Arthur Peter Wunderlich1,2, Stephan Kannengießer3, Lena Kneller1, Berthold Kiefer3, Holger Cario4, Meinrad Beer1, and Stefan Andreas Schmidt1
1Dept. for Diagnostic and Interventional Radiology, Ulm University, Medical Center, Ulm, Germany, 2Section for Experimental Radiology, Ulm University, Medical Center, Ulm, Germany, 3Siemens Healthcare GmbH, Erlangen, Germany, 4Dept. for Pediatric and Adolescent Medicine, Ulm University, Medical Center, Ulm, Germany
Synopsis
To study pancreatic iron accumulation in liver
overloaded patients in relation to hepatic and splenic iron content, 90 patients
were investigated at 1.5 T MRI with a prototype breath hold volumetric 3D GRE sequence with
in-line R2* calculation. Mean R2* values were determined
in liver, spleen and pancreas by manually drawn ROIs. Pancreatic R2*
values were related to hepatic and splenic R2* by multiple linear
regression, yielding significant correlation in two subgroups: a) frequently
transfused patients, and b) regular transfused patients. Correlation, and
therefore, ability to predict pancreatic R2*, improved by including splenic R2*
compared to solely hepatic R2*.
Purpose
To study pancreatic iron accumulation in relation
to hepatic and splenic iron in iron overloaded patients, divided in subgroups
according to transfusion frequency.Methods
89 patients (41 f, 48 m, age range 2 to 60 years,
mean ± SD: 19.9 ± 13.7 years) suspected for liver iron overload were
investigated with 1.5 T MRI (MAGNETOM Avanto, Siemens Healthcare, Erlangen, Germany) in a study approved by our local ethics
committee.
Patients after splenectomy were excluded from this study. By means of a breath hold
3D GRE protocol, fifty-six transversal partitions of 4 mm thickness (no gap) at
2.5x2.5 mm voxel size were acquired at minimum TE and TE spacing of 1.2 ms for
the first five echoes (TE=1.2 to 6 ms), while a sixth echo was acquired at TE
of 9 ms. CAIPIRINHA technique (Controlled Aliasing In Parallel Imaging Results
IN Higher Acceleration) 1 was used with an acceleration factor of three
to enable acquisition in a single breath hold of 13 sec. The prototype implementation
of this sequence determined R2* in-line for each voxel, accounting
for signal modulation by fat/water-dephasing 2. To obtain mean
hepatic, splenic and pancreatic R2* values for each patient, three
regions of interest (ROI) were manually placed in tissue free of vessels and artifacts
of each organ. Patients were divided into four subgroups according to transfusion
frequency: 1) no transfusion, 2) frequent transfusion, 3) regular transfusion,
and 4) after bone marrow transplant (condition after transfusion). Multiple
linear regression parameters, i.e. coefficient of determination R2,
slope and intercept of splenic and hepatic R2* vs. pancreatic R2* were determined,
and linear regression was tested for significance. For comparison, linear
regression between solely hepatic and pancreatic R2* was also evaluated.
Finally, accuracy of pancreatic R2* calculation based on hepatic and splenic
R2* was evaluated.Results
In group 1 of patients with no transfusion (13
patients), we found splenic R2* values between 15 and 39 s-1 with
two exceptions (78 and 110 s-1), pancreatic R2* varied between 18 to
41 s-1, while hepatic R2* ranged up to 486 s-1. No significant
correlation of splenic and hepatic R2* vs. pancreatic R2* was found (p >
0.05). A highly significant correlation (R2=0.83, p<0.001) of pancreatic R2*
(14-80 s-1) vs. liver R2* (32-750 s-1) and splenic
R2* (39-469 s-1) was observed in group 2 of frequently transfused
patients (11 patients). For regular transfused patients (group 3, 51 patients),
pancreatic R2* values of 16-496 s-1, hepatic R2*
of 36-930 s-1 and splenic R2* between 12 and 381 s-1 were
found with a moderate correlation (R2 = 0.41, p < 0.001). In
patients with previous blood transfusions (group 4, 14 patients), pancreatic R2*
was below 67 s-1 with two exceptions, independent of hepatic R2*
(104-790 s-1) and splenic R2* (58-634 s-1; p > 0.05).
Compared to relationship of pancreatic R2* with merely hepatic R2* in group 2
and 3, correlation improved when incorporating splenic R2*, cf. Table 1. In sporadic
and frequently transfused patients, analysis of linear correlation between
liver and pancreas yielded R2=0.66 and p=0.002, in the group
receiving regular transfusion we got R2=0.37 at p<0.001. Linear
correlation between pancreatic and only splenic R2*, shown in Table 1, was even
worse.
For a scatterplot of pancreatic R2* values calculated based on hepatic
and splenic R2* and the associated regression line, refer to Fig. 1.Discussion
Pancreatic R2*, reflecting
pancreatic iron accumulation, is an important clinical parameter. Yet, a
correlation to exocrine and endocrine function has not been proven. R2* can be determined
with 3D Multi-GRE imaging and in line R2* calculation, but, due to its anatomy, it is challenging to
get reliable pancreatic values. This is much easier in spleen and
liver. We proposed a method which allows to estimate pancreatic R2*, and
thereby pancreatic iron content, from hepatic and splenic R2*. Yet, reliable
results can be achieved only in the group of frequently transfused patients,
suffering from leukemia (n=4), anemia (n=4), or MDS (n=3).
Further
studies are needed to evaluate probable relation of pancreatic R2*
to its exocrine and endocrine function. Furthermore, in analogy to 3,
it may be evaluated whether cardiac R2*, which can be determined directly, but
requires lengthy MR procedures due to heart motion, can be calculated from R2*
values obtained in spleen and liver.Acknowledgements
No acknowledgement found.References
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