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Serum chromogranin A as a screening test for gastric enterochromaffin‐like cell hyperplasia during acid‐suppressive therapy
Author(s) -
Sanduleanu S.,
De Bruïne A.,
Stridsberg M.,
Jonkers D.,
Biemond I.,
Hameeteman W.,
Lundqvist G.,
Stockbrügger R. W.
Publication year - 2001
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.2001.00890.x
Subject(s) - enterochromaffin like cell , medicine , gastrin , gastroenterology , atrophic gastritis , chromogranin a , gastric acid , hyperplasia , pentagastrin , endocrinology , proton pump inhibitor , gastrinoma , gastritis , stomach , immunohistochemistry , secretion
Background Serum chromogranin A (CgA), a marker of neuroendocrine neoplasia, increases during profound gastric acid inhibition, possibly reflecting the trophic effect of gastrin on the enterochromaffin‐like (ECL) cells. Aims This study investigated the clinical value of serum CgA as a screening test for gastric fundic enterochromaffin‐like (ECL) cell hyperplasia during acid‐suppressive therapy. Method A consecutive series of 230 dyspeptic patients referred for upper gastrointestinal endoscopy was investigated in a cross‐sectional design. They were 154 patients on continuous medium‐term (6 weeks to one year) or long‐term (longer than one year) acid inhibition with either proton pump inhibitors (PPIs, n = 117) or histamine 2 ‐receptor antagonists (H 2 RAs, n = 37) for gastro‐oesophageal reflux disease, and 76 nontreated subjects, with normal endoscopic findings (control group). Fasting blood samples were analysed for gastrin and CgA. Gastric biopsy specimens (oxyntic mucosa) were examined for histological evaluation of gastritis (Sydney classification) and of ECL cell hyperplasia (Solcia classification). Results Serum CgA levels correlated positively with serum gastrin, following a quadratic function ( r = 0·78, P < 0·0001). Elevated serum CgA values during long‐term acid inhibition correlated with the presence and severity of fundic ECL cell hyperplasia. Multivariate analysis identified hypergastrinaemia ( P < 0·0001), duration of acid inhibition ( P < 0·0001), H. pylori infection ( P = 0·008) , ECL cell hyperplasia ( P = 0·012), and body gland atrophy ( P = 0·043) as independent predictors of elevated serum CgA. In subjects on long‐term acid inhibition ( n = 123), serum CgA was equally sensitive but more specific than serum gastrin for the detection of ECL cell hyperplasia (sensitivity, 91·3% for both; specificity, 73% vs. 43%, P < 0·0001). Conclusions During long‐term gastric acid inhibition, serum CgA levels reflect the presence and severity of fundic ECL cell hyperplasia. Serum CgA is therefore a useful screening test for gastric ECL cell proliferative changes within this context.