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(Radiology. 1999;212:213-218.)
© RSNA, 1999


Gastrointestinal Imaging

Pancreatic Carcinoma versus Chronic Pancreatitis: Dynamic MR Imaging1

Pamela T. Johnson, MD and Eric K. Outwater, MD

1 From the Department of Radiology, Thomas Jefferson University Hospital, 132 S 11th St, 7th Floor Main Bldg, Philadelphia, PA 19107. From the 1997 RSNA scientific assembly. Received May 21, 1998; revision requested July 14; revision received October 9; accepted December 16. Address reprint requests to P.T.J. (e-mail: johnson5@jeflin.tju.edu).


    Abstract
 TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
PURPOSE: To determine if dynamic gadolinium-enhanced magnetic resonance (MR) imaging can distinguish chronic pancreatitis from pancreatic carcinoma.

MATERIALS AND METHODS: A retrospective review of MR and pathology examination findings was performed for 24 patients with pancreatic ductal adenocarcinoma and seven with chronic pancreatitis who underwent dynamic gadolinium-enhanced breath-hold spoiled gradient-echo imaging. Arterial, portal, and delayed phase images were obtained after injection of gadopentatate dimeglumine. The MR images of 14 patients without clinical evidence of pancreatic disease were also reviewed as controls. Signal intensity (SI) was measured on the precontrast (pre) and gadolinium-enhanced (post) images of the area of the pancreas sampled at biopsy and of the nontumorous pancreas. Percentage enhancement was defined as SIpre/SIpost x 100.

RESULTS: Normal pancreas showed rapid enhancement that peaked in the arterial or portal phase. For both diseases, T1-weighted images showed hypointense masses with progressive enhancement (differences were significant [P < .05] on only delayed fat-saturated images). Differences in enhancement between either disease state and normal pancreas were significant for at least one phase. Nontumorous pancreas in patients with carcinoma showed gradual enhancement that was significantly different from that of normal pancreas.

CONCLUSION: Chronic pancreatitis and pancreatic carcinoma show abnormal pancreatic enhancement, but the two were not distinguished on the basis of degree and time of enhancement.

Index terms: Pancreas, MR, 77.121411, 77.121412, 77.121415, 77.12143 • Pancreas, neoplasms, 77.321 • Pancreatitis, 77.291


    Introduction
 TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Advances in technology for magnetic resonance (MR) imaging and computed tomography (CT) have improved the ability to detect pancreatic carcinoma (14). Findings in several studies have suggested that MR imaging may be superior to CT in pancreatic lesion detection and preoperative staging (5,6). However, chronic pancreatitis remains difficult to distinguish from pancreatic carcinoma on the basis of imaging criteria because both demonstrate low signal intensity on T1-weighted images and are associated with ductal obstruction (7,8).

A recent study compared images of the pancreas obtained with dynamic gadolinium-enhanced fast multiplanar spoiled gradient-echo (GRE), T1- and T2-weighted spin-echo (SE), and gadolinium-enhanced T1-weighted SE sequences. Dynamic gadolinium-enhanced multiplanar fast spoiled GRE images were found to result in more accurate and specific diagnoses of pathologic conditions in the pancreas (2). The purpose of this study was to determine if the contrast enhancement pattern on dynamic gadolinium-enhanced multiplanar fast spoiled GRE images of the pancreas could distinguish masses due to chronic pancreatitis from those due to pancreatic carcinoma.


    MATERIALS AND METHODS
 TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
A computer search identified 145 MR imaging examinations performed between 1992 and 1996 at our institution in which a pancreatic mass was detected. In 43 patients, pathologic confirmation of the diagnosis was obtained by means of ultrasonography (US)-guided biopsy, intraoperative biopsy, or resection of the pancreatic mass. Twelve of these 43 patients were excluded because the original MR imaging archive could not be retrieved, no intravenous contrast material was administered, an inadequate arterial bolus was used, the MR imaging protocol varied from the standard dynamic breath-hold fast multiplanar spoiled GRE sequence, or the mass could not be defined and measured when the image was reviewed. Of the remaining 31 patients, 24 (13 men and 11 women; age range, 52–77 years; mean age, 66 years) had pancreatic carcinoma and seven (five men and two women; age range, 46–66 years; mean age, 55 years) had chronic pancreatitis.

