eMedicine Specialties > Gastroenterology > Stomach
Gastrinoma
Updated: Aug 29, 2009
Introduction
Background
A gastrinoma is a gastrin-secreting tumor that can occur in the pancreas, although it is most commonly found in the duodenum. Duodenal wall gastrinomas have been identified in 40-50% of patients. These duodenal wall tumors are frequently small and multiple. Sporadic tumors occurring in the pancreas tend to be solitary and have greater malignant potential as compared to duodenal gastrinomas.1
More than 80% of gastrinomas arise within the triangle defined as the confluence of the cystic and common bile duct superiorly, the second and third portions of the duodenum inferiorly, and the neck and body of the pancreas medially.
Rarely, primary tumors also occur in a variety of ectopic sites, including the body of the stomach, jejunum, peripancreatic lymph nodes, splenic hilum, omentum, liver, gallbladder, common bile duct, and the ovary.
Over 50% of gastrinomas are malignant and can metastasize to regional lymph nodes and the liver. One fourth of gastrinomas are related to multiple endocrine neoplasia (MEN) type I and are associated with hyperparathyroidism and pituitary adenomas. These MEN I associated tumors have been observed to occur at an earlier age than sporadic tumors and often follow a more benign course.
The triad of nonbeta islet cell tumors of the pancreas (gastrinomas), hypergastrinemia, and severe ulcer disease was described by Zollinger and Ellison in 1955, hence the eponym Zollinger-Ellison syndrome (ZES).
Pathophysiology
Enormous secretion of gastrin from the tumor cells leads to hyperplasia of fundic parietal cells and increased basal acid secretion. This results in severe ulcer disease. Ulceration might even extend into the small intestine. The acidic content of the small intestine causes the release of secretin, which is responsible for the diarrhea, in part, caused by the outpouring of water and bicarbonate from the pancreas and small intestine.
A recent small study by Kohan et al describes duodenal bulb mucosa with hypertrophic heterotopia in patients with ZES.2 The investigators evaluated the incidence of duodenal gastric oxyntic hypertrophic heterotopia in 7 patients with ZES over an average period of 5 years. The patients underwent endoscopic examinations with methylene blue staining and biopsy of the gastric and duodenal mucosa every 3-6 months.
Of the 7 patients with ZES and an intact stomach and duodenum, 2 had no evidence of duodenal mucosal hypertrophic heterotopia, but 5 did, in whom bowel mucosa biopsies revealed patchy replacement of surface epithelium by gastric-type epithelium with hypertrophic oxyntic glands in the lamina propria.2 In addition, the patients with gastric oxyntic hypertrophic heterotopia had higher levels of average serum gastrin and basal acid output levels than those without gastric oxyntic hypertrophic heterotopia, a finding that Kohan et al suggest not only could hypertrophic and heterotopic gastric mucosa result from increased gastrin levels but that an increased incidence of postbulbar ulcers may result in affected patients.2
Frequency
International
The true incidence of ZES is not known. ZES constitutes 0.1% or more of cases of peptic ulcer disease. Although rare, gastrinomas are the most common pancreatic islet cell tumors.
Mortality/Morbidity
With the advent of antiulcer medications, the number of deaths secondary to ulcer complications decreased significantly. The primary determinants of survival for patients with gastrinomas are the size of the primary tumor and the occurrence of tumor metastasis.
- Patients with hepatic metastases may have a remaining life span of less than 1 year.
- In patients with liver metastasis, the 5-year survival rate is 20-30%.
- In patients with localized disease or metastasis to local lymph nodes without liver metastasis, the 5-year survival rate is 90%.
Sex
Gastrinomas are more common in males than in females, with ratios from 1.5:1 to 2:1.
Age
Although gastrinomas can occur at any age, the initial clinical manifestation usually appears in people aged 30-50 years.
Clinical
History
- The symptoms in 90-95% of patients with gastrinomas are similar to the symptoms of common peptic ulcer disease. Usually, persistent abdominal pain exists that is less responsive to medical treatment.
- Sometimes, symptoms may relate to a complication of peptic ulcer disease, such as bleeding (eg, melena, hematemesis), gastric outlet obstruction (eg, vomiting), and perforation (eg, peritoneal irritation).
