PROGNOSTIC IMPLICATIONS OF DIABETIC KETOACIDOSIS ON LONG-TERM MORTALITY AND DIABETES-RELATED COMPLICATIONS.

Journal

Canadian journal of diabetes
ISSN: 2352-3840
Titre abrégé: Can J Diabetes
Pays: Canada
ID NLM: 101148810

Informations de publication

Date de publication:
26 Jul 2024
Historique:
received: 04 05 2024
revised: 18 07 2024
accepted: 22 07 2024
medline: 29 7 2024
pubmed: 29 7 2024
entrez: 28 7 2024
Statut: aheadofprint

Résumé

Diabetic ketoacidosis (DKA) occurring after diabetes diagnosis is often associated with risk factors for other diabetes-related complications. We aimed to determine the prognostic implications of DKA on all-cause mortality and complications in type 1 diabetes (T1D). Previously collected data from the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) Study was obtained through the NIDDK central repository. Using Cox proportional-hazards models with time-dependent covariates, we examined age- and sex-, HbA1c-, and fully-adjusted associations of DKA with all-cause mortality, cardiovascular disease, microvascular, and acute complications over 34 years. Of 1441 participants, 297 had 488 DKA events. Prior DKA was associated with a higher risk of age- and sex-adjusted all-cause mortality (hazard ratio (HR) 8.28, 95% confidence interval (CI) 3.74-18.32, p<0.001), major adverse cardiovascular events (MACE) (HR 2.05, 95%CI 1.34-3.13, p<0.001), and all advanced microvascular and acute complications compared to no prior DKA. Most associations except retinopathy were significant even after adjustment for covariates. In our fully-adjusted analysis, prior DKA was associated with a significantly higher risk of subsequent all-cause mortality (HR 9.13, 95%CI 3.87-21.50; p<0.001), MACE (HR 1.66, 95%CI 1.07-2.59; p=0.03), advanced kidney disease (HR 2.10, 95%CI 1.00-4.22; p=0.049), advanced neuropathy (HR 1.49, 95%CI 1.05 to 2.13; p=0.03), severe hypoglycemia (HR 1.53, 95%CI 1.28-1.81; p<0.001) and recurrent DKA (HR 3.24, 95%CI 2.41-4.36, p<0.001) compared to person-time without DKA. DKA is a prognostic marker for diabetes complications, including excess all-cause mortality. Intensified clinical interventions such as cardiovascular prevention strategies may be warranted following the diagnosis of DKA.

Sections du résumé

BACKGROUND BACKGROUND
Diabetic ketoacidosis (DKA) occurring after diabetes diagnosis is often associated with risk factors for other diabetes-related complications. We aimed to determine the prognostic implications of DKA on all-cause mortality and complications in type 1 diabetes (T1D).
METHODS METHODS
Previously collected data from the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) Study was obtained through the NIDDK central repository. Using Cox proportional-hazards models with time-dependent covariates, we examined age- and sex-, HbA1c-, and fully-adjusted associations of DKA with all-cause mortality, cardiovascular disease, microvascular, and acute complications over 34 years.
FINDINGS RESULTS
Of 1441 participants, 297 had 488 DKA events. Prior DKA was associated with a higher risk of age- and sex-adjusted all-cause mortality (hazard ratio (HR) 8.28, 95% confidence interval (CI) 3.74-18.32, p<0.001), major adverse cardiovascular events (MACE) (HR 2.05, 95%CI 1.34-3.13, p<0.001), and all advanced microvascular and acute complications compared to no prior DKA. Most associations except retinopathy were significant even after adjustment for covariates. In our fully-adjusted analysis, prior DKA was associated with a significantly higher risk of subsequent all-cause mortality (HR 9.13, 95%CI 3.87-21.50; p<0.001), MACE (HR 1.66, 95%CI 1.07-2.59; p=0.03), advanced kidney disease (HR 2.10, 95%CI 1.00-4.22; p=0.049), advanced neuropathy (HR 1.49, 95%CI 1.05 to 2.13; p=0.03), severe hypoglycemia (HR 1.53, 95%CI 1.28-1.81; p<0.001) and recurrent DKA (HR 3.24, 95%CI 2.41-4.36, p<0.001) compared to person-time without DKA.
INTEPRETATION CONCLUSIONS
DKA is a prognostic marker for diabetes complications, including excess all-cause mortality. Intensified clinical interventions such as cardiovascular prevention strategies may be warranted following the diagnosis of DKA.

Identifiants

DOI: 10.1016/j.jcjd.2024.07.002 PMID: 39069232
pubmed: 39069232
pii: S1499-2671(24)00142-4
doi: 10.1016/j.jcjd.2024.07.002
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024. Published by Elsevier Inc.

Auteurs

Dalton R Budhram (DR)

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital. Toronto, Ontario, Canada; Division of General Internal Medicine, Department of Medicine, University Health Network and Sinai Health, University of Toronto, Canada.

Priya Bapat (P)

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital. Toronto, Ontario, Canada; Division of Endocrinology, Department of Medicine, University of Toronto, Canada.

Abdulmohsen Bakhsh (A)

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital. Toronto, Ontario, Canada; Division of Endocrinology, Department of Medicine, University of Toronto, Canada; Kidney & Pancreas Health Centre, Organ Transplant Centre of Excellence, King Faisal Specialist Hospital & Research Centre, Riyadh, Kingdom of Saudi Arabia.

Mohammad I Abuabat (MI)

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital. Toronto, Ontario, Canada; Division of Endocrinology, Department of Medicine, University of Toronto, Canada; Internal Medicine and Critical Care Department, King Abdullah bin Abdulaziz University Hospital, Princess Norah University, Riyadh, Saudi Arabia.

Natasha J Verhoeff (NJ)

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital. Toronto, Ontario, Canada; Temerty Faculty of Medicine, University of Toronto, Toronto, Canada.

Doug Mumford (D)

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital. Toronto, Ontario, Canada; Patient-partner (person with lived type 1 diabetes experience).

Andrej Orszag (A)

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital. Toronto, Ontario, Canada; Division of Endocrinology, Department of Medicine, University of Toronto, Canada.

Akshay Jain (A)

TLC Diabetes and Endocrinology, Surrey, British Columbia, Canada; Division of Endocrinology, Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada.

David Z I Cherney (DZI)

Temerty Faculty of Medicine, University of Toronto, Toronto, Canada; Division of Nephrology, Department of Medicine, University Health Network, Toronto, Ontario, Canada.

Michael Fralick (M)

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital. Toronto, Ontario, Canada; Division of General Internal Medicine, Department of Medicine, University Health Network and Sinai Health, University of Toronto, Canada.

Alanna Weisman (A)

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital. Toronto, Ontario, Canada; Division of Endocrinology, Department of Medicine, University of Toronto, Canada; Institute of Health Policy, Management, and Evaluation, University of Toronto, Canada.

Leif Erik Lovblom (LE)

Biostatistics Department, University Health Network, Toronto, Canada.

Bruce A Perkins (BA)

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital. Toronto, Ontario, Canada; Division of Endocrinology, Department of Medicine, University of Toronto, Canada; Institute of Health Policy, Management, and Evaluation, University of Toronto, Canada. Electronic address: bruce.perkins@sinaihealth.ca.

Classifications MeSH