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1.
Nutr Clin Pract ; 2023 Oct 10.
Artículo en Inglés | MEDLINE | ID: mdl-37817534

RESUMEN

BACKGROUND: The Academy of Nutrition and Dietetics/American Society for Parenteral and Enteral Nutrition (AND/ASPEN) published malnutrition guidelines in 2014. In 2015, our institution implemented a quality improvement project focused on malnutrition identification with the goal to improve the diagnosis of malnutrition in hospitalized children. METHODS: Our project included three approaches: education, nutrition assessment, and documentation initiatives. Education initiatives focused on physicians at all levels of training. Nutrition screening was completed on all patients admitted to our institution. Registered dietitians (RDs) conducted nutrition assessments and identified and documented malnutrition based on AND/ASPEN guidelines. Documentation initiatives included development of automatic text and template changes to allow import of RD-assigned malnutrition diagnosis into physician documentation. We met with members of our clinical documentation integrity team regularly to review the results of these initiatives starting in 2016. RESULTS: The total diagnosed cases of malnutrition increased from 208 cases in 2016 at the start of our monitoring to >800 cases per year in 2020-2022. Unspecified (no severity assigned) protein calorie malnutrition as a percentage of total malnutrition diagnoses decreased from 36.9% in 2016 to <10% since 2018. Children with severe malnutrition have remained the largest portion of children with a malnutrition diagnosis, with >40% of children with malnutrition diagnosed with severe malnutrition. CONCLUSION: Our education and documentation initiatives have led to both improved diagnosis of malnutrition and accurate identification and documentation of malnutrition severity. These initiatives could be utilized to improve malnutrition diagnosis and documentation at other institutions caring for hospitalized children.

2.
J Pediatr Gastroenterol Nutr ; 75(6): 709-716, 2022 12 01.
Artículo en Inglés | MEDLINE | ID: mdl-36399175

RESUMEN

OBJECTIVES: Perianal fistulas are among the most severe complications of Crohn disease, but limited data regarding their outcomes are available in children. Our objective was to determine predictors of perianal fistula healing among pediatric patients newly diagnosed with Crohn disease. METHODS: This single-center retrospective study followed patients with perianal fistulas at Crohn disease diagnosis until fistula healing. Time to healing was analyzed using Cox proportional hazard regression models considering relevant covariates including patient demographics, disease characteristics, medical therapies [no anti-tumor necrosis factor (TNF)α therapy, anti-TNFα therapy ±therapeutic drug monitoring], and perianal surgical procedures including fistulotomy, fistulectomy, removal of perianal lesions, seton placement, and incision and drainage. RESULTS: Of 485 patients identified, 107 (22%) had a perianal fistula at Crohn disease diagnosis. Multivariate analysis identified that perianal fistulotomy, fistulectomy, and lesion removal [hazard ratio (HR) 0.46; P = 0.028], non-White race (HR 0.30, P < 0.01), and male sex (HR 0.42; P = 0.02) were associated with delayed fistula healing. Faster fistula healing was associated with treatment with anti-TNFα with therapeutic drug monitoring (HR 1.78, P = 0.009). There were no other differences in healing by treatment. CONCLUSIONS: Fistulotomy, fistulectomy, and perianal lesion removal as well as non-White race were associated with delayed fistula healing. Anti-TNFα therapy was associated with faster fistula healing when combined with therapeutic drug monitoring, compared to all other medical treatment groups, including anti-TNFα therapy without therapeutic drug monitoring.


Asunto(s)
Enfermedad de Crohn , Fístula Rectal , Humanos , Niño , Masculino , Enfermedad de Crohn/tratamiento farmacológico , Estudios Retrospectivos , Resultado del Tratamiento , Fístula Rectal/etiología , Fístula Rectal/cirugía , Fístula Rectal/diagnóstico , Cicatrización de Heridas
4.
PLoS Pathog ; 10(7): e1004280, 2014 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-25032698

RESUMEN

Mammalian Peptidoglycan Recognition Proteins (PGRPs) are a family of evolutionary conserved bactericidal innate immunity proteins, but the mechanism through which they kill bacteria is unclear. We previously proposed that PGRPs are bactericidal due to induction of reactive oxygen species (ROS), a mechanism of killing that was also postulated, and later refuted, for several bactericidal antibiotics. Here, using whole genome expression arrays, qRT-PCR, and biochemical tests we show that in both Escherichia coli and Bacillus subtilis PGRPs induce a transcriptomic signature characteristic of oxidative stress, as well as correlated biochemical changes. However, induction of ROS was required, but not sufficient for PGRP killing. PGRPs also induced depletion of intracellular thiols and increased cytosolic concentrations of zinc and copper, as evidenced by transcriptome changes and supported by direct measurements. Depletion of thiols and elevated concentrations of metals were also required, but by themselves not sufficient, for bacterial killing. Chemical treatment studies demonstrated that efficient bacterial killing can be recapitulated only by the simultaneous addition of agents leading to production of ROS, depletion of thiols, and elevation of intracellular metal concentrations. These results identify a novel mechanism of bacterial killing by innate immunity proteins, which depends on synergistic effect of oxidative, thiol, and metal stress and differs from bacterial killing by antibiotics. These results offer potential targets for developing new antibacterial agents that would kill antibiotic-resistant bacteria.


Asunto(s)
Bacillus subtilis/metabolismo , Proteínas Portadoras/metabolismo , Escherichia coli/metabolismo , Regulación Bacteriana de la Expresión Génica , Metales/metabolismo , Estrés Oxidativo , Especies Reactivas de Oxígeno/metabolismo , Compuestos de Sulfhidrilo/metabolismo , Bacillus subtilis/genética , Proteínas Portadoras/genética , Escherichia coli/genética , Humanos
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