Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/32932
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dc.contributor.authorMårtensson, Johan-
dc.contributor.authorCutuli, Salvatore Lucio-
dc.contributor.authorOsawa, Eduardo A-
dc.contributor.authorYanase, Fumitaka-
dc.contributor.authorToh, Lisa-
dc.contributor.authorCioccari, Luca-
dc.contributor.authorLuethi, Nora-
dc.contributor.authorMaeda, Akinori-
dc.contributor.authorBellomo, Rinaldo-
dc.date2023-
dc.date.accessioned2023-06-07T02:25:17Z-
dc.date.available2023-06-07T02:25:17Z-
dc.date.issued2023-05-16-
dc.identifier.citationCritical Care (London, England) 2023en_US
dc.identifier.issn1466-609X-
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/32932-
dc.description.abstractSodium glucose co-transporter-2 (SGLT2) inhibitors improve long-term cardiovascular and renal outcomes in individuals with type 2 diabetes. However, the safety of SGLT2 inhibitors in ICU patients with type 2 diabetes is uncertain. We aimed to perform a pilot study to assess the relationship between empagliflozin therapy and biochemical, and clinical outcomes in such patients. We included 18 ICU patients with type 2 diabetes receiving empagliflozin (10 mg daily) and insulin to target glucose range of 10-14 mmol/l according to our liberal glucose control protocol for patients with diabetes (treatment group). Treatment group patients were matched on age, glycated hemoglobin A1c, and ICU duration with 72 ICU patients with type 2 diabetes exposed to the same target glucose range but who did not receive empagliflozin (control group). We compared changes in electrolyte and acid-base parameters, hypoglycemia, ketoacidosis, worsening kidney function, urine culture findings, and hospital mortality between the groups. Median (IQR) maximum increase in sodium and chloride levels were 3 (1-10) mmol/l and 3 (2-8) mmol/l in the control group and 9 (3-12) mmol/l and 8 (3-10) mmol/l in the treatment group (P = 0.045 for sodium, P = 0.059 for chloride). We observed no differences in strong ion difference, pH or base excess. Overall, 6% developed hypoglycemia in each group. No patient in the treatment group and one patient in the control group developed ketoacidosis. Worsening kidney function occurred in 18% and 29% of treatment and control group patients, respectively (P = 0.54). Urine cultures were positive in 22% of treatment group patients and 13% of control group patients (P = 0.28). Overall, 17% of treatment group patients and 19% of control group patients died in hospital (P = 0.79). In our pilot study of ICU patients with type 2 diabetes, empagliflozin therapy was associated with increases in sodium and chloride levels but was not significantly associated with acid-base changes, hypoglycemia, ketoacidosis, worsening kidney function, bacteriuria, or mortality.en_US
dc.language.isoeng-
dc.subjectDiabetesen_US
dc.subjectEmpagliflozinen_US
dc.subjectIntensive careen_US
dc.subjectSGLT2 inhibitoren_US
dc.titleSodium glucose co-transporter-2 inhibitors in intensive care unit patients with type 2 diabetes: a pilot case control study.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleCritical Careen_US
dc.identifier.affiliationDepartment of Physiology and Pharmacology, Section of Anaesthesia and Intensive Care, Karolinska Institutet, Stockholm, Swedenen_US
dc.identifier.affiliationDipartimento di Scienze dell'Emergenza, Anestesiologiche e della Rianimazione, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italyen_US
dc.identifier.affiliationCardiology Intensive Care Unit, Hospital DF-Star, Brasília, Brazilen_US
dc.identifier.affiliationIntensive Careen_US
dc.identifier.affiliationDepartment of Intensive Care, Royal Melbourne Hospital, Melbourne, Australiaen_US
dc.identifier.affiliationDepartment of Intensive Care Medicine, Kantonsspital Aarau, Aarau, Switzerland.en_US
dc.identifier.affiliationAustralian and New Zealand Intensive Care Research Centre, Monash University, Melbourne, VIC, Australia.en_US
dc.identifier.affiliationDepartment of Emergency and Critical Care Medicine, The University of Tokyo Hospital, Tokyo, Japan.en_US
dc.identifier.affiliationDepartment of Critical Care, Melbourne University, Melbourne, VIC, Australiaen_US
dc.identifier.affiliationDepartment of Perioperative Medicine and Intensive Care, Karolinska University Hospital, 171 76, Stockholm, Swedenen_US
dc.identifier.affiliationDipartimento di Scienze Biotecnologiche di Base, Cliniche Intensivologiche e Perioperatorie, Università Cattolica del Sacro Cuore, L.Go F. Vito 1, 00168, Rome, Italyen_US
dc.identifier.doi10.1186/s13054-023-04481-yen_US
dc.type.contentTexten_US
dc.identifier.pubmedid37194077-
dc.description.volume27-
dc.description.issue1-
dc.description.startpage189-
dc.subject.meshtermssecondaryDiabetes Mellitus, Type 2/complications-
dc.subject.meshtermssecondaryDiabetes Mellitus, Type 2/drug therapy-
dc.subject.meshtermssecondaryHypoglycemia/drug therapy-
dc.subject.meshtermssecondaryHypoglycemic Agents/therapeutic use-
dc.subject.meshtermssecondarySodium-Glucose Transporter 2 Inhibitors/therapeutic use-
local.name.researcherBellomo, Rinaldo
item.grantfulltextnone-
item.openairetypeJournal Article-
item.languageiso639-1en-
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
crisitem.author.deptIntensive Care-
crisitem.author.deptIntensive Care-
crisitem.author.deptIntensive Care-
crisitem.author.deptData Analytics Research and Evaluation (DARE) Centre-
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