Early versus late intravenous insulin administration in critically ill patients

Honiden, Shyoko; Schultz, Atara; Im, Shelly A.; Nierman, David M.; Gong, Michelle N.

doi:10.1007/s00134-007-0978-3

Cited by 20 publications

(9 citation statements)

References 27 publications

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“…Hyperglycemia early in trauma predicts worse outcomes than hyperglycemia in later stages of the ICU stay (122). Initiation of intensive insulin therapy in critically ill hyperglycemic patients within 48 hrs of ICU admission was associated with better outcomes compared with delayed initiation of insulin (123). …”

Section: Resultsmentioning

confidence: 99%

Diabetes, insulin, and development of acute lung injury

Honiden

Gong

2009

Critical Care Medicine

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113

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Objectives-Recently, many studies have investigated the immunomodulatory effects of insulin and glucose control in critical illness. This review examines evidence regarding the relationship between diabetes and the development of acute lung injury/acute respiratory distress syndrome (ALI/ARDS), reviews studies of lung injury related to glycemic and nonglycemic metabolic features of diabetes, and examines the effect of diabetic therapies.Data Sources and Study Selection-A MEDLINE/PubMed search from inception to August 1, 2008, was conducted using the search terms acute lung injury, acute respiratory distress syndrome, hyperglycemia, diabetes mellitus, insulin, hydroxymethylglutaryl-CoA reductase inhibitors (statins), angiotensin-converting enzyme inhibitor, and peroxisome proliferatoractivated receptors, including combinations of these terms. Bibliographies of retrieved articles were manually reviewed.Data Extraction and Synthesis-Available studies were critically reviewed, and data were extracted with special attention to the human and animal studies that explored a) diabetes and ALI; b) hyperglycemia and ALI; c) metabolic nonhyperglycemic features of diabetes and ALI; and d) diabetic therapies and ALI.Conclusions-Clinical and experimental data indicate that diabetes is protective against the development of ALI/ARDS. The pathways involved are complex and likely include effects of hyperglycemia on the inflammatory response, metabolic abnormalities in diabetes, and the interactions of therapeutic agents given to diabetic patients. Multidisciplinary, multifaceted studies, involving both animal models and clinical and molecular epidemiology techniques, are essential. Keywordsacute respiratory distress syndrome; acute lung injury; hyperglycemia; diabetes mellitus; insulin Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is a devastating condition defined by the American-European Consensus Committee on ARDS as an acute syndrome of lung inflammation and increased permeability associated with severe hypoxia and bilateral infiltrates on chest radiographs with no evidence of left heart failure (1). Decades of animal and clinical studies have identified several pathophysiologic mechanisms important in the development of ALI/ARDS. Acute inflammation is a key feature, as evidenced by the central role of neutrophil recruitment and activation and the increased expression and release of inflammatory mediators, such as proinflammatory and antiinflammatory cytokines and chemokines. Disturbances in surfactant function and edema Copyright © 2009 clearance are present, and ample evidence supports imbalances in oxidant/antioxidant activity (2), coagulation/fibrinolysis, and fibrosis/repair. The relative balance of these interacting pathways either exacerbates or ameliorates further lung injury (3,4).ALI/ARDS is a commonly encountered condition, with 190,600 cases of ALI per year in the United States and an associated 74,500 deaths and 3.6 million hospital days (5). Of the predisposing injuries for ALI/ARDS, ...

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Section: Resultsmentioning

confidence: 99%

Diabetes, insulin, and development of acute lung injury

Honiden

Gong

2009

Critical Care Medicine

Self Cite

113

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“…In clinical situations, insulin is usually used when hyperglycemia occurred, which sometimes as a result of insulin resistance. Honiden et al conducted a clinical trial comparing timing of intensive insulin therapy in critically ill patients [7]. Their data suggests that insulin therapy within 48 h of ICU admission is associated with better outcomes.…”

Section: Discussionmentioning

confidence: 98%

Timing of Insulin Therapy Affects the Inflammatory Response in Endotoxemic Rats

et al. 2011

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The aim of the present study was to determine whether timing of insulin administration influences the hepatic and serum proinflammatory and anti-inflammatory cytokines during endotoxemia stimulated by lipopolysaccharide (LPS). Eighty-one male Sprague-Dawley rats were divided into different time groups and insulin was given 30 min pre-LPS administration or hour 0, 1, 3, 6, 12, 24 after the induction of endotoxemia, respectively. Hepatic and serum proinflammatory cytokines IL-1β, IL-6, and TNF-α, and anti-inflammatory cytokine IL-10 were detected 24 and 48 h after the induction of endotoxemia. Compared with sham control rats, serum concentrations of proinflammatory cytokines IL-1β, IL-6, and TNF-α and anti-inflammatory cytokine IL-10 significantly increased on 24 and 48 h after induction of endotoxemia. Similarly, LPS administration also significantly increased the hepatic IL-1β, TNF-α, IL-6, and IL-10 protein concentration 48 h after LPS injection. Compared with levels in positive LPS controls animals receiving saline, on 24 and 48 h after LPS injection, insulin administrated ahead of 6 h after LPS injection significantly decreased the serum IL-1β, IL-6, and TNF-a concentration (P < 0.05), and significantly increased anti-inflammatory cytokine IL-10 concentration (P < 0.05); hepatic IL-1β and IL-6 expression were (P < 0.05) significantly decreased compared with levels in positive LPS controls. But, the significant decrease of hepatic TNF-a expression and significant increase of hepatic IL-10 were only seen in the animals in which insulin was administrated at 30 min pre-LPS or coadministrated with LPS. Insulin administrated 6 h after LPS injection lost the ability to significantly reduce serum or hepatic IL-1β, TNF-α, and IL-6 concentrations. Insulin has a protective role in systemic inflammatory response syndrome related to sepsis, such as downregulation of proinflammatory cytokines and upregulation of anti-inflammatory cytokine production. However, timing of insulin administrated may change its effect of inflammatory response in endotoxemic rats. Insulin administrated 6 h after LPS injection weaken the ability to protect inflammatory response related to sepsis.

