Red cell distribution width and mortality in newly hospitalized patients

ObjectivePrevious studies suggest that red cell distribution width, a measure of erythrocyte size variability, may predict long-term mortality, particularly in cardiovascular disease. Less research has focused on the prognostic utility of red cell distribution width in an acutely hospitalized population.MethodsWe performed a secondary analysis of prospectively collected data on 74,784 consecutive hospitalized adults with red cell distribution width measured on admission. The primary outcome of interest was in-hospital mortality; a secondary outcome was unplanned transfer to the intensive care unit. We calculated multivariable logistic models adjusted for age, gender, race, and comorbid conditions.ResultsThe overall in-hospital mortality rate was 1.3% (95% confidence interval [CI], 1.2-1.4). As red cell distribution width increased, so did mortality, from 0.2% (lowest red cell distribution width decile) to 4.4% (highest red cell distribution width decile). Unadjusted red cell distribution width significantly discriminated between hospital survivors and nonsurvivors (area under the curve 0.74). In multivariate analyses, for every 1% increment in red cell distribution width at the time of admission, the odds for in-hospital mortality increased by 24% (odds ratio 1.24; 95% CI, 1.20-1.27); findings were robust across comorbidity subgroups. The rate of unplanned intensive care unit transfer was 7.0% (95% CI, 6.8-7.2) and in unadjusted analyses increased more than 2-fold from 4.5% in the lowest to 11.6% in the highest red cell distribution width decile. This relationship was significantly confounded but remained significant in multivariate analysis (odds ratio 1.04 per 1% red cell distribution width increment; 95% CI, 1.03-1.06).ConclusionRed cell distribution width strongly and independently predicted in-hospital mortality in this large cohort of hospitalized patients. It also was associated with acute decompensation among patients on the general ward, but to a lesser degree. The mechanisms underlying these findings are unknown.     

Inanspruchnahme kostenfreier verschreibungspflichtiger Verhütungsmittel durch Frauen

Bundesgesundheitsblatt - Gesundheitsforschung - Gesundheitsschutz - Der Bezug staatlicher Transferleistungen (STL) in Deutschland ist mit dem Verzicht auf sichere Verhütung assoziiert. Die...     

Potential neuroprotective role of astroglial exosomes against smoking-induced oxidative stress and HIV-1 replication in the central nervous system

Introduction: HIV-1-infected smokers are at risk of oxidative damage to neuronal cells in the central nervous system by both HIV-1 and cigarette smoke. Since neurons have a weak antioxidant defense system, they mostly depend on glial cells, particularly astrocytes, for protection against oxidative damage and neurotoxicity. Astrocytes augment the neuronal antioxidant system by supplying cysteine-containing products for glutathione synthesis, antioxidant enzymes such as SOD and catalase, glucose for antioxidant regeneration via the pentose-phosphate pathway, and by recycling of ascorbic acid.

Areas covered: The transport of antioxidants and energy substrates from astrocytes to neurons could possibly occur via extracellular nanovesicles called exosomes. This review highlights the neuroprotective potential of exosomes derived from astrocytes against smoking-induced oxidative stress, HIV-1 replication, and subsequent neurotoxicity observed in HIV-1-positive smokers.

Expert opinion: During stress conditions, the antioxidants released from astrocytes either via extracellular fluid or exosomes to neurons may not be sufficient to provide neuroprotection. Therefore, we put forward a novel strategy to combat oxidative stress in the central nervous system, using synthetically developed exosomes loaded with antioxidants such as glutathione and the anti-aging protein Klotho.