• Atherosclerosis
• Cardiovascular disease
• Cerebrovascular disease
• Coronary heart disease
• Hepatitis C

Platelet microparticles (PMPs) are platelet-derived membrane vesicles involved in cardiovascular diseases and atherosclerosis. Chronic hepatitis C (CHC) is associated with increased atherosclerosis, but the effect of therapy on its atherogenic potential has not been adequately studied.

We evaluated PMP levels before and after treatment with pegylated-interferon-alfa and ribavirin in 28 CHC patients compared with 20 non-alcoholic fatty liver disease (NAFLD) patients and 20 healthy volunteers (HV).

Twenty-four (86%) CHC patients achieved sustained virological response (SVR). PMP levels were determined at baseline in CHC, NAFLD patients, and HV, and at end-of-treatment (EOT) and 24 weeks post-treatment (SVR24) in CHC patients. PMP levels at baseline were higher in CHC than NAFLD patients (P<0.001) and HV (P=0.007). Higher PMPs at baseline were observed in smokers than non-smokers with CHC (P=0.006). Among smokers from all groups, PMPs at baseline were higher in CHC than NAFLD patients (P=0.001) and HV (P=0.024). In CHC patients, PMPs declined from baseline to both EOT (P=0.035) and SVR24 (P=0.006). Only CHC patients with SVR had a significant decline in PMPs from baseline to SVR24 (P=0.018). PMPs at ΕΟΤ and SVR24 in all CHC patients were similar to PMPs in NAFLD patients and HV.

PMP levels are increased in CHC patients, particularly smokers, which further supports the atherosclerotic potential of CHC and suggests a potentially synergistic effect of smoking and CHC on the atherosclerotic process. Since PMP levels in CHC patients with SVR were similar to NAFLD patients and HV, the atherosclerotic potential of CHC seems to be abolished by effective antiviral treatment.

• Atherosclerosis
• hepatitis C
• interferon
• platelet microparticles
• smoking

• extrahepatic manifestations
• hepatitis C virus
• treatment

The opportunity for total joint arthroplasty (TJA) in patients with chronic infectious liver disease is rapidly expanding. This is the product of both superior survival of chronic hepatitis patients, evolving implant technologies, and improvement of techniques in TJA. Unfortunately, treating this group of patients is not without significant challenges that can stem from both intrahepatic and extrahepatic clinical manifestations. Moreover, many subclinical changes occur in this cohort that can alter hemostasis, wound healing, and infection risk even in the asymptomatic patient. In this review, we discuss the various clinical presentations of chronic infectious liver disease and summarize the relevant literature involving total joint arthroplasty for this population. Hopefully, through appropriate patient selection and perioperative optimization, treating surgeons should see continued improvement in outcomes for patients with chronic infectious liver disease.

• Cirrhosis
• Hepatitis B
• Hepatitis C
• Total joint arthroplasty

Hepatitis C virus (HCV) infection is considered a systemic disease because of involvement of other organs and tissues concomitantly with liver disease. Among the extrahepatic manifestations, neuropsychiatric disorders have been reported in up to 50% of chronic HCV infected patients. Both the central and peripheral nervous system may be involved with a wide variety of clinical manifestations. Main HCV-associated neurological conditions include cerebrovascular events, encephalopathy, myelitis, encephalomyelitis, and cognitive impairment, whereas “brain fog”, depression, anxiety, and fatigue are at the top of the list of psychiatric disorders. Moreover, HCV infection is known to cause both motor and sensory peripheral neuropathy in the context of mixed cryoglobulinemia, and has also been recently recognized as an independent risk factor for stroke. These extrahepatic manifestations are independent of severity of the underlying chronic liver disease and hepatic encephalopathy. The brain is a suitable site for HCV replication, where the virus may directly exert neurotoxicity; other mechanisms proposed to explain the pathogenesis of neuropsychiatric disorders in chronic HCV infection include derangement of metabolic pathways of infected cells, alterations in neurotransmitter circuits, autoimmune disorders, and cerebral or systemic inflammation. A pathogenic role for HCV is also suggested by improvement of neurological and psychiatric symptoms in patients achieving a sustained virologic response following interferon treatment; however, further ad hoc trials are needed to fully assess the impact of HCV infection and specific antiviral treatments on associated neuropsychiatric disorders.

• Hepatitis C virus
• Neurological disorders
• Psychiatric disorders
• Stroke
• Inflammation

• Animals
• Antiviral Agents/therapeutic use
• Central Nervous System/drug effects
• Central Nervous System/physiopathology
• Central Nervous System/virology
• Central Nervous System Viral Diseases/drug therapy
• Central Nervous System Viral Diseases/physiopathology
• Central Nervous System Viral Diseases/psychology
• Central Nervous System Viral Diseases/virology
• Hepacivirus/drug effects
• Hepacivirus/pathogenicity
• Hepatitis C, Chronic/complications
• Hepatitis C, Chronic/drug therapy
• Humans
• Mental Disorders/drug therapy
• Mental Disorders/physiopathology
• Mental Disorders/psychology
• Mental Disorders/virology
• Treatment Outcome

• cardiovascular
• chronic
• hepatitis C virus
• inflammation
• meta-analysis

• Extra hepatic manifestations
• HCV
• Treatment

Chronic infection and associated inflammation may play a role in various unfavorable pathologic conditions, including atherosclerosis. Chronic hepatitis C virus (HCV) infection is thought to be associated with a higher prevalence of atherosclerotic vascular changes in the coronary artery, cerebrovascular artery, and carotid artery; however, little is known about the precise mechanisms by which HCV enhances atherogenic processes. Furthermore, some studies have found no association, or even an inverse association, between HCV infection and atherosclerotic vascular changes or cardiovascular events. Differences in data regarding the mode of association may be because of variations in sample size, target population, and study design. Nevertheless, physicians should be aware of cardiovascular disorders as a possible comorbidity – owing to their considerable consequences – among patients with chronic HCV infection.

