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Does Hepatitis C Affect The Kidneys

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Does Hepatitis C Affect The Kidneys – Chaudhari R, Fouda S, Sainu A, Pappachan JM. Metabolic complications of hepatitis C virus infection. World J Gastroenterol2021;27(13): 1267-1282 [PMID: 33833481 DOI: 10.3748/w71.]3v2.1.

Joseph M Pappachan, FRCP, MD, Consultant, Honorary Researcher, Senior Researcher, Department of Endocrinology and Metabolism, Lancashire Teaching Hospitals NHS Trust, Royal Preston Hospital, Preston PR2 9HT, UK. [email protected]

Does Hepatitis C Affect The Kidneys

This article is an open access article, selected by an internal editor and fully reviewed by external reviewers. It is distributed under the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which allows others to non-commercially distribute, remix, adapt, build upon, and license derivative works of this work under various terms. original work is properly cited and use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

New Research At Croi 2016: How Prep Changes Kidney Function

Joseph M Pappachan, Department of Endocrinology and Metabolism, Lancashire Teaching Hospitals NHS Trust, Preston PR2 9HT, UK

Joseph M Pappachan, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PL, UK

Author Contributions: Chaudhari R and Fouda S performed the extensive literature review and drafted the manuscript and share first authorship; Sainu A added to the hepatological aspect of the work especially by reviewing and revising the additional literature; Pappachan JM conceived the idea, incorporated additional scientific points, especially metabolic aspects, critically revised the entire work and approved the final version for publication.

Open Access: This article is an open access article selected by an internal editor and reviewed exclusively by external reviewers. It is distributed under the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which allows others to non-commercially distribute, remix, adapt, build upon, and license their derivative works under various terms. the work is properly cited and its use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/

Hepatitis C Complications To Know About

Author: Joseph M Pappachan, FRCP, MD, Senior Research Fellow, Honorary Fellow, Senior Fellow, Department of Endocrinology and Metabolism, Lancashire Teaching Hospitals NHS Trust, Royal Preston Hospital, Preston PR2 9HT, UK.

Hepatitis C virus (HCV) infection is a systemic disease associated with multiple extrahepatic organ dysfunctions that contribute to protein manifestations. HCV is associated with a number of extrahepatic diseases, including atherosclerosis, glucose and lipid metabolism disorders, changes in iron metabolism pathways, and traditional liver manifestations such as lymphoproliferative diseases, cirrhosis, and hepatocellular carcinoma. The orchestration between HCV core proteins and the liver-muscle-fat axis, if not adequately addressed, imposes an enormous burden on the global health of human body organs. The close and inextricable relationship between chronic HCV infection, metabolic diseases and cardiovascular diseases is particularly important given the increasing prevalence of obesity and metabolic syndrome and their economic burden on patients, health systems and society. The cellular and molecular mechanisms that regulate the interaction between these organs and tissues in health and disease are therefore of great interest. Coexistence of metabolic disorders and chronic hepatitis C infection also increases the progression of liver fibrosis and hepatocellular carcinoma. The presence of metabolic disturbances is thought to influence the chronicity and virulence of HCV, leading to the progression of liver disease. This comprehensive review highlights the current knowledge of the metabolic manifestations of hepatitis C and the potential ways in which these metabolic changes may influence the natural history of the disease.

Key tip: Current evidence shows a strong association between hepatitis C virus (HCV) and metabolic complications such as hyperlipidemia, fatty liver, insulin resistance, metabolic syndrome, and diabetes mellitus. The development of insulin resistance and hepatic steatosis in chronic HCV infection affects the course of the disease in the liver and increases overall morbidity and mortality. The effect of metabolic diseases on HCV infection can increase the severity of the disease. The interaction between HCV core proteins and the liver-muscle-fat axis is complex and still not fully elucidated. Coexistence of metabolic diseases such as diabetes and HCV infection is also known to result in adverse outcomes for both disorders. There is evidence that successful treatment halts the progression of liver disease, but more research is needed on how treatment affects metabolic outcomes.

