Noninvasive Diagnosis of Focal Hyperinsulinism of Infancy With [18F]-DOPA Positron Emission Tomography

Otonkoski, Timo; Näntö‐Salonen, Kirsti; Seppänen, Marko; Veijola, Riitta; Huopio, Hanna; Hussain, Khalid; Tapanainen, Päivi; Eskola, Olli; Parkkola, Riitta; Ekström, Klas; Guiot, Yves; Rahier, Jacques; Laakso, Markku; Rintala, Risto J.; Nuutila, Pirjo; Minn, Heikki

doi:10.2337/diabetes.55.01.06.db05-1128

Cited by 236 publications

(126 citation statements)

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“…The pancreatic uptake of 111 In-labelled exendin was clearly decreased in patients with type 1 diabetes, with marked differences between diabetic patients and healthy individuals. To date, no other radiotracer tested for BCM determination has shown such large maximum differences between healthy individuals and patients with type 1 diabetes, nor has such a high interindividual variability of the uptake been reported previously [37][38][39][40][41][42][43][44]. A recent study in healthy individuals and patients with type 1 diabetes, involving PET after injection of [ 18 F]fluoropropyl-dihydrotetrabenazine ([ 18 F]FP-(+)-DTBZ), showed a maximum difference in pancreatic uptake of <40% [45].…”

Section: Discussionmentioning

confidence: 99%

Non-invasive quantification of the beta cell mass by SPECT with 111In-labelled exendin

et al. 2014

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Aims/hypothesis A reliable method for in vivo quantification of pancreatic beta cell mass (BCM) could lead to further insight into the pathophysiology of diabetes. The glucagonlike peptide 1 receptor, abundantly expressed on beta cells, may be a suitable target for imaging. We investigated the potential of radiotracer imaging with the GLP-1 analogue exendin labelled with indium-111 for determination of BCM in vivo in a rodent model of beta cell loss and in patients with type 1 diabetes and healthy individuals. MethodsThe targeting of 111 In-labelled exendin was examined in a rat model of alloxan-induced beta cell loss. Rats were injected with 15 MBq 111 In-labelled exendin and single photon emission computed tomography (SPECT) acquisition was performed 1 h post injection, followed by dissection, biodistribution and ex vivo autoradiography studies of pancreatic sections. BCM was determined by morphometric analysis after staining with an anti-insulin antibody. For clinical evaluation SPECT was acquired 4, 24 and 48 h after injection of 150 MBq 111 In-labelled exendin in five patients with type 1 Maarten Brom and Wietske Woliner-van der Weg contributed equally to this study. Diabetologia (2014) 57:950-959 DOI 10.1007 diabetes and five healthy individuals. The tracer uptake was determined by quantitative analysis of the SPECT images. Results In rats, 111 In-labelled exendin specifically targets the beta cells and pancreatic uptake is highly correlated with BCM. In humans, the pancreas was visible in SPECT images and the pancreatic uptake showed high interindividual variation with a substantially lower uptake in patients with type 1 diabetes. Conclusions/interpretation These studies indicate that 111 Inlabelled exendin may be suitable for non-invasive quantification of BCM.

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Section: Discussionmentioning

confidence: 99%

Non-invasive quantification of the beta cell mass by SPECT with 111In-labelled exendin

et al. 2014

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“…In diffuse CHI, histologically there is an increase in the b-cell nuclear size throughout the pancreas. Diffuse CHI is genetically heterogeneous and most commonly due to mutations in ABCC8 or KCNJ11 genes (3,12,13,14,15). Diazoxide, an agonist that targets the SUR1 subunit, is usually ineffective in patients with autosomal recessive form of ABCC8 or KCNJ11 mutations.…”

Section: Introductionmentioning

confidence: 99%

Clinical and histological heterogeneity of congenital hyperinsulinism due to paternally inherited heterozygous ABCC8/KCNJ11 mutations

Arya

Güemes

Nessa

et al. 2014

European Journal of Endocrinology

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Context: Congenital hyperinsulinism (CHI) has two main histological types: diffuse and focal. Heterozygous paternally inherited ABCC8/KCNJ11 mutations (depending upon whether recessive or dominant acting and occurrence of somatic maternal allele loss) can give rise to either phenotype. However, the relative proportion of these two phenotypes in a large cohort of CHI patients due to paternally inherited heterozygous ABCC8/KCNJ11 mutations has not been reported. Objective: The purpose of this study is to highlight the variable clinical phenotype and to characterise the distribution of diffuse and focal disease in a large cohort of CHI patients due to paternally inherited heterozygous ABCC8/KCNJ11 mutations. Design: A retrospective chart review of the CHI patients due to heterozygous paternally inherited ABCC8/KCNJ11 mutations from 2000 to 2013 was conducted. Results: Paternally inherited heterozygous ABCC8/KCNJ11 mutations were identified in 53 CHI patients. Of these, 18 (34%) either responded to diazoxide or resolved spontaneously. Fluorine-18 L-3, 4-dihydroxyphenylalanine positron emission tomography computerised tomography ( 18 F DOPA-PET CT) scanning in 3/18 children showed diffuse disease. The remaining 35 (66%) diazoxide-unresponsive children either had pancreatic venous sampling (nZ8) or 18

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“…Ribeiro et al (10)(11)(12) were the first to report on the use of 18 F-DOPA PET for differentiating between focal and diffuse hyperinsulinemia of infancy, and their findings were subsequently verified by other investigators (13)(14)(15)(16)(17)(18). When uptake of 18 F-DOPA was focal, immunocytochemical analysis of surgical specimens confirmed the diagnosis of focal disease.…”

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confidence: 82%

Pancreatic Imaging with ¹¹C-Dihydrotetrabenazine PET: A Perspective

Fagan

Fischman²

2009

J Nucl Med

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Noninvasive Diagnosis of Focal Hyperinsulinism of Infancy With [18F]-DOPA Positron Emission Tomography

Abstract: Congenital hyperinsulinism of infancy (CHI) is character-

Cited by 236 publications

References 27 publications

Non-invasive quantification of the beta cell mass by SPECT with 111In-labelled exendin

Non-invasive quantification of the beta cell mass by SPECT with 111In-labelled exendin

Clinical and histological heterogeneity of congenital hyperinsulinism due to paternally inherited heterozygous ABCC8/KCNJ11 mutations

Pancreatic Imaging with ¹¹C-Dihydrotetrabenazine PET: A Perspective

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Noninvasive Diagnosis of Focal Hyperinsulinism of Infancy With [18F]-DOPA Positron Emission Tomography

Abstract: Congenital hyperinsulinism of infancy (CHI) is character-

Cited by 236 publications

References 27 publications

Non-invasive quantification of the beta cell mass by SPECT with 111In-labelled exendin

Non-invasive quantification of the beta cell mass by SPECT with 111In-labelled exendin

Clinical and histological heterogeneity of congenital hyperinsulinism due to paternally inherited heterozygous ABCC8/KCNJ11 mutations

Pancreatic Imaging with 11C-Dihydrotetrabenazine PET: A Perspective

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Pancreatic Imaging with ¹¹C-Dihydrotetrabenazine PET: A Perspective