eMedicine Specialties > Pediatrics: General Medicine > Endocrinology

Multiple Endocrine Neoplasia: Differential Diagnoses & Workup

Author: Robert J Ferry Jr, MD, Chief, Division of Pediatric Endocrinology and Diabetes, Le Bonheur Children's Medical Center, University of Tennessee Health Science Center at Memphis and St Jude Children's Research Hospital; Lieutenant Colonel (Medical Corps), 162nd Area Support Medical Company, Army National Guard
Coauthor(s): Klaus Radebold, MD, PhD, Research Associate, Department of Surgery, Yale University School of Medicine; Christian A Koch, MD, PhD, FACP, FACE, Professor and Director, Division of Endocrinology, University of Mississippi Medical Center; George P Chrousos, MD, FAAP, MACP, MACE, Professor and Chair, Department of Pediatrics, Athens University Medical School
Contributor Information and Disclosures

Updated: Jun 12, 2008

Differential Diagnoses

Carcinoid Tumor
Gastroesophageal Reflux
Hypercalcemia
Pheochromocytoma
VIPoma
Zollinger-Ellison Syndrome

Other Problems to Be Considered

Mastocytosis
Type 1 multiple endocrine neoplasia (MEN): Gastrinoma, adrenal adenoma, and glucagonomas
Type 2B MEN: Medullary carcinoma of the thyroid, mucosal neuromas, and ganglioneuromas

Other conditions associated with elevated gastrin levels

Massive small-bowel resection
Hypercalcemia
Treatment with histamine 2 (H2) blockers or proton-pump inhibitors (PPIs), such as omeprazole
Gastric-outlet obstruction

Workup

Laboratory Studies

Laboratory studies include investigations of the different tumor-expression patterns.

  • Gastrinomas (ZES): Serum gastrin levels exceed 115 ng/mL and increase more than 200 ng/mL from baseline after secretin challenge (ie, intravenous injection of 2 U/kg of secretin). Approximately two-thirds of patients have basal gastrin levels of 150-1000 ng/mL.
  • Insulinoma
    • Results may reveal fasting hypoglycemia with inappropriately elevated serum insulin, C-peptide, or proinsulin concentrations.
    • When the serum glucose level is less than 60 mg/dL, the serum insulin level should be less than 2 µU/mL. A serum insulin level of less than 2 µU/mL during hypoglycemia is consistent with hyperinsulinism.
    • Additional diagnostic criteria include the following:
      • Decreased fasting tolerance (defined during a controlled inpatient fast)
      • Inappropriate glycemic response to glucagon challenge when the patient is hypoglycemic (ie, increase in serum glucose level by >30 mg/dL from a baseline of <60 mg/dL within 20 min after 1 mg of glucagon is intravenously or subcutaneously administered)
      • Suppressed lipolysis (free fatty acid concentration <20 mM)
      • Suppressed ketogenesis (undetectable plasma acetoacetate or beta-hydroxybutyrate) when the patient has hypoglycemia
      • Acute insulin response to peripheral venous or intra-arterial calcium challenge (performed at centers including the University of Texas Health Science Center at San Antonio and the Children's Hospital of Philadelphia)
  • Glucagonoma: Findings are hyperglycemia with elevated serum glucagon levels.
  • Watery diarrhea syndrome: Serum levels of vasoactive intestinal peptide are elevated. Serum K levels may be low.
  • Carcinoids: levels of serotonin, urinary 5-hydroxyindoleacetic acid (5-HIAA), calcitonin, and 24-hour urinary free cortisol and corticotropin may be elevated.
  • Pituitary tumors: Tests reveal persistent elevation of serum somatotropin (growth hormone [GH]) during oral glucose challenge; serum free or total insulinlike growth factor (IGF)-I level more than 2 standard deviations (for age, sex, and Tanner stage); or elevated serum prolactin levels.
  • Type 2 multiple endocrine neoplasia
    • MTC: Patients frequently have elevated calcitonin levels.
    • Pheochromocytoma: Total urine catecholamine excretion exceeds 100-300 μg/d (over 24 h). Serum levels of more than 2000 μg/mL are pathognomonic. Measuring plasma free and urinary fractionated metanephrines with a 24-hour collection is best.

Imaging Studies

  • Type 1 multiple endocrine neoplasia
    • Gastrinomas: Somatostatin-receptor scintigraphy (SRS) has a sensitivity of 70-90%, which is more than that of any other imaging procedure. SRS depends on the SSR receptor profile (types 2 and 5, rarely type 3) and tumors size (exceeding 5 mm). Endoscopic ultrasonography can depict tumors in the pancreatic head but rarely in the duodenal wall.
    • Insulinomas: Perform high-resolution CT scanning and MRI first. SRS findings are positive in about 50% of patients. Intraoperative ultrasonography of the pancreas is highly recommended to detect additional tumors.
    • Pituitary tumors: Perform MRI, CT scanning, or both after biochemical evaluation.
  • Pheochromocytoma: Radiologic imaging for pheochromocytomas includes CT scanning, MRI, metaiodobenzylguanidine (MIBG) scanning, OctreoScan imaging, and positive emission tomography (PET).
  • Nonfunctioning pancreatic endocrine tumors: After type 1 multiple endocrine neoplasia (MEN) is confirmed, perform pancreatic endoscopic ultrasonography to monitor progression of nonfunctioning pancreatic endocrine tumors. Their incidence is high (54.9%), although their clinical significance remains uncertain. Follow-up of lesions discovered should be coordinated with experienced subspecialists.

