Localization of Insulinomas to Regions of the Pancreas by Intra-arterial Stimulation with Calcium

Jl, Doppman; Chang, Richard; Dl, Fraker; Ja, Norton; Hr, Alexander; Dl, Miller; Collier, Elaine; Mc, Skarulis; Gorden, Philip

doi:10.7326/0003-4819-123-4-199508150-00004

Cited by 255 publications

(177 citation statements)

References 6 publications

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“…Localization is more precise, although accuracy is not increased. 20 If laparoscopic surgery is contemplated for older children with insulinoma, such precise localization can be significant. In contrast to SUR1-defective patients, children with HI/HA had no acute insulin response to calcium.…”

Section: Discussionmentioning

confidence: 99%

“…ASVS was performed with the patients under general endotracheal anesthesia after an overnight fast with the method of Doppman et al 20 and Brown et al 21 In brief, under fluoroscopic visualization by the right internal jugular vein, a diagnostic vascular catheter was advanced selectively into the right hepatic vein for venous blood sampling. Thereafter, by way of retrograde catheterization of the right common femoral artery, another catheter was superselectively negotiated into the right hepatic artery (as a negative control), gastroduodenal artery, superior mesenteric artery, and splenic artery.…”

Section: Peripheral Intravenous Caair and Asvsmentioning

confidence: 99%

“…18 The acute insulin response to rapid peripheral intravenous infusion of calcium has been used to diagnose insulinomas in adults, 19 and selective arterial calcium stimulation of the pancreas with hepatic venous sampling has been used in adults to localize insulinomas. 20,21 We hypothesized that children with hyperinsulinism caused by SUR1 defects would also hyper-respond to calcium because of constitutive activation of β-cell Ltype calcium channels. The purpose of this study was to determine whether children with focal and diffuse forms of SUR1 hyperinsulinism would respond to calcium and whether calcium ASVS could be used to localize congenital focal (SUR1 p-) lesions.…”

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confidence: 99%

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Calcium-stimulated insulin secretion in diffuse and focal forms of congenital hyperinsulinism

Ferry

Kelly

Grimberg

et al. 2000

The Journal of Pediatrics

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Objectives-To identify infants with hyperinsulinism caused by defects of the β-cell adenosine triphosphate-dependent potassium channel complex and to distinguish focal and diffuse forms of hyperinsulinism caused by these mutations.Study design-The acute insulin response to intravenous calcium stimulation (CaAIR) was determined in 9 patients <20 years with diffuse hyperinsulinism caused by defective β-cell sulfonylurea receptor (SUR1 −/− ), 3 patients with focal congenital hyperinsulinism (6 weeks to 18 months), a 10-year-old with insulinoma, 5 with hyperinsulinism/hyperammonemia syndrome caused by defective glutamate dehydrogenase (6 months to 28 years), 4 SUR1 +/− heterozygotes with no symptoms, and 9 normal adults. Three infants with congenital focal disease, 1 with diffuse hyperinsulinism, and the child with insulinoma underwent selective pancreatic intra-arterial calcium stimulation with hepatic venous sampling.Results-Children with diffuse SUR1 −/− disease and infants with congenital focal hyperinsulinism responded to CaAIR, whereas the normal control group, patients with hyperinsulinism/hyperammonemia syndrome, and SUR1 +/− carriers did not. Selective arterial calcium stimulation of the pancreas with hepatic venous sampling revealed selective, significant step-ups in insulin secretion that correlated anatomically with the location of solitary lesions confirmed surgically in 2 of 3 infants with congenital focal disease and in the child with insulinoma. Selective arterial calcium stimulation of the pancreas with hepatic venous sampling demonstrated markedly elevated baseline insulin levels throughout the pancreas of the infant with diffuse hyperinsulinism. Congenital hyperinsulinism, the most common cause of persistent hypoglycemia in infants beyond the first few days of life, 1 can result from genetic defects of the pancreatic β-cell including autosomal recessive mutations of the sulfonylurea receptor gene 2 or inwardrectifying 6.2-kDa potassium channel, 3,4 which together compose the β-cell adenosine triphosphate-de-pendent potassium channel complex. Other defects that can cause congenital hyperinsulinism are autosomal dominant mutations of islet glucokinase 5 or glutamate dehydrogenase, the latter causing the hyperinsulinism/hyperammonemia syndrome. 6 Recessive SUR mutations (SUR1 −/− ) compose the most common and most severe form of congenital hyperinsulinism. 7,8 Affected infants are usually large for gestational age and have hypoglycemia in the first few postnatal days. 1 Children with SUR1 −/− hyperinsulinism usually fail to respond to treatment with diazoxide, a drug that acts on the SUR to suppress insulin secretion 9 and may require near total pancreatectomy to control hypoglycemia. 10 More than a third of patients with congenital hyperinsulinism requiring surgery have focal adenomatous hyperplasia of islet cells. [10][11][12] Surrounded by normal pancreas, these cells express a paternally derived SUR1 mutation in association with specific loss of imprinted maternal alleles of chromosome 1...

