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islet cell tumor; pancreatic neuroendocrine neoplasm; nesidioblastoma

Pathology: - 75-90% of pancreatic neuroendocrine tumors are non-functional - 10-25% of pancreatic neuroendocrine tumors are functional [1] - insulinomas ~60% (beta-cell tumors) - APUDomas (alpha-cell tumors) - gastrinomas ~20% - glucagonoma - somatostatinoma - VIPoma (vasoactive intestinal polypeptide) - GRFoma - CRFoma - PPoma - neurotensinoma - may be benign or malignant - cannot be determined on basis of histology Genetics: - YY1 gene mutation Clinical manifestations: 1) secretion of gastrointestinal hormones a) vasoactive intestinal polypeptide (VIP) 1] secretory diarrhea 2] hypokalemia 3] flushing b) glucagon 1] diabetes mellitus 2] skin rash, especially migrating necrotizing erythema c) somatostatin 1] gallstones 2] diabetes mellitus 3] steatorrhea d) gastrin 1] esophagitis 2] peptic ulcer e) pancreatic polypeptide (P-Poma) -> no characteristic clinical syndrome 2) secretion of other endocrine peptides a) GRFoma b) CRFoma c) neurotensinoma d) vasopressinoma e) MSHoma 3) 80% of tumors are multiple or malignant Laboratory: -> serum chemistries a) serum gastrin b) serum vasoactive intestinal polypeptide (VIP) c) serum glucagon d) serum somatostatin e) serum pancreatic polypeptide f) serum chromogranin A may serve as a marker for all APUDomas Special laboratory: - endoscopic ultrasonography Radiology: 1) computed tomography (CT) & spiral CT 2) octreotide radioisotope scan - most APUDomas express cell surface somatostatin receptors 3) gadolinium-enhanced magnetic resonance imaging (MRI) 4) angiography Management: 1) treatment is not indicated for asymptomatic patients [5] 2) surgical resection for single & benign tumors 3) high dose proton pump inhibitor for gastrinoma - omeprazole 40-240 mg/day 4) surgical debulking of tumor a) VIPoma b) glucagonoma c) somatostatinoma e) P-Poma 4) octreotide injections 50-300 ug SQ QD can control hormonal effects & lead to tumor regression in some patients 5) chemotherapy minimally effective [1] 6) sunitinib & everolimus are active [1] 7) capecitabine plus temozolomide is active [1] 8) chemoembolization can be used to reduce tumor volume in cases of liver metastasis [5] 9) prognosis is better than for adenocarcinoma of the pancreas

Interactions

disease interactions

Related

amine precursor uptake & decarboxylation tumor (APUDoma)

Specific

benign islet cell tumor CRFoma glucagonoma GRFoma; GRHoma insulinoma neurotensinoma pancreatic polypeptideoma (PPoma) somatostatinoma Zollinger-Ellison (ZE) syndrome (gastrinoma)

General

carcinoma neuroendocrine neoplasm pancreatic neoplasm

References

  1. Medical Knowledge Self Assessment Program (MKSAP) 15, 16, 17, 18, 19. American College of Physicians, Philadelphia 2009, 2012, 2015, 2018, 2021.
  2. ARUP Consult: Pancreatic Neuroendocrine Tumors - NET The Physician's Guide to Laboratory Test Selection & Interpretation https://arupconsult.com/content/pancreatic-neuroendocrine-tumors
  3. Davies K, Conlon KC. Neuroendocrine tumors of the pancreas. Curr Gastroenterol Rep. 2009 Apr;11(2):119-27. PMID: 19281699
  4. Burns WR1, Edil BH. Neuroendocrine pancreatic tumors: guidelines for management and update. Curr Treat Options Oncol. 2012 Mar;13(1):24-34 PMID: 22198808
  5. Kleynberg RL, Guralnik G Pancreatic Cancer: Difficult Diagnosis, Ominous Outlook. Medscape. March 24, 2016 http://reference.medscape.com/features/slideshow/pancreatic-cancer