S. Sanduleanu et al., Serum chromogranin A as a screening test for gastric enterochromaffin-likecell hyperplasia during acid-suppressive therapy, EUR J CL IN, 31(9), 2001, pp. 802-811
Citations number
40
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research General Topics
Background Serum chromogranin A (CgA), a marker of neuroendocrine neoplasia
, increases during profound gastric acid inhibition, possibly reflecting th
e 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 durin
g acid-suppressive therapy.
Method A consecutive series of 230 dyspeptic patients referred for upper ga
strointestinal 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 inhibit
ors (PPIs, n = 117) or histamine(2)-receptor antagonists (H2RAs, n = 37) fo
r gastro-esophageal reflux disease, and 76 nontreated subjects, with normal
endoscopic findings (control group). Fasting blood samples were analysed f
or gastrin and CgA. Gastric biopsy specimens (oxyntic mucosa) were examined
for histological evaluation of gastritis (Sydney classification) and of EC
L cell hyperplasia (Solcia classification).
Results Serum CgA levels correlated positively with serum gastrin, followin
g a quadratic function (r = 0.78, P < 0.0001). Elevated serum CgA values du
ring long-term acid inhibition correlated with the presence and severity of
fundic ECL cell hyperplasia. Multivariate analysis identified hypergastrin
aemia (P < 0.0001), duration of acid inhibition (P < 0.0001), H. pylori inf
ection (P = 0.008), ECL cell hyperplasia (P = 0.012), and body gland atroph
y (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 refl
ect the presence and severity of fundic ECL cell hyperplasia. Serum CgA is
therefore a useful screening test for gastric ECL cell proliferative change
s within this context.