Pancreas MRI segmentation into head, body, and tail enables regional quantitative analysis of heterogeneous disease

Pancreatic disease can be spatially inhomogeneous. For this reason, quantitative imaging studies of the pancreas have often targeted the 3 main anatomical pancreatic parts, head, body, and tail, traditionally using a balanced region of interest (ROI) strategy. Existing automated analysis methods have implemented whole-organ segmentation, which provides an overall quantification, but fails to address spatial heterogeneity in disease. A method to automatically refine a whole-organ segmentation of the pancreas into head, body, and tail subregions is presented for abdominal magnetic resonance imaging (MRI). The subsegmentation method is based on diffeomorphic registration to a group average template image, where the parts are manually annotated. For a new whole-pancreas segmentation, the aligned template's part labels are automatically propagated to the segmentation of interest. The method is validated retrospectively on the UK Biobank imaging substudy (scanned using a 2-point Dixon protocol at 1.5 tesla), using a nominally healthy cohort of 100 subjects for template creation, and 50 independent subjects for validation. Pancreas head, body, and tail were annotated by multiple experts on the validation cohort, which served as the benchmark for the automated method's performance. Good intra-rater (Dice overlap mean, Head: 0.982, Body: 0.940, Tail: 0.961, N=30) as well as inter-rater (Dice overlap mean, Head: 0.968, Body: 0.905, Tail: 0.943, N=150) agreement was observed. No significant difference (Wilcoxon rank sum test, DSC, Head: p=0.4358, Body: p=0.0992, Tail: p=0.1080) was observed between the manual annotations and the automated method's predictions. Results on regional pancreatic fat assessment are also presented, by intersecting the 3-D parts segmentation with one 2-D multi-echo gradient-echo slice, available from the same scanning session, that was used to compute MRI proton density fat fraction (MRI-PDFF). Initial application of the method on a type 2 diabetes cohort showed the utility of the method for assessing pancreatic disease heterogeneity.

Comparison of pancreatic fat content measured by different methods employing MR mDixon sequence

Objective To compare the reliability of different methods for measuring fat content of pancreas by MR modified Dixon(mDixon) Sequence and accurately evaluate pancreatic fat in as simple a way as possible. Methods This is a retrospective study, 64 patients were included in this study who underwent abdominal MR scan that contained the mDixon sequence from June 2019 to May 2020(Included 7 patients with type 2 diabetes and 4 patients with impaired glucose tolerance (IGT), they were admitted to hospital through the obesity clinic set up by endocrine department, all of them were initially diagnosed and untreated). All of the 64 patients were scanned in 3.0T MR (Philips Ingenia II) due to their condition, 10–34 slice pancreas images were obtained, which were different from each other. Three different methods of measurement were employed by two observers using Philips Intellispace Portal software: (1) All images (whole-pancreas) measurement, the whole-pancreatic fat fraction (wPFF) was calculated by software. (2) Interval slices measurement, that is half-pancreatic slices fat fraction (hPFF) measured in the same way, fat fraction obtained by the interlayer assay was calculated. (3) As usual, the fat content of pancreatic head, body and tail fat was measured respectively, and in order to improve credibility, we also measured head、 body and tail in every layer, and its average value was taken. The elapsed time of the above different measurement methods was recorded. Intra-group correlation coefficient (ICC) was used to analyze the consistency of the measured data within and between observers. T-tests and Friedman tests were applied to compare the difference of measured values among groups. Results No matter in normal person or diabetic or IGT, hPFF has shown good stability (ICChPFF = 0.988), and there was no significant difference compared with wPFF. But the average fat percentage composition of head, body and tail were significantly different from wPFF and hPFF (P < 0.01). At the same time, compared with normal person, pancreatic fat content in IGT and diabetic patients showed progressive significance(P<0.05). Conclusion The distribution of pancreatic fat is not uniform, the method of measuring half pancreas by interlayer data collection can reflect the fat content of the entire pancreas, this suggests that measuring 50% of the pancreas is sufficient, this method effectively saves time and effort without affecting the results, which may have a better clinical application prospect.