Histologic Findings

  • Parathyroid glands: The glands show hyperplasia and diffuse or nodular proliferations of chief cells, mixed with some oncocytic cells. All glands are involved.
  • Pancreas: Numerous microadenomas (mostly in the pancreatic tail) are present. The tumors display a trabecular pattern. Immunohistochemically, tumor cells stain with antibodies directed to pancreatic polypeptide, glucagon, insulin, and gastrin.
  • Duodenum: Duodenal tumors are most often gastrinomas in the first part of the duodenum. They stain positive for gastrin and may metastasize to regional lymph nodes.
  • Stomach: In the stomach, diffuse hyperplasia of enterochromaffinlike (ECL) cells is found and is associated with tumors of considerable size but rarely of metastatic potential.
  • Pituitary: Most tumors are single, are found in the anterior part of the gland, and produce prolactin and/or GH, and, occasionally, corticotropin.

More on Multiple Endocrine Neoplasia

Overview: Multiple Endocrine Neoplasia
Differential Diagnoses & Workup: Multiple Endocrine Neoplasia
Treatment & Medication: Multiple Endocrine Neoplasia
Follow-up: Multiple Endocrine Neoplasia
References
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Further Reading

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Keywords

multiple endocrine neoplasia, MEN syndrome, MEN 1, MEN 2A, MEN 2B, Wermer syndrome, Wermer's syndrome, Sipple syndrome, Sipple's syndrome, multiple endocrine adenopathy, MEA, pluriglandular syndrome, Carney complex, vasoactive intestinal peptide tumor, VIPoma, pancreatic polypeptide–producing tumor, PPoma, medullary thyroid carcinoma, MTC, gastrinoma, insulinoma, glucagonoma, prolactinoma, somatotropinoma, corticotropinoma, nonfunctioning tumors, lipomas, angiofibromas, pheochromocytoma, hyperparathyroidism, parathyroid gland hyperplasia, thyroid cancer, mucosal neuroma, medullated corneal nerve fibers, marfanoid habitus, peptic ulcer disease, coronary heart disease, hypercalcemia, stroke, heart failure, Zollinger-Ellison syndrome, ZES, Hirschsprung disease

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Contributor Information and Disclosures

Author

Robert J Ferry Jr, MD, Chief, Division of Pediatric Endocrinology and Diabetes, Le Bonheur Children's Medical Center, University of Tennessee Health Science Center at Memphis and St Jude Children's Research Hospital; Lieutenant Colonel (Medical Corps), 162nd Area Support Medical Company, Army National Guard
Robert J Ferry Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, American Medical Association, Endocrine Society, Lawson-Wilkins Pediatric Endocrine Society, Society for Pediatric Research, and Texas Pediatric Society
Disclosure: Nutropin Speakers Bureau Honoraria Speaking and teaching

Coauthor(s)

Klaus Radebold, MD, PhD, Research Associate, Department of Surgery, Yale University School of Medicine
Klaus Radebold, MD, PhD is a member of the following medical societies: American Gastroenterological Association and New York Academy of Sciences
Disclosure: Nothing to disclose.

Christian A Koch, MD, PhD, FACP, FACE, Professor and Director, Division of Endocrinology, University of Mississippi Medical Center
Christian A Koch, MD, PhD, FACP, FACE is a member of the following medical societies: American Academy of Neurology, American Association of Clinical Endocrinologists, American College of Clinical Endocrinologists, American College of Physicians-American Society of Internal Medicine, American Society for Clinical Pharmacology and Therapeutics, American Society for Dermatologic Surgery, Endocrine Society, and German Diabetes Society
Disclosure: Nothing to disclose.

George P Chrousos, MD, FAAP, MACP, MACE, Professor and Chair, Department of Pediatrics, Athens University Medical School
George P Chrousos, MD, FAAP, MACP, MACE is a member of the following medical societies: American Academy of Pediatrics, American College of Endocrinology, American College of Physicians, American Pediatric Society, American Society for Clinical Investigation, Association of American Physicians, Endocrine Society, Lawson-Wilkins Pediatric Endocrine Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Medical Editor

Arlan L Rosenbloom, MD, Adjunct Distinguished Service Professor Emeritus of Pediatrics, University of Florida; Fellow of the American Academy of Pediatrics; Fellow of the American College of Epidemiology
Arlan L Rosenbloom, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Epidemiology, American Pediatric Society, Endocrine Society, Florida Pediatric Society, Lawson-Wilkins Pediatric Endocrine Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Lynne Lipton Levitsky, MD, Chief, Pediatric Endocrine Unit, Massachusetts General Hospital; Associate Professor, Department of Pediatrics, Harvard University Medical School
Lynne Lipton Levitsky, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Diabetes Association, American Pediatric Society, Endocrine Society, Lawson-Wilkins Pediatric Endocrine Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

CME Editor

Merrily P M Poth, MD, Professor, Department of Pediatrics and Neuroscience, Uniformed Services University of the Health Sciences
Merrily P M Poth, MD is a member of the following medical societies: American Academy of Pediatrics, Endocrine Society, and Lawson-Wilkins Pediatric Endocrine Society
Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD, Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas and Arkansas Children's Hospital
Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, and Southern Society for Pediatric Research
Disclosure: Genentech, Inc. Honoraria Speaking and teaching; Pfiser, Inc. Honoraria Consulting

 
 
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