- Other symptoms include gastroesophageal reflux, diarrhea, steatorrhea, and weight loss, all of which are secondary to acid hypersecretion. Vitamin B-12 malabsorption, which is not correctable by oral intrinsic factor, may also be observed.
- Chronic acid reflux may lead to esophageal complications (eg, esophagitis, stricture formation, Barrett esophagus) in up to two thirds of patients with Zollinger-Ellison syndrome.
Physical
- Epigastric tenderness is the most frequent abnormal physical finding. Depending on the possible ulcer complications, signs may vary.
- Nearly 75% of ulcers in patients with gastrinomas are present in the first portion of the duodenum. These ulcers usually are single or multiple and are indistinguishable from peptic ulcer disease.
- Nearly 10% of patients with ZES have no demonstrable ulcer. Ulcers located in the second, third, or fourth portion of the duodenum or jejunum should increase the possibility of gastrinoma.
- The other factors that alert one to the presence of underlying gastrinomas are the following:
- Ulcers that are refractory to standard therapy
- Multiple ulcers
- Giant ulcers, larger than 2 cm
- Recurrent ulcers
- Ulcers with unexplained diarrhea
- Strong family history of ulcers
- Hypercalcemia
- Duodenal ulcer that is not related to Helicobacter pylori infection or nonsteroidal anti-inflammatory drug use
Differential Diagnoses
Achlorhydria
Gastric Outlet Obstruction
Gastritis, Atrophic
Peptic Ulcer Disease
Pernicious Anemia
Zollinger-Ellison Syndrome
Other Problems to Be Considered
Antral G-cell hyperfunction
Massive small intestine resection
Workup
Laboratory Studies
- Due to the elusive nature of the neoplasm, the diagnosis is based on the following 3 criteria:
- Fasting hypergastrinemia is present (>150 pg/mL with levels >100,000 pg/mL in some patients; a serum gastrin level >1,000 pg/mL in the appropriate clinical setting is virtually diagnostic of Zollinger-Ellison syndrome).
- Basal acid output (BAO) is greater than 10 mEq/h.
- Results from a secretin stimulation test are positive.
- Fasting serum gastrin measurement is discussed as follows:
- This is the most sensitive test for the diagnosis of ZES.
- This screening test is indicated for patients strongly considered to have gastrinoma (see History).
- Stop histamine 2 (H2) blockers 1 day or omeprazole 6 days prior to performing the study.
- The reference range for fasting serum gastrin usually is 50-60 pg/mL, with an upper limit as high as 150 pg/mL.
- Levels higher than 1000 pg/mL with acid hypersecretion are highly suggestive of ZES.
- Because low gastric acid output (eg, in atrophic gastritis, pernicious anemia, or postvagotomy state) can lead to hypergastrinemia, check patients for the following:
- A gastric pH level higher than 3.0 excludes gastrinoma.
- A BAO of greater than 15 mEq/h and even as high as 150 mEq/h is indicative of gastrinoma.
- In patients with intermediate gastrin levels (150-1000 pg/mL) and acid secretion, the secretin stimulation test can help diagnose the presence of gastrinoma. Intravenous secretin (2 U/kg) raises serum gastrin levels to higher than 200 pg/mL within 2 minutes and, virtually always, within 10 minutes in patients with gastrinomas.
Imaging Studies
- Imaging studies are helpful to help localize the tumor. They also are helpful for assessing surgical resectability by helping reveal liver metastasis.
- Somatostatin receptor scintigraphy (SRS) is very useful for helping identify the primary lesions preoperatively. SRS is the most sensitive noninvasive method for localizing primary tumors and metastases. It also is helpful for detecting the presence of liver or bone metastasis. The findings from this technique can be used to differentiate small liver metastases from small liver hemangiomas. Occasionally, false-positive SRS localization results can occur.
- Endoscopic ultrasound also has been found to be useful in helping detect primary tumor, with a reported overall sensitivity and accuracy of higher than 90% for intrapancreatic gastrinomas. For extrapancreatic gastrinomas in the duodenal wall, endoscopic ultrasound is useful but somewhat less sensitive.
- CT scan and selective angiogram also are helpful for detecting gastrinoma.
- MRI can be used as an adjunct to the imaging studies already discussed. MRI has great value in identifying liver metastases but has not been shown to be useful in detecting extrahepatic tumors less than 1 cm in diameter.
- Because of the large proportion of primary gastrinomas in the proximal duodenum, upper endoscopy may also be a useful tool in the localization of tumors in these patients.
