed significant increase of CTLA-4. Furthermore, HCV peptide-stimulated CD4+ T cells of CHC patients also displayed relatively higher levels of PD-1 and TRAIL, whereas TIM-3 was up-regulated on HCV peptide-stimulated CD8+ T cells. Whereas the levels of IL-10 and TGF-β1 were significantly increased, the levels of pro-inflammatory cytokines IL-2, TNF-α, IL-17A and IL-6 were markedly decreased in the T cell cultures of CHC patients. Chronic HCV infection results in functional exhaustion of CD4+ and CD8+ T cells likely contributing to viral persistence.
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3.
Risk factors for hepatic decompensation in patients with HIV/HCV coinfection and liver cirrhosis during interferon-based therapy.
Mauss, S, Valenti, W, DePamphilis, J, Duff, F, Cupelli, L, Passe, S, Solsky, J, Torriani, FJ, Dieterich, D, Larrey, D
AIDS (London, England). 2004;(13):F21-5
Abstract
OBJECTIVE Hepatic decompensation was reported from two recent trials (APRICOT and RIBAVIC) assessing interferon (IFN)-based treatment of hepatitis C virus (HCV) in HIV/HCV-coinfected patients. This paper identifies risk factors associated with hepatic decompensation in APRICOT. METHODS APRICOT is a randomized, partially-blinded, controlled trial comparing treatment with peg-IFN alpha-2a 180 microg once weekly plus ribavirin/placebo 400 mg twice daily with IFN alpha-2a 3 million units three times weekly plus ribavirin 400 mg twice daily for 48 weeks in a total of 859 patients. Multiple logistic regression analysis was performed comparing the baseline characteristics of those cirrhotic patients who experienced decompensation with those of the other cirrhotic patients enrolled. RESULTS Fourteen patients, all cirrhotic, experienced hepatic decompensation during the study. The incidence in the cirrhotic subgroup of the study was 10.4% (14/134). Six of the 14 patients died as a result of hepatic decompensation. The risk factors associated with hepatic decompensation were increased bilirubin, decreased haemoglobin, increased alkaline phosphatase or decreased platelets, and treatment with didanosine. Markers of viral replication, histological activity, cellular immune status or HCV-therapy, treatment with ribavirin and pegylated versus non-pegylated IFN were not associated with hepatic decompensation. CONCLUSIONS The results from APRICOT indicate that the overall risk of hepatic decompensation in HIV/HCV-coinfected patients without cirrhosis receiving IFN-based treatment is low. In contrast, patients with markers of advanced cirrhosis, despite the absence of a history of hepatic decompensation, should be monitored closely during IFN-based therapy, because they are at risk of hepatic decompensation. Treatment with antiretrovirals such as didanosine may increase the risk further.
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4.
Nutritional guidelines for persons infected with the hepatitis C virus: a review of the literature.
Wendland, BE
Canadian journal of dietetic practice and research : a publication of Dietitians of Canada = Revue canadienne de la pratique et de la recherche en dietetique : une publication des Dietetistes du Canada. 2001;(1):7-15
Abstract
Hepatitis C virus (HCV) is one of the leading causes of chronic liver disease. It was first identified in 1989, as being distinct from hepatitis A and hepatitis B. The HCV does not attack the immune system, but rather causes an inflammatory reaction that is localized within the liver, involving the entire organ. About 80% of patients with acute hepatitis C will develop chronic HCV, of which about 20-30% will progress to cirrhosis and its consequences, over 10-20 years. After 20-40 years, a smaller proportion of patients with chronic disease will develop hepatocellular carcinoma. The course and outcome of the disease vary considerably. In some individuals, spontaneous remission occurs over a few years; in others, the disease is more severe, progressing to cirrhosis and end-stage liver disease. Despite biochemical and pathological confirmation of the diagnosis, patients are often asymptomatic for many years. Hepatic failure occurs late in the disease. Factors suggesting a poor prognosis include high serum transaminase levels, active cirrhosis on liver biopsy, and an increased viral load (HCV RNA), as well as associated medical conditions such as alcoholic liver disease, hepatitis B viral (HBV) infection, or human immunodeficiency virus (HIV). Nutrition has been recognized as a prognostic indicator in patients with chronic liver failure. However, standardized approaches for the diagnosis and classification of malnutrition in this population have not been consistently applied before implementing nutrition intervention. Common criteria for the assessment of malnutrition, weight and body mass index (BMI) for example, do not give accurate data in patients with chronic liver disease, complicated by ascites and edema. In addition, the chronic inflammatory reaction of liver failure progresses slowly, so that subtle nutritional deficits are not obvious at early stages of the disease. A review of the literature has been undertaken to identify current nutritional guidelines for patients with hepatitis C as well as chronic hepatitis.