The diagnosis of pancreatic carcinoma was confirmed at surgical excision of the mass by means of a Whipple procedure in seven of the 24 patients. Intraoperative biopsy was performed in 12 patients with unresectable tumors. The remaining five patients underwent US-guided fine-needle aspiration (n = 4) or core biopsy (n = 1); their tumors were deemed unresectable at preoperative imaging.

In the seven patients with the diagnosis of chronic pancreatitis, the pathologic correlation was obtained by means of US-guided fine-needle aspiration (n = 2), surgical resection of the mass (n = 1), or intraoperative biopsy (n = 4). Two of the patients who underwent intraoperative biopsy also underwent fine-needle aspiration or pancreatic duct brushing. Findings at follow-up (range, 3–17 months) MR imaging, CT, or endoscopic retrograde cholangiopancreatography confirmed no change in two patients. Two patients underwent follow-up MR imaging that depicted enlargement of the mass, but no further biopsies were performed. Three patients did not undergo follow-up imaging.

Fourteen patients who underwent dynamic imaging of the liver for indications unrelated to pancreatic disease served as control subjects. Their examinations were performed to evaluate hemangioma, fatty liver, or parenchymal liver disease.

All examinations were performed on a 1.5-T system (GE Medical Systems, Milwaukee, Wis). The following parameters were used in the multiplanar fast spoiled GRE sequence: repetition time msec/echo time msec, 100–170/1.3–2.9; flip angle, 90°; matrix, 256 x 128 to 256 x 192; one signal acquired; section thickness, 7–9 mm; gap, 1–2 mm; field of view, 24–38 cm. Gadopentatate dimeglumine (Magnevist; Berlex Laboratories, Wayne, NJ) was administered (0.1 mmol/L per kilogram of body weight) intravenously at approximately 2 mL/sec by means of hand injection followed by a 20-mL saline solution flush. Imaging was initiated after 10 mL of the flush had been infused.

Imaging was performed with four breath-hold gadolinium-enhanced sequences in most patients. These sequences correlated approximately with arterial dominant (n = 45), portal venous (n = 45), parenchymal (n = 38), and delayed (n = 42) phases of contrast enhancement. Eight patients with pancreatic cancer underwent imaging with only three gadolinium-enhanced sequences (only one delayed sequence was performed). Five of the eight patients did not undergo imaging with the third gadolinium-enhanced sequence, and three did not undergo imaging with the final delayed fat-saturated sequence. All seven of the patients with chronic pancreatitis underwent imaging with all four sequences.

During review of each case, an adequate bolus was confirmed on the basis of the presence of a moiré pattern in the spleen, absence of hepatic vein contrast enhancement, and corticomedullary differentiation of the kidneys. On the basis of these criteria, two patients were excluded because of an inadequate bolus. The final delayed fat-saturated sequence usually required two breath holds.

The original MR imaging data were loaded onto a workstation (Cannon; Sun Microsystems, Palo Alto, Calif) by means of software (RATIONAL IMAGING; Intuitive Software, West Hills, Calif). Each study was reviewed with the pathology report and US-guided biopsy report or intraoperative note to confirm the location of the mass sampled at biopsy. In the patients with pancreatic carcinoma or chronic pancreatitis, the largest possible region of interest was drawn when the signal intensity of the mass or the nontumorous pancreas was measured proximal to tumor. In the control subjects, region-of-interest measurements were obtained from the pancreatic head and body or tail. The signal intensity was measured on the precontrast and gadolinium-enhanced multiplanar fast spoiled GRE images (n = 31). All regions of interest were placed by one author (P.T.J.).

Percentage enhancement values for the pancreatic mass, nontumorous pancreas, and normal pancreas were calculated by dividing the gadolinium-enhanced signal intensity by the precontrast signal intensity and multiplying by 100. A Student two-tailed t test was performed to compare the percentage enhancement of carcinoma, nontumorous pancreas proximal to tumor, chronic pancreatitis, and normal pancreas.


    RESULTS
 TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
The normal pancreas enhanced rapidly after infusion of gadopentatate dimeglumine and remained enhanced on the portal venous and first delayed images (Fig 1). The percentage enhancement of the normal pancreatic head peaked on the arterial dominant or portal venous phase images. The percentage enhancement of the pancreatic body did not differ significantly from that of the head.



