Prospective Cohort Study
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2021 ◽  
Vol 46 ◽  
pp. S619
J.R. Rey-Garcia ◽  
C. Donat-Vargas ◽  
H. Sandoval-Insausti ◽  
A. Bayan-Bravo ◽  
J.R. Banegas ◽  

Amy Tyler ◽  
Mersine A. Bryan ◽  
Chuan Zhou ◽  
Rita Mangione-Smith ◽  
Derek Williams ◽  

OBJECTIVES: Evaluate the association between dexamethasone dosing and outcomes for children hospitalized with croup. METHODS: This study was nested within a multisite prospective cohort study of children aged 6 months to 6 years admitted to 1 of 5 US children’s hospitals between July 2014 and June /2016. Multivariable linear and logistic mixed-effects regression models were used to examine the association between the number of dexamethasone doses (1 vs >1) and outcomes (length of stay [LOS], cost, and 30-day same-cause reuse). All multivariable analyses included a site-specific random effect to account for clustering within hospital and were adjusted for age, sex, race and ethnicity, presenting severity, medical complexity, insurance, caregiver education, and hospital. In cost analyses, we controlled for LOS. RESULTS: Among 234 children hospitalized with croup, patient characteristics did not differ by number of doses. The proportion receiving >1 dose varied by hospital (range 27.9%–57.1%). In adjusted analyses, >1 dose was not associated with same-cause reuse (odds ratio 0.87 [95% confidence interval (CI): 0.26 to 2.95]) but was associated with 45% longer LOS (relative risk = 1.45 [95% CI: 1.30 to 1.62]). When we controlled for LOS, >1 dose was not associated with differential cost ($−31.2 [95% CI $−424.4 to $362.0]). Eighty-two (35%) children received dexamethasone before presentation. CONCLUSIONS: We found significant interhospital variation in dexamethasone dosing and LOS. When we controlled for severity on presentation, >1 dexamethasone dose was associated with longer LOS but not reuse. Although incomplete adjustment for severity is one possible explanation, some providers may routinely keep children hospitalized to administer multiple dexamethasone doses.

2021 ◽  
Vol 42 ◽  
pp. 101190
Shepherd R. Singer ◽  
Frederick J. Angulo ◽  
David L. Swerdlow ◽  
John M. McLaughlin ◽  
Itay Hazan ◽  

2021 ◽  
Haozhe Cui ◽  
Qian Liu ◽  
Yuntao Wu ◽  
Liying Cao

Abstract Background Previous studies has shown a significant relationship between baseline triglyceride-glucose (TyG) index and cardiovascular disease (CVD). However, the long-term effect of TyG index and incident CVD remains uncertain. This study aimed to investigate the association between cumulative TyG index and the risk of CVD.Method In this study, we recruited individuals participating in Kailuan Study from 2006 to 2013 without stroke, myocardial infarction, and cancer in the four consecutive examinations. Cumulative TyG index was calculated by multiplying the average TyG index and the time between the two consecutive examinations. Cumulative TyG index levels were categorized into four quartile groups: Q1 group, ≤50.65 (as reference group), Q2 group, 50.65-53.86, Q3 group, 53.86-57.44, Q4 group, >57.44. The effect of Cumulative TyG index on CVD incidence was estimated by multivariable-adjusted Cox proportional hazard models.Result A total of 44,087 individuals participated in the final analysis. After a mean follow-up of 6.52±1.14 years, incident CVD, MI and stroke occurred in 2057, 395 and 1695, respectively. The multivariable-adjusted COX regression model showed the HR (95% CI) of CVD were Q2 1.25(1.08-1.44), Q3 1.22(1.05-1.40) and Q4 1.39(1.21-1.61), compared to Q1 group. Consistent results were obtained in the subgroup analyses and sensitivity analyses.Conclusion Cumulative TyG index was associated with increased risk of CVD. Maintaining a healthy level of TyG index within the desirable range and better control of cumulative TyG index is important for prevention of CVD.

2021 ◽  
Jennifer L. Rosenbaum ◽  
Susan J. Melhorn ◽  
Stefan Schoen ◽  
Mary F. Webb ◽  
Mary Rosalynn B. De Leon ◽  

Objective: Preclinical research implicates hypothalamic glial cell responses in the pathogenesis of obesity and type 2 diabetes. The current study sought to translate such findings into humans by testing if radiologic markers of gliosis in the mediobasal hypothalamus (MBH) were greater in persons with obesity and impaired glucose homeostasis or type 2 diabetes. <p>Research Design and Methods: Using cross-sectional and prospective cohort study designs, we applied a validated, quantitative magnetic resonance imaging (MRI) approach to assess gliosis in 67 adults with obesity and normal glucose tolerance, impaired glucose tolerance, or type 2 diabetes. Assessments of glucose homeostasis were conducted via oral glucose tolerance tests (OGTT) and β-cell modeling. </p> <p> Results: We found significantly greater T2 relaxation times (a marker of gliosis by MRI), that were independent of adiposity, in the impaired glucose tolerance and type 2 diabetes groups as compared to the normal glucose tolerance group. Findings were present in the MBH, but not control regions. Moreover, positive linear associations were present in the MBH but not control regions between T2 relaxation time and glucose area under the curve during an OGTT, fasting glucose concentrations, hemoglobin A1c, and visceral adipose tissue mass, whereas negative linear relationships were present in the MBH for markers of insulin sensitivity and β-cell function. In a prospective cohort study, greater MBH T2 relaxation times predicted declining insulin sensitivity over one year. </p> Conclusions: Findings support a role for hypothalamic gliosis in the progression of insulin resistance in obesity and, thus, type 2 diabetes pathogenesis in humans.

Émilie Richer-Séguin ◽  
Christian Ayoub ◽  
Jean-Sébastien Lebon ◽  
Jennifer Cogan ◽  
Stéphanie Jarry ◽  

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