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Sterken C.,Clinical Division and Laboratory of Intensive Care Medicine | Lemiere J.,University Psychiatric Center | Lemiere J.,University Hospitals Leuven | Van Den Berghe G.,Clinical Division and Laboratory of Intensive Care Medicine | Mesotten D.,Clinical Division and Laboratory of Intensive Care Medicine
Pediatrics | Year: 2016

OBJECTIVES: Children with congenital heart disease (CHD) often have neurocognitive deficits, sometimes with a detrimental impact on daily and school functioning. These deficits may increase through childhood. In this study, we investigated whether children with CHD, who underwent heart surgery as infants, show more neurocognitive deficits, especially in the executive functions, as they get older, compared with healthy controls. METHODS: In this longitudinal follow-up study, 107 children with CHD and 77 healthy control children underwent extensive neurocognitive testing at 4 years of age. Ninety-three percent of the children (100 patients with CHDs and 72 controls) underwent a second neurocognitive testing 3 years later. Intelligence, visual-motor integration (VMI), alertness, motor coordination, executive functions, and psychosocial functioning were assessed. RESULTS: IQ scores were consistently lower in the CHD group (P < .001); however, the difference of 11.7 IQ points between both groups at follow-up 1 decreased to 7 IQ points at follow-up 2 (P = .003). Inhibition reaction time had improved in both study groups at follow-up 2 (P < .001) and did not differ between both groups from follow-up 1 to follow-up 2 (P = .849). Deficits in VMI, alertness, motor coordination, and psychosocial functioning also did not worsen for patients with CHDs at follow-up 2, compared with healthy controls. CONCLUSIONS: Children with CHD, who underwent heart surgery as infants, do not show an increase of neurocognitive deficits between the ages of 4 and 7 years, compared with healthy controls. Patients with CHDs keep deficits in intelligence, VMI, and psychosocial functioning, but seem to partially grow out of their deficits. Copyright © 2016 by the American Academy of Pediatrics. Source


Boonen E.,Clinical Division and Laboratory of Intensive Care Medicine | Langouche L.,Clinical Division and Laboratory of Intensive Care Medicine | Janssens T.,Clinical Division and Laboratory of Intensive Care Medicine | Meersseman P.,Catholic University of Leuven | And 7 more authors.
Journal of Clinical Endocrinology and Metabolism | Year: 2014

Context: Adrenal insufficiency is considered to be prevalent during critical illness, although the pathophysiology, diagnostic criteria, and optimal therapeutic strategy remain controversial. During critical illness, reduced cortisol breakdown contributes substantially to elevated plasma cortisol and low plasma ACTH concentrations.Objective: Because ACTH has a trophic impact on the adrenal cortex, we hypothesized that with a longer duration of critical illness, subnormal ACTH adrenocortical stimulation predisposes to adrenal insufficiency.Design, Setting and Participants: Adrenal glands were harvested 24 hours or sooner after death from 13 long intensive care unit (ICU)-stay patients, 27 short ICU-stay patients, and13 controls. Prior glucocorticoid treatment was excluded.Main Outcome and Measure(s): Microscopic adrenocortical zonational structure was evaluated by hematoxylin and eosin staining. The amount of adrenal cholesterol esters was determined by Oil-Red-O staining, and mRNA expression of ACTH-regulated steroidogenic enzymes was quantified.Conclusion and Relevance: Lipid depletion and reduced ACTH-regulated gene expression in prolonged critical illness suggest that sustained lack of ACTH may contribute to the risk of adrenal insufficiency in long-stay ICU patients.Results: The adrenocortical zonational structure was disturbed in patients as compared with controls (P<.0001), with indistinguishable adrenocortical zones present only in long ICU-stay patients (P= .003 vs. controls). Adrenal glands from long ICU-stay patients, but not those of short ICU-stay patients, contained21%less protein (P=.03) and9%more fluid (P=.01) than those from controls, whereas they tended to weigh less for comparable adrenal surface area. There was 78% less Oil-Red-O staining in long ICU-stay patients than in controls and in short-stay patients (P=.03), the latter similar to controls (P= .31). The mRNA expression of melanocortin 2 receptor, scavengerreceptor class B, member 1, 3-hydroxy-3-methylglutaryl-CoA reductase, steroidogenic acute regulatory protein, and cytochrome P450 cholesterol side-chain cleavage enzyme was at least 58% lower in long ICU-stay patients than in controls (all P= .03) and of melanocortin 2 receptor, scavenger-receptor class B, member 1, steroidogenic acute regulatory protein, and cytochrome P450 cholesterol side-chain cleavage enzyme at least 53% lower than in short ICU-stay patients (all P= .04), whereas gene expression in short ICU-stay patients was similar to controls. Copyright © 2014 by the Endocrine Society. Source

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