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Figure 1. Bar graph depicts mean percentage enhancement after injection of gadopentatate dimeglumine for normal pancreas in control subjects (black bars), chronic pancreatitis (gray bars), and pancreatic cancer (dotted black bars). Error bars represent mean plus or minus SD. The series represents the percentage enhancement before injection of gadopentatate dimeglumine (Pre Gad) and after injection in the arterial (Post #1), portal venous (Post #2), parenchymal(Post #3), or delayed (Post #4) phases. In the normal pancreas, the percentage enhancement peaks in the arterial dominant or portal venous phase. Pancreatic carcinoma and chronic pancreatitis demonstrate more gradual enhancement.

 
Twenty-four of the patients had biopsy-proved pancreatic carcinoma (mean transverse diameter, 3.2 cm ± 1.2). Seventeen masses were located in the pancreatic head, two in the uncinate process, and five in the pancreatic body. After infusion of gadopentatate dimeglumine, these masses showed gradual progressive enhancement (Fig 2). The percentage enhancement was statistically different from normal on the second (P = .015), third (P = .001), and delayed fat-saturated (P < .001) gadolinium-enhanced images (Fig 1).



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Figure 2a. Contrast enhancement of pancreatic carcinoma. (a) Reconstructed MR cholangiogram (1,2000/255) depicts distal obstruction of the common bile duct (straight arrows) and pancreatic duct (curved arrow) with ductal dilatation due to a pancreatic adenocarcinoma near the ampulla. (b, c) T1-weighted GRE images (155/2.2) were obtained (b) before injection of gadopentatate dimeglumine and (c) during the arterial phase of contrast enhancement. In c, enhancement of the tumor (arrow) is less than that of normal pancreatic parenchyma (arrowheads). (d) Photomicrograph shows extensive fibrosis (F) throughout the tumor, which borders normal pancreatic parenchyma (N).

 


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Figure 2b. Contrast enhancement of pancreatic carcinoma. (a) Reconstructed MR cholangiogram (1,2000/255) depicts distal obstruction of the common bile duct (straight arrows) and pancreatic duct (curved arrow) with ductal dilatation due to a pancreatic adenocarcinoma near the ampulla. (b, c) T1-weighted GRE images (155/2.2) were obtained (b) before injection of gadopentatate dimeglumine and (c) during the arterial phase of contrast enhancement. In c, enhancement of the tumor (arrow) is less than that of normal pancreatic parenchyma (arrowheads). (d) Photomicrograph shows extensive fibrosis (F) throughout the tumor, which borders normal pancreatic parenchyma (N).

 


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Figure 2c. Contrast enhancement of pancreatic carcinoma. (a) Reconstructed MR cholangiogram (1,2000/255) depicts distal obstruction of the common bile duct (straight arrows) and pancreatic duct (curved arrow) with ductal dilatation due to a pancreatic adenocarcinoma near the ampulla. (b, c) T1-weighted GRE images (155/2.2) were obtained (b) before injection of gadopentatate dimeglumine and (c) during the arterial phase of contrast enhancement. In c, enhancement of the tumor (arrow) is less than that of normal pancreatic parenchyma (arrowheads). (d) Photomicrograph shows extensive fibrosis (F) throughout the tumor, which borders normal pancreatic parenchyma (N).

 


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Figure 2d. Contrast enhancement of pancreatic carcinoma. (a) Reconstructed MR cholangiogram (1,2000/255) depicts distal obstruction of the common bile duct (straight arrows) and pancreatic duct (curved arrow) with ductal dilatation due to a pancreatic adenocarcinoma near the ampulla. (b, c) T1-weighted GRE images (155/2.2) were obtained (b) before injection of gadopentatate dimeglumine and (c) during the arterial phase of contrast enhancement. In c, enhancement of the tumor (arrow) is less than that of normal pancreatic parenchyma (arrowheads). (d) Photomicrograph shows extensive fibrosis (F) throughout the tumor, which borders normal pancreatic parenchyma (N).

 
Seven masses were pathologically proved chronic pancreatitis (mean transverse diameter, 3.3 cm ± 1.7). All seven were located in the pancreatic head. After infusion of gadopentatate dimeglumine, these masses showed a more gradual enhancement compared with that of the normal pancreas (Fig 3), with peak enhancement on the third gadolinium-enhanced series (Fig 1). The percentage enhancement was statistically different from normal on the delayed fat-saturated gadolinium-enhanced images (P = .01).