• atherosclerosis
• coronary artery disease
• hepatitis C virus

• Atherosclerosis/complications
• Atherosclerosis/epidemiology
• Atherosclerosis/pathology
• Atherosclerosis/virology
• Hepacivirus/pathogenicity
• Hepatitis C/complications
• Hepatitis C/epidemiology
• Hepatitis C/pathology
• Hepatitis C/virology
• Humans
• Risk Factors

The relationship between hepatitis C virus infection and risk of stroke remains inconsistent. This study evaluates the risk of stroke in association with chronic hepatitis C infection in a longitudinal population-based cohort.

We identified 4,094 adults newly diagnosed with hepatitis C infection in 2002–2004 from the Taiwan National Health Insurance Research Database. Comparison group consisted of 16,376 adults without hepatitis C infection randomly selected from the same dataset, frequency matched by age and sex. Events of stroke from 2002–2008 were ascertained from medical claims (International Classification of Diseases, Ninth Revision, Clinical Modification, ICD-9-CM, codes 430–438). Multivariate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated for potential associated factors including HCV infection, age, sex, low-income status, urbanization, cessation of cigarette smoking, alcohol-related illness, obesity, history of chronic diseases and medication use.

During 96,752 person-years of follow-up, there were 1981 newly diagnosed stroke cases. The HRs of stroke associated with medical conditions such as hypertension, diabetes and heart disease were 1.48 (95% CI 1.33 to 1.65), 1.23 (95% CI 1.11 to 1.36) and 1.17 (95% CI 1.06 to 1.30), respectively, after adjustment for covariates. The cumulative risk of stroke for people with hepatitis C and without hepatitis C infections was 2.5% and 1.9%, respectively (p<0.0001). Compared with people without hepatitis C infection, the adjusted HR of stroke was 1.27 (95% CI 1.14 to 1.41) for people with hepatitis C infection.

Chronic hepatitis C infection increases stroke risk and should be considered an important and independent risk factor.

• Adult
• Aged
• Cohort Studies
• Confidence Intervals
• Demography
• Female
• Hepacivirus/physiology
• Hepatitis C/complications
• Hepatitis C/virology
• Humans
• Incidence
• Male
• Middle Aged
• Multivariate Analysis
• Proportional Hazards Models
• Risk Factors
• Stroke/epidemiology
• Stroke/etiology
• Stroke/virology
• Taiwan/epidemiology
• Young Adult

• Adult
• Case-Control Studies
• Cholesterol, HDL/blood
• Cholesterol, LDL/blood
• Cross-Sectional Studies
• Female
• Genotype
• Hepacivirus/genetics
• Hepatitis C, Chronic/blood
• Hepatitis C, Chronic/pathology
• Hepatitis C, Chronic/virology
• Humans
• Lipids/blood
• Liver/pathology
• Liver/virology
• Male
• Middle Aged
• Multivariate Analysis
• Prospective Studies
• RNA, Viral/blood
• Retrospective Studies
• Triglycerides/blood
• Viral Load

Information concerning lipid disturbances in HIV-infected women on antiretroviral therapy (ART) is scarce. The objective of the study is to describe the lipid profile in a large cohort of HIV-infected women on contemporary ART and analyse differences between regimes and patient's characteristics.

Observational, multicentre, cross-sectional study from the Spanish VACH Cohort. 922 women on stable ART without lipid-lowering treatment were included.

Median age was 42 years, median CD4 lymphocyte count was 544 cells/mm3, and 85.6% presented undetectable HIV-1 viral load. Median total cholesterol (TC) was 189 mg/dL (interquartile range, IQR, 165-221), HDL cholesterol 53 mg/dL (IQR, 44-64), LDL cholesterol 108 mg/dL (IQR, 86-134), and triglycerides 116 mg/dL (IQR, 85-163). Mean accumulated time on ART was 116 months; 47.4% were on NNRTI-based regimes, 44.7% on PI, and 6.7% on only-NRTI therapy. 43.8% were also hepatitis C (HCV) coinfected. Patients on PI treatment presented higher TC/HDL ratio than those on NNRTI (p < 0.001). Significantly higher HDL values were observed in NNRTI-treated patients. HCV-coinfected patients presented lower TC/HDL ratio than the non HCV-coinfected. In multivariate analysis, factors independently associated with TC/HDL ratio were age, triglyceride levels and HCV co-infection. PI treatment presented a non-significant association with higher TC/HDL ratio.

In HIV-infected women, the NNRTI-based ART is associated with a better lipid profile than the PI-based. Factors unrelated to ART selection may also exert an independent, significant influence on lipids; in particular, age, and triglyceride levels are associated with an increased TC/HDL ratio while HCV co-infection is associated with a reduced TC/HDL ratio.