ENDOCRINE SURGERY - PART 8 potx

Figure 7 Lymph node with metastatic pancreatic neuroendocrine tumor. (Hemotoxylin/eosin Â 10.) Figure 8 Pancreatic small-cell carcinoma. The tumor is composed of uniform cells with finely clumped chromatin and minimal cytoplasm. (Hemotoxylin/eosin Â 40.) Pathology of Pancreatic Endocrine Neoplasia 493 3 GASTRINOMAS Gastrinomas are the second most common of the functional pancreatic endocrine tumors. In addition to the pancreas, these tumors may arise in extrapancreatic sites and give rise to the Zollinger-Ellison syndrome due to gastrin hypersecretion. These tumors can be found in any pancreatic site but are more common in the gastrinoma triangle, defined by the cystic-hepatic duct confluence, the junction of the second and third portion of the duodenum, and the body of the pancreas. They may be solitary or multiple particularly in MEN I patients. Tumors average in size 2 cm, but lesions smaller than 1 cm can occur. Histologically, there is usually lymphatic/vascular invasion present. Gastrin immunohistochemistry will be positive in the tumor cells, and there may be reaction for other hormones. Ultrstructurally there are electron dense granules of varying size and shape. These are slow-growing tumors, which usually have a malignant course. Meta- stases may occur many years following detection of the primary tumor. 4 GLUCAGONOMAS Glucagonomas comprise approximately 5% of the functional pancreatic endocrine tumors and arise from the a cells. These tumor s are usually solitary and found in the tail portion of the pancreas. The average size is 7 cm. Immunohistochemical stain for glucagon or a pro- glucagon peptide will be positive in these tumors and there may be focal positivity for other hormones. The typical a granule on ultrastructural examination will be 180–300 nm with a dense inner core and a surrounding paler rim. Approximately 80% of these cases are malignant, the liver being most often the first site of metastatic spread. Other functional pancreatic tumors which rarely occur include somatostatinomas and VIPomas (watery diarrhea syndrome) (1–21). 5 SMALL-CELL CARCINOMA OF THE PANCREAS Small-cell carcinoma is an uncommon primary pancreatic tumor representing approximately 1% of all tumors. It is considered a poorly differentiated endocrine tumor. Elderly men are the usual patient population. Most tumors occur in the head of the pancreas. Grossly, they are large, infiltrative masses with areas of hemmo- rhage and necrosis and are soft or grey in appearance. Histologically they are similar to the more commonly occurring lung tumors (Fig. 8). The cells are arranged in solid sheets or nests with little appreciable cytoplasm. Nuclei have dense coarse chromatin without prominent nucleoli and may have nuclear moldi ng. Mitotic figures are numerous. Ultrastructurally, there are rare dense core neurosecretory granules. Immunohistochemically, they will react with neuroendocrine markers such as chromogranin and synaptophysin. Hormones are usually not detected. Metastases to either liver lymph nodes or other structures are generally found at the time of presentation (22–24). REFERENCES 1. Solcia E, Capella C, Kloppel G. Tumors of the pancreas. Atlas of Tumor Pathology, 3rd Series, Fascicle 20. Washington, DC: Armed Forces Institute of Pathology, 1997;145–180. 2. Kloppel G, Heitz PU. Pancreatic endocrine tumors in man. In: Polak JM, ed. Diagnostic Histopathology of Neuroendocrine Tumors. Edinburgh: Churchill Living- stone, 1993:91–121. 3. Howard JN, Moss NH, Rhoads JE. Collective review: hyperinsulinism and islet cell tumors of the pancreas. Int Abstr Surg 1950; 90:417–455. 4. Frantz VK. Tumors of the pancreas. In: Atlas of Tumor Pathology: 1st Series, Fasicle 27–28. Washington, DC: Armed Forces Institute of Pathology, 1959;79–149. 5. Eberle F, Grun R. Multiple endocrine neoplasia, type I (MEN I). Erge Inn Med Kinderheil 1981; 46:76–149. 6. Majewski JT, Wilson SD. The MEN I syndrome: an all or none phenomenon. Surgery 1979; 475–484. 7. Heitz PU, Kasper M, Polak JM, Kloppel G. Pancreatic endocrine tumors. Hum Pathol 1982; 13:263–271. 