Other Tests
- Selective arterial secretin injection, involving gastroduodenal, splenic, and superior mesenteric arteries, with hepatic vein serum gastrin concentrations is one among some other diagnostic procedures proposed for helping identify gastrinomas. However, this test has been shown to be of value primarily in localizing gastrinomas to the head of the pancreas and proximal duodenum and, therefore, is infrequently recommended.
- The calcium infusion test, calcium gluconate, is infused intravenously over 180 minutes with serum gastrin levels obtained at set intervals. In most patients with gastrinomas, this should substantially increase serum gastrin levels (>400 pg/mL increase).
- Serum chromogranin A, a nonspecific marker for neuroendocrine tumors, has been shown to be increased in gastrinoma patients with serum levels correlating with tumor burden.
Treatment
Medical Care
Individualize the selection of treatment. Base treatment on factors related to ulcer disease, diarrhea, and malignant properties of the tumor. Antisecretory medications are helpful for controlling the manifestations of peptic acid disease and secretory diarrhea (secondary to hyperacidity).
- Proton pump inhibitors (eg, omeprazole, lansoprazole)
- These are highly effective drugs and are the drugs of choice for suppressing acid secretion. Long duration of action, fewer adverse effects, and high potency make them superior to H2 blockers.
- In 60% of patients, ulcer healing occurs within 2 weeks. In 90-100% of patients, healing occurs within 4 weeks.
- The recommended initial dose of omeprazole is 60 mg/d. Divided, twice-a-day dosing is suggested for doses greater than 80 mg/d. Once an effective maintenance dose is achieved, tapering of the medication, while monitoring symptoms and acid output, is suggested.
- H2-receptor antagonists
- The dose usually is 4-8 times higher than the dose administered to patients with peptic ulcer disease.
- Although a good success rate exists, this treatment has been reported to fail in 50% of patients.
- Chemotherapy
- This is indicated in patients with metastatic disease and in patients who are not candidates for surgery; however, it is not indicated for metastatic disease confined to the lymph nodes.
- Chemotherapy reduces tumor size and improves the symptoms secondary to metastatic effects of the tumor.
- A combination of streptozocin, 5-fluorouracil, and doxorubicin has been used, with the response rate reported to be as high as 65%.
- Granberg et al described a patient with almost complete response on treatment with Sandostatin LAR, a long-acting somatostatin analog.3
- Interferon or targeted radiotherapy may also be considered in patients who are not candidates for chemotherapy.
Surgical Care
- Surgical care is indicated for localized disease. Surgical resection of localized disease leads to a complete cure without any recurrence in 20-25% of patients with gastrinomas.
- Patients who have an isolated lesion or patients in whom the preoperative workup fails to localize the tumor should undergo laparotomy (by an experienced surgeon) with the intent to resect.
- It has been reported that Whipple pancreaticoduodenectomy affords the greatest probability for cure, particularly for MEN I associated gastrinomas, though also for sporadic tumors, since it results in removal of the entire gastrinoma triangle. However, the excellent long-term survival in patients with less complicated surgeries and the increased morbidity and mortality associated with the Whipple procedure make its general utility still unclear and recommended primarily for large, advanced tumors.
Consultations
- Gastroenterologist
- Endocrinologist
- Oncologist
- Surgeon
Medication
Immediate and sustained control of gastric acid hypersecretion is the most important aspect of disease management in patients with ZES because acid hypersecretion is the cause of essentially all symptoms and early morbidity and mortality.
Once ZES is considered and while appropriate diagnostic tests are conducted, acute acid secretion usually is best controlled with oral administration of a proton pump inhibitor (eg, omeprazole, lansoprazole, rabeprazole, esomeprazole). However, continuous infusion of an H2 antagonist (eg, ranitidine, cimetidine, famotidine), often at high doses, may be necessary for a small proportion of patients requiring rapid control of acid secretion who are unable to take oral medication.
Long-term management of acid secretion with a high dose of a proton pump inhibitor (or H2 blocker) is safe and effective.
Proton pump inhibitors
These agents bind to the proton pump of the parietal cell, inhibiting secretion of hydrogen ions into the gastric lumen. These agents are more effective than H2 blockers in relieving pain and healing ulcers. They are the drugs of choice in ZES. Although the drugs in this class are equally effective, omeprazole is used most commonly. Efficacy and tolerability of parenterally administered proton pump inhibitors in the acute treatment of patients with suspected ZES have not been established.