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Figure 3a. Contrast enhancement of chronic pancreatitis. (a–c) T1-weighted GRE images (140/2.5) were obtained (a) before injection of gadopentatate dimeglumine and during the (b) arterial and (c) portal venous phases of contrast enhancement. b and c depict only slight enhancement of the pancreatic head mass (arrow). (d) Photomicrograph shows extensive fibrosis (F) throughout the chronic pancreatitis.

 


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Figure 3b. Contrast enhancement of chronic pancreatitis. (a–c) T1-weighted GRE images (140/2.5) were obtained (a) before injection of gadopentatate dimeglumine and during the (b) arterial and (c) portal venous phases of contrast enhancement. b and c depict only slight enhancement of the pancreatic head mass (arrow). (d) Photomicrograph shows extensive fibrosis (F) throughout the chronic pancreatitis.

 


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Figure 3c. Contrast enhancement of chronic pancreatitis. (a–c) T1-weighted GRE images (140/2.5) were obtained (a) before injection of gadopentatate dimeglumine and during the (b) arterial and (c) portal venous phases of contrast enhancement. b and c depict only slight enhancement of the pancreatic head mass (arrow). (d) Photomicrograph shows extensive fibrosis (F) throughout the chronic pancreatitis.

 


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Figure 3d. Contrast enhancement of chronic pancreatitis. (a–c) T1-weighted GRE images (140/2.5) were obtained (a) before injection of gadopentatate dimeglumine and during the (b) arterial and (c) portal venous phases of contrast enhancement. b and c depict only slight enhancement of the pancreatic head mass (arrow). (d) Photomicrograph shows extensive fibrosis (F) throughout the chronic pancreatitis.

 
The pattern of gradual enhancement of chronic pancreatitis and cancer was similar. However, a statistically significant difference was detected between the two pathologic conditions when the percentage enhancement was compared on the delayed fat-saturated images (P = .04). Considerable overlap was noted when peak percentage enhancement was compared between masses due to chronic pancreatitis or pancreatic cancer. Of the seven masses due to chronic pancreatitis, peak percentage enhancement occurred during the portal venous phase in one, parenchymal phase in four, and delayed phase in two. Of the 24 masses due to pancreatic carcinoma, peak percentage enhancement occurred during the portal venous phase in five, parenchymal phase in four, and delayed phase in 15.

In the setting of a pancreatic head carcinoma, the nontumorous pancreatic body or tail (n = 19) showed gradual progressive enhancement after administration of gadopentatate dimeglumine that peaked on the delayed fat-saturated images (Fig 4). The percentage enhancement of the body or tail was significantly different from that of the normal pancreatic body on the portal venous phase (P = .003), parenchymal (P = .005), and delayed fat-saturated (P < .001) gadolinium-enhanced images. The nontumorous body and tail demonstrated a decreased precontrast signal intensity (Fig 5), which accounted in part for the differences in percentage enhancement.



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Figure 4. Bar graph depicts mean percentage enhancement after injection of gadopentatate dimeglumine in the normal pancreas of control patients (black bars) and nontumorous portion of the pancreas in patients with pancreatic carcinoma (gray bars). The series represents the percentage enhancement before injection of gadopentatate dimeglumine (Pre Gad) and after injection during the arterial (Post #1), portal venous (Post #2), parenchymal (Post #3), and delayed (Post #4) phases. The nontumorous pancreas demonstrates gradually increasing enhancement over time that is significantly different from that of normal pancreas ({star} = P < .005) and peaks on the delayed fat-saturated image (Post #4). Error bars represent mean plus or minus SD.

 


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Figure 5a. Enhancement of chronic pancreatitis due to obstructing pancreatic head carcinoma. (a) Gadolinium-enhanced T1-weighted GRE image shows the pancreatic carcinoma (arrow) in the head of the pancreas. (b–d) In the same patient, T1-weighted GRE images (115/2.2) of the pancreatic body and tail obtained (b) before injection of gadopentatate dimeglumine and after injection during the (c) arterial and (d) portal venous phases of enhancement. Enhancement of the pancreatic parenchyma (arrows) is lower than that of the normal pancreas. In c, the dilated pancreatic duct appears as a beaded low-signal-intensity structure in the parenchyma of the body and tail.

