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. 2019 Mar;48(3):420-426.
doi: 10.1097/MPA.0000000000001252.

Association of Pancreatic Steatosis With Chronic Pancreatitis, Obesity, and Type 2 Diabetes Mellitus

Affiliations

Association of Pancreatic Steatosis With Chronic Pancreatitis, Obesity, and Type 2 Diabetes Mellitus

Temel Tirkes et al. Pancreas. 2019 Mar.

Abstract

Objective: The aim of this study was to determine the association of the pancreatic steatosis with obesity, chronic pancreatitis (CP), and type 2 diabetes mellitus.

Methods: Patients (n = 118) were retrospectively identified and categorized into no CP (n = 60), mild (n = 21), moderate (n = 27), and severe CP (n = 10) groups based on clinical history and magnetic resonance cholangiopancreatography using the Cambridge classification as the diagnostic standard. Visceral and subcutaneous compartments were manually segmented, and fat tissue was quantitatively measured on axial magnetic resonance imaging.

Results: Pancreatic fat fraction showed a direct correlation with fat within the visceral compartment (r = 0.54). Patients with CP showed higher visceral fat (P = 0.01) and pancreatic fat fraction (P < 0.001): mild, 24%; moderate, 23%; severe CP, 21%; no CP group, 15%. Patients with type 2 diabetes mellitus showed higher pancreatic steatosis (P = 0.03) and higher visceral (P = 0.007) and subcutaneous fat (P = 0.004). Interobserver variability of measuring fat by magnetic resonance imaging was excellent (r ≥ 0.90-0.99).

Conclusions: Increased visceral adipose tissue has a moderate direct correlation with pancreatic fat fraction. Chronic pancreatitis is associated with higher pancreatic fat fraction and visceral fat. Type 2 diabetes mellitus is associated with higher pancreatic fat fraction and visceral and subcutaneous adiposity.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

FIGURE 1.
FIGURE 1.
Patient selection algorithm. Categorization of the patient groups was done by secretin-enhanced MRCP using the Cambridge classification as the diagnostic standard. Cambridge 0 patients comprised the no CP group.
FIGURE 2.
FIGURE 2.
Correlation of pancreatic fat fraction and visceral fat amount. This plot shows the moderate correlation between the pancreatic and visceral fat (r = 0.54, P < 0.0001), which is stronger than the SAT and V/S.
FIGURE 3.
FIGURE 3.
Correlation of abdominal fat content within the visceral (VAT) and subcutaneous (SAT) compartments, V/S, and pancreatic fat fraction (PS). Low to moderate correlations were observed between each pair. The highest correlation was between the VAT and pancreatic fat. NA indicates not applicable.
FIGURE 4.
FIGURE 4.
Box-and-whisker plot showing the distribution of pancreatic fat fraction in the no CP, mild, moderate, and severe CP groups. Patients with CP showed significantly higher percentage of pancreatic fat compared with the no CP group. Pancreatic fat fractions in the mild (average, 24%), moderate (23%), and severe CP (21%) groups were significantly higher than normal group (15%), with the highest difference between the no CP and mild CP group. There was no statistically significant difference in the fat fraction between the CP groups (P = 0.48).
FIGURE 5.
FIGURE 5.
Multivariate logistic regression analysis is showing the association between the pancreatic steatosis (PS) and distribution of the abdominal fat with CP (A) and T2DM (B). A, Multivariate logistic model analysis of CP with base model, PS, VAT, SAT, and V/S. Base model included these conventional risk factors: alcohol, smoking, and BMI. Pancreatic steatosis has the highest diagnostic potential for CP (AUC,0.83), followed by VAT (AUC, 0.72) and SAT (AUC, 0.70). Using pancreatic fat fraction of 56% as the threshold, PS was 74% sensitive and 85% specific for CP. B, Multivariate logistic regression analysis of T2DM with PS, VAT, SAT, and V/S. Base model included these conventional risk factors: alcohol, hyperlipidemia, and BMI. Pancreatic steatosis has the highest diagnostic potential for T2DM (AUC, 0.85), closely followed by VAT (0.84), SAT (AUC, 0.82), and V/S (AUC, 0.79). Using pancreatic fat fraction of 24% as the threshold, PS was 69% sensitive and 87% specific for T2DM.
FIGURE 6.
FIGURE 6.
These 3 diagrams are created using probit regression to analyze the dose-response analysis between the visceral adiposity, pancreatic fat fraction, and T2DM. The probit regression procedure fits a probit sigmoid dose-response curve and calculates values (with 95% CI) of the dose variable that corresponds to a series of probabilities. A, Predicted probability curve of visceral adiposity (VAT measured as cm2) and CP. B, Predicted probability curve of pancreatic fat fraction and CP. C, Predicted probability curve of pancreatic fat fraction and T2DM.

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