scholarly journals Correction: Netazepide, a Gastrin Receptor Antagonist, Normalises Tumour Biomarkers and Causes Regression of Type 1 Gastric Neuroendocrine Tumours in a Nonrandomised Trial of Patients with Chronic Atrophic Gastritis

Author(s):  
Andrew R. Moore ◽  
Malcolm Boyce ◽  
Islay A. Steele ◽  
Fiona Campbell ◽  
Andrea Varro ◽  
...  
2016 ◽  
Vol 28 (11) ◽  
pp. 1345-1352 ◽  
Author(s):  
Liv Sagatun ◽  
Patricia Mjønes ◽  
Constantin S. Jianu ◽  
Malcolm Boyce ◽  
Hege L. Waldum ◽  
...  

2012 ◽  
Vol 142 (5) ◽  
pp. S-15 ◽  
Author(s):  
Reidar Fossmark ◽  
Øystein Sørdal ◽  
Constantin S. Jianu ◽  
Gunnar Qvigstad ◽  
Malcolm J. Boyce ◽  
...  

Endocrine ◽  
2009 ◽  
Vol 35 (3) ◽  
pp. 420-428 ◽  
Author(s):  
Núria Alonso ◽  
María Jesús Martínez-Arconada ◽  
María Luisa Granada ◽  
Berta Soldevila ◽  
Ana Cantón ◽  
...  

2005 ◽  
Vol 152 (3) ◽  
pp. 443-448 ◽  
Author(s):  
M Peracchi ◽  
C Gebbia ◽  
G Basilisco ◽  
M Quatrini ◽  
C Tarantino ◽  
...  

Objective: In atrophic body gastritis (ABG) chronic hypergastrinaemia stimulates enterochromaffin-like (ECL) cell proliferation with development of cell hyperplasia, dysplasia and possibly type-1 gastric carcinoids. As circulating chromogranin A (CgA) levels are a marker of neuroendocrine tumours, we evaluated the clinical usefulness of CgA assay in ABG patients to detect those with carcinoids. Design and methods: Plasma CgA levels were measured using a commercial ELISA in 45 healthy volunteers, nine patients with type-1 gastric carcinoids and 43 consecutive ABG patients (21 without and 22 with ECL cell hyperplasia/dysplasia). Results: CgA levels were significantly higher in ABG patients with and without gastric carcinoids than in healthy subjects (P < 0.001). The highest values occurred in patients with carcinoids (median (interquartile range): 58.1 (44.5–65.3) U/l) and with ECL cell hyperplasia/dysplasia (35.5 (31.8–48.65) U/l) but there were no significant differences in CgA among the various subgroups of ABG patients classified according to ECL cell status. Nevertheless, in ABG patients without carcinoids CgA values correlated with the presence and severity of ECL cell lesions (r s = 0.428, P < 0.01). The sensitivity and specificity of the CgA assay in identifying patients with carcinoids were 100 and 23% respectively. Conclusions: CgA plasma levels reflect the histological degree of ECL cell lesions in patients with ABG but the assay specificity is too low to detect among these patients those with gastric carcinoids.


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