Insulinomas: Localization with selective intraarterial injection of calcium

Diagnostic Radiology Department, Warren G. Magnuson Clinical Center, National Institutes of Health, Bethesda, MD 20892.
Radiology (Impact Factor: 6.21). 02/1991; 178(1):237-41. DOI: 10.1148/radiology.178.1.1984311
Source: PubMed

ABSTRACT To facilitate the noninvasive preoperative localization of islet cell tumors less than 15 mm in diameter, the authors examined the use of calcium as an insulin secretagogue in an arterial stimulation venous sampling (ASVS) technique. In four patients with episodic hypoglycemia, calcium gluconate (0.01-0.025 mEq Ca2+/kg) was injected directly into branches of the celiac plexus (gastroduodenal, splenic, and hepatic arteries) and the superior mesenteric artery. In all patients, serum levels of insulin rose abruptly in blood samples taken from the right hepatic vein 30 and 60 seconds after the infusion of calcium into the artery supplying the tumor; injection into an artery not supplying the tumor did not result in a similar rise. Accurate localization of the insulinomas was verified at surgery in three patients. In the fourth patient, who did not undergo surgery, arteriographic results were positive for insulinoma at the predicted site. On the basis of these results, the authors believe noninvasive ASVS may replace invasive portal venous sampling as the most effective method for the localization of occult insulinomas.

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    • "However, abdominal arteriography revealed a vague area of hypervascularity in the tail of the pancreas. Due to this finding and the severity of her symptoms, she underwent selective arterial calcium stimulation with hepatic venous sampling for insulin as described by Doppman et al. [7]. This test did not localize a region of insulin hypersecretion, and thus was not consistent with a diagnosis of insulinoma (Table 1). "
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    ABSTRACT: Objective. We evaluated a 47-year-old woman with a history of type 2 diabetes and severe obesity who developed postprandial hypoglycemia after undergoing Roux-en-Y gastric bypass surgery and losing 60% of her total body weight. We studied her insulin secretion and blood glucose dynamics and were able to tailor a therapeutic regimen involving insulin that eliminated episodes of hypoglycemia. Methods. We studied blood glucose levels during a prolonged fast, performed continuous glucose monitoring studies using a subcutaneous glucose sensor, and evaluated regional pancreatic insulin secretion using selective arterial calcium stimulation. Results. Continuous glucose monitoring revealed that the patient had early (1-2 hr) postprandial hyperglycemia followed by late (3-4 hr) postprandial hypoglycemia. Biochemical studies confirmed endogenous pancreatogenous insulin secretion as the cause of episodic hypoglycemia, but imaging studies and selective arterial calcium stimulation failed to localize an insulinoma. The patient was treated with preprandial doses of insulin aspart in order to attenuate the early postprandial hyperglycemia, and the late hypoglycemic episodes were avoided. Conclusion. We describe an interesting and novel nonsurgical approach to the prevention of postprandial hypoglycemia in a patient with noninsulinoma pancreatogenous hypoglycemia after gastric bypass.
    06/2012; 2012:427565. DOI:10.1155/2012/427565
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    • "By contrast, arterial stimulation and venous sampling (ASVS) is an important technique for determining the localization of insulinomas (1, 2). The ASVS method was originally reported by Doppman et al. in 1991 (1), and there have been several subsequent reports of its success in localizing insulinomas (3, 4). The principle behind ASVS is that insulin secretion is promoted from insulinoma cells by the injection of calcium into the insulinoma-feeding artery (5). "
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    ABSTRACT: Arterial stimulation and venous sampling (ASVS) is an important technique for localizing insulinoma. The principle behind ASVS is that insulin secretion is promoted from insulinoma cells by the injection of calcium into the insulinoma-feeding artery. However, the mechanism for ASVS-induced insulin secretion remains unclear. Both insulinoma and familial hypocalciuric hypercalcemia (FHH) are rare diseases. This study reports on a case in which both of these diseases occur concurrently. The patient with FHH also suffered from insulinoma. We reasoned that insulin secretion for ASVS is dependent on the calcium-sensing receptor (CaSR). ASVS was performed on this patient. The expression of the CaSR protein and corresponding mRNA were confirmed. No significant changes in the plasma levels of insulin and C-peptide were observed during ASVS. The patient was clinically diagnosed as having FHH. We confirmed that a mutation in the CaSR gene was present in the genomic DNA of this patient and that there were no mutations in the multiple endocrine neoplasia type 1 gene. In addition, expression of both CaSR mRNA and CaSR protein was confirmed in the insulinoma samples. These results suggest that the CaSR gene is involved in ASVS-induced insulin secretion.
    European Journal of Endocrinology 08/2008; 159(1):81-6. DOI:10.1530/EJE-08-0069 · 3.69 Impact Factor
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    • "gastrin or insulin). In the presence of a tumour, the hormone levels double after 30 s, whereas the normal effect is a reduction in levels (Doppman et al. 1990, 1991, Fedorak et al. 1993, Goldstone et al. 1996, O'Shea et al. 1996). The tremendous advantage of this technique is that it allows biochemical localization of the tumour (e.g. a very small insulinoma) even if the radiology appears Table 5 Imaging modalities for gastroenteropancreatic neuroendocrine tumours. "
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    ABSTRACT: Neuroendocrine tumours are a heterogeneous group including, for example, carcinoid, gastroenteropancreatic neuroendocrine tumours, pituitary tumours, medullary carcinoma of the thyroid and phaeochromocytomas. They have attracted much attention in recent years, both because they are relatively easy to palliate and because they have indicated the chronic effect of the particular hormone elevated. As neuroendocrine phenotypes became better understood, the definition of neuroendocrine cells changed and is now accepted as referring to cells with neurotransmitter, neuromodulator or neuropeptide hormone production, dense-core secretory granules, and the absence of axons and synapses. Neuroendocrine markers, particularly chromogranin A, are invaluable diagnostically. Study of several neuroendocrine tumours has revealed a genetic etiology, and techniques such as genetic screening have allowed risk stratification and prevention of morbidity in patients carrying the particular mutation. Pharmacological therapy for these often slow-growing tumours, e.g. with somatostatin analogues, has dramatically improved symptom control, and radiolabelled somatostatin analogues offer targeted therapy for metastatic or inoperable disease. In this review, the diagnosis and management of patients with carcinoid, gut neuroendocrine tumours, multiple endocrine neoplasia types 1 and 2, and isolated phaeochromocytoma are evaluated.
    Endocrine Related Cancer 04/2004; 11(1):1-18. · 4.91 Impact Factor
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