18 research outputs found

    Prevalence, associated factors and outcomes of pressure injuries in adult intensive care unit patients: the DecubICUs study

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    Funder: European Society of Intensive Care Medicine; doi: http://dx.doi.org/10.13039/501100013347Funder: Flemish Society for Critical Care NursesAbstract: Purpose: Intensive care unit (ICU) patients are particularly susceptible to developing pressure injuries. Epidemiologic data is however unavailable. We aimed to provide an international picture of the extent of pressure injuries and factors associated with ICU-acquired pressure injuries in adult ICU patients. Methods: International 1-day point-prevalence study; follow-up for outcome assessment until hospital discharge (maximum 12 weeks). Factors associated with ICU-acquired pressure injury and hospital mortality were assessed by generalised linear mixed-effects regression analysis. Results: Data from 13,254 patients in 1117 ICUs (90 countries) revealed 6747 pressure injuries; 3997 (59.2%) were ICU-acquired. Overall prevalence was 26.6% (95% confidence interval [CI] 25.9–27.3). ICU-acquired prevalence was 16.2% (95% CI 15.6–16.8). Sacrum (37%) and heels (19.5%) were most affected. Factors independently associated with ICU-acquired pressure injuries were older age, male sex, being underweight, emergency surgery, higher Simplified Acute Physiology Score II, Braden score 3 days, comorbidities (chronic obstructive pulmonary disease, immunodeficiency), organ support (renal replacement, mechanical ventilation on ICU admission), and being in a low or lower-middle income-economy. Gradually increasing associations with mortality were identified for increasing severity of pressure injury: stage I (odds ratio [OR] 1.5; 95% CI 1.2–1.8), stage II (OR 1.6; 95% CI 1.4–1.9), and stage III or worse (OR 2.8; 95% CI 2.3–3.3). Conclusion: Pressure injuries are common in adult ICU patients. ICU-acquired pressure injuries are associated with mainly intrinsic factors and mortality. Optimal care standards, increased awareness, appropriate resource allocation, and further research into optimal prevention are pivotal to tackle this important patient safety threat

    Autocrine negative feed-back regulation of lipolysis through sensing of NEFAs by FFAR4/GPR120 in WAT

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    Objectives: Long-chain fatty acids (LCFAs) released from adipocytes inhibit lipolysis through an unclear mechanism. We hypothesized that the LCFA receptor, FFAR4 (GPR120), which is highly expressed in adipocytes, may be involved in this feedback regulation. Methods and results: Liquid chromatography mass spectrometry (LC-MS) analysis of conditioned media from isoproterenol-stimulated primary cultures of murine and human adipocytes demonstrated that most of the released non-esterified free fatty acids (NEFAs) are known agonists for FFAR4. In agreement with this, conditioned medium from isoproterenol-treated adipocytes stimulated signaling strongly in FFAR4 transfected COS-7 cells as opposed to non-transfected control cells. In transfected 3T3-L1 cells, FFAR4 agonism stimulated Gi- and Go-mini G protein binding more strongly than Gq, effects which were blocked by the selective FFAR4 antagonist AH7614. In primary cultures of murine white adipocytes, the synthetic, selective FFAR4 agonist CpdA inhibited isoproterenol-induced intracellular cAMP accumulation in a manner similar to the antilipolytic control agent nicotinic acid acting through another receptor, HCAR2. In vivo, oral gavage with the synthetic, specific FFAR4 agonist CpdB decreased the level of circulating NEFAs in fasting lean mice to a similar degree as nicotinic acid. In agreement with the identified anti-lipolytic effect of FFAR4, plasma NEFAs and glycerol were increased in FFAR4-deficient mice as compared to littermate controls despite having elevated insulin levels, and cAMP accumulation in primary adipocyte cultures was augmented by treatment with the FFAR4 antagonist conceivably by blocking the stimulatory tone of endogenous NEFAs on FFAR4. Conclusions: In white adipocytes, FFAR4 functions as an NEFA-activated, autocrine, negative feedback regulator of lipolysis by decreasing cAMP though Gi-mediated signaling
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