Omeprazole (Prilosec)
Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ -ATP pump.
Titrate dose to achieve a BAO of 10 mEq/h. Gastric acid hypersecretion usually is controlled with doses <80 mg/d, but doses up to and even >200 mg/d have been used in some patients.
Dosing
Adult
40-120 mg/d PO
Pediatric
Not established
Interactions
May decrease effects of itraconazole and ketoconazole; may increase toxicity of warfarin, digoxin, and phenytoin
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Bioavailability may increase in elderly persons
Lansoprazole (Prevacid)
Inhibits gastric acid secretion. Titrate dose to achieve a BAO of 10 mEq/h. Efficacy and tolerability of IV administration in acute treatment of patients with suspected ZES have not been established.
Dosing
Adult
30 mg PO qd
Pediatric
Not established
Interactions
May decrease effects of ketoconazole and itraconazole; may increase theophylline clearance
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
B - Usually safe but benefits must outweigh the risks.
Precautions
Consider adjusting dose in patients with liver impairment
Rabeprazole (Aciphex)
Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ -ATP pump. Titrate dose to achieve a BAO of 10 mEq/h.
Dosing
Adult
20-mg tab PO qd for 4-8 wk
Pediatric
Not established
Interactions
May decrease effects of itraconazole and ketoconazole; may increase toxicity of warfarin, digoxin, and phenytoin
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
B - Usually safe but benefits must outweigh the risks.
Precautions
Symptomatic relief with proton pump inhibitors may mask symptoms of gastric malignancy
Esomeprazole magnesium (Nexium)
S-isomer of omeprazole. Inhibits gastric acid secretion by inhibiting H+/K+ -ATP pump at secretory surface of gastric parietal cells. Titrate dose to achieve a BAO of 10 mEq/h.
Dosing
Adult
20 mg PO qd for 4 wk
Pediatric
Not established
Interactions
Amoxicillin or clarithromycin may increase plasma levels when used concurrently; may reduce absorption of dapsone; may increase levels of diazepam and GI absorption of digoxin; may decrease absorption of iron, ketoconazole, and itraconazole
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Symptomatic relief with proton pump inhibitors may mask symptoms of gastric malignancy
H2-receptor antagonists
Inhibit the action of histamine on the parietal cell, which inhibits acid secretion. All agents in this class are equally effective. Intravenous administration may be helpful in patients who are unable to take oral medication.
Ranitidine (Zantac)
Inhibits histamine stimulation of the H2 receptor in gastric parietal cells, which, in turn, reduces gastric acid secretion, gastric volume, and hydrogen concentrations. Titrate dose to achieve BAO <10 mEq/h.
Dosing
Adult
150 mg PO bid; not to exceed 600 mg/d
Alternatively, 50 mg/dose IV/IM q6-8h
Pediatric
<12 years: Not established
>12 years: 1.25-2.5 mg/kg/dose PO q12h; not to exceed 300 mg/d; alternatively, 0.75-1.5 mg/kg/dose IV/IM q6-8h; not to exceed 400 mg/d
Interactions
May decrease effects of ketoconazole and itraconazole; may alter serum levels of ferrous sulfate, diazepam, nondepolarizing muscle relaxants, and oxaprozin
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
B - Usually safe but benefits must outweigh the risks.
Precautions
Caution in renal or liver impairment; if changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment
Cimetidine (Tagamet)
Inhibits histamine at H2 receptors of the gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen concentrations. Titrate dose to achieve BAO <10 mEq/h.
Dosing
Adult
150 mg PO qid; not to exceed 600 mg/d; 50 mg/dose IV/IM q6-8h; not to exceed 400 mg/d
Pediatric
Not established
Interactions
Can increase blood levels of theophylline, warfarin, tricyclic antidepressants, triamterene, phenytoin, quinidine, propranolol, metronidazole, procainamide, and lidocaine
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
B - Usually safe but benefits must outweigh the risks.
Precautions
Elderly persons may experience confusional states; may cause impotence and gynecomastia in young males; may increase levels of many drugs; adjust dose or discontinue treatment if changes in renal function occur
Famotidine (Pepcid)
Competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen concentrations. Titrate dose to achieve a BAO of 10 mEq/h.
