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People with diabetes are at an increased risk for worse postoperative outcomes, compared to people without diabetes. Notably, up to one in 10 people who undergo surgery have unrecognized diabetes and an additional 10% may have postoperative hyperglycemia without meeting the criteria for a diagnosis of diabetes. Management of postoperative hyperglycemia has been demonstrated to reduce the incidence of poor outcomes, but evidence demonstrates that postoperative hyperglycemia remains a quality gap for surgical patients. In this review, we will outline the evidence for preoperative screening for postoperative hyperglycemic risk, review the evidence for perioperative glycemic management, and examine the barriers to these best practices. RÉSUMÉLes personnes atteintes de diabète courent un risque accru de voir leurs résultats postopératoires moins bons que ceux des personne non atteinte de diabète. En particulier, près d’une personne sur dix qui subit une intervention chirurgicale présente un diabète non diagnostiqué et dix pour cent supplémentaires peuvent présenter une hyperglycémie postopératoire sans pour autant répondre aux critères de diagnostic du diabète. Il a été démontré que le traitement de l’hyperglycémie postopératoire réduit l’incidence des mauvais résultats, mais les données probantes montrent que l’hyperglycémie postopératoire demeure une lacune chez les patients opérés. Dans cette revue, nous présentons les données probantes relatives au dépistage préopératoire du risque d’hyperglycémie postopératoire, nous passons en revue les données probantes relatives à la gestion de la glycémie périopératoire et nous examinons les obstacles à ces meilleures pratiques.

ATOX1 is a cytoplasmic copper chaperone that interacts with the copper-binding domain of the membrane copper transporters ATP7A and ATP7B. ATOX1 has also been suggested to have a potential anti-oxidant activity. This study investigates the tissue-specific localization of the mouse homolog, Atox1, in mouse liver and kidney. Immunohistochemical studies in the liver localize the copper chaperone to hepatocytes surrounding both hepatic and central veins. In the kidney, Atox1 is localized to the cortex and the medulla. Cortex immunostaining is specific to glomeruli in both the juxtamedullary and cortical nephrons. Expression in the medulla appears to be associated with the loops of Henle. These data suggest that localized regions in the liver and kidney express Atox1 and have a role in copper homeostasis and/or anti-oxidant protection. Twenty-seven patients with Wilson disease-like phenotypes and two patients with Menkes disease-like phenotypes were screened for ATOX1 mutations with no alterations detected. The human phenotype resulting from mutations in ATOX1 remains unidentified.

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