No abstract

Antiviral therapy of CHC possibly induces de novo or exacerbates pre-existing silent TD. TD does not seem to correlate with any pretreatment virological parameter; it is probably not related to dose or treatment duration, nor linked to viral kinetics or virological outcome. The role of chronic hepatitis C per se in TD remains to be determined.

In hypertensive patients free of cardiovascular disease, CKD and LVH are both independent prognosticators of the composite end point of all-cause death and cardiovascular morbidity, whereas LVH but not CKD is a major predictor for stroke.

Serum procalcitonin levels remain below the threshold of 0.5 ng/ml in all patients with uncomplicated cirrhosis, irrespective of the cause of the disease, while they are significantly elevated when bacterial infection complicates the course of the disease. A significant proportion of patients with acute alcoholic hepatitis on a cirrhotic background as well as of patients with acute on chronic viral hepatitis, without bacterial infection, exhibit serum procalcitonin levels above 0.5 ng/ml, suggesting that this cut-off value is probably not enough to discriminate between patients with or without bacterial infection within these subgroups of patients with liver disease.

The role of serum uric acid (SUA) in the context of adverse cardiovascular events in hypertensive subjects is controversial. Additionally, the relationship between SUA and indices of target organ damage is not well defined in this setting. Towards this end, we studied 842 consecutive nondiabetic patients with stage I-II essential hypertension (office blood pressure ¼ 148/95 mmHg, aged 53.4 years), referred to our outpatient hypertensive unit within a period of 4 years. According to the urinary albumin excretion (UAE), the study population was classified into those with microalbuminuria [MA( þ ), UAE ¼ 20-200 mg/24 h, n ¼ 222] and those without MA [MA (À), UAEo 20 mg/24 h, n ¼ 620]. Moreover, according to the presence of left ventricular hypertrophy (LVH) the participants were subdivided into two additional groups: [LVH ( þ ), n ¼ 305 and LVH (À), n ¼ 537]. SUA levels were higher by 0.4 mg/dl, (P ¼ 0.04) in group MA ( þ ) compared with the group MA (À), while no difference was observed between groups LVH ( þ ) and LVH (À) (P ¼ NS). In the entire population, SUA was correlated with body mass index (BMI) (r ¼ 0.17, Po0.001), waist/hip ratio (r ¼ 0.3, Po0.001), office systolic blood pressure (SBP) (r ¼ 0.14, Po0.05), triglycerides levels (r ¼ 0.25, Po0.001), UAE (r ¼ 0.35, Po0.001) and HDL (r ¼ À0.26, Po0.001). Multiple regression analysis demonstrated that SUA was significantly related with BMI, office SBP and UAE (Po0.05). In conclusion, increased SUA levels are associated with MA but not with LVH in essential hypertensive subjects. Whether these inter-relationships may elucidate the clinical positioning of augmented SUA in this setting remains to be clarified in future studies.

Pregnant women were found to be at higher risk for SPB if they had circulating HBsAg, and the risk did not seem to be influenced by the levels of HBsAg or HBV DNA.

The immunogenicity of HBV vaccine seems to be lower in CHC patients compared to healthy subjects. SVR following IFN plus RIB treatment does not affect the antibody response to HBV vaccine. Infection by genotype-1 seems to negatively influence the seroconversion rates. Vaccination against HBV during PEG plus RIB combination treatment is not beneficial in terms of anti-HBs seroconversion rates.

Pegylated IFN-α will remain the basis of anti-HCV therapy during the next decade, since new IFN formulation are not proven to be superior or are in early stages of development and directly acting antivirals show limited antiviral activity as monotherapy.