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  1. Article ; Online: Nutrition and autophagy deficiency in critical illness.

    Vanhorebeek, Ilse / Casaer, Michaël / Gunst, Jan

    Current opinion in critical care

    2023  Volume 29, Issue 4, Page(s) 306–314

    Abstract: Purpose of review: Critical illness imposes a severe insult on the body, with various stressors triggering pronounced cell damage. This compromises cellular function, leading to a high risk of multiple organ failure. Autophagy can remove damaged ... ...

    Abstract Purpose of review: Critical illness imposes a severe insult on the body, with various stressors triggering pronounced cell damage. This compromises cellular function, leading to a high risk of multiple organ failure. Autophagy can remove damaged molecules and organelles but appears insufficiently activated during critical illness. This review discusses insight into the role of autophagy in critical illness and the involvement of artificial feeding in insufficient autophagy activation in critical illness.
    Recent findings: Animal studies manipulating autophagy have shown its protective effects against kidney, lung, liver, and intestinal injury after several critical insults. Autophagy activation also protected peripheral, respiratory, and cardiac muscle function, despite aggravated muscle atrophy. Its role in acute brain injury is more equivocal. Animal and patient studies showed that artificial feeding suppressed autophagy activation in critical illness, particularly with high protein/amino acid doses. Feeding-suppressed autophagy may explain short and long-term harm by early enhanced calorie/protein feeding in large randomized controlled trials.
    Summary: Insufficient autophagy during critical illness is at least partly explained by feeding-induced suppression. This may explain why early enhanced nutrition failed to benefit critically ill patients or even induced harm. Safe, specific activation of autophagy avoiding prolonged starvation opens perspectives for improving outcomes of critical illness.
    MeSH term(s) Animals ; Humans ; Critical Illness ; Autophagy/physiology ; Nutritional Support ; Nutritional Status ; Liver
    Language English
    Publishing date 2023-06-08
    Publishing country United States
    Document type Review ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1235629-3
    ISSN 1531-7072 ; 1070-5295
    ISSN (online) 1531-7072
    ISSN 1070-5295
    DOI 10.1097/MCC.0000000000001056
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The epigenetic legacy of ICU feeding and its consequences.

    Vanhorebeek, Ilse / Van den Berghe, Greet

    Current opinion in critical care

    2023  Volume 29, Issue 2, Page(s) 114–122

    Abstract: Purpose of review: Many critically ill patients face physical, mental or neurocognitive impairments up to years later, the etiology remaining largely unexplained. Aberrant epigenetic changes have been linked to abnormal development and diseases ... ...

    Abstract Purpose of review: Many critically ill patients face physical, mental or neurocognitive impairments up to years later, the etiology remaining largely unexplained. Aberrant epigenetic changes have been linked to abnormal development and diseases resulting from adverse environmental exposures like major stress or inadequate nutrition. Theoretically, severe stress and artificial nutritional management of critical illness thus could induce epigenetic changes explaining long-term problems. We review supporting evidence.
    Recent findings: Epigenetic abnormalities are found in various critical illness types, affecting DNA-methylation, histone-modification and noncoding RNAs. They at least partly arise de novo after ICU-admission. Many affect genes with functions relevant for and several associate with long-term impairments. As such, de novo DNA-methylation changes in critically ill children statistically explained part of their disturbed long-term physical/neurocognitive development. These methylation changes were in part evoked by early-parenteral-nutrition (early-PN) and statistically explained harm by early-PN on long-term neurocognitive development. Finally, long-term epigenetic abnormalities beyond hospital-discharge have been identified, affecting pathways highly relevant for long-term outcomes.
    Summary: Epigenetic abnormalities induced by critical illness or its nutritional management provide a plausible molecular basis for their adverse effects on long-term outcomes. Identifying treatments to further attenuate these abnormalities opens perspectives to reduce the debilitating legacy of critical illness.
    MeSH term(s) Child ; Humans ; Critical Illness/therapy ; Parenteral Nutrition/methods ; Epigenesis, Genetic ; Intensive Care Units ; DNA
    Chemical Substances DNA (9007-49-2)
    Language English
    Publishing date 2023-02-15
    Publishing country United States
    Document type Review ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1235629-3
    ISSN 1531-7072 ; 1070-5295
    ISSN (online) 1531-7072
    ISSN 1070-5295
    DOI 10.1097/MCC.0000000000001021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Our Scientific Journey through the Ups and Downs of Blood Glucose Control in the ICU.