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“…Hyperglycemia is commonly observed during acute and critical illness (18). Controlling hyperglycemia with insulin is crucial in the management of critically ill patients.…”

Section: Afif Nakhleh and Naim Shehadehmentioning

confidence: 99%

“…Controlling hyperglycemia with insulin is crucial in the management of critically ill patients. Early administration of insulin in acute illness is associated with better outcomes and lower mortality rates (18). Early insulin therapy in patients with type 2 diabetes with COVID-19 disease that warrant hospital care appears to have several advantages.…”

Section: Afif Nakhleh and Naim Shehadehmentioning

confidence: 99%

Glycemic control of type 2 diabetic patients with coronavirus disease during hospitalization: a proposal for early insulin therapy

Nakhleh

Shehadeh

2020

American Journal of Physiology-Endocrinology and Metabolism

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TO THE EDITOR: The world is watching the progress of coronavirus disease (COVID᎑19) pandemic. Older age and pre-existing medical conditions, specifically diabetes mellitus, hypertension, ischemic heart disease, and chronic lung disease, are associated with a more severe course of . Diabetes mellitus is one of the most prevalent comorbidities among patients hospitalized due to . Data obtained from 21 hospitals in Wuhan, China, showed that 25% of the reported COVID-19 fatalities had a history of diabetes mellitus (33). Diabetes and ambient hyperglycemia were independent predictors for death and morbidity in patients with severe acute respiratory syndrome (14,34). In this letter, we discuss the putative roles of angiotensin-converting enzyme II (ACE2) in glucose homeostasis in patients with type 2 diabetes and COVID-19 and introduce the proposed benefit of early insulin therapy in patients that warrant hospital care.The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) uses angiotensin-converting enzyme II (ACE2) receptor for host cell entry and the serine protease TMPRSS2 for virus spike protein priming (16). The binding of SARS-CoV-1 Spike protein to ACE2 activates disintegrin and metalloprotease-17 (ADAM17) and induces ACE2 shedding via a process tightly coupled with TNF-␣ production (15). AD-AM17-mediated ACE2 shedding facilitates SARS-CoV-1 entry and induces tissue damage by TNF-␣ production (15). Interestingly, Kuba et al. (22) found that SARS-CoV-1 infection downregulates ACE2 expression in the mice lungs, and this downregulation was associated with the severity of lung injury. Considering that SARS-CoV-1 and SARS-CoV-2 share Ͼ70% sequence in the Spike protein (31), SARS᎑CoV᎑2 infection might also downregulate the ACE2 expression in the same manner and play a role in the pathological process of the lung injury. ADAM17-mediated ACE2 ectodomain shedding might compromise the renin-angiotensin system (RAS) compensatory axis by impairing ACE2 enzymatic activity or its ability to process angiotensin II on the cell surface. Recently, Monteil et al. (23) showed that human recombinant soluble ACE2 significantly blocks SARS-CoV-2 infections, providing a rationale that soluble ACE2 might not only protect from lung injury but also block the SARS-CoV-2 from entering target cells.ACE2 is expressed in several tissues including the kidney and recognized to be renoprotective by degrading angiotensin II to angiotensin(1-7) (9). The ACE2 receptor protects against lung injury by modulating of the RAS and decreasing angio-tensin II levels (19). Accumulating evidence supports the protective roles of ACE2 in diabetes. ACE2 is expressed in the pancreas and several insulin-sensitive tissues and might play important roles in glucose homeostasis. First, ACE2 deficiency leads to altered glucose metabolism; ACE2-knockout mice showed a ␤-cell defect associated with a decrease in insulin secretion in a manner that is not dependent on angiotensin II but may reflect the collectrin-like action of ACE2 (2, 24). In the db/db mouse...

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Early versus late intravenous insulin administration in critically ill patients

Cited by 20 publications

References 27 publications

Diabetes, insulin, and development of acute lung injury

Diabetes, insulin, and development of acute lung injury

Timing of Insulin Therapy Affects the Inflammatory Response in Endotoxemic Rats

Glycemic control of type 2 diabetic patients with coronavirus disease during hospitalization: a proposal for early insulin therapy

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