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Original Report |
1
Department of Radiology, D1, Osaka University Medical School. 2-2 Yamadaoka,
Suita City, Osaka 565-0871, Japan.
2
Department of Surgery and Clinical Oncology, Osaka University Medical School,
2-2 Yamadaoka, Suita City, Osaka 565-0871, Japan.
3
Department of Surgical Oncology, Osaka University Medical School, Suita City,
Osaka 565-0871, Japan.
4
Department of Pathology, Osaka City University Medical School, Suita City,
Osaka 565-0871, Japan.
Received November 2, 2000;
accepted after revision February 22, 2001.
Address correspondence to T. Kim.
Abstract
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CONCLUSION. When histologic fibrosis is uniformly present through the pancreas in patients with chronic pancreatitis, there is no demarcation of masses due to chronic pancreatitis. When there is a greater degree of histologic fibrosis in the masslike part of the pancreas, the mass is often demarcated from the remaining pancreas, and the enhancement pattern on two-phase helical CT and dynamic gadolinium-enhanced MR imaging mimics that of pancreatic adenocarcinoma.
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The purpose of this study was to clarify helical CT and MR imaging features of pancreatic mass due to chronic pancreatitis and to correlate these features with pathologic findings.
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All seven patients underwent two-phase helical CT (HiSpeed Advantage; General Electric Medical Systems, Milwaukee, WI) of the pancreas. After we obtained unenhanced CT scans, the pancreatic and portal venous phase helical CT scans were obtained respectively, starting 35 and 70 sec after the initiation of IV injection of 100 mL of noniodinated 300 mg I/mL iohexol (Omnipaque 300; Daiichi Pharmaceutical, Tokyo, Japan) at a rate of 3 mL/sec. Each helical scan was obtained with a single 20- to 25-sec breath-hold with a slice collimation of 5 mm and a table pitch of 1:1.
Six patients (Table 1) underwent MR imaging with a 1.5-T superconducting unit (Signa Advantage or Horizon; General Electric Medical Systems). For the unenhanced study, T1-weighted spin-echo images (TR/TE, 600/28) with and without fat-suppression technique and T2-weighted spin-echo images (2000/80) were acquired. For the dynamic study, fast spoiled gradient-recalled acquisition in the steady state sequence (12.8/2.6; flip angle, 30°; or 6.2/1.4; flip angle, 40°) was used with the three-dimensional Fourier transformation technique. After obtaining unenhanced images, we obtained pancreatic phase images, starting 30 sec after the initiation of IV bolus injection of 0.1 mmol/kg of gadopentetate dimeglumine (Magnevist; Nihon Schering, Osaka, Japan). Portal venous and late phase images were obtained starting 60 and 90 sec later, respectively.
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Both CT and MR imaging were performed less than 2 months before surgery or biopsy. Surgical excision involved a Whipple procedure for one of the four patients with a pancreatic mass in the pancreatic head and pylorus-preserving duodenopancreatectomy for the other three patients. Excision of the pancreatic body and tail was performed in one patient who had a pancreatic mass in that region.
Two experienced abdominal radiologists retrospectively reviewed the CT scans and MR images of the seven patients for the imaging findings, including attenuation, signal intensity, and calcifications of the mass and pancreas, pancreatic duct dilatation, and bile duct dilatation, and reached a consensus. The attenuation on CT scans and the signal intensity on MR images of the pancreatic mass due to chronic pancreatitis were compared with those of the nonenlarged portion of the pancreas in each patient.
For the five patients who underwent surgical resection of the pancreatic mass, the pathologic findings in the tissues of the pancreatic mass due to chronic pancreatitis and in the tissues of the nonenlarged portion of the resected pancreas were assessed by an experienced pathologist without knowledge of CT and MR imaging findings. The pathologist examined the histopathologic specimens for pathologic changes and rated the degree of fibrosis, infiltration of lymphocytes, and reduction of glandular elements on a 4-point scaleabsent, mild, moderate, and severefor both the pancreatic mass and the nonenlarged portion of the pancreas. In the two patients who underwent tumor biopsy, only the pathologic findings for the tissues of the pancreatic mass were assessed.
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Four pancreatic masses showed isoattenuation on all CT scans and isointensity on all MR images, relative to the nonenlarged portion of the pancreas (Table 1 and Fig. 3A,3B,3C,3D), and these masses were not clearly demarcated from the nonenlarged portions of the pancreas on any of the CT scans or MR images. The other three masses exhibited hypoattenuation relative to the nonenlarged portion of the pancreas on pancreatic phase CT scans and were visibly demarcated from the nonenlarged portions (Figs. 1A,1B,1C,1D,1E,1F and 2A,2B), although they showed isoattenuation on unenhanced and portal venous phase CT scans. Two of the three demarcated masses underwent MR imaging. One demarcated mass showed isointensity on T1-weighted spin-echo MR images and hypointensity on T2-weighted spin-echo MR images (Fig. 1A,1B,1C,1D,1E,1F), relative to the nonenlarged portion of the pancreas. The other demarcated mass revealed hypointensity on T1-weighted spin-echo MR images and heterogeneous mixed intensity composed of hypo- to hyperintensity on T2-weighted spin-echo MR images (Fig. 2A,2B). These masses showed hypointensity relative to the nonenlarged portion of the pancreas on the pancreatic phase images of dynamic MR imaging and were visibly demarcated from the nonenlarged portions (Figs. 1A,1B,1C,1D,1E,1F and 2A,2B), although the masses showed isointensity on portal venous and late phase images.