Hepatitis C virus (HCV) is the leading cause of liver disease worldwide, and according to the World Health Organization, 130-170 million people are infected[1]. About 10-20% of chronically infected patients experience persistent inflammation and develop liver cirrhosis and ultimately hepatocellular carcinoma[1]. Well-known extrahepatic manifestations include, but are not limited to; disorders of glucose and lipid metabolism, atherogenic disease, mixed cryoglobulinemia, lymphoproliferative disorders, kidney diseases, insulin resistance (IR), type 2 diabetes (T2DM), polyarthritis such as sicca syndrome, rheumatoid arthritis and autoimmune diseases[2, 3]. In addition, patients with chronic HCV are at increased risk of developing metabolic bone disease and osteopenia, as this has been observed in more than 50% of infected subjects[4]. The detrimental effect of metabolic complications resulting from HCV infection is mainly related to the disruption of glucose and lipid metabolism [5]. Regardless of the stage of liver fibrosis, IR and DM are more common during HCV infection and after liver transplantation in patients with chronic HCV (CHC) infection[ 6 – 8 ]. Interestingly, the prevalence of HCV infection among patients with diabetes mellitus is higher than in the general population of this age [9]. CHC induces systemic and hepatic inflammation that contributes to the development of atherosclerosis through elevated levels of pro-atherogenic cytokines and chemokines[10]. Atherosclerosis has also been shown to be associated with a high tumor necrosis factor alpha (TNF-α)/adiponectin ratio, which is found in HCV-infected patients and is associated with IR [ 11 ].

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The systemic burden of hepatitis C infection exceeds the burden of liver disease due to its metabolic spectrum, and it is likely that the virus stimulates other mechanisms of liver injury by disrupting glucose and lipid homeostasis and contributes to the pathogenesis of extrahepatic diseases[ 12] ] . Therefore, a comprehensive understanding of the metabolic impact of this enigmatic disease on the human body is essential for optimal management of the disease and its sequelae. This evidence-based review highlights the current understanding of CHC infection and its metabolic complications.

Most people infected with HCV are unaware of their condition because they are asymptomatic. About a third of infections resolve spontaneously within the first year, while the remaining infections persist and become chronic. CHC infection can progress to end-stage liver disease, including cirrhosis and hepatocellular carcinoma (HCC). HCV can also cause serious problems in organ systems other than the liver, including cryoglobulinemic vasculitis, metabolic bone disease, kidney disease, cardiovascular disease, and hematologic malignancies. In the United States, HCV is one of the leading causes of end-stage liver disease requiring liver transplantation, and HCV-attributable mortality is expected to continue to increase over the next 10 years. Figure 1 shows the metabolic disorders associated with HCV, which mainly target the liver, skeletal muscle and adipose tissue, as indicated by current evidence[13].

Hepatic steatosis in the background of HCV virus infection is considered a distinct entity with specific clinical and prognostic implications. The prevalence of fatty liver in patients with HCV infection is 55.54%, which remains higher than non-infected individuals[14]. Unlike nonalcoholic fatty liver disease, which is associated with hyperlipidemia, CHC is associated with hypolipidemia, including hypocholesterolemia, hypotriglyceridemia, and low low-density lipoprotein (LDL) cholesterol levels. The coexistence of nonalcoholic fatty liver disease in HCV-infected patients is associated with features of the metabolic syndrome (MetS) and is an independent risk factor for advanced liver fibrosis[15-17].

Genotype 3 has the highest prevalence of fatty liver in patients with CHC (40–86%) compared to approximately 50% in patients with other genotypes [ 18 , 19 ]. There is a direct correlation between genotype 3 HCV (G3-HCV) and the development of steatosis, while IR in non-genotype 3 CHC plays a key role in the pathophysiology of hepatic steatosis [20, 21].

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The term “viral steatosis” is used especially in G3-HCV infection when hepatic steatosis is associated with viral load rather than MetS and when “metabolic steatosis” occurs secondary to IR/MetS in G1, G2 and G4 genotypes[22- 24] ] . Studies of G3-HCV-infected patients have shown that steatosis can improve or even disappear after successful antiviral treatment with interferon and ribavirin; however, data from direct-acting antivirals (DAAs) are limited [ 25 , 26 ]. The risk of progression of fibrosis increases with pre-existing steatosis and decreased response to antiviral treatment [27–29]. CHC is involved in the development and progression of non-alcoholic steatohepatitis (NASH). NASH is a chronic condition of liver damage that can result from CHC infection or coexist with HCV, and biopsies have shown that the association leads to progressive fibrosis and is a predictor of liver disease progression in patients with CHC, regardless of genotype[ 30 , 31 ] ]. Both “viral” and “metabolic” steatosis stimulate the development of fibrosis and liver disease, which is influenced by increased insulin levels and inflammatory cytokines in hepatic stellate cells (Figure 2).

Adv: Advanced; HCV: Hepatitis C virus; NAFLD: Non-alcoholic fatty liver disease; FFA: Free fatty acid; IR: insulin resistance; HCC: Hepatocellular carcinoma.

Iron is a central component for HCV viral replication and translation, although whether iron promotes HCV viral replication is controversial. Elevated serum ferritin levels associated with hepatic iron overload have been found in CHC patients and have been considered an independent risk factor for advanced liver fibrosis [ 32 , 33 ]. Changes in iron metabolism in CHC are thought to be associated with decreased hepcidin levels. Hepcidin, a peptide hormone, is important in its strict regulation

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