8. Solcia E, Capella C, Buffa R, Tenti P, Rindi G, Cornaggia M. Antigenic markers of neuroendocrine tumors: their diagnostic and prognostic value. In: Fenoglio CM, Weinstein RS, Kaufman N, eds. New Concepts in Neoplasia as Applied to Diagnostic Pathology. Balti- more: Williams & Wilkins, 1986:242–261. 9. Wilson BS, Lloyd RV. Detection of chromogranin in neuroendocrine cells with a monoclonal antibody. Am J Pathol 1984; 115:458–468. 10. Buffa R, Rindi G, Sessa F, et al. Synaptophysin immuno- reactivity and small clear vesicles in neuroendocrine cells and related tumors. Mol Cell Probes 1987; 1:367– 381. 11. Cheijfec G, Faulkner S, Grimelius L, et al. Synaptophy- sin. A new marker for pancreatic neuroendocrine tumors. Am J Surg Pathol 1987; 11:241–247. 12. Bordi C, Bussolati G. Immunoflourescence, histochem- Unger494 ical and ultrastructural studies for the detection of multiple endocrine polypeptide tumors of the pancreas. Virchows Arch (Cell Pathol) 1974; 17:13–27. 13. Heitz PU. Pancreatic endocrine tumors. In: Kloppel G, Heitz PU, eds. Pancreatic Pathology. Edinburgh: Churchill-Livingstone, 1984:206–232. 14. Mukai K, Grotting JC, Greider MH, Rosai J. Retrospec- tive study of 77 pancreatic endocrine tumors using the immunoperoxidase method. Am J Surg Pathol 1982; 6:387–399. 15. Broder LE, Carter SK. Pancreatic islet cell carcinoma. I. Clinical features of 52 patients. Am Intern Med 1973; 79:101–107. 16. Cubilla AL, Hajdu SI. Islet cell carcinoma of the pancreas. Arch Pathol 1975; 99:204–207. 17. Kloppel G, Heitz PU. Pancreatic endocrine tumors in man. In: Polak JM, ed. Diagnostic Histopathology of Neuroendocrine Tumors. Edinburgh: Churchill Living- stone, 1993:91–121. 18. Solcia E, Sessa F, Rindi G, Bonato M, Capella C. Pan- creatic endocrine tumors: nonfunctioning tumors and tumors with uncommon function. In: Dayal Y, ed. Endocrine Pathology of the Gut and Pancreas. Boca Raton, FL: CRC Press, 1991:105–132. 19. Stefanini P, Carboni M, Patrassi N, Basoli A. Beta islet cell tumors of the pancreas: results of a statistical study on 1,067 cases collected. Surgery 1974; 75:597–609. 20. Greider MH, Rosai J, McGuigan JE. The human pancreatic islet cells and their tumors. II. Ulcerogenic and diarrheogenic tumors. Cancer 1974; 33:1423–1443. 21. Niewenhuijzen Kruseman AC, Knijnenburg G, Brutel de la Rivera G, Bosman FT. Morphology and immunohistochemically defined endocrine function of pancreatic islet cell tumours. Histopathology 1978; 2:389–399. 22. Cubilla AL, Fitzgerald PJ. Tumors of the exocrine pancreas. In: Atlas of Tumor Pathology. Washington, DC: Armed Forces Institute of Pathology, 1984:196–201. 23. O’Connor TP, Held G, Kloppel G. Exocrine pancreatic tumours and their histological classification. A study based on 167 autopsies and 97 surgical cases. Histo- pathology 1983; 645–661. 24. Reyes CV, Wang T. Undifferentiated small cell carcinoma of the pancreas. Report of a patient with tumor marker studies. Cancer 1992; 70:2500–2502. Pathology of Pancreatic Endocrine Neoplasia 495 41 Ultrasonography of the Pancreas Hsu-Chong Yeh Mount Sinai School of Medicine, New York University, New York, New York, U.S.A. 1 ULTRASONOGRAPHIC FEATURES OF THE NORMAL PANCREAS The pancreas is located in the subdiaphragmatic retroperitoneal space at the level of the first and second lumbar vertebrae. The pancreatic head is located to the right of superior mesenteric vein and medial to the second portion of the duodenum, which can be identi- fied as a fluid- or air-containing structure. The pancreatic body is anterior to the aorta, separated from the latter by retropancreatic and periaortic fat. The superior mesenteric artery and vein pass anterior to the uncinate process and/or posterior to the pancreatic neck and body. The tail of the pancreas extends to near the splenic hilum. The common bile duct runs anterior to the portal vein and enters the inferior aspect of the pancreatic head, then runs inferiorly to join the pancreatic duct close to ampulla. Normal pancreatic echotexture is hyperechoic rela- tive to that of the liver. The degree of echogenicity is determined mostly by the amount of the fat between the lobules and acinar cells, but to a lesser extent by interlobular fibrous tissue. In the adult, a highly echogenic pancreas is quite common, especially in older age. When echogenicity is similar to peripancreatic fat, the pancreas may not be easily recognized. Visual- ization of the splenic vein may be greatly helpful in identifying the pancreas in such cases since a large part of pancreas lies immediately anterior to the splenic vein. The endocrine portion of pancreas is the islets of Langerhans, which are groups of cells scattered throughout the pancreas. They are usually not identifi- able on ultrasonography. 