Dosing
Adult
40 mg PO bid
Pediatric
Not established
Interactions
May decrease the effects of ketoconazole and itraconazole
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
B - Usually safe but benefits must outweigh the risks.
Precautions
If changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment
Chemotherapeutic agents
Indicated in metastatic disease and in patients who are not candidates for surgery. Reduce tumor size and improve symptoms secondary to metastatic effects of the tumor. A combination of streptozocin, 5-fluorouracil, and doxorubicin has been used, with a response rate of as high as 65%.
Streptozocin (Zanosar)
Inhibits DNA synthesis without significantly affecting bacterial or mammalian RNA or protein synthesis.
Dosing
Adult
Administer under direction of oncologist experienced in both use of medication and treatment of this disease
Pediatric
Not established
Interactions
None reported
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Monitor closely for evidence of renal, hepatic, or hematopoietic toxicity; perform CBC count and LFTs weekly
5-Fluorouracil (Adrucil)
Interferes with DNA synthesis by blocking methylation of deoxyuridylic acid, inhibiting thymidylate synthetase, and, subsequently, inhibiting cell proliferation.
Dosing
Adult
Administer under direction of oncologist experienced in both use of medication and treatment of this disease
Pediatric
Not established
Interactions
Leucovorin may enhance toxicity
Contraindications
Documented hypersensitivity; poor nutritional status; depressed bone marrow function; potentially serious infections
Precautions
Pregnancy
D - Unsafe in pregnancy
Precautions
Discontinue use if stomatitis or esophagopharyngitis, rapidly falling WBC count, leukopenia (WBC <3500/mm3), intractable vomiting, diarrhea, GI ulceration and bleeding, thrombocytopenia (platelets <100,000/mm3), or hemorrhage occurs
Doxorubicin (Adriamycin, Rubex)
Inhibits topoisomerase II and produces free radicals, which may cause the destruction of DNA. The combination of these 2 events can, in turn, inhibit the growth of neoplastic cells.
Dosing
Adult
Administer under direction of oncologist experienced in both use of medication and treatment of this disease
Pediatric
Not established
Interactions
May decrease phenytoin and digoxin plasma levels; phenobarbital may decrease plasma levels; cyclosporine may induce coma or seizures; mercaptopurine increases toxicity; cyclophosphamide increases cardiac toxicity
Contraindications
Documented hypersensitivity; severe heart failure, cardiomyopathy, impaired cardiac function, preexisting myelosuppression
Precautions
Pregnancy
D - Unsafe in pregnancy
Precautions
Irreversible cardiac toxicity and myelosuppression may occur; extravasation may result in severe local tissue necrosis; reduce dose in patients with impaired hepatic function
Follow-up
Further Outpatient Care
- Follow-up of patients with gastrinomas that have been resected is directed at the diagnosis and treatment of recurrence.
- Measurement of the fasting serum gastrin level is the best screening test to monitor these patients.
- Disease recurrence might present as a recurrent peptic ulceration, diarrhea, or abdominal pain.
- If recurrent disease is identified, reoperation may be considered and undertaken if no evidence of metastasis exists.
- Metastatic disease can be managed with chemotherapy and long-term acid suppression.
Prognosis
- The primary determinants of survival for patients with gastrinomas are the size of the primary tumor and the development of tumor metastasis.
- Patients with hepatic metastases may have a remaining life span of less than 1 year.
- In patients with liver metastasis, the 5-year survival rate is 20-30%.
- In patients with localized disease or metastasis to local lymph nodes without liver metastasis, the 5-year survival rate may be 90%.
- Surgical resection of localized disease leads to a complete cure without any recurrence in 20-25% of patients with gastrinomas.
Miscellaneous
Medicolegal Pitfalls
- Gastrinoma can be a difficult diagnosis. However, delay in diagnosis or misdiagnosis can lead to incorrect treatment or less successful treatment secondary to any such delay. Thus, gastrinoma always should be included in the differential diagnosis in those patients with the appropriate symptoms (see Clinical).
- Risks exist regarding medication-induced adverse effects and the surgical procedures associated with the treatment of this disease.
References
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Feldman M, Sleisenger MW, McGuigan JE. Zollinger-Ellison syndrome and other hypersecretory states. In: Feldman M, Scharschmidt BF, Sleisenger M, Zorab R, eds. Sleisenger & Fordtran's Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management. 6th ed. Philadelphia, Pa: WB Saunders; 1998:. 679-90.