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Section: Discussionmentioning

confidence: 99%

Section: Peripheral Intravenous Caair and Asvsmentioning

confidence: 99%

mentioning

confidence: 99%

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Calcium-stimulated insulin secretion in diffuse and focal forms of congenital hyperinsulinism

Ferry

Kelly

Grimberg

et al. 2000

The Journal of Pediatrics

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“…On the other hand, IOUS combined with palpation is reported to detect up to 100% of the tumors (1,14,15). Recently, it was noted that selective intraarterial calcium injection could be used to localize occult insulinoma (1,(16)(17)(18). The technique is based upon the use of intraarterial secretin injections for the localization of gastrinomas ( 19).…”

Section: Discussionmentioning

confidence: 99%

Usefulness of the Combination of Pre- and Intraoperative Selective Intraarterial Calcium Injection to Detect Residual Insulinomas.

et al. 2001

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In a 35-year-old womandiagnosed with insulinoma selective intraarterial calcium injection was positive for proximal gastroduodenal artery and inferior pancreaticoduodenal artery involvement preoperatively. Although non-invasive imaging studies were negative, a mass was detected at the pancreatic uncus by intraoperative ultrasonography. Gastroduodenal artery calcium injection was performed after enucleation of the tumor. Following calcium injection, the insulin level was inappropriately increased and further pancreaticoduodenectomy was performed. After excision, another tumor was detected at the head of the pancreas by histopathological examination. As shown, selective intraarterial calcium injection is useful to localize tumors preoperatively and intraoperatively. (Internal Medicine 40: 48-51, 2001) Key words: gastroduodenal artery, enucleation, pancreaticoduodenectomy,another adenoma Case ReportA 35-year-old Japanese female had episodes of loss of awareness over 10 months. She had had a traffic accident while driving alone and was brought to our hospital on May 13, 1997. Family and past histories were not remarkable. The patient weighed 57.0 kg and her body height was 158 cm (body mass index; 22.8 kg/m2). The level of consciousness was E1V2M5(by Glasgow ComaScale). Results of routine laboratory tests including blood chemistry, hemogram, and serology were normal except for a plasma glucose of 27 mg/dl (70-110 mg/dl) and an immunoreactive insulin (IRI) of 8.7 jiU/ml (0-17 |llU/ ml). Anti-insulin antibody and anti-insulin receptor antibody tests were negative. Continuous intravenous injection of 10% glucose was given to maintain a plasma glucose level of over 70 mg/dl in order to prevent hypoglycemia and associated symptoms. Then, a fasting glucose tolerance test was performed. Based upon the collected data, the biochemical criteria for the diagnosis of insulinoma were met. Namely, the patient had symptomatic hypoglycemia (plasma glucose 47 mg/ dl) with inappropriately elevated IRI (1 1 |iU/ml) (0-17 |LiU/ ml) and C-peptide (2.2 ng/ml) (0.6-2.8 ng/ml) after 6 hours. Serum levels of HCGand HCG-pwere normal. Function of the pituitary, adrenal, thyroid, and parathyroid glands were normal. Ultrasonography (US), endoscopic ultrasonography (EUS), computed tomography (CT), magnetic resonance imaging, digital subtraction angiography, and CT angiography failed to localize the tumors. There was no evidence of hepatic metastasis on CT scan or by angiography. The percutaneous transhepatic venous sampling (PTVS) was also negative. Finally, selective intraarterial calcium injection was performed. We used the method described by O'shea et al (1). A catheter was placed in the right hepatic vein close to its junction with the inferior vena cava via a femoral vein. Each artery [proximal gastroduodenal artery (GDA), inferior pancreatico-duodenal artery (IPDA), proximal splenic artery, left hepatic artery, superior mesenteric artery] was catheterized in turn. After samples were taken twice from the hepatic vein as contr...

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“…Endoscopic retrograde cholangiopancreatography (ERCP) indicated no abnormalities in the pancreatic duct. To localize and diagnose the tumor as an insulinoma, we employedintra-arterial stimulation with calcium and hepatic venous sampling to measure the insulin Myotonic Dystrophy with Insulinoma level (7). In this method, calcium is infused through a conventional intravenous sampling catheter, and it stimulates insulin secretion from the insulinoma.…”

Section: Introductionmentioning

confidence: 99%

Myotonic Dystrophy Associated with Insulinoma.

et al. 1999

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Wedescribe a 51-year-old man with myotonic dystrophy (MyD) associated with insulinoma. In addition to the typical symptomsof MyD,he showedhypoglycemicattacks after meals. The radiological examination and selective blood sampling revealed an insulinoma in the head of the pancreas. The tumor was resected and histopathologically diagnosed as an insulinoma. In Southern blot analysis, CTGrepeat of the myotonin protein kinase gene in the insulinoma showed the longest expansion, followed by normal tissue of the pancreas, muscle and white blood cells. Therefore, microsatellite instability was the most prominent in the tumor cells. (Internal Medicine 38: 504-506, 1999)

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Localization of Insulinomas to Regions of the Pancreas by Intra-arterial Stimulation with Calcium

Abstract: Intra-arterial calcium stimulation with right hepatic vein sampling for insulin gradients is the most sensitive preoperative test for localizing insulinomas.

Cited by 255 publications

References 6 publications

Calcium-stimulated insulin secretion in diffuse and focal forms of congenital hyperinsulinism

Calcium-stimulated insulin secretion in diffuse and focal forms of congenital hyperinsulinism

Usefulness of the Combination of Pre- and Intraoperative Selective Intraarterial Calcium Injection to Detect Residual Insulinomas.

Myotonic Dystrophy Associated with Insulinoma.

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