2 SCANNING TECHNIQUE Ideally the patient should fast overnight or for at least 6–8 hour s, although in many patients the pancreas is very well visualized without fasting. The purpose of fasting is to prevent gastric contents, especially gas bubbles from obscuring the pancreas. Since the stomach is usually slightly inferior and anterior to the pancreas, scanning from above the pancreas and angling the transducer downward may allow one to visualize the pancreas even if some gas is present in the stomach. Less commonly, the stomach may overlie the pancreas. A firm compression with the transducer during scanning is frequently helpful for visualizing the pancreas in such instances. Sometimes, scanning from below the gas- filled stomach and transverse colon and angling the transducer upward may also be helpful in visualizing the pancreas in such cases. When the volume of gas in the stomach is excessive or difficult to compress because of the large size of the abdomen, drinking a large amount of degassed water or contrast material may sometimes be helpful. Since the distal part of the tail of the pancreas is located near the splenic hilum, scanning the splenic hilar 497 area usually clearly visualizes the tail of the pancreas that usually lies immediately inferior to splenic vein. A tumor in the pancreatic tail (Fig. 1) may be seen by this approach. Intraoperative scanning can be done with a high- frequency (7.5–10 MHz) linear transducer. This will show very good detail of the pancreas and adjacent structures (Fig. 2). The transducer is covered with a sterile sheath, which contains sterile gel. The pancreatic area is filled with sterile saline, and the transducer is placed on or approximately 1 cm above the pancreas (1). The entire pancreas, the pancreatic duct, common bile duct, superior mesenteric artery and vein as well as the inferior vena cava and aorta are usually seen with very good detail. 3 ISLET CELL TUMORS The islets of Langerhans are the endocrine part of the pancreas. The majority of islet cell tumors are functional, but about one third are non-functioning (2). The most common functional islet cell tumor is insulinoma (60%), followed by gastrinoma (18%), which may cause Zollinger-Ellison syndrome, VIPoma, which produce the WDHA syndrome (watery diarrhea, hypokalemia, and achlorhydria), glucagonomas, somatostatinomas (delta-cell tumors), and carcinoid tumors (Fig. 1), which produce serotonin and an atypical carcinoid syndrome. The functional tumors are frequently small and difficult to detect because hormonal hypersecretion leads to early discovery. About 90% of insulinomas are le ss than 2 cm in diameter (3) (Fig. 2). Although islet cell tumors have been reported to be most common in the tail of pancreas (54% of 82 tumors) (4), others reported that insulinoma is most commonly foun d in the pancreatic head (62% of 44 solitary tumors) (1). The detection rate by convetional ultrasonography is only 30–61%. Some small tumors may be difficult to palpate even during surgery. Intraoperative ultrasonography may be very helpful in such instances. In a series of 28 cases of intraoperative ultrasound scanning, 4 insulinomas, which were not palpable, were visualized by ultrasonography. On the other hand, 2 superficial tumors were obscured in the near field of a 10 MHz transducer, and 2 in the distal pancreatic tail were not scanned because of lack of surgical mobilization of the tail. The sensitivity for detecting insulinomas by intr aoperative ultr asonogra- phy is 84% compared to 54% for angiography and 30% for computed tomography (CT) (1). The combined sensitivity of intraoperative ultrasonography and surgi- Figure 1 A carcinoid tumor in the tail of pancreas. (Left) Coronal scan from left upper flank region shows