Chronic hepatitis C infection induces cardiovascular disease and type 2 diabetes: mechanisms and management.

Despite the availability of effective treatments, hepatitis C virus (HCV) still remains a threat to public health. HCV is capable to trigger, behind liver damage, extrahepatic manifestations, including cardiovascular disease and type 2 diabetes (T2DM). A close association has been reported between HCV infection and cardiovascular disease due to imbalances in metabolic pathways and chronic inflammation. HCV through both direct and indirect mechanisms causes a higher incidence of ischemic stroke, acute coronary syndrome, heart failure and peripheral arterial disease. In addition, a higher risk of death from cardiovascular events has been showed in HCV patients. Insulin resistance is a hallmark of HCV infection and represents the link between HCV and T2DM, which is one of the most frequent HCV-associated extrahepatic manifestations. The pathological basis of the increased risk of T2DM in HCV infection is provided by the alterations of the molecular mechanisms of IR induced both by the direct effects of the HCV proteins, and by the indirect effects mediated by chronic inflammation, oxidative stress and hepatic steatosis. T2DM increases the risk of compensated and decompensate cirrhosis and hepatocellular carcinoma as well as increases the risk of cardiovascular disease, lower limb amputation and end stage renal disease. Current evidence suggests that HCV eradication reduces the incidence and mortality of cardiovascular disease and T2DM, further underling the importance of public health strategies for eradication the infection. The aim of this review was to update evidence and management of interaction between HCV, cardiovascular disease, and T2DM in the era of DAA treatment.

Metabolic and renal changes in patients with chronic hepatitis C infection after hepatitis C virus clearance by direct-acting antivirals.

BACKGROUND AND AIM: The impact of hepatitis C virus (HCV) clearance by direct-acting antiviral agents (DAAs) on HCV-related extrahepatic manifestations is not well known. We evaluated the effect of viral clearance on metabolic and renal parameters. METHODS: In this prospective study, HCV patients who achieved a sustained virologic response (SVR) by DAAs were evaluated before, at the end, and 24 weeks after treatment for glycemic (serum glucose and insulin, HOMA-IR, HOMA-ß, and HOMA-S) and lipid (serum cholesterol, triglycerides, low-density lipoprotein [LDL], high-density lipoprotein) metabolism and renal function (serum creatinine, estimated glomerular filtration rate [eGFR]). RESULTS: A total of 343 consecutive HCV patients were evaluated. At 24 weeks of post-follow-up, an increase in body mass index (BMI) was observed (P < 0.05). Regardless of hepatic fibrosis levels and BMI, a reduction in serum glucose (P = 0.001), HOMA-IR (P < 0.001) and HOMA-ß (P < 0.001) and an increase in HOMA-S (P < 0.001) values were observed at 24 weeks after HCV clearance as compared to pretreatment values; 32.4% of patients with impaired fasting glucose normalized serum glucose values and 44.6% of diabetics showed an improvement in glycemic control. In contrast, serum cholesterol (P < 0.001) and LDL cholesterol (P < 0.001) values were increased. Renal function was improved with about 10% reduction of serum creatinine values (P < 0.02) and an increase of eGFR (P < 0.001). A baseline eGFR of ≤60 mL/min/1.73 m2 was a negative predictor of renal function improvement. HCV clearance was an independent factor improving glucose metabolism and renal function. CONCLUSIONS: Our study shows an occurrence of changes in metabolic and renal parameters in HCV patients with SVR, anticipating possible future clinical scenarios that the clinician must know for proper management.