Fibrosis, infiltration of lymphocytes, and reduction of glandular elements of the pancreas were pathologically observed in the pancreatic mass due to chronic pancreatitis in all seven patients. Table 2 shows the degree of pathologic changes in the pancreatic masses due to chronic pancreatitis and in the nonenlarged portion of the pancreas in the five patients who underwent surgical resection of the pancreatic masses. Various degrees of fibrosis, infiltration of lymphocytes, or reduction of glandular elements of the pancreas were observed in the pancreatic masses of all five patients (Figs. 1A,1B,1C,1D,1E,1F,2A,2B,3A,3B,3C,3D). Reduction of the glandular elements of the pancreas was observed in the nonenlarged portions of the pancreata in the five patients who underwent surgery. Mild-to-moderate fibrosis in the nonenlarged portion of the pancreas was observed in the three patients with the nondemarcated masses on CT scans or MR images (Fig. 3A,3B,3C,3D), whereas fibrosis was not observed in the nonenlarged portion of the pancreata in the two patients with demarcated masses (Fig. 1A,1B,1C,1D,1E,1F).
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Two-phase helical CT and dynamic MR imaging have been reported useful for detecting and characterizing pancreatic tumors [9,10,11,12]. Pancreatic ductal adenocarcinoma is usually hypovascular and appears as a hypoenhanced lesion relative to surrounding pancreatic parenchyma on pancreatic phase images of helical CT and on dynamic MR imaging [9, 10]. On the other hand, islet cell tumors and acinar cell carcinomas are usually hypervascular, and these tumors appear as hyperenhanced lesions on such images [12].
Johnson and Outwater [11] found that masses of pancreatic carcinoma and those due to chronic pancreatitis showed more gradual progressive enhancement on dynamic MR imaging than did normal pancreatic parenchyma, and they histologically found abundant fibrosis in both pathologic conditions, which was thought to account for the similar imaging appearances of the two kinds of masses. However, they did not assess enhancement or histology of pancreatic parenchyma other than that of masses due to chronic pancreatitis. In our experience, demarcation of a pancreatic mass is more suggestive of a mass due to pancreatic neoplasm, including pancreatic carcinoma, than of a mass due to chronic pancreatitis. It is, therefore, important to compare enhancement and histologic changes in a mass due to chronic pancreatitis with those in a nonenlarged portion of the pancreas.
Our results revealed two different enhancement patterns in pancreatic masses due to chronic pancreatitis as seen on two-phase helical CT and on dynamic MR imaging: pancreatic masses due to chronic pancreatitis appeared as hypoenhanced demarcated masses or as isoenhancing nondemarcated masses on pancreatic phase images. The two different enhancement patterns in masses due to chronic pancreatitis might be explained by the difference in the degree of fibrosis between the mass and the nonenlarged portion of the pancreas. Fibrosis was pathologically identified in the nonenlarged portion of the pancreas in patients with nondemarcated masses on CT scans or MR images, whereas fibrosis was not found in the nonenlarged portion of the pancreas in patients with demarcated masses. Fibrosis is one of the main pathologic changes characteristic of chronic pancreatitis [2]. Therefore, when chronic pancreatitis occurs focally, the inflammatory mass is visibly demarcated on CT scans or on MR images. On the other hand, when chronic pancreatitis occurs throughout the pancreas, the mass is not demarcated.
It is thought that the hypoenhanced and demarcated pancreatic mass due to chronic pancreatitis on pancreatic phase contrast-enhanced helical CT or MR imaging is not distinguishable from pancreatic carcinoma, whereas the isoenhanced and nondemarcated masses may be distinguishable from hypovascular pancreatic adenocarcinoma or other hypervascular pancreatic tumors. However, histologic examination or close interval follow-up is needed for such isoenhanced and nondemarcated pancreatic masses. Tumor-free pancreatic parenchyma located proximally to a pancreatic carcinoma obstructing the pancreatic duct may undergo atrophy and fibrosis and thus may show the same gradual enhancement pattern as pancreatic carcinoma [11], whereas pancreatic carcinoma located in the pancreatic head may show isoenhancement and no demarcation.
In conclusion, two different enhancement patterns on two-phase helical CT and dynamic MR imaging were identified in masses due to chronic pancreatitis. When histologic fibrosis is uniformly present through the gland in patients with chronic pancreatitis, there is no demarcation of masses due to chronic pancreatitis. When there is a greater degree of histologic fibrosis in the masslike part of the gland, the mass is often demarcated from the remaining pancreas, and the enhancement pattern on two-phase helical CT and dynamic gadolinium-enhanced MR imaging mimics that of pancreatic adenocarcinoma. Further work is needed to improve the rate of correct diagnosis of masses due to chronic pancreatitis.
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