HBV vaccination in HIV-positive, HBVcAb-positive patients

Morsica et al 1 looked at 25 HIV-positive patients with isolated antibodies to hepatitis B core antigen (HBVcAb). The 25 patients, 80% male and 50% intravenous drug users, were tested at baseline and then vaccinated for hepatitis B and their response was monitored. Those with hepatitis B surface antibody <100 IU/L continued to have the full vaccination course with subsequent vaccines at weeks 5 and 24. Antibody titres were measured for all patients at baseline, and at 4 (postvaccination) 24 and 48 weeks. In addition hepatitis B virus (HBV) DNA quantification was also taken at these time points and hepatitis C antibody status was measured.

Their results show that 6/25 (24%) developed an antibody response and 4/6 had anti-HBs levels of >100 IU/L. Of the 19 remaining patients, 10 (52.6%) developed adequate immunity (>10 IU/L) after the third vaccine dose. Occult HBV infection was seen in four out of six patients who developed an antibody response after one vaccine, in two out of ten patients with a partial response after one vaccine, and in none of the patients who did not respond. Eleven of the thirteen who responded still had adequate immunity at 24 weeks, but this had dropped to five patients by 48 weeks. Two of the patients who responded with an antibody titre >100 IU/L after the initial vaccine still maintained this level of immunity out to 48 weeks. Hepatitis C antibody positivity was also associated in univariate and multivariate analyses with obtaining a partial response (HBsAb >10 IU/L) (P=0.0191). Longer duration of HIV infection with a median of 27 vs 12 years (partial responders vs non-responders) was associated in univariate analysis with partial response to vaccine (P=0.044).

Atazanavir effect on atherosclerotic risk factors in stable HIV

Bilirubin is known to be a potent antioxidant and has been associated with lower rates of cardiovascular disease. Beckman et al 2 hypothesised that increasing bilirubin levels using atazanavir (ATZ) would improve cardiometabolic risk factors and vascular function in older patients with HIV (>45 years). They recruited 60 participants undetectable on a non-ATZ regimen (TDF/FTC backbone). In stage 1 individuals underwent tests looking at markers of inflammation, thrombosis and conduit artery endothelial function. Participants were then randomly assigned to continue their current antiretroviral regimen (29 patients) not containing ATZ or to switch to an ATZ-containing regimen (TDF/FTC/ATZ). Measurements were made at baseline and then at 28 days.

In a second protocol 30 patients who had taken ATZ for more than 1 year were compared with the baseline subjects in the first protocol (non-ATZ regimen). The group found that ATZ significantly increased bilirubin levels (P<0.001) and acutely increased total plasma antioxidant capacity (P<0.001). In addition von Willebrand factor was seen to increase (P<0.001), and there was a significant reduction in hs-CRP (P=0.034) but no changes were seen in vasodilation. Comparing the ATZ vs the non-ATZ participants at baseline, there were few differences seen. The study team concluded that the increase in bilirubin associated with ATZ use does reduce highly sensitive CRP and reduced oxidative stress on a temporary basis, but von Willebrand factor was increased. They found no measurable benefit in terms of endothelial function, a finding this study group had also seen previously in patients with type 1 but not type 2 diabetes.

Predictors of frailty in ageing patients living with HIV

Interest in the ‘frailty’ phenotype has increased dramatically in the past few years, in particular how this relates to our ageing cohorts of patients with HIV. Brothers et al 3 aimed to identify longitudinal predictors of frailty severity and mortality in patients enrolled in the Modena HIV Metabolic Clinic Cohort, which started in 2004. There were 963 participants followed for 4 years from their first available visit. Of the participants, 29% were female and the median age was 46.8 years. Patients enrolled had an undetectable HIV viral load, median CD4 count of 549 (IQR 405–720) and a nadir CD4 of 180 (81–280). Frailty was measured using the 31-item Frailty Index using the deficit accumulation approach, where the score is calculated as a proportion of the deficits that are present out of all the health variables, for example, signs, symptoms, laboratory abnormalities and self-reported measures, in the model. The study found that 4-year mortality was 3.0% (n=29), and the independent predictors for frailty at 4 years of follow-up were baseline Frailty Index score (RR 1.06, 95% CI 1.0 to 1.07), being female (RR 0.93, 95% CI 0.87 to 0.98), duration of HIV infection (RR 1.06, 95% CI 1.01 to 1.12), nadir CD4 (RR 0.96, 95% CI 0.93 to 0.99), duration of antiretroviral exposure (RR 1.08, 95% CI 1.02 to 1.14) and smoking pack-years (RR 1.03, 95% CI 1.03 (1.01 to 1.05)). The independent predictors of mortality were current CD4 count (OR 0.34, 0.2–0.6), baseline Frailty Index (OR 1.19, 1.02–1.38) and injecting drug use (OR 2.89, 0.30–6.42). Research is continuing in this field.