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New-Onset Diabetes After Acute and Critical Illness

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Presentation on theme: "New-Onset Diabetes After Acute and Critical Illness"— Presentation transcript:

1 New-Onset Diabetes After Acute and Critical Illness
Chirag J. Jivanji, MHSc, Varsha M. Asrani, MHSc, John A. Windsor, MBChB, MD, Maxim S. Petrov, MD, MPH, PhD  Mayo Clinic Proceedings  Volume 92, Issue 5, Pages (May 2017) DOI: /j.mayocp Copyright © 2017 Mayo Foundation for Medical Education and Research Terms and Conditions

2 Figure 1 Flowchart of study selection.
Mayo Clinic Proceedings  , DOI: ( /j.mayocp ) Copyright © 2017 Mayo Foundation for Medical Education and Research Terms and Conditions

3 Figure 2 A, Prevalence of new-onset diabetes for patients with normoglycemia. Normoglycemia was classified as a hospital admission plasma glucose (PG) level less than 124 mg/dL (to convert to mmol/L, multiply by ) in the study by McAllister et al.34 B, Prevalence of new-onset diabetes for patients with mild hyperglycemia. Patients with random PG levels of 140 mg/dL or greater were classified as having mild hyperglycemia in the studies by Van Ackerbroeck et al,28 Gornik et al,30 and Shore et al36 because data were not available for patients with severe hyperglycemia (random PG levels ≥200 mg/dL). Mild hyperglycemia was classified as a hospital admission PG level of 126 to 198 mg/dL in the study by McAllister et al34 and 128 mg/dL or greater in the study by Meisinger et al.35 C, Prevalence of new-onset diabetes for patients with severe hyperglycemia. Mayo Clinic Proceedings  , DOI: ( /j.mayocp ) Copyright © 2017 Mayo Foundation for Medical Education and Research Terms and Conditions

4 Figure 3 Hypothesized changes in glucose homeostasis after acute and critical illness. aAcute and critical stress is a systemic response to injury associated with hypermetabolism and increased circulating glucose, cytokine, and counterregulatory hormone levels. bOvert in-hospital stress hyperglycemia is characterized by disturbed carbohydrate metabolism, peripheral insulin resistance, and decreased insulin secretion. cGut injury results in impaired motility, disturbed barrier function, luminal translocation of bacteria, or altered endocrine and immune function. dPersistent stress signaling describes the production of reactive oxygen species, DNA methylation and histone acetylation, and modulation of anti-inflammatory and antioxidant genes. eAltered microbiota can lead to the loss of health-promoting bacteria and the proliferation of pathogenic bacteria. Pathogenic bacteria may promote further gut dysfunction (dashed arrow). NF-kB = nuclear factor-κβ; SCFA = short-chain fatty acid. Mayo Clinic Proceedings  , DOI: ( /j.mayocp ) Copyright © 2017 Mayo Foundation for Medical Education and Research Terms and Conditions


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