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Passaro E, Howard TJ, Sawicki MP. The origin of sporadic gastrinomas within the gastrinoma triangle: a theory. Arch Surg. Jan 1998;133(1):13-6; discussion 17. [Medline].
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Keywords
gastrinoma, Zollinger-Ellison syndrome, ZES, ZE syndrome, pancreatic tumor, pancreas tumor, duodenal tumor, duodenal wall tumor, lymph node tumor, gastrin-secreting tumor, tumor, pancreatic islet cell tumors, malignancy, malignant tumor, basal acid output, BAO, ulcer, severe ulcer disease, multiple endocrine neoplasia type I, MEN type I, ulcerogenic islet cell tumor
Contributor Information and Disclosures
Author
Jennifer Lynn Bonheur, MD, Attending Physician, Division of Gastroenterology, Lenox Hill Hospital
Jennifer Lynn Bonheur, MD is a member of the following medical societies: American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, New York Academy of Sciences, New York Society for Gastrointestinal Endoscopy, and Sigma Xi
Disclosure: Nothing to disclose.
Coauthor(s)
Senthil Nachimuthu, MD, FACP, Fellow in Cardiology, Heart and Vascular Institute, Tulane University School of Medicine
Senthil Nachimuthu, MD, FACP is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.
Medical Editor
Manoop S Bhutani, MD, FACG, FACP, Professor, Department of Medicine, Division of Gastroenterology, Director, Center for Endoscopic Ultrasound, Co-Director, Center for Endoscopic Research, Training and Innovation, University of Texas Medical Branch at Galveston
Manoop S Bhutani, MD, FACG, FACP is a member of the following medical societies: American Association for the Advancement of Science, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Institute of Ultrasound in Medicine, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.
Pharmacy Editor
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Managing Editor
Simmy Bank, MD, Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine
Disclosure: Nothing to disclose.
CME Editor
Rajalaxmi McKenna, MD, FACP, Consulting Staff, Department of Medicine, Southwest Medical Consultants, SC, Good Samaritan Hospital, Advocate Health Systems
Rajalaxmi McKenna, MD, FACP is a member of the following medical societies: American Society of Clinical Oncology, American Society of Hematology, and International Society on Thrombosis and Haemostasis
Disclosure: Nothing to disclose.
Chief Editor
Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.
Related eMedicine Topics
- Gastric Ulcers
- Multiple Endocrine Neoplasia [in the Pediatrics: General Medicine section]
- Neoplasms of the Endocrine Pancreas [in the Oncology section]
- Pancreas, Islet Cell Tumors [in the Radiology section]
- Zollinger-Ellison Syndrome [in the Gastroenterology section]
- Zollinger-Ellison Syndrome [in the Pediatrics: General Medicine section]
Clinical Trials
- Combination Chemotherapy and Bevacizumab in Treating Patients With Advanced Neuroendocrine Tumors
- Radiolabeled Octreotide in Treating Children With Advanced or Refractory Solid Tumors
- Treatment of Zollinger-Ellison Syndrome With Prevacid
- ACR Appropriateness Criteria® acute abdominal pain and fever or suspected abdominal abscess. American College of Radiology - Medical Specialty Society. 1996 (revised 2006). 7 pages. NGC:005138
- ASCO 2006 update of recommendations for the use of tumor markers in gastrointestinal cancer. American Society of Clinical Oncology - Medical Specialty Society. 996 (revised 2006 Nov 20). 15 pages. NGC:005328
- ASGE guideline: the role of endoscopy in the diagnosis and the management of cystic lesions and inflammatory fluid collections of the pancreas. American Society for Gastrointestinal Endoscopy - Medical Specialty Society. 2005 Mar. 8 pages. NGC:004190
- ASGE guideline: the role of ERCP in diseases of the biliary tract and the pancreas. American Society for Gastrointestinal Endoscopy - Medical Specialty Society. 2005 Jul. 8 pages. NGC:004486
- Quality indicators for endoscopic retrograde cholangiopancreatography. American College of Gastroenterology - Medical Specialty Society; American Society for Gastrointestinal Endoscopy - Medical Specialty Society. 2006 Apr. 6 pages. NGC:004967
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