    Van den Berghe, Greet / Vanhorebeek, Ilse / Langouche, Lies / Gunst, Jan

    American journal of respiratory and critical care medicine

    2023  Volume 209, Issue 5, Page(s) 497–506

    Abstract: This article tells the story of our long search for the answer to one question: Is stress hyperglycemia in critically ill patients adaptive or maladaptive? Our earlier work had suggested the lack of hepatic insulin effect and hyperglycemia as jointly ... ...

    Abstract This article tells the story of our long search for the answer to one question: Is stress hyperglycemia in critically ill patients adaptive or maladaptive? Our earlier work had suggested the lack of hepatic insulin effect and hyperglycemia as jointly predicting poor outcome. Therefore, we hypothesized that insulin infusion to reach normoglycemia, tight glucose control, improves outcome. In three randomized controlled trials (RCTs), we found morbidity and mortality benefit with tight glucose control. Moving from the bed to the bench, we attributed benefits to the prevention of glucose toxicity in cells taking up glucose in an insulin-independent, glucose concentration gradient-dependent manner, counteracted rather than synergized by insulin. Several subsequent RCTs did not confirm benefit, and the large Normoglycemia in Intensive Care Evaluation-Survival Using Glucose Algorithm Regulation, or "NICE-SUGAR," trial found increased mortality with tight glucose control associated with severe hypoglycemia. Our subsequent clinical and mechanistic research revealed that early use of parenteral nutrition, the context of our initial RCTs, had been a confounder. Early parenteral nutrition (early-PN) aggravated hyperglycemia, suppressed vital cell damage removal, and hampered recovery. Therefore, in our next and largest "TGC-fast" RCT, we retested our hypothesis, without the use of early-PN and with a computer algorithm for tight glucose control that avoided severe hypoglycemia. In this trial, tight glucose control prevented kidney and liver damage, though with much smaller effect sizes than in our initial RCTs without affecting mortality. Our quest ends with the strong recommendation to omit early-PN for patients in the ICU, as this reduces need of blood glucose control and allows cellular housekeeping systems to play evolutionary selected roles in the recovery process. Once again, less is more in critical care.
    MeSH term(s) Humans ; Glycemic Control ; Blood Glucose ; Insulin/therapeutic use ; Glucose ; Hyperglycemia/prevention & control ; Hypoglycemia/prevention & control ; Intensive Care Units
    Chemical Substances Blood Glucose ; Insulin ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2023-11-22
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1180953-x
    ISSN 1535-4970 ; 0003-0805 ; 1073-449X
    ISSN (online) 1535-4970
    ISSN 0003-0805 ; 1073-449X
    DOI 10.1164/rccm.202309-1696SO
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: ICU-acquired weakness.

    Vanhorebeek, Ilse / Latronico, Nicola / Van den Berghe, Greet

    Intensive care medicine

    2020  Volume 46, Issue 4, Page(s) 637–653

    Abstract: Critically ill patients often acquire neuropathy and/or myopathy labeled ICU-acquired weakness. The current insights into incidence, pathophysiology, diagnostic tools, risk factors, short- and long-term consequences and management of ICU-acquired ... ...