a mass (between ‘‘+’’) with central calcifications located in the tail of pancreas (arrowheads), which is inferior to the splenic hilar vessels (arrows). The mass represents a carcinoid tumor. S = spleen. (Right) Transverse scan from left upper flank region shows the mass (between ‘‘+’’) located anterior to the left kidney (K). S = spleen. Figure 2 A 1.5 cm insulinoma detected on intraoperative ultrasonography. (Left) Transverse scan shows a small mass (arrowhead) in the head of the pancreas. smv = superior mesenteric vein; V = inferior vena cava; A = aorta. (Right) Longitudinal scan shows the 1.5 cm mass (arrowhead) in the head of pancreas anterior to the inferior vena cava (V). Yeh498 cal palpation fo r detecting solitary insulinomas was 100%. Intraoperative ultrasonography may also con- tribute significantly to the surgical management by precisely demonstrating the relationship of insulinoma to the pancreatic and common bile ducts and pancreatic blood vessels. Intraoperative ultrasonography may differentiate malignant from benign islet cell tumors by demonstrating ill-defined tumor borders, invasion of surrounding pancreatic tissue or the pancreatic duct (5). Approximately 10% of islet cell tumors are multiple. The sensitivity for detecting multiple islet cell masses is low because many of these tumors may be smaller than 1 cm (1). In a series of 59 insulinomas in 9 patients, the sensitivity for detecting these tumors was as follows: conventional ultrasonography, 15%; intraoperative ultrasonography, 36%; angiography, 29%; CT, 8% (1). The nonfunctional tumors are easier to detect because they reach a larger size before causing symptoms. They usually range in size from 1 to 20 cm, frequently being more than 10 cm in diameter (5). The small islet cell tumors are usually hypoechoic homogeneous solid masses, but some larger tumors may be moderately echogenic, heterogeneous, and may con- tain fluid-filled areas or cystic changes or calcifications (5–9). The homogeneous solid masses are more likely to be functional, and heterogeneous masses with cystic or necrotic areas are more likely to be nonfunctiona l (2). Solid islet cell tumors were usually indistinguishable from those of adenocarcinoma of the pancreas except that islet cell tumors tend to be hypervascular on color Doppler study, although this is not always true (Fig. 3). Five to 10% of insulomas are malignant. Histologically, these tumor s display little evidence of anaplasia and may be impossible to differentiate from benign tumors. The diagnosis is made in the presence of metastases or local invasion (9). The metastases to the liver may appear hypoechoic, near-isoechoic, or hyperechoic and may have cystic changes. Different ultrasono- Figure 3 An islet cell carcinoma in the tail of the pancreas with liver metastases. (Top left) Transverse scan shows a mass (arrows) in the tail of the pancreas. The mass contains a small calcification. Arrows = normal head and body of pancreas. Color Doppler study (not shown) did not show hypervascularity in the tumor. (Top right) Sagittal scan shows a near isoechoic mass (arrowheads) in the anterior surface of the left lobe of the liver. (Bottom left) Sagittal scan of right lobe of the liver shows a hyperechoic mass (arrowhead) with a central cavity in the posterior surface of the liver. (Bottom right) Sagittal scan more lateral toward the right shows a small hypoechoic mass (arrowhead) in the liver. The masses in the tail of the pancreas and left lobe of the liver were biopsied under ultrasound guidance, and both proved to be islet cell carcinoma. Ultrasonography of the Pancreas 499 graphic features of metastatic lesions may be present in the same liver (Fig. 3). REFERENCES 1. Galiber AK, Reading CC, Charboneau JW, Sheedy PF, James EM, Gorman B, Grant CS, Heerden JAV, Telander RL. Localization of pancreatic insulinoma: comparison of pre- and intraoperative US with CT and angiography. Radiology 1988; 166:405–408. 2. Gold J, Rosenfield AT, Sostman D, Burrell M, Taylor KJW. Nonfunctioning islet cell tumors of the pancreas: radiographic and ultrasonographic appearances of two cases. Am J Roentgenol 1978; 131:715–717. 