Manuel Taso1, Koenraad J Mortele1, Fotini Papadopoulou1, Martin P Smith1, and David C Alsop1
1Division of MRI research, Radiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boson, MA, United States
Synopsis
Being able to non-invasively monitor pancreatic perfusion changes
is essential for its clinical translation, but it can also prove useful in the
evaluation of endocrine disorders such as diabetes. While some perfusion
modification following a glucose challenge was observed with PET, ASL has not
yet succeeded. We propose here an investigation of pancreatic perfusion
modulation following an oral glucose challenge with background-suppressed pCASL
at 3T, highlighting perfusion modulation that could be linked to pancreatic
endocrine function.
Such paradigm could either serve as a tool for studying
endocrine disorders or provide a glucose-enhanced scan that increases SNR for
diagnostic purposes.
Introduction
Non-invasive pancreatic perfusion assessment with ASL has
recently become feasible1,2 and may prove useful for
studying endocrine disorders such as diabetes mellitus. PET-based studies have
reported a significant pancreatic perfusion increase after endocrine
stimulation by glucose challenge3 that might be linked to
dynamics of insulin secretion and release in the bloodstream. Such observations have not yet been made with
ASL4, however, potentially because
of signal instabilities and/or insufficient sensitivity. Therefore, we performed
an investigation of pancreas perfusion modulation following a glucose challenge
with a background-suppressed pCASL sequence on a 3T scanner. Such a paradigm could
either serve as a tool for studying endocrine disorders or just provide a
glucose-enhanced scan of the pancreas that increases SNR for diagnostic
purposes. Material and Methods
Thirteen fasting (4 hours
minimum) healthy volunteers (9F/4M, 32±7y, BMI=26±4kg/m2) were scanned
at 3T (Discovery MR750, GE Healthcare) with a 32-ch body array coil.
A first pilot scan was performed
including fat-suppressed 3D T1-w GRE and T2-w SSFSE to
locate the pancreas, as well as an ASL measurement to estimate baseline
perfusion.
As an exploratory study, we
investigated different glucose stimuli including:
- Oral
absorption of commercially available grape juice (N=7)
-
Over
the counter glucose tablets (N=3)
- Over
the counter glucose gel (N=3)
The glucose quantity was of ≈24mg
for the fruit juice and glucose gel and ≈12g for the tablet due to practical
constraints.
Upon completion of glucose
administration, the same single-slice ASL was acquired for 2min followed by
2min breaks over 20min for the fruit-juice group (N=7) or 30min for tablets/gel
(7 time points, Fig1).
All ASL data were acquired with a
background-suppressed pCASL preparation with a single axial slice SSFSE readout
(TR/TE=6000/40ms, 128x128 matrix, 10-mm slice thickness) as described
previously5, using a $$$\tau$$$=1.5s
labeling duration followed by w=1.5s post-labeling delay. A
synchronized-breathing approach was used. Three reference images (PD-w and 2-IR
for M0/T1 estimation) were acquired at the beginning of
each sequence followed by either 14 (baseline) or 7 (post-stimulation) ASL
pairs.
All images were reconstructed on
the scanner. We looked at both absolute ASL-derived pancreatic blood-flow (PBF) temporal evolution at each time point and relative compared to the baseline perfusion to assess the temporal dynamics of perfusion modulation following glucose intake. To do so, the PBF was quantified using a standard
kinetic model for continuous ASL6, with a labeling efficiency of $$$\alpha$$$=0.6, $$$\lambda$$$=0.9, T1,b=1.66s, M0,t/T1,t estimated from the reference scans and a transit-time $$$\delta$$$=1.03s2:
$$$dM=2M_t^0\alpha T_{1,t}PBFe^{-\delta/T_{1,b}}(e^{-max(w-\delta,0)/T_{1,t}}-e^{-max(\tau+w-\delta,0)/T_{1,t}})/\lambda$$$
Results and Discussion
Baseline ASL perfusion values were in the range of those previously
reported2,7, with an average blood-flow
of 200±60mL/100g/min, ranging from 135 to 305 mL/100g/min, showing significant
variability. We noticed a positive correlation (Pearson’s $$$\rho$$$=0.7) between BMI and
baseline perfusion that might partially explain this variability.
Following glucose stimuli, a blood-flow increase was systematically
observed as seen in Figure 2 and illustrated on one case in Figure 3 (on
average +31%). Interestingly, the relative perfusion change with regards to
baseline flow seems to follow a marked biphasic pattern; insulin secretion
following glucose challenge has been shown to follow a biphasic pattern in
animal and human experiments. A negative correlation was found ($$$\rho$$$=-0.68) between baseline
perfusion and maximal relative increase.
Although a single-ROI encompassing the whole gland was used
for quantification, visual inspection shows an interesting enhancement
predominantly in the tail at later timepoints. Conclusions
This study shows that our background-suppressed pCASL
implementation is sufficiently sensitive to detect blood-flow changes in the
pancreas induced by a glucose challenge. This might be an interesting and very
practical paradigm for enhanced SNR of pancreas ASL perfusion in a clinical
setting, especially knowing that the actual glucose dose remains low (1/3rd
of what is given to suspected diabetic patients in a glucose-tolerance test). Further
comparisons of the glucose administration methods and the corresponding blood
glucose and insulin curves is planned, as well as investigation of the dose
effect.
A standardized protocol for reproducible stimulation could
provide some new insights into pancreatic functional alterations encountered in
type 2 diabetes throughout the different stages of the disease, especially at
pre-diabetic stages for which the diagnosis and evolution assessment remains
problematic. With 113 million adults in the US suffering from pre-diabetes or
diagnosed type 2 diabetes, non-invasive pancreatic endocrine function
assessment with ASL can potentially have tremendous clinical impact. Acknowledgements
No acknowledgement found.References
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