    Abstract Critically ill patients often acquire neuropathy and/or myopathy labeled ICU-acquired weakness. The current insights into incidence, pathophysiology, diagnostic tools, risk factors, short- and long-term consequences and management of ICU-acquired weakness are narratively reviewed. PubMed was searched for combinations of "neuropathy", "myopathy", "neuromyopathy", or "weakness" with "critical illness", "critically ill", "ICU", "PICU", "sepsis" or "burn". ICU-acquired weakness affects limb and respiratory muscles with a widely varying prevalence depending on the study population. Pathophysiology remains incompletely understood but comprises complex structural/functional alterations within myofibers and neurons. Clinical and electrophysiological tools are used for diagnosis, each with advantages and limitations. Risk factors include age, weight, comorbidities, illness severity, organ failure, exposure to drugs negatively affecting myofibers and neurons, immobility and other intensive care-related factors. ICU-acquired weakness increases risk of in-ICU, in-hospital and long-term mortality, duration of mechanical ventilation and of hospitalization and augments healthcare-related costs, increases likelihood of prolonged care in rehabilitation centers and reduces physical function and quality of life in the long term. RCTs have shown preventive impact of avoiding hyperglycemia, of omitting early parenteral nutrition use and of minimizing sedation. Results of studies investigating the impact of early mobilization, neuromuscular electrical stimulation and of pharmacological interventions were inconsistent, with recent systematic reviews/meta-analyses revealing no or only low-quality evidence for benefit. ICU-acquired weakness predisposes to adverse short- and long-term outcomes. Only a few preventive, but no therapeutic, strategies exist. Further mechanistic research is needed to identify new targets for interventions to be tested in adequately powered RCTs.
    MeSH term(s) Critical Care ; Critical Illness ; Humans ; Intensive Care Units ; Muscle Weakness/etiology ; Quality of Life ; Respiration, Artificial
    Keywords covid19
    Language English
    Publishing date 2020-02-19
    Publishing country United States
    Document type Journal Article ; Meta-Analysis ; Review
    ZDB-ID 80387-x
    ISSN 1432-1238 ; 0340-0964 ; 0342-4642 ; 0935-1701
    ISSN (online) 1432-1238
    ISSN 0340-0964 ; 0342-4642 ; 0935-1701
    DOI 10.1007/s00134-020-05944-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Abnormal DNA methylation within genes of the steroidogenesis pathway two years after paediatric critical illness and association with stunted growth in height further in time.

    Vanhorebeek, Ilse / Coppens, Grégoire / Güiza, Fabian / Derese, Inge / Wouters, Pieter J / Joosten, Koen F / Verbruggen, Sascha C / Van den Berghe, Greet

    Clinical epigenetics

    2023  Volume 15, Issue 1, Page(s) 116

    Abstract: Background: Former critically ill children show an epigenetic age deceleration 2 years after paediatric intensive care unit (PICU) admission as compared with normally developing healthy children, with stunted growth in height 2 years further in time as ... ...

    Abstract Background: Former critically ill children show an epigenetic age deceleration 2 years after paediatric intensive care unit (PICU) admission as compared with normally developing healthy children, with stunted growth in height 2 years further in time as physical correlate. This was particularly pronounced in children who were 6 years or older at the time of critical illness. As this age roughly corresponds to the onset of adrenarche and further pubertal development, a relation with altered activation of endocrine pathways is plausible. We hypothesised that children who have been admitted to the PICU, sex- and age-dependently show long-term abnormal DNA methylation within genes involved in steroid hormone synthesis or steroid sulphation/desulphation, possibly aggravated by in-PICU glucocorticoid treatment, which may contribute to stunted growth in height further in time after critical illness.
    Results: In this preplanned secondary analysis of the multicentre PEPaNIC-RCT and its follow-up, we compared the methylation status of genes involved in the biosynthesis of steroid hormones (aldosterone, cortisol and sex hormones) and steroid sulphation/desulphation in buccal mucosa DNA (Infinium HumanMethylation EPIC BeadChip) from former PICU patients at 2-year follow-up (n = 818) and healthy children with comparable sex and age (n = 392). Adjusting for technical variation and baseline risk factors and corrected for multiple testing (false discovery rate < 0.05), former PICU patients showed abnormal DNA methylation of 23 CpG sites (within CYP11A1, POR, CYB5A, HSD17B1, HSD17B2, HSD17B3, HSD17B6, HSD17B10, HSD17B12, CYP19A1, CYP21A2, and CYP11B2) and 4 DNA regions (within HSD17B2, HSD17B8, and HSD17B10) that were mostly hypomethylated. These abnormalities were partially sex- (1 CpG site) or age-dependent (7 CpG sites) and affected by glucocorticoid treatment (3 CpG sites). Finally, multivariable linear models identified robust associations of abnormal methylation of steroidogenic genes with shorter height further in time, at 4-year follow-up.
    Conclusions: Children who have been critically ill show abnormal methylation within steroidogenic genes 2 years after PICU admission, which explained part of the stunted growth in height at 4-year follow-up. The abnormalities in DNA methylation may point to a long-term disturbance in the balance between active sex steroids and mineralocorticoids/glucocorticoids after paediatric critical illness, which requires further investigation.
    MeSH term(s) Child ; Humans ; Child, Preschool ; Critical Illness/therapy ; Glucocorticoids ; DNA Methylation ; Time Factors ; Growth Disorders ; DNA ; Steroid 21-Hydroxylase
    Chemical Substances Glucocorticoids ; DNA (9007-49-2) ; CYP21A2 protein, human (EC 1.14.14.16) ; Steroid 21-Hydroxylase (EC 1.14.14.16)
    Language English
    Publishing date 2023-07-19
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553921-8
    ISSN 1868-7083 ; 1868-7075
    ISSN (online) 1868-7083
    ISSN 1868-7075
    DOI 10.1186/s13148-023-01530-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Abnormal DNA methylation within HPA-axis genes years after paediatric critical illness.

