In critically ill non-immunosuppressed patients, the presence of functional CMV-specific CD8+ T lymphocyte response at intensive care unit admission provides protection against CMV reactivation.

We retrospectively investigated the impact of high vancomycin minimum inhibitory concentration (MIC > 2 μg/ml) on the outcome of 53 patients with bacteremia caused by methicillin-susceptible Staphylococcus aureus (MSSA). Vancomycin MIC was determined by broth microdilution according to CLSI methods. The primary outcome was 30-day all-cause mortality from the date of the first positive blood culture. The mortality rate was 22.6% (12 of 53 patients). High vancomycin MIC (odds ratio (OR) = 9.3; 95% confidence interval (95% CI) = 1.31-63.20; p = 0.027), Charlson comorbidity index ≥ 3 (OR = 10.3; 95% CI = 1.3-102.04; p = 0.03), advanced age (OR = 35.8; 95% CI = 2.3-659.2; p = 0.01), and severe sepsis (OR = 8.5; 95% CI = 1.2-61.4; p = 0.03) were associated with mortality.

Objective: To evaluate the progression of liver stiffness after treatment with direct antiviral agents (DAAs), to identify predictive factors of fibrosis regression and to analyze the changes of scores AST-to-platelet ratio index (APRI) and Fibrosis-4 (FIB-4) after treatment. Design: Multicenter prospective cohort study of HIV/HCV co-infected patients conducted within the GECMEI cohort, Spain. Methods: Individuals were eligible if they were willing to start DAAs and underwent two transient elastographies: at baseline and after the end of treatment (EOT). All patients with detectable HCV RNA naïve to DAAs were consecutively enrolled from nine medical hospitals. Liver stiffness results were categorized in four Metavir stages (F1: <7.1; F2 : 7.1--9.5; F3 : 9.5--2.4; F4: >12.4 kPa). The APRI and FIB-4 scores were calculated at baseline, EOT and 12 weeks after EOT. Results: One hundred and seventy-eight patients were examined throughout a follow-up of 16.3 months (IQR: 12.5–25). The median of liver stiffness decrease was 2.6 kPa (IQR: 0–6.3). A greater improvement was observed in F3–F4 compared with F1–F2, (6.4 vs. 0.91 kPa, P < 0.001; P = 0.001, respectively). A decline between baseline and EOT measures was observed in APRI and FIB-4 (P < 0.001). Sustained virological response (SVR12) achievement was the only predictor of fibrosis regression [OR:17.4 (95% CI: 1.8–164.6; P = 0.013)]. Conclusion: Most patients experienced a significant reduction of liver stiffness and APRI and FIB-4 scores. This improvement was greater in those with advanced liver disease. SVR12 was the only predictor of fibrosis regression. The significance of this reduction is unclear and could reflect a decline in inflammation rather than true fibrosis regression.

HCV treatment in coinfected patients is highly successful in terms of SVR rate in the real-life setting and toxicity is exceptional. We identified no specific predictors of an unfavorable outcome.