A Comparative Study on the Presence and Reversibility of Subclinical Arterial Damage in HCV-Infected Individuals and Matched Controls

Abstract

Background: The arterial pathology and mechanisms of increased cardiovascular disease (CVD) risk in HCV-infected individuals are not yet clear. The aim of this study was to identify types of arterial pathology in treatment-naive chronic HCV patients and to test their reversibility after successful treatment. Methods: Consecutive, never-treated, HCV-infected patients were compared with age and CVD-related risk factors, matched controls, healthy individuals (HI), patients with rheumatoid arthritis (RA) and people living with HIV (PLWH), in terms of arterial stiffening by pulse wave velocity, arterial atheromatosis/hypertrophy by carotid plaques/intima-media thickness and impaired pressure wave reflections by augmentation index. After three months of sustained virological response (SVR) administered using direct-acting antivirals, vascular examination was repeated in HCV-infected patients to test drug and viral-elimination effect in subclinical CVD. Results: Thirty HCV patients were examined at baseline; fourteen of them were re-examined post-SVR. Compared with HI, HCV patients had significantly more plaques, which is similar to that of RA patients and the PLWH group. No other differences were found in all other vascular biomarkers, and regression among HCV patients also revealed no differences 3 months post-SVR. Conclusions: Accelerated atheromatosis, rather than arterial stiffening, arterial remodeling and peripheral impaired hemodynamics is the underlying pathology leading to increased CVD risk in HCV patients.

Peripheral Neuropathy in Patients with Hepatitis C Infection—Reversibility after HCV Eradication: A Single Center Study

“…HCV-related neuropathies include symmetrical axonal sensorimotor neuropathy, accounting for over 50% of cases; distal symmetric painful small-fiber neuropathy, with predominantly sensory features; mononeuritis multiplex; pure motor polyneuropathy; or, rarely, demyelinating and autonomic neuropathies, leading to a reduced quality of life [ 10 , 40 , 41 ]. The introduction of an all-oral DAA treatment for HCV has led to impressive results regarding viral eradication; however, the impact on HCV-related EHM is still in doubt, even though most studies have revealed an ameliorating effect [ 42 , 43 , 44 , 45 ]. We conducted a prospective, single-center study to estimate the prevalence and impact of HCV eradication in HCV-associated neuropathy in the absence of MCG.…”

Cholestatic HCV Cryoglobulinemia: A New Clinical and Pathological Entity before and after Direct-Acting Antiviral Therapies—A Case-Control Study

“…Cryoglobulinemic vasculitis is a systemic disorder, determined by the deposition of cryoglobulins within vessel walls associated with increased mortality and high healthcare costs in patients with chronic hepatitis C (CHC) [9], and HCV eradication is not always followed by a resolution of the damage caused by MC. Indeed, as documented for other extrahepatic manifestations of CHC, such as lymphoproliferative disorders [10,11], renal and ocular involvement, and cardiovascular and cerebrovascular disorders [10,12], after clearance of HCV via antiviral therapy, in particular with Direct-Acting Antiviral (DAA) therapies, disappearance of cryoglobulinemia is observed in only about 50% of cases [10], which highlights how the aforementioned therapy does not have consistent effects on the presence of MC. A correlation between HCV infection and cholestasis has already been established [13,14]; indeed, the onset of cholestasis in CHC is thought to be determined by direct viral cytotoxicity of hepatocytes and is associated with a weak HCV-specific T-cell response, which is predominantly carried out by Th2 cells, leading to increasingly higher levels of viral replication and amplification of the intrahepatic damage [15].…”

Surface antigen serocleared hepatitis B virus infection increases the risk of mixed cryoglobulinemia vasculitis in male patients with chronic hepatitis C

“…Besides MCV and B-cell NHL, chronic HCV infection causes a spectrum of extrahepatic manifestations that include diabetes and cardiovascular disease, which is an important cause of mortality in infected people. Although HCV-associated B-cell lymphoproliferative disorders and cardiovascular disease are driven by different mechanisms, inflammation vs antigenic pressure and gene mutation, they share the characteristic of regressing after antiviral therapy as especially illustrated by the recent use of highly effective direct-acting antivirals ( 4 , 6 – 8 ). While in the case of HCV-associated cardiovascular disease no risk factor have been identified except for those canonical such as diabetes, smoking and hypertension ( 9 ), the fact that only a minority of CHC patients develop HCV pos MCV suggests specific risk factor(s) that, however, remain elusive.…”