Infectious Complications in Obese Patients Following Trauma

Background Obesity is a public health concern in the United States due to its increasing prevalence, especially in younger age groups. Trauma is the most common cause of death for people under aged 40 y. The purpose of this study is to determine the association between obesity and specific infectious complications after traumatic injury. Materials and methods A retrospective analysis was conducted using data from the 2012 National Trauma Data Bank. The National Trauma Data Bank defined obesity as having a body mass index of 30 or greater. Descriptive statistics were calculated and stratified by obesity status. A hierarchical regression model was used to determine the odds of experiencing an infectious complication in patients with obesity while controlling for age, gender, diabetes, number of comorbidities, injury severity, injury mechanism, head injury, and surgical procedure. Results Patients with a body mass index of 30 or greater compared with nonobese patients had increased odds of having an infectious complication (Odds Ratio, 1.59; 1.49-1.69). In addition to obesity, injury severity score greater than 29, age 40 y or older, diabetes, comorbid conditions, and having a surgical procedure were also predictive of an infectious complication. Conclusions Our results indicate that trauma patients with obesity are nearly 60% more likely to develop an infectious complication in the hospital. Infection prevention and control measures should be implemented soon after hospital arrival for patients with obesity, particularly those with operative trauma

Neonatal iron deficiency causes abnormal phosphate metabolism by elevating FGF23 in normal and ADHR mice.

Fibroblast growth factor 23 (FGF23) gain of function mutations can lead to autosomal dominant hypophosphatemic rickets (ADHR) disease onset at birth, or delayed onset following puberty or pregnancy. We previously demonstrated that the combination of iron deficiency and a knock-in R176Q FGF23 mutation in mature mice induced FGF23 expression and hypophosphatemia that paralleled the late-onset ADHR phenotype. Because anemia in pregnancy and in premature infants is common, the goal of this study was to test whether iron deficiency alters phosphate handling in neonatal life. Wild-type (WT) and ADHR female breeder mice were provided control or iron-deficient diets during pregnancy and nursing. Iron-deficient breeders were also made iron replete. Iron-deficient WT and ADHR pups were hypophosphatemic, with ADHR pups having significantly lower serum phosphate (p 50 fold; p < 0.01). WT and ADHR pups receiving low iron had elevated intact serum FGF23; ADHR mice were affected to a greater degree (p < 0.01). Iron-deficient mice also showed increased Cyp24a1 and reduced Cyp27b1, and low serum 1,25-dihydroxyvitamin D (1,25D). Iron repletion normalized most abnormalities. Because iron deficiency can induce tissue hypoxia, oxygen deprivation was tested as a regulator of FGF23, and was shown to stimulate FGF23 mRNA in vitro and serum C-terminal FGF23 in normal rats in vivo. These studies demonstrate that FGF23 is modulated by iron status in young WT and ADHR mice and that hypoxia independently controls FGF23 expression in situations of normal iron. Therefore, disturbed iron and oxygen metabolism in neonatal life may have important effects on skeletal function and structure through FGF23 activity on phosphate regulation

"Smoker's Paradox" in Patients Treated for Severe Injuries: Lower Risk of Mortality After Trauma Observed in Current Smokers

BACKGROUND: Studies evaluating the effect of smoking status on mortality outcomes in trauma patients have been limited, despite the fact that survival benefits of smoking have been reported in other critical care settings. The phenomenon "smoker's paradox" refers to the observation that following acute cardiovascular events, such as acute myocardial infarction and cardiac arrest, smokers often experience decreased mortality in the hospital setting. The objective of our study was to determine whether smoking imparts a survival benefit in patients with traumatic injuries. METHODS: We performed a retrospective cohort study that analyzed cases included in the National Trauma Data Bank research dataset. Hierarchical logistic regression analyses were used to determine whether smoking alters the risk of mortality and complications in patients who smoke. RESULTS: The percentage of patients experiencing mortality differed significantly between smokers (n = 38,564) and nonsmokers (n = 319,249) (1.8% vs. 4.3%, P < .001); however, the percentage experiencing a major complication did not (9.7% vs. 9.6%, P = .763). Regression analyses indicated that smokers were significantly less likely to die during the hospital stay compared to nonsmokers after adjusting for individual and hospital factors (OR = 0.15; CI = 0.10, 0.22). Additionally, smokers were also less likely to develop a major complication than nonsmokers (OR = 0.73, CI = 0.59-0.91). CONCLUSIONS: Patients who smoke appear to have a much lower risk of in-hospital mortality than nonsmokers. Further investigation into biological mechanisms responsible for this effect should be carried out in order to potentially develop therapeutic applications