    Coppens, Grégoire / Vanhorebeek, Ilse / Güiza, Fabian / Derese, Inge / Wouters, Pieter J / Téblick, Arno / Dulfer, Karolijn / Joosten, Koen F / Verbruggen, Sascha C / Van den Berghe, Greet

    Clinical epigenetics

    2024  Volume 16, Issue 1, Page(s) 31

    Abstract: Background: Critically ill children suffer from impaired physical/neurocognitive development 2 years later. Glucocorticoid treatment alters DNA methylation within the hypothalamus-pituitary-adrenal (HPA) axis which may impair normal brain development, ... ...

    Abstract Background: Critically ill children suffer from impaired physical/neurocognitive development 2 years later. Glucocorticoid treatment alters DNA methylation within the hypothalamus-pituitary-adrenal (HPA) axis which may impair normal brain development, cognition and behaviour. We tested the hypothesis that paediatric-intensive-care-unit (PICU) patients, sex- and age-dependently, show long-term abnormal DNA methylation within the HPA-axis layers, possibly aggravated by glucocorticoid treatment in the PICU, which may contribute to the long-term developmental impairments.
    Results: In a pre-planned secondary analysis of the multicentre PEPaNIC-RCT and its 2-year follow-up, we identified differentially methylated positions and differentially methylated regions within HPA-axis genes in buccal mucosa DNA from 818 former PICU patients 2 years after PICU admission (n = 608 no glucocorticoid treatment; n = 210 glucocorticoid treatment) versus 392 healthy children and assessed interaction with sex and age, role of glucocorticoid treatment in the PICU and associations with long-term developmental impairments. Adjusting for technical variation and baseline risk factors and correcting for multiple testing (false discovery rate < 0.05), former PICU patients showed abnormal DNA methylation of 26 CpG sites (within CRHR1, POMC, MC2R, NR3C1, FKBP5, HSD11B1, SRD5A1, AKR1D1, DUSP1, TSC22D3 and TNF) and three DNA regions (within AVP, TSC22D3 and TNF) that were mostly hypomethylated. These abnormalities were sex-independent and only partially age-dependent. Abnormal methylation of three CpG sites within FKBP5 and one CpG site within SRD5A1 and AKR1D1 was partly attributable to glucocorticoid treatment during PICU stay. Finally, abnormal methylation within FKBP5 and AKR1D1 was most robustly associated with long-term impaired development.
    Conclusions: Two years after critical illness in children, abnormal methylation within HPA-axis genes was present, predominantly within FKBP5 and AKR1D1, partly attributable to glucocorticoid treatment in the PICU, and explaining part of the long-term developmental impairments. These data call for caution regarding liberal glucocorticoid use in the PICU.
    MeSH term(s) Child ; Humans ; DNA Methylation ; Critical Illness/therapy ; Glucocorticoids/adverse effects ; Receptors, Glucocorticoid/genetics ; DNA
    Chemical Substances Glucocorticoids ; Receptors, Glucocorticoid ; DNA (9007-49-2)
    Language English
    Publishing date 2024-02-23
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553921-8
    ISSN 1868-7083 ; 1868-7075
    ISSN (online) 1868-7083
    ISSN 1868-7075
    DOI 10.1186/s13148-024-01640-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Nonthyroidal illness in critically ill children.