 


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Figure 5b. Enhancement of chronic pancreatitis due to obstructing pancreatic head carcinoma. (a) Gadolinium-enhanced T1-weighted GRE image shows the pancreatic carcinoma (arrow) in the head of the pancreas. (b–d) In the same patient, T1-weighted GRE images (115/2.2) of the pancreatic body and tail obtained (b) before injection of gadopentatate dimeglumine and after injection during the (c) arterial and (d) portal venous phases of enhancement. Enhancement of the pancreatic parenchyma (arrows) is lower than that of the normal pancreas. In c, the dilated pancreatic duct appears as a beaded low-signal-intensity structure in the parenchyma of the body and tail.

 


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Figure 5c. Enhancement of chronic pancreatitis due to obstructing pancreatic head carcinoma. (a) Gadolinium-enhanced T1-weighted GRE image shows the pancreatic carcinoma (arrow) in the head of the pancreas. (b–d) In the same patient, T1-weighted GRE images (115/2.2) of the pancreatic body and tail obtained (b) before injection of gadopentatate dimeglumine and after injection during the (c) arterial and (d) portal venous phases of enhancement. Enhancement of the pancreatic parenchyma (arrows) is lower than that of the normal pancreas. In c, the dilated pancreatic duct appears as a beaded low-signal-intensity structure in the parenchyma of the body and tail.

 


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Figure 5d. Enhancement of chronic pancreatitis due to obstructing pancreatic head carcinoma. (a) Gadolinium-enhanced T1-weighted GRE image shows the pancreatic carcinoma (arrow) in the head of the pancreas. (b–d) In the same patient, T1-weighted GRE images (115/2.2) of the pancreatic body and tail obtained (b) before injection of gadopentatate dimeglumine and after injection during the (c) arterial and (d) portal venous phases of enhancement. Enhancement of the pancreatic parenchyma (arrows) is lower than that of the normal pancreas. In c, the dilated pancreatic duct appears as a beaded low-signal-intensity structure in the parenchyma of the body and tail.

 

    DISCUSSION
 TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
The ability to detect and stage pancreatic carcinoma has improved owing to advances in MR imaging and CT technology. Findings in comparative studies suggest that fast MR imaging sequences may be superior to helical CT for preoperative tumor detection and determination of tumor extension (4,6). Administration of antiperistaltic agents and imaging with fast breath-hold sequences have resulted in images with less motion artifact. Use of faster sequences has also facilitated dynamic gadolinium-enhanced imaging of the pancreas during multiple phases of contrast enhancement. Data continue to emerge about which dynamic sequences are optimal for lesion detection (9).

In many studies, CT has been used in an attempt to distinguish chronic pancreatitis from pancreatic carcinoma. Karawasa et al (10) evaluated the pancreatic duct caliber and contour and found that smooth or beaded dilatations of the duct are more common with an obstructing neoplasm. Chronic pancreatitis more frequently results in an irregularly dilated duct, often with intraductal calcification. Additionally, they found a statistically significant difference in the ratio of duct caliber to pancreatic gland width, which is higher in patients with cancer (10). Megibow et al (11) originally described thickening of the celiac artery or superior mesenteric artery as specific for carcinoma. However, more recent work by Baker (8) and Shulte et al (12) demonstrates that acute and chronic inflammatory processes can result in infiltration of the fat around the superior mesenteric artery and encasement of the vessel by a mass or periarterial adenopathy. Recognizing that periarterial findings are nonspecific, Elmas et al (13) measured the diameter of the superior mesenteric artery and vein in patients with chronic pancreatitis or pancreatic carcinoma. They found that the artery enlarges in the setting of cancer, and carcinoma should be suspected if the artery-to-vein ratio is greater than 1.0.

As MR imaging techniques improve, findings in comparative studies reveal potentially higher diagnostic accuracy compared to that with other modalities in the evaluation of pancreatic disease (3,5). The study by Semelka et al (3) compared MR imaging with CT and revealed significantly diminished delayed contrast enhancement at MR imaging in chronic pancreatitis compared to nonnecrotic acute pancreatitis or normal pancreas. The more recent work by Gohde et al (2) compared a dynamic gadolinium-enhanced multiplanar fast spoiled GRE sequence to T1- and T2-weighted SE sequences and a gadolinium-enhanced T1-weighted SE sequence with fat saturation. The multiplanar fast spoiled GRE sequence has higher sensitivity, specificity, and accuracy for detection of pancreatic disease and yields images of higher quality with better delineation of pancreatic anatomy.