3. Fink IJ, Krudy AG, Shawker TH, Norton JA, Gordon P, Doppman JL. Demonstration of an angiographically hypovascular insulinoma with intra-arterial dynamic CT. Am J Roentgenol 1985; 144:555–556. 4. Kruger RL, Dockerty MP. Tumors of the islets of Langerhans. Surg Gyn Obst 1947; 85:495–511. 5. Norton JA, Cromack DR, Shawker TH, Doppman JL, Comi R, Gorden P, Maton PN, Gardna JD. Intra- operative ultrasound localization of islet cell tumors, a prospective comparison to palpation. Ann Surg 1988; 270:160. 6. Raghavendra BN, Glickstein ML. Sonography of islet cell tumor of the pancreas: report of two cases. J Clin Ultrasound 1981; 9:331–333. 7. Fugazzola C, Procacci C, Andreis JCB, Iacono C, Portuese A, Mansueto G, Rasidori E, Zampieri P, Jannucci A, Serio G. The contribution of ultrasonography and computed tomography in the diagnosis of nonfunctioning islet cell tumors of the pancreas. Gastrointest Radiol 1990; 15:139–144. 8. Shawker TH, Doppman JL, Dunnick NR, McCarthy DM. Ultrasonic investigation of pancreatic islet cell tumors. J Ultrasound Med 1982; 1:193–200. 9. Gunther RW, Klose KJ, Ruckert K, Kuhn FP, Beyer J, Klotter HI. Islet-cell tumors: detection of small lesions with computed tomography. Radiology 1983; 148:485– 488. 10. Crawford JM, Cotran RS. The pancreas. In: Cotran RS, Kuman SL, Robbins SL, Schoen FJ, eds. Robbins Path- ologic Basis of Diseases. 5th ed. Philadelphia: W.B. Saunders, 1994:923. Yeh500 42 Computed Tomography of the Pancreas William L. Simpson, Jr. and David S. Mendelson Mount Sinai School of Medicine, New York University, New York, New York, U.S.A. 1 ANATOMY OF THE PANCREAS The pancreas is a tongue-shaped retroperitoneal organ (Fig. 1). It is located within the anterior pararenal space along with the ascending and descending colon as well as the duodenum. The pancreas is divided into the uncinate process, head, neck, body, and tail. The long axis of the gland most commonly follows an oblique course with the head at the 8 o’clock position and the tail at 2 o’clock. The normal dimensions of the pancreas depend on many factors, the most important of which is age. The head should measure up to 3.0–3.5 cm, the body up to 2.5 cm, and the tail up to 2.0 cm. Generally the gland tapers in size from head to tail. Fatty infiltra- tion of the gland lobules is common with age. This gives the gland a more lace-like or feathery appearance. The pancreatic duct runs through the entire length of the gland and may measure up to 3.0 mm in the head and gradually tapers to the tail. It is often partially visualized, more commonly in thin section computed tomography (CT). The common bile duct passes through the pancreatic head before it joins the pancreatic duct near the ampulla of Vater. The size of the common bile duct (CBD) in the pancreatic head varies with age as well but should never exceed 10 mm, often attaining the larger diameters on patients post-cholecystectomy. Anatomically the organ sits posterior to the stomach with the potential space of the lesser sac between them. The left lobe of the liver is anterior as well. The spine, aorta, and inferior vena cava are posterior to the pancreas. The head of the organ sits within the duodenal sweep. The tail extends up into the splenic hilum. The transverse mesocolon attaches to the anterior aspect of the gland. There are important vascular landmarks related to the pancreas. The splenic vein lies along the dorsal aspect. The splenic vein and superior mesenteric vein join at the portal confluence posterior to the pancreatic head. The uncinate process extends between the superior mesenteric vein and the inferior vena cava (IVC). The splenic artery usu-ally follows a tortuous, serpige- nous course behind the organ. It can easily be mistaken for pancreatic cysts or a dilated pancreatic duct on a noncontrast scan by novice observers. Splenic artery calcifications can also be mistaken for pancreatic calcifications. The superior mesenteric artery originates off of the aorta posterior to the body of the pancreas with a fat plane separating the two. The gastroduodenal artery runs along the anterior surface of the pancreatic neck. 2 IMAGING TECHNIQUE CT imaging of the pancreas has changed with the new developments in CT technology. The goal of scanning a patient