    Jacobs, An / Vanhorebeek, Ilse / Van den Berghe, Greet

    Current opinion in endocrinology, diabetes, and obesity

    2019  Volume 26, Issue 5, Page(s) 241–249

    Abstract: Purpose of review: This review summarizes recent literature on nonthyroidal illness syndrome (NTI) and outcome of pediatric critical illness, to provide insight in pathophysiology and therapeutic implications.: Recent findings: NTI is typically ... ...

    Abstract Purpose of review: This review summarizes recent literature on nonthyroidal illness syndrome (NTI) and outcome of pediatric critical illness, to provide insight in pathophysiology and therapeutic implications.
    Recent findings: NTI is typically characterized by lowered triiodothyronine levels without compensatory TSH rise. Although NTI severity is associated with poor outcome of pediatric critical illness, it remains unclear whether this association reflects an adaptive protective response or contributes to poor outcome. Recently, two metabolic interventions that improved outcome also altered NTI in critically ill children. These studies shed new light on the topic, as the results suggested that the peripheral NTI component, with inactivation of thyroid hormone, may represent a beneficial adaptation, whereas the central component, with suppressed TSH-driven thyroid hormone secretion, may be maladaptive. There is currently insufficient evidence for treatment of NTI in children. However, the recent findings raised the hypothesis that reactivation of the central NTI component could offer benefit, which should be tested in RCTs.
    Summary: NTI in critically ill children can be modified by metabolic interventions. The peripheral, but not the central, component of NTI may be a beneficial adaptive response. These findings open perspectives for the development of novel strategies to improve outcome of critical illness in children.
    MeSH term(s) Child ; Critical Illness ; Euthyroid Sick Syndromes/etiology ; Euthyroid Sick Syndromes/metabolism ; Euthyroid Sick Syndromes/therapy ; Humans
    Language English
    Publishing date 2019-08-30
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2272017-0
    ISSN 1752-2978 ; 1752-296X
    ISSN (online) 1752-2978
    ISSN 1752-296X
    DOI 10.1097/MED.0000000000000494
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Predicting adverse long-term neurocognitive outcomes after pediatric intensive care unit admission.

    Nakano, Felipe Kenji / Dulfer, Karolijn / Vanhorebeek, Ilse / Wouters, Pieter J / Verbruggen, Sascha C / Joosten, Koen F / Güiza Grandas, Fabian / Vens, Celine / Van den Berghe, Greet

    Computer methods and programs in biomedicine

    2024  Volume 250, Page(s) 108166

    Abstract: Background and objective: Critically ill children may suffer from impaired neurocognitive functions years after ICU (intensive care unit) discharge. To assess neurocognitive functions, these children are subjected to a fixed sequence of tests. ... ...

    Abstract Background and objective: Critically ill children may suffer from impaired neurocognitive functions years after ICU (intensive care unit) discharge. To assess neurocognitive functions, these children are subjected to a fixed sequence of tests. Undergoing all tests is, however, arduous for former pediatric ICU patients, resulting in interrupted evaluations where several neurocognitive deficiencies remain undetected. As a solution, we propose using machine learning to predict the optimal order of tests for each child, reducing the number of tests required to identify the most severe neurocognitive deficiencies.
    Methods: We have compared the current clinical approach against several machine learning methods, mainly multi-target regression and label ranking methods. We have also proposed a new method that builds several multi-target predictive models and combines the outputs into a ranking that prioritizes the worse neurocognitive outcomes. We used data available at discharge, from children who participated in the PEPaNIC-RCT trial (ClinicalTrials.gov-NCT01536275), as well as data from a 2-year follow-up study. The institutional review boards at each participating site have also approved this follow-up study (ML8052; NL49708.078; Pro00038098).
    Results: Our proposed method managed to outperform other machine learning methods and also the current clinical practice. Precisely, our method reaches approximately 80% precision when considering top-4 outcomes, in comparison to 65% and 78% obtained by the current clinical practice and the state-of-the-art method in label ranking, respectively.
    Conclusions: Our experiments demonstrated that machine learning can be competitive or even superior to the current testing order employed in clinical practice, suggesting that our model can be used to severely reduce the number of tests necessary for each child. Moreover, the results indicate that possible long-term adverse outcomes are already predictable as early as at ICU discharge. Thus, our work can be seen as the first step to allow more personalized follow-up after ICU discharge leading to preventive care rather than curative.
    Language English
    Publishing date 2024-04-10
    Publishing country Ireland
    Document type Journal Article
    ZDB-ID 632564-6
    ISSN 1872-7565 ; 0169-2607
    ISSN (online) 1872-7565
    ISSN 0169-2607
    DOI 10.1016/j.cmpb.2024.108166
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  9. Article: Pro-opiomelanocortin and ACTH-cortisol dissociation during pediatric cardiac surgery.