In several studies, MR imaging was used in an attempt to distinguish pancreatic diseases. Jenkins et al (14) found that there is no statistically significant difference in T1 and T2 between chronic pancreatitis and pancreatic carcinoma, although the relaxation times for cancer differed from normal findings in control subjects. More recently, Sittek et al (15) used fast multiplanar MR imaging to demonstrate that chronic pancreatitis and cancer enhance differently from normal pancreas or unaffected pancreatic parenchyma in patients with a mass. Semelka et al (3) compared calcific versus noncalcific chronic pancreatitis imaged with fast GRE and fat-suppressed SE sequences. Percentage contrast enhancement is significantly different between the two groups (16).

The promising work in CT and MR imaging combined with the higher diagnostic accuracy of the dynamic multiplanar fast spoiled GRE sequence prompted us to compare the dynamic multiplanar MR characteristics of chronic pancreatitis with those of pancreatic carcinoma. Both pathologic entities resulted in gradual progressive enhancement of the involved pancreatic parenchyma that would be difficult to distinguish subjectively. Although there was a significant difference in percentage enhancement between the two diseases with the delayed fat-saturated sequence, the amount of overlap would preclude distinguishing the two subjectively on this basis.

Evaluation of the histology of chronic pancreatitis and carcinoma reveals abundant fibrosis in both pathologic conditions (Figs 2, 3), which likely accounts for their similar imaging appearance. Additionally, the pancreas proximal to an obstructing mass may undergo atrophy and fibrosis that lead to an altered pattern of enhancement when compared to that of normal pancreatic parenchyma. Interestingly, this pattern of gradual enhancement in the nontumorous body of a pancreas with a pancreatic head mass was more similar to the enhancement of the cancer itself than to that of chronic pancreatitis. This may be due to the lack of inflammation that accompanies typical chronic pancreatitis.

In conclusion, masses due to pancreatic carcinoma and chronic pancreatitis show a pattern of contrast enhancement after dynamic infusion of gadopentatate dimeglumine that is altered compared to that of normal pancreas. The similar gradual pattern of enhancement and overlap in peak enhancement preclude distinction of the two entities on the basis of gadolinium-enhanced MR findings. Further work must address other dynamic MR imaging features that may help distinguish the two pathologic entities.


    Footnotes
 
Abbreviations: GRE = gradient echo SE = spin echo

Author contributions: Guarantor of integrity of entire study, P.T.J.; study concepts and design, P.T.J., E.K.O.; definition of intellectual content, P.T.J., E.K.O.; literature research, P.T.J.; clinical studies, P.T.J., E.K.O.; data acquisition and analysis, P.T.J., E.K.O.; statistical analysis, P.T.J., E.K.O.; manuscript preparation, P.T.J.; manuscript editing, P.T.J., E.K.O.


