ARDS is severe form of respiratory failure with significant impact on the morbidity and mortality of critical care patients. Epidemiological data are crucial for evaluating the efficacy of therapeutic interventions, designing studies, and optimizing resource distribution. The goal of this review is to present general aspects of mortality data published over the past decades. A systematic search of the MEDLINE/PubMed was performed. The articles were divided according to their methodology, type of reported mortality, and time. The main outcome was mortality. Extracted data included study duration, number of patients, and number of centers. The mortality trends and current mortality were calculated for subgroups consisting of in-hospital, ICU, 28/30-d, and 60-d mortality over 3 time periods (A, before 1995; B, 1995–2000; C, after 2000). The retrospectivity and prospectivity were also taken into account. Moreover, we present the most recent mortality rates since 2010. One hundred seventy-seven articles were included in the final analysis. General mortality rates ranged from 11 to 87% in studies including subjects with ARDS of all etiologies (mixed group). Linear regression revealed that the study design (28/30-d or 60-d) significantly influenced the mortality rate. Reported mortality rates were higher in prospective studies, such as randomized controlled trials and prospective observational studies compared with retrospective observational studies. Mortality rates exhibited a linear decrease in relation to time period ( P < .001). The number of centers showed a significant negative correlation with mortality rates. The prospective observational studies did not have consistently higher mortality rates compared with randomized controlled trials. The mortality trends over 3 time periods (before 1995, 1995–2000, and after 2000) yielded variable results in general ARDS populations. However, a mortality decrease was present mostly in prospective studies. Since 2010, the overall rates of in-hospital, ICU, and 28/30-d and 60-d mortality were 45, 38, 30, and 32%, respectively.

To determine the quantitative variances in peripheral blood lymphocyte subsets during sepsis, and their clinical significance. Peripheral blood lymphocyte subsets were enumerated in 32 non-surgical septic patients during the first 14 days of hospitalization; results from septic patients were compared with those from 34 healthy controls. Influences of the severity and the bacterial etiology of sepsis on changes in lymphocyte subsets were also assessed. Significant decreases (P < 0.05) from normal values of CD4+, CD8+ and total T-lymphocytes were observed in septic patients, but the decline persisted only for CD4+ T-lymphocytes and natural killer (NK) cells for 3 and 7 days, respectively. In addition, the numbers of CD3+/DR+ lymphocytes were significantly elevated on day 14. There were no correlations between these alterations and the severity of sepsis. Gram-positive sepsis (n = 10), which was mainly due to Streptococcus pneumoniae and Staphylococcus aureus, caused prolonged decreases in CD4+, CD8+ and total T-lymphocytes, and a reduction in NK cells, that lasted for >or=14 days. Conversely, patients with sepsis due to Gram-negative pathogens (Neisseria meningitidis, n = 8; enterobacteria, n = 2) achieved full recovery of the subsets within 3 days. Moreover, the patients with Gram-negative sepsis demonstrated a significant increase in B-lymphocytes, and a rise in the numbers of CD3+/DR+ and CD4+ T-lymphocytes, which were more rapid than in patients with Gram-positive sepsis. Our results indicate that Gram-positive sepsis causes stronger suppression of peripheral blood lymphocyte subsets in comparison to sepsis due to Gram-negative pathogens.

SUMMARY: To determine changes in incidence of reactivation ofToxoplasma gondiiinfection, manifesting as toxoplasmic encephalitis, and to assess the immunological mechanisms controlling reactivation in HIV-infected patients, a Czech cohort of 502 HIV/T. gondiico-infected patients was followed for 2909·3 person-years. The incidence of toxoplasmic encephalitis between the periods before and after the introduction of combination antiretroviral therapy (cART) was compared. Toxoplasmic encephalitis was diagnosed in 21 patients. In those patients the geometric mean value of CD4⁺T lymphocytes was 12·6 times lower than in patients with non-reactivatedT. gondiiinfection but an additionally significant decline in CD8⁺T lymphocytes (3·3-fold) and natural killer cells (4·3-fold) was observed. This confirms the significance of these parameters. A twelvefold decrease inToxoplasmareactivation incidence (40·2vs. 3·4/1000 person-years) between monitored periods was seen. In the cART era,Toxoplasmareactivation was observed only in patients with unrecognized HIV infection or refusing therapy.

Routinely used biomarkers of bacterial etiology of infection, such as C-reactive protein and procalcitonin, have limited usefulness for evaluation of infections since their expression is enhanced by a number of different conditions. Therefore, several inflammatory cytokines and chemokines were analyzed with sera from patients hospitalized for moderate bacterial and viral infectious diseases. In total, 57 subjects were enrolled: 21 patients with community-acquired bacterial infections, 26 patients with viral infections, and 10 healthy subjects (control cohorts). The laboratory analyses were performed using Luminex technology, and the following molecules were examined: IL-1Ra, IL-2, IL-4, IL-6, IL-8, TNF-α, INF-γ, MIP-1β, and MCP-1. Bacterial etiology of infection was associated with significantly (P<0.001) elevated serum concentrations of IL-1Ra, IL-2, IL-6, and TNF-αin comparison to levels observed in the sera of patients with viral infections. In the patients with bacterial infections, IL-1Ra and IL-8 demonstrated positive correlation with C-reactive protein, whereas, IL-1Ra, TNF-α, and MCP-1 correlated with procalcitonin. Furthermore, elevated levels of IL-1Ra, IL-6, and TNF-αdecreased within 3 days of antibiotic therapy to levels observed in control subjects. The results show IL-1Ra as a potential useful biomarker of community-acquired bacterial infection.