1. Presence of “peripancreatic radiating thick-stands” on MDCT
a) Frequency
Positive finding in 13(76%) of 17 cases
b) Frequency in each 4 area (Fig.2)
(A: abdominal aorta,IVC: inferior vena cava,PV: portal vein,S: superior mesenteric artery)
The “peripancreatic radiating thick-strands” was seen at the anterior area in nine cases (69%),
the posterior in eight cases (62%),
the superior area in 10 cases (77%),
and at the posterior area in 13 cases (100%),
respectively.
The difference in detectability was mainly due to the amount of adipose tissues in the peripancreatic areas.
2. Correlation with pathological findings
The “peripancreatic radiating thick-strands” seen on MDCT was well correlated with the extrapancreatic carcinoma invasion with marked fibrotic thickening (icicle-like appearance) of adipose tissue septa,
including micro-vessels (Fig.3).
This pathological finding was confirmed in all of 13 cases with positive “peripancreatic radiating thick-strands”.
In addition,
minimum fibroses around the carcinoma invasion to the extrapancreatic adipose tissues was also identified,
pathologically.
On the other hand,
there were negative “peripancreatic radiating thick-strands” in 4 cases (24%).
Of these cases,
three showed minimum carcinoma invasion to the extrapancreatic adipose tissues with little fibrosis (Fig.4) and remaining one did not show carcinoma invasion to the extrapancreatic adipose tissues.
3. Clinical evaluation regarding the tumor recurrence
Positive recurrence* was identified in 10 (67%) of 15 cases who could be followed-up*.
* Soft tissue density lesion recurred at the surgical region,
showing interval progression and increase in values of tumor markers during follow-up periods.
4. Comparison to control cases
As control groups,
we retrospectively reviewed MDCT images in normal
cases of 20 cases and in autoimmune pancreatitis of 9 cases.
In normal control group,
there was no “peripancreatic radiating thick-strands” in all cases,
although thin and short (less than 1mm in length) -linear structures were identified at the peripancreatic areas (Fig.5-A).
In autoimmune pancreatitis (Fig.5-B),
the “peripancreatic radiating thick-strands” was seen in 3(33%) of 9 cases but these were relatively thin compared to those of pancreatic carcinoma.
*Case presentation*
Case.1
A 60-year-old man with pancreatic body-tail carcinoma.
On preoperative MDCT images (axial images; Fig.6-A,
coronal images: Fig.
6-B),
the “peripancreatic thick-strands appearance” (arrows) is seen around the pancreatic body-tail carcinoma (arrowheads).
Pathologically,
the extrapancreatic carcinoma invasion with micro-vessels and fibrotic thickening of adipose tissue septa is identified (Fig.6-C).
Case.2
A 63-year-old man with pancreatic body-tail carcinoma.
On preoperative MDCT images (axial,
coronal,
oblique sagittal images: Fig.
7-A),
the “peripancreatic thick-strands appearance” (arrowheads) is seen around the pancreatic body-tail carcinomas identified.
Pathologically,
the extrapancreatic carcinoma invasion with marked fibrotic thickening of adipose tissue septa is identified.
The immunestaining shows micro-vessels (arrow) without tumor cells,
which are positive endothelial marker (cytokeratin 7) and vascular endothelial marker (CD-34),
in fibrotic stroma of adipose tissue septa. However,
the tumor cells are found at adjacent lymphatics (arrowheads),
showing positive endothelial marker (cytokeratin 7) and lymphatic endothelial marker (D2-40).
<Discussion>
In this study,
the “peripancreatic radiating thick-strands” was identified in 13 (76%) of 17 patients with pancreatic body and tail carcinoma on MDCT.
This CT finding was correlated with the extrapancreatic carcinoma invasion with marked fibrotic thickening of adipose tissue septa,
including micro-vessels.
Tumor desmoplasia is one of the representative histopathological findings in pancreatic carcinoma.
Pancreatic stellate cells (PSCs) play an important role in the pathogenesis of pancreatic fibrosis in chronic pancreatitis and in carcinoma-associated desmoplastic reaction3,4).
Bachem et.al4) reported that (PSCs) were stimulated and proliferated by pancreatic caricinoma cells.
In their study,
high numbers of desmin and alfa-smooth muscle actin-positive cells were detected 96% in pancreatic carcinomas.
Carcinoma cell-induced activation of PSCs has the potential to lead to increased production of angiogenic factors3,5).
The resulting stimulation of new blood vessels formation in the stroma would encourage carcinoma progression by delivering nutrients and oxygen to carcinoma cells to promote local growth.
Therefore,
the “peripancreatic radiating thick-strands” reflecting the extrapancreatic carcinoma invasion with micro-vessels and fibrotic thickening of adipose tissue septa,
would be due to desmoplastic reaction and angiogensis caused by activated PSCs,
which means aggressive local invasiveness.