    References
 TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 

  1. Semelka RC, Ascher SM. MR imaging of the pancreas. Radiology 1993; 188:593-602.[Abstract/Free Full Text]
  2. Gohde SC, Toth J, Krestin GP, Debatin JF. Dynamic contrast-enhanced FMPSPGR of the pancreas: impact on diagnostic performance. AJR 1997; 168:689-696.[Abstract/Free Full Text]
  3. Semelka RC, Kroeker MA, Shoenut JP, Kroeker R, Yaffe CS, Micflikier AB. Pancreatic disease: prospective comparison of CT, ERCP, and 1.5-T MR imaging with dynamic gadolinium enhancement and fat suppression. Radiology 1991; 181:785-791.[Abstract/Free Full Text]
  4. Gabata T, Masui S, Kadoya M, et al. Small pancreatic adenocarcinomas: efficacy of MR imaging with fat suppression and gadolinium enhancement. Radiology 1994; 193:683-688.[Abstract/Free Full Text]
  5. Vellet AD, Romano W, Bach DB, Passi RB, Taves DH, Munk PL. Adenocarcinoma of the pancreatic ducts: comparative evaluation with CT and MR imaging at 1.5 T. Radiology 1992; 183:87-95.[Abstract/Free Full Text]
  6. Ichikawa T, Haradome H, Hachiya J, et al. Pancreatic ductal adenocarcinoma: preoperative assessment with helical CT versus dynamic MR imaging. Radiology 1997; 202:655-662.[Abstract/Free Full Text]
  7. DelMaschio A, Vanzulli A, Sironi S, et al. Pancreatic cancer versus chronic pancreatitis: diagnosis with Ca 19-9 assessment, US, CT, and CT-guided fine-needle biopsy. Radiology 1991; 178:95-99.[Abstract/Free Full Text]
  8. Baker ME. Pancreatic adenocarcinoma: are there pathognomonic changes in the fat surrounding the superior mesenteric artery?. Radiology 1991; 180:613-614.[Free Full Text]
  9. Lu DS, Vedantham S, Krasny RM, Kadell B, Berger WL, Reber HA. Two-phase helical CT for pancreatic tumors: pancreatic versus hepatic phase enhancement of tumor, pancreas, and vascular structures. Radiology 1996; 199:697-701.[Abstract/Free Full Text]
  10. Karawasa E, Goldberg HI, Moss AA, Federle MP, London SS. CT pancreatogram in carcinoma of the pancreas and chronic pancreatitis. Radiology 1983; 148:489-493.[Abstract/Free Full Text]
  11. Megibow AJ, Bosniak MA, Ambos MA, Beranbaum ER. Thickening of the celiac axis and/or superior mesenteric artery: a sign of pancreatic carcinoma on computed tomography. Radiology 1981; 141:449-453.[Free Full Text]
  12. Shulte SH, Baron RL, Freeny PC, Patten RM, Gorell HA, Maclin ML. Root of the superior mesenteric artery in pancreatitis and pancreatic carcinoma: evaluation with CT. Radiology 1991; 180:659-662.[Abstract/Free Full Text]
  13. Elmas N, Yorulmaz I, Oran I, Oyar O, Ozutemiz O, Ozer H. A new criterion in differentiation of pancreatitis and pancreatic carcinoma: artery-to-vein ratio using the superior mesenteric vessels. Abdom Imaging 1996; 21:331-333.[Medline]
  14. Jenkins JP, Braganza JM, Hickey DS, Isherwood I, Machin M. Quantitative tissue characterisation in pancreatic disease using magnetic resonance imaging. Br J Radiol 1987; 60:333-341.[Abstract/Free Full Text]
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P Manoharan and M B Sheridan
Neoplasms of the pancreas
Imaging, September 1, 2004; 16(4): 323 - 337.
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J Ultrasound MedHome page
Y. Ozawa, K. Numata, K. Tanaka, N. Ueno, T. Kiba, K. Hara, M. Morimoto, T. Sakaguchi, H. Sekihara, T. Kubota, et al.
Contrast-Enhanced Sonography of Small Pancreatic Mass Lesions
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RadiologyHome page
E. Lopez Hanninen, H. Amthauer, N. Hosten, J. Ricke, M. Bohmig, J. Langrehr, R. Hintze, P. Neuhaus, B. Wiedenmann, S. Rosewicz, et al.
Prospective Evaluation of Pancreatic Tumors: Accuracy of MR Imaging with MR Cholangiopancreatography and MR Angiography
Radiology, July 1, 2002; 224(1): 34 - 41.
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RadioGraphicsHome page
C. Matos, O. Cappeliez, C. Winant, E. Coppens, J. Deviere, and T. Metens
MR Imaging of the Pancreas: A Pictorial Tour
RadioGraphics, January 1, 2002; 22(1): e2 - e2.
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RadiologyHome page
P. M. McMahon, E. F. Halpern, C. Fernandez-del Castillo, J. W. Clark, and G. S. Gazelle
Pancreatic Cancer: Cost-Effectiveness of Imaging Technologies for Assessing Resectability
Radiology, October 1, 2001; 221(1): 93 - 106.
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Am. J. Roentgenol.Home page
T. Kim, T. Murakami, M. Takamura, M. Hori, S. Takahashi, S. Nakamori, M. Sakon, Y. Tanji, K. Wakasa, and H. Nakamura
Pancreatic Mass Due to Chronic Pancreatitis: Correlation of CT and MR Imaging Features with Pathologic Findings
Am. J. Roentgenol., August 1, 2001; 177(2): 367 - 371.
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