2022
DOI: 10.1007/s12664-022-01288-7
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New-onset prediabetes, diabetes after acute pancreatitis: A prospective cohort study with 12-month follow-up

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Cited by 7 publications
(6 citation statements)
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“…Overall, our results highlight the lack of definitive knowledge about and the complexity of postacute pancreatitis diabetes and suggest that likely diabetes in pancreatitis subjects has multifactorial etiologies. Prospective studies dedicated to The frequency of prediabetes or diabetes after a single episode of acute pancreatitis that we observed is higher than previously reported in pediatric studies [11] and similar to adult studies examining glucose homeostasis over the firstyear postacute pancreatitis attack [1][2][3]. As previously stated, severity of pancreatitis appeared to mediate an increased risk of abnormal glucose testing within the first-year postacute pancreatitis in our patients.…”
Section: Discussionsupporting
confidence: 78%
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“…Overall, our results highlight the lack of definitive knowledge about and the complexity of postacute pancreatitis diabetes and suggest that likely diabetes in pancreatitis subjects has multifactorial etiologies. Prospective studies dedicated to The frequency of prediabetes or diabetes after a single episode of acute pancreatitis that we observed is higher than previously reported in pediatric studies [11] and similar to adult studies examining glucose homeostasis over the firstyear postacute pancreatitis attack [1][2][3]. As previously stated, severity of pancreatitis appeared to mediate an increased risk of abnormal glucose testing within the first-year postacute pancreatitis in our patients.…”
Section: Discussionsupporting
confidence: 78%
“…Hyperglycemia was historically considered a transient complication of acute pancreatitis with permanent diabetes only occurring after chronic disease as the pancreas undergoes necrosis and fibrosis from long-term disease. Over the last 10 years, diabetes has become an increasingly recognized complication after a single episode of acute pancreatitis in adults [1][2][3][4] and there are ongoing efforts to understand the underlying pathophysiology and natural history [5]. Diabetes after acute pancreatitis is likely a heterogenous entity with multiple pathophysiological mechanisms contributing to its development in pancreatitis patients, including insulin resistance, insulin deficiency, altered metabolism of gut hormones and iron, and islet cell autoimmunity [6,7].…”
Section: Introductionmentioning
confidence: 99%
“…Similarly, only a statistically non-significant tendency could be observed in case of any organ failure (regardless of organ and duration of impairment) and DM [OR: 3.19; CI: 0.55–18.64; ( 36 , 40 , 45 , 52 )] or PD/DM [OR: 2.14; CI: 0.51–9.06; ( 31 , 32 , 46 ); Figure 4 ].…”
Section: Resultsmentioning
confidence: 99%
“…We found a significantly greater odds of developing PD/DM with necrotizing AP [OR: 5.53; CI: 1.59-19.21; (22,31,(46)(47)(48)] and a statistically non-significant tendency with DM [OR: 3.09; CI: 0.98-9.72; (24,30,36,40,41,49,50)] compared to non-necrotizing AP (Figure 4). Sensitivity analysis revealed that leaving out Takeyama (24) from the analysis would lead to a statistically significant OR (4.17; CI: 2.08-8.37) of developing DM in AP patients who had necrosis compared to its absence (Supplementary Figure S28).…”
Section: Ap Severity and Complicationsmentioning
confidence: 91%
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