Referral and utilization of paediatric bariatric surgery in an academic freestanding children's hospital with dedicated paediatric bariatric programme.

OBJECTIVE: This report estimates the percent of medically eligible adolescents who are referred for metabolic and bariatric surgery (MBS) evaluation or factors associated with referral. METHODS: This cross-sectional retrospective review evaluated patients aged 13 to 18 years seen between 2017 and 2019 for demographics, insurance status, body mass index (BMI), obesity-related comorbidities, and compared these data to patients whom had been referred and received MBS. RESULTS: Half of the patients (86 411/163137, 53%) between ages of 13 and 18 years identified had BMI documented, of which, 1974 (2.3%) were medically eligible for MBS, 238 (12%) were referred for MBS and 52 (22%) underwent MBS. Females had similar odds of being eligible for MBS [odds ratio (OR) = 1.01, 95% confidence interval (CI) 0.92-1.11, P = .9], but greater odds of referral (OR = 1.58, 95% CI 1.13-2.23, P = .009). Independently, miniorities and patients with public insurance had higher odds of being eligible for MBS, but similar odds of being referred as non-Hispanic white patients. Black patients with public insurance had greater odds of being referred for MBS (OR = 12.22, 95% CI 2.08-235.15, P = .022). Patients' multiple comorbidities had greater odds of being referred for MBS (OR = 2.16, 95% CI 1.29-3.68, P = .004). CONCLUSIONS: Referral is barrier for patients medically eligible for MBS; however, this barrier is not uniformly faced by all patients.

Outcomes of Bariatric Surgery in Older Versus Younger Adolescents.

OBJECTIVES: In this report, we compare weight loss, comorbidity resolution, nutritional abnormalities, and quality of life between younger and older adolescents after metabolic and bariatric surgery. METHODS: From March 2007 to December 2011, 242 adolescents (≤19 years of age) who underwent bariatric surgery at 5 clinical centers in the United States were enrolled in the prospective, multicenter, long-term outcome study Teen-Longitudinal Assessment of Bariatric Surgery. Outcome data from younger (13-15 years; n = 66) and older (16-19 years; n = 162) study participants were compared. Outcomes included percent BMI change, comorbidity outcomes (hypertension, dyslipidemia, and type 2 diabetes mellitus), nutritional abnormalities, and quality of life over 5 years post surgery. RESULTS: Baseline characteristics, except for age, between the 2 cohorts were similar. No significant differences in frequency of remission of hypertension (P = .84) or dyslipidemia (P = .74) were observed between age groups. Remission of type 2 diabetes mellitus was high in both groups, although statistically higher in older adolescents (relative risk 0.86; P = .046). Weight loss and quality of life were similar in the 2 age groups. Younger adolescents were less likely to develop elevated transferrin (prevalence ratio 0.52; P = .048) and low vitamin D levels (prevalence ratio 0.8; P = .034). CONCLUSIONS: The differences in outcome of metabolic and bariatric surgery between younger and older adolescents were few. These data suggest that younger adolescents with severe obesity should not be denied consideration for surgical therapy on the basis of age alone and that providers should consider adolescents of all ages for surgical therapy for obesity when clinically indicated.

Corrigendum: Experimental Traumatic Brain Injury Induces Chronic Glutamatergic Dysfunction in Amygdala Circuitry Known to Regulate Anxiety-Like Behavior.

[This corrects the article DOI: 10.3389/fnins.2019.01434.].

Experimental Traumatic Brain Injury Induces Chronic Glutamatergic Dysfunction in Amygdala Circuitry Known to Regulate Anxiety-Like Behavior.

Up to 50% of traumatic brain injury (TBI) survivors demonstrate persisting and late-onset anxiety disorders indicative of limbic system dysregulation, yet the pathophysiology underlying the symptoms is unclear. We hypothesize that the development of TBI-induced anxiety-like behavior in an experimental model of TBI is mediated by changes in glutamate neurotransmission within the amygdala. Adult, male Sprague-Dawley rats underwent midline fluid percussion injury or sham surgery. Anxiety-like behavior was assessed at 7 and 28 days post-injury (DPI) followed by assessment of real-time glutamate neurotransmission in the basolateral amygdala (BLA) and central nucleus of the amygdala (CeA) using glutamate-selective microelectrode arrays. The expression of anxiety-like behavior at 28 DPI coincided with decreased evoked glutamate release and slower glutamate clearance in the CeA, not BLA. Numerous factors contribute to the changes in glutamate neurotransmission over time. In two additional animal cohorts, protein levels of glutamatergic transporters (Glt-1 and GLAST) and presynaptic modulators of glutamate release (mGluR2, TrkB, BDNF, and glucocorticoid receptors) were quantified using automated capillary western techniques at 28 DPI. Astrocytosis and microglial activation have been shown to drive maladaptive glutamate signaling and were histologically assessed over 28 DPI. Alterations in glutamate neurotransmission could not be explained by changes in protein levels for glutamate transporters, mGluR2 receptors, astrocytosis, and microglial activation. Presynaptic modulators, BDNF and TrkB, were significantly decreased at 28 DPI in the amygdala. Dysfunction in presynaptic regulation of glutamate neurotransmission may contribute to anxiety-related behavior and serve as a therapeutic target to improve circuit function.

Does time heal all wounds? Experimental diffuse traumatic brain injury results in persisting histopathology in the thalamus.

BACKGROUND: Thalamic dysfunction has been implicated in overall chronic neurological dysfunction after traumatic brain injury (TBI), however little is known about the underlying histopathology. In experimental diffuse TBI (dTBI), we hypothesize that persisting histopathological changes in the ventral posteromedial (VPM) nucleus of the thalamus is indicative of progressive circuit reorganization. Since circuit reorganization in the VPM impacts the whisker sensory system, the histopathology could explain the development of hypersensitivity to whisker stimulation by 28days post-injury; similar to light and sound hypersensitivity in human TBI survivors. METHODS: Adult, male Sprague-Dawley rats underwent craniotomy and midline fluid percussion injury (FPI) (moderate severity; 1.8-2.0atm) or sham surgery. At 1d, 7d, and 28days post-FPI (d FPI) separate experiments confirmed the cytoarchitecture (Giemsa stain) and evaluated neuropathology (silver stain), activated astrocytes (GFAP), neuron morphology (Golgi stain) and microglial morphology (Iba-1) in the VPM. RESULTS: Cytoarchitecture was unchanged throughout the time course, similar to previously published data; however, neuropathology and astrocyte activation were significantly increased at 7d and 28d and activated microglia were present at all time points. Neuron morphology was dynamic over the time course with decreased dendritic complexity (fewer branch points; decreased length of processes) at 7d FPI and return to sham values by 28d FPI. CONCLUSIONS: These data indicate that dTBI results in persisting thalamic histopathology out to a chronic time point. While these changes can be indicative of either adaptive (recovery) or maladaptive (neurological dysfunction) circuit reorganization, they also provide a potential mechanism by which maladaptive circuit reorganization could contribute to the development of chronic neurological dysfunction. Understanding the processes that mediate circuit reorganization is critical to the development of future therapies for TBI patients.