Trial reportFrontiers in endocrinology2022
Establishment and validation of a clinical model for predicting diabetic ketosis in patients with type 2 diabetes mellitus.
Trial report in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Loss of melatonin signaling increases the risk of T2DM caused by metabolic disorders.Cell communication and signaling : CCS · 2025Article
- Retrospective derivation of a causal pathway for diabetic ketoacidosis in adult patients with type 2 diabetes mellitus.BMJ open diabetes research & care · 2024Article
- International dietary quality index and its association with diabetes in RaNCD cohort study.Scientific reports · 2024Article
- Development and validation of a nomogram for screening patients with type 2 diabetic ketoacidosis.BMC endocrine disorders · 2024Article
- The role of C-peptide in diabetes and its complications: an updated review.Frontiers in endocrinology · 2023Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Diabetic ketosis (DK) is one of the leading causes of hospitalization among patients with diabetes. Failure to recognize DK symptoms may lead to complications, such as diabetic ketoacidosis, severe neurological morbidity, and death. Purpose: This study aimed to develop and validate a model to predict DK in patients with type 2 diabetes mellitus (T2DM) based on both clinical and biochemical characteristics. Methods: A cross-sectional study was conducted by evaluating the records of 3,126 patients with T2DM, with or without DK, at The Affiliated Hospital of Qingdao University from January 2015 to May 2022. The patients were divided randomly into the model development (70%) or validation (30%) cohorts. A risk prediction model was constructed using a stepwise logistic regression analysis to assess the risk of DK in the model development cohort. This model was then validated using a second cohort of patients. Results: The stepwise logistic regression analysis showed that the independent risk factors for DK in patients with T2DM were the 2-h postprandial C-peptide (2hCP) level, age, free fatty acids (FFA), and HbA1c. Based on these factors, we constructed a risk prediction model. The final risk prediction model was L= (0.472 Conclusion: This study identified independent risk factors for DK in patients with T2DM and constructed a prediction model based on these factors. The present findings provide an easy-to-use, easily interpretable, and accessible clinical tool for predicting DK in patients with T2DM.
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