Associations between Intra-Pancreatic Fat Deposition, Pancreas Size, and Pancreatic Enzymes in Health and after an Attack of Acute Pancreatitis

<b><i>Introduction:</i></b> Ectopic fat deposition in the pancreas is involved in the pathogenesis of metabolic sequelae following an attack of pancreatitis. However, its relationship with the exocrine pancreas has never been explored in this setting. The aim was to investigate the associations between intra-pancreatic fat deposition (IPFD), pancreas size, and pancreatic enzymes. <b><i>Methods:</i></b> This cross-sectional study recruited individuals with a history of acute pancreatitis and healthy controls. All participants underwent 3T magnetic resonance imaging, from which IPFD, total pancreas volume (TPV), and pancreas diameters (across the head, body, and tail) were measured independently by 2 raters in a blinded fashion. Circulating levels of pancreatic amylase, pancreatic lipase, and chymotrypsin were measured in a fasted state. A series of linear regression analyses was conducted, accounting for possible confounders. <b><i>Results:</i></b> A total of 108 individuals with pancreatitis and 60 healthy controls were studied. There was a statistically significant difference in IPFD (<i>p</i> &#x3c; 0.001), but not in TPV (<i>p</i> = 0.389), between the groups. In the post-pancreatitis group, IPFD was significantly inversely associated with pancreas tail diameter (β = −0.736, <i>p</i> = 0.036 in the most adjusted model). In the control group, IPFD was significantly inversely associated with TPV (β = −3.557, <i>p</i> = 0.026 in the most adjusted model). Levels of pancreatic amylase were significantly directly associated with pancreas tail diameter in the post-pancreatitis group (β = 3.891, <i>p</i> = 0.042 in the most adjusted model), whereas levels of pancreatic lipase were significantly inversely associated with TPV in the control group (β = −10.533, <i>p</i> = 0.024 in the most adjusted model). <b><i>Conclusion:</i></b> Increased IPFD in individuals after an attack of pancreatitis is associated with reduced pancreas tail diameter, which is in turn associated with reduced circulating levels of pancreatic amylase. The relationship between IPFD and the exocrine pancreas warrants further investigations.

Pancretic Fat Accummulation is Associated with Subclinical Atherosclerosis

We investigated the relationship between pancreatic fat accumulation and markers of atherosclerosis among patients with nonalcoholic fatty liver disease (NAFLD). Patients with NAFLD have been reported to be at an increased risk of vascular events. We grouped 183 patients in whom we detected and graded hepatosteatosis (HS) on transabdominal ultrasonography into 2 groups based on the presence/absence of pancreatic fat. There were 85 participants (50 female; mean age: 53.6 ± 9.7 years) who were nonalcoholic fatty pancreas disease (NAFPD) positive and 98 participants (56 female; mean age: 51.4 ± 9.3 years) who were NAFPD negative. Carotid intima media thickness (cIMT) was significantly greater in the group where HS was accompanied by NAFPD (0.51 [0.40–0.62] vs 0.45 [0.35–0.55] mm; P < .001). Multivariable analyses showed that the independent predictors of increased cIMT were age (odds ratio [OR]: 1.108; 95% CI: 1.059–1.158, P = .001), hypertension (OR: 2.244; 95% CI: 1.099–4.579, P = .026), and the presence of NAFPD (OR: 3.078; CI 95% CI: 1.531–6.190, P = .0002). In the present study we demonstrated that, in patients with NAFLD, pancreatic fat accumulation was significantly associated with cIMT, a marker of early atherosclerosis. NAFPD may increase the risk of vascular events associated with NAFLD.

Genome-wide association study of pancreatic fat: The Multiethnic Cohort Adiposity Phenotype Study

Several studies have found associations between higher pancreatic fat content and adverse health outcomes, such as diabetes and the metabolic syndrome, but investigations into the genetic contributions to pancreatic fat are limited. This genome-wide association study, comprised of 804 participants with MRI-assessed pancreatic fat measurements, was conducted in the ethnically diverse Multiethnic Cohort-Adiposity Phenotype Study (MEC-APS). Two genetic variants reaching genome-wide significance, rs73449607 on chromosome 13q21.2 (Beta = -0.67, P = 4.50x10-8) and rs7996760 on chromosome 6q14 (Beta = -0.90, P = 4.91x10-8) were associated with percent pancreatic fat on the log scale. Rs73449607 was most common in the African American population (13%) and rs79967607 was most common in the European American population (6%). Rs73449607 was also associated with lower risk of type 2 diabetes (OR = 0.95, 95% CI = 0.89–1.00, P = 0.047) in the Population Architecture Genomics and Epidemiology (PAGE) Study and the DIAbetes Genetics Replication and Meta-analysis (DIAGRAM), which included substantial numbers of non-European ancestry participants (53,102 cases and 193,679 controls). Rs73449607 is located in an intergenic region between GSX1 and PLUTO, and rs79967607 is in intron 1 of EPM2A. PLUTO, a lncRNA, regulates transcription of an adjacent gene, PDX1, that controls beta-cell function in the mature pancreas, and EPM2A encodes the protein laforin, which plays a critical role in regulating glycogen production. If validated, these variants may suggest a genetic component for pancreatic fat and a common etiologic link between pancreatic fat and type 2 diabetes.