Incidence and Predictors of Acute Pancreatitis in Patients With Diabetic Ketoacidosis (DKA) and Hyperosmolar Hyperglycemic State (HHS): A Multicenter Retrospective Study > 2026

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2026

Incidence and Predictors of Acute Pancreatitis in Patients With Diabet…

작성자 채식영양
작성일 26-01-01 00:00 | 조회 0 | 댓글 0

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E. Cho, JH. Lee, GR. You, MW. Chung, G. Kim, SW. Park, M. Haque, RA. Liddle, et al. (2026). Incidence and Predictors of Acute Pancreatitis in Patients With Diabetic Ketoacidosis (DKA) and Hyperosmolar Hyperglycemic State (HHS): A Multicenter Retrospective Study. Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists. https://doi.org/10.1016/j.eprac.2026.04.015

PubMed 42061649


[Abstract]
OBJECTIVES: Acute pancreatitis (AP) complicates hyperglycemic crisis, yet incidence and predictors remain unclear. We evaluated the incidence and predictors of AP in patients with diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS).

METHODS: This retrospective multicenter study included patients with hyperglycemic crisis between January 2015 and August 2025 at 3 tertiary hospitals. DKA/HHS and AP were diagnosed per American Diabetes Association and revised Atlanta criteria, respectively. Multivariable analysis was performed for the total cohort and DKA subgroup.

RESULTS: Among 406 patients (303 with DKA, 103 with HHS), 60 (14.8%) developed AP, more frequently in DKA than in HHS (17.5% vs6.8%). Patients with AP more often presented with abdominal pain and shock and had higher serum γ-glutamyl transferase (γ-GTP) and triglyceride levels. Higher body mass index, abdominal pain, shock, elevated γ-GTP, and hypertriglyceridemia independently predicted AP. In the DKA subgroup, alcohol consumption, type 2 diabetes, abdominal pain, shock, and γ-GTP were independent predictors. While AP was associated with increased intensive care unit admission, it did not result in increased hospital stay or in-hospital mortality.

CONCLUSION: AP occurs in a substantial proportion of hyperglycemic crises. Its development is linked to specific metabolic and hemodynamic stressors, suggesting a multifactorial pathophysiology.

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