Joshua Shur1, Stephan A R Kannengiesser2, Ravi Menezes1, Richard Ward3, Kevin Kuo3, Kartik Jhaveri4. 1. Joint Department of Medical Imaging, University Health Network, Mount Sinai Hospital, and Women's College Hospital, University of Toronto, 610 University Ave, 3-957, Toronto, ON, M5G 2M9, Canada. 2. MR Applications Predevelopment, Siemens Healthcare, Erlangen, Germany. 3. Division of Medical Oncology & Hematology, University Health Network, University of Toronto, Toronto, ON, Canada. 4. Joint Department of Medical Imaging, University Health Network, Mount Sinai Hospital, and Women's College Hospital, University of Toronto, 610 University Ave, 3-957, Toronto, ON, M5G 2M9, Canada. kartik.jhaveri@uhn.ca.
Abstract
OBJECTIVES: The aim was to investigate the relationship between pancreatic and hepatic iron and fat to glucose metabolism in patients with iron overload and address conflicting results in literature as regards the relationship between pancreas iron and glucose dysregulation. METHODS: We retrospectively evaluated pancreatic and hepatic R2*, fat fraction (FF), liver iron concentration (LIC), and glucose metabolism in 105 patients with iron overload obtained with a multi-echo gradient echo R2* technique and assessed the correlation between pancreatic R2* and FF to glucose dysregulation. RESULTS: There were no significant differences in pancreatic R2*, liver R2*, and FF in patients with iron overload and glucose dysregulation compared to those with normoglycemia (p = 0.435, p = 0.674, and p = 0.976), whereas pancreatic FF was significantly higher, 23.5% vs 16.7% respectively (p = 0.011). Pancreatic FF and R2* demonstrated an area under the curve of 0.666 and 0.571 for discriminating glucose dysregulation. Pancreatic FF of 26.2% yielded specificity and sensitivity of 80% and 45% for prediction of glucose dysregulation. Pancreatic R2* weakly correlated with pancreatic FF, r = 0.388 (p < 0.001), and liver R2*, r = 0.201 (p = 0.033), and showed no correlation with hepatic FF r = -0.013 (p = 0.892) or LIC categories (p = 0.493). CONCLUSION: Pancreatic FF but not pancreatic R2* was associated with glucose dysregulation in patients with iron overload. Prior studies reporting correlation of pancreatic R2* to glucose dysregulation likely relate from inadequate MRI technique or analysis employed, which unlike our study did not perform simultaneous measurements of fat and iron essential to avoid their confounding effects during quantitative analysis. KEY POINTS: • Pancreatic fat fraction, unlike iron, is associated with glucose dysregulation in iron overload. • Simultaneous measurement of pancreatic iron and fat content with MRI is essential to avoid confounding effects of one another during quantitative analysis. • Pancreatic fat fraction could be utilized to predict glucose dysregulation in iron overload states.
OBJECTIVES: The aim was to investigate the relationship between pancreatic and hepatic iron and fat to glucose metabolism in patients with iron overload and address conflicting results in literature as regards the relationship between pancreasiron and glucose dysregulation. METHODS: We retrospectively evaluated pancreatic and hepatic R2*, fat fraction (FF), liver iron concentration (LIC), and glucose metabolism in 105 patients with iron overload obtained with a multi-echo gradient echo R2* technique and assessed the correlation between pancreatic R2* and FF to glucose dysregulation. RESULTS: There were no significant differences in pancreatic R2*, liver R2*, and FF in patients with iron overload and glucose dysregulation compared to those with normoglycemia (p = 0.435, p = 0.674, and p = 0.976), whereas pancreatic FF was significantly higher, 23.5% vs 16.7% respectively (p = 0.011). Pancreatic FF and R2* demonstrated an area under the curve of 0.666 and 0.571 for discriminating glucose dysregulation. Pancreatic FF of 26.2% yielded specificity and sensitivity of 80% and 45% for prediction of glucose dysregulation. Pancreatic R2* weakly correlated with pancreatic FF, r = 0.388 (p < 0.001), and liver R2*, r = 0.201 (p = 0.033), and showed no correlation with hepatic FF r = -0.013 (p = 0.892) or LIC categories (p = 0.493). CONCLUSION:Pancreatic FF but not pancreatic R2* was associated with glucose dysregulation in patients with iron overload. Prior studies reporting correlation of pancreatic R2* to glucose dysregulation likely relate from inadequate MRI technique or analysis employed, which unlike our study did not perform simultaneous measurements of fat and iron essential to avoid their confounding effects during quantitative analysis. KEY POINTS: • Pancreatic fat fraction, unlike iron, is associated with glucose dysregulation in iron overload. • Simultaneous measurement of pancreatic iron and fat content with MRI is essential to avoid confounding effects of one another during quantitative analysis. • Pancreatic fat fraction could be utilized to predict glucose dysregulation in iron overload states.
Entities:
Keywords:
Diabetes mellitus; Iron; Magnetic resonance imaging; Pancreas
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