    Téblick, Arno / Vanhorebeek, Ilse / Derese, Inge / Jacobs, An / Haghedooren, Renata / Maebe, Sofie / Zeilmaker-Roest, Gerdian A / Wildschut, Enno D / Langouche, Lies / Van den Berghe, Greet

    Endocrine connections

    2024  

    Abstract: In critically ill adults, high plasma cortisol in face of low ACTH coincides with high pro-opiomelanocortin (POMC) levels. Glucocorticoids further lower ACTH without affecting POMC. We hypothesized that in pediatric cardiac surgery-induced critical ... ...

    Abstract In critically ill adults, high plasma cortisol in face of low ACTH coincides with high pro-opiomelanocortin (POMC) levels. Glucocorticoids further lower ACTH without affecting POMC. We hypothesized that in pediatric cardiac surgery-induced critical illness, plasma POMC is elevated, plasma ACTH transiently rises intraoperatively but becomes suppressed post-operatively, and glucocorticoid administration amplifies this phenotype. From 53 patients (0-36 months), plasma was obtained pre-operatively, intraoperatively and on post-operative day 1 and 2. Plasma was also collected from 24 healthy children. In patients, POMC was supra-normal pre-operatively (p<0.0001) but no longer thereafter (p<0.05). ACTH was never high in patients. While in glucocorticoid-naive patients ACTH became suppressed by post-operative day 1 (p<0.0001), glucocorticoid-treated patients had suppressed ACTH already intraoperatively (p≤0.0001). Pre-operatively high POMC, not accompanied by increased plasma ACTH, suggests a centrally-activated HPA-axis with reduced pituitary processing of POMC into ACTH. Increasing systemic glucocorticoid availability with glucocorticoid treatment accelerated the suppression of plasma ACTH.
    Language English
    Publishing date 2024-04-01
    Publishing country England
    Document type Journal Article
    ZDB-ID 2668428-7
    ISSN 2049-3614
    ISSN 2049-3614
    DOI 10.1530/EC-24-0078
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Critical Care Management of Stress-Induced Hyperglycemia.

    Vanhorebeek, Ilse / Gunst, Jan / Van den Berghe, Greet

    Current diabetes reports

    2018  Volume 18, Issue 4, Page(s) 17

    Abstract: Purpose of review: We discuss key studies that have set the scene for the debate on the efficacy and safety of tight glycemic control in critically ill patients, highlighting important differences among them, and describe the ensuing search towards ... ...

    Abstract Purpose of review: We discuss key studies that have set the scene for the debate on the efficacy and safety of tight glycemic control in critically ill patients, highlighting important differences among them, and describe the ensuing search towards strategies for safer glucose control.
    Recent findings: Differences in level of glycemic control, glucose measurement and insulin administration, expertise, and nutritional management may explain the divergent outcomes of the landmark studies on tight glycemic control in critical illness. Regarding strategies towards safer glucose control, several computerized algorithms have shown promise, but lack validation in adequately powered outcome studies. Real-time continuous glucose monitoring and closed loop blood glucose control systems are not up to the task yet due to technical challenges, though recent advances are promising. Alternatives for insulin have only been investigated in small feasibility studies. Severe hyperglycemia in critically ill patients generally is not tolerated anymore, but the optimal blood glucose target may depend on the specific patient and logistic context.
    MeSH term(s) Blood Glucose/analysis ; Critical Care ; Humans ; Hyperglycemia/therapy ; Stress, Psychological/complications
    Chemical Substances Blood Glucose
    Language English
    Publishing date 2018-02-26
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2065167-3
    ISSN 1539-0829 ; 1534-4827
    ISSN (online) 1539-0829
    ISSN 1534-4827
    DOI 10.1007/s11892-018-0988-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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