with a suspected tumor is not onl y to establish the diagnosis but also to localize the mass and evaluate for the extent of disease. Noncontrast images of the pancreas are useful for detecting calcifications as eval- 501 uating the size and contour of the gland. For most diagnostic studies intraven ous contrast enhancement is necessary. The pancreas should be imaged with thin sections—3 mm or less. Helical scanners can cover the pancreas with 3 mm slices in a single breath hold. Mul- tislice scanners can cover the pancreas with as thin as 1 mm slices in one breath hold. The pancreas should be scanned in both the arterial and portal venous phases. An arterial phase scan is obtained by beginning scanning 20–30 seconds after intravenous contrast is injected. The portal venous phase occurs after a 70- second delay. Since the pancreas is a very vascular gland, it enhances readily with contrast. Therefore, most tumors appear as hypo-attenuating lesions in both the arterial and venous phases. However, there are a few tumors that enhance more than the surrounding glan- dular tissue on the arterial phase—particularly neuroendocrine tumors. 3 NEUROENDOCRINE TUMORS Most tumors of the pancreas arise from the ductal portion of the gland. These comprise the adenomas and adenocarcinomas. The pancreatic parenchyma gives rise to the neuroendocrine tumors. The majority arises from the islet of Langerhans cells and are also known as islet cell tumors (Fig. 2). They are rare tumors with an incidence of 1.0–1.5 per 100,000 in the general population (1). Approximately half of these tumors are functional, meaning that they produce clinical symptoms from the overproduction of a hormone. The remainder are nonfunctional and come to medical attention due to symptoms from tumor size. The functional tumors include insulinoma, gastrinoma, glucagonoma, vasoactive intestinal peptide-oma (VIPoma), somatostatinoma, growth hormone–releas- ing factor-oma (GFRoma), adrenocorticotropic hormone-oma (ACTH oma), parathyroid hormone– like- oma (PTHoma), and neurotensinoma. There is only one nonfunctional tumor, namely the pancreatic peptide-oma (PPoma). It produces pancreatic polypeptide and neuron-specific enolase, both of which have no biological activity. Many islet cell tumors are composed of a mixture of more than one cell type. Insulinomas (Fig. 3) are the most common neuroendocrine tumors of the pancreas. They are predom- inantly benign (90%) and tend to be solitary and small (<2 cm) (2). Due to their small size they are difficult to localize with CT preoperatively. Sensitivities ranging from 12.5 to 36% have been reported (3–7). However, these studies were performed on conventional dynamic CT scanners using a single phase technique. More recent studies performed on helical scanners with a dual phase technique report sensitivities ranging from 82 to 86% (8,9). Five to 10% of patients with an insulinoma have multiple endocrine neoplasia (MEN)-1 syndrome. MEN-associated insulinomas are more frequently multiple (10). Gastrimomas are the second most common neuroendocrine tumors (11). The clinical manifestation of the tumor is known as Zollinger-Ellison syndrom e. As Figure 1 Normal CT appearance of the pancreas. Figure 2 A large nonfunctioning islet cell tumor in the neck/body of the pancreas. The tumor is large as is typical of these tumors since they produce no symptoms except by mass effect. There is both hypervascularity around the pe- riphery of the mass (long arrow) as well as calcification within it (short arrow). Simpson, Jr. and Mendelson502 [...]... localization of insulinomas necessary? Lancet 1 981 ; 1: 483 – 486 Doherty GM, Doppman JL, Shawker JH, et al Results of a prospective strategy to diagnose, localize and resect insulinomas Surgery 1991; 110: 989 –997 Grant CS, van Heerden JA, Charboneau JW, et al Insulinoma: the value of intraoperative ultrasonography Arch Surg 1 988 ; 123 :84 3 84 8 Jensen RT, Norton JA Endocrine neoplasms of the pancreas In: Yamada... modalities to localize tumors in patients with Zollinger-Ellison syndrome Dig Dis Sci 1993; 38( 7):13 18 13 28 46 Tjon ATRT, et al CT and MR imaging of advanced Zollinger-Ellison syndrome J Comput Assist Tomogr 1 989 ; 13(5) :82 1 82 8 47 Frucht H, et al Gastrinomas: comparison of MR imaging with CT, angiography, and US Radiology 1 989 ; 171 (3):713–717 48 Prinz RA Localization of gastrinomas Int J Pancreatol... Endocrinol Metab 2001; 86 :89 5–902 Pasquali C, Rubello D, Sperti C, Gasparoni P, Liessi G, Chierichetti F, Ferlin G, Pedrazzoli S Neuroendocrine tumor imaging: can 18F-fluorodeoxyglucose positron emission tomography detect tumors with poor prognosis and aggressive behavior? World J Surg 19 98; 22: 588 –592 Adams S, Baum R, Rink T, Schumm-Drager PM, Usadel KH, Hor G Limited value of fluorine- 18 fluorodeoxyglucose... Gastroenterol 19 98; 93(9):1559–1562 59 Vogl TJ, Hammerstingl R, Schwartz W, et al Superparamagnetic iron oxide-enhanced MR imaging for differential diagnosis of focal liver lesions Radiology 1996; 1 98: 881 88 7 60 Mathieu D, et al Unexpected MR-T1 enhancement of endocrine liver metastases with mangafodipir J Magn Reson Imaging 1999; 10(2):193–195 61 Ahlstrom H, Gehl HB Overview of MnDPDP as a pancreas-specific... Acta Radiol 1997; 38( 4 Pt 2):660–664 62 Gehl HB, et al Mn-DPDP in MR imaging of pancreatic adenocarcinoma: initial clinical experience Radiology 1993; 186 (3):795–7 98 63 Gehl HB, et al Pancreatic enhancement after lowdose infusion of Mn-DPDP Radiology 1991; 180 (2):337–339 64 Vasseur B, et al Peritoneal carcinomatosis in patients with digestive endocrine tumors Cancer 1996; 78( 8): 1 686 –1692 65 Chatziioannou... management of patients with neuroendocrine gastroenteropancreatic tumors J Nucl Med 1997; 38: 853 85 8 Alexander HR, Fraker DL, Norton JA, Bartlett DL, Tio L, Benjamin SB, Doppman JL, Goebel SU, Serrano J, Gibril F, Jensen RT Prospective study of somatostatin receptor scintigraphy and its effect on operative outcome in patients with Zollinger-Ellison syndrome Ann Surg 19 98; 2 28: 2 28 2 38 Frilling A, Malago M, tin... 19(2):79–91 49 Krenning EP, et al Somatostatin receptor scintigraphy with [111In-DTPA-D-Phe1 ]- and [123I- Tyr3]-octreotide: the Rotterdam experience with more than 1000 patients Eur J Nucl Med 1993; 20 (8) :716–731 519 50 Debray MP, et al Imaging appearances of metastases from neuroendocrine tumours of the pancreas Br J Radiol 2001; 74 (88 7):1065–1070 51 Sutliff VE, et al Growth of newly diagnosed, untreated metastatic... Kelekis NL, et al ACTH-secreting islet cell tumor: appearances on dynamic gadolinium-enhanced MRI Magn Reson Imaging 1995; 13(4):641–644 Amikura K, et al Role of surgery in management of adrenocorticotropic hormone-producing islet cell tumors of the pancreas Surgery 1995; 1 18( 6):1125–1130 Hes FJ, Feldberg MA Von Hippel-Lindau disease: strategies in early detection (renal-, adrenal-, pancreatic masses)... neuroendorine tumors include iodine-131 (or iodine-123) meta-iodobenzylguanidine (MIBG), a norepinephrine analogue, and fluorine- 18 fluorodeoxyglucose (F- 18 FDG), a positron-emitting radiotracer More detailed information regarding these radiotracers is presented in Chapter 31 This chapter discusses the role of radionuclide imaging in the diagnostic evaluation of pancreatic endocrine tumors Therapeutic applications... REFERENCES 18 1 2 3 4 5 6 7 8 9 10 11 12 13 Megibow AJ, Lavelle MT, Rofsky NM MR imaging of the pancreas Surg Clin North Am 2001; 81 (2):307–320, ix–x Martin DR, Semelka RC MR imaging of pancreatic masses Magnet Reson Imaging Clin North Am 2000; 8( 4): 787 81 2 Murphy KJ, Brunberg JA, Cohan RH Adverse reactions to gadolinium contrast media: a review of 36 cases AJR Am J Roentgenol 1996; 167(4) :84 7 84 9 Prince . T1-weighted, GRE, fat-suppressed sequence both with and without contrast (9, 18) , a T2-weighted FSE or single-shot (SS) sequence with or without fat suppression, and a thin- slice, single-shot. resect insulinomas. Surgery 1991; 110: 989 –997. 6. Grant CS, van Heerden JA, Charboneau JW, et al. Insu- linoma: the value of intraoperative ultrasonography. Arch Surg 1 988 ; 123 :84 3 84 8. 7. Jensen RT,. sensitivities ranging from 82 to 86 % (8, 9). Five to 10% of patients with an insulinoma have multiple endocrine neoplasia (MEN )-1 syndrome. MEN-associated insulinomas are more frequently multiple (10). Gastrimomas

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