Argyrophil Cell Hyperplasia of Fundic Mucosa in Patients with Chronic Atrophic Gastritis

Bordi, Cesare; Pilato, Francesco Paolo; Carfagna, G.; Ferrari, C.; D’Adda, Tiziana; Sivelli, R; Bertelè, A.; Missale, G.

doi:10.1159/000199389

Cited by 47 publications

(12 citation statements)

References 8 publications

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“…Moreover, the infiltration of inflammatory cells was mild and characterized by the persistence of mononuclear cells and by the virtual disappearance of neutrophils, corresponding to an inflammatory process close to extinction. In agreement with previous observations, 20 intestinal metaplasia was not a prominent finding in these patients.…”

Section: Discussionsupporting

confidence: 93%

Endocrine cell growths in atrophic body gastritis. Critical evaluation of a histological classification

et al. 1997

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The aim of the present study was to evaluate the correspondence of the classification of non‐antral endocrine cell growths proposed by Solcia and co‐workers with clinical features and non‐endocrine mucosal changes. For this purpose, 94 cases of newly diagnosed atrophic body gastritis were investigated using endoscopic biopsies and compared with 18 control subjects. The patients were subdivided into the following four groups according to the most severe pattern of endocrine cell proliferation found in the body mucosa, as shown by chromogranin A immunostaining: group 1, normal pattern (7 cases, 7·5 per cent); group 2, simple hyperplasia (6 cases, 6·5 per cent); group 3, linear hyperplasia (24 cases, 25·8 per cent); group 4; micronodular hyperplasia (56 cases, 60·2 per cent). Adenomatoid hyperplasia was found in only one case, thus precluding further analysis. Patients in groups 1 and 2 had lower acid secretion, higher gastrin level, and higher mean scores in all histopathological variables of chronic gastritis considered by the Sydney system when compared with controls, but did not differ among them in any parameter investigated. When compared with groups 1 and 2, patients of groups 3 and 4 showed higher values of circulating gastrin, higher scores of glandular atrophy, and lower values of acid secretion and of mononuclear and neutrophil inflammatory cell infiltration. Moreover, group 4 patients differed significantly from those of group 3 in their higher gastrin levels and atrophy scores, and lower scores of neutrophil cell infiltration. On the basis of these results, it is proposed that for practical purposes the normal and the simple hyperplasia patterns may be incorporated into a single group. It is concluded that this classification in its simplified form, based on a qualitative histological approach, shows clinical relevance without the need to perform expensive, time‐consuming morphometric evaluations. © 1997 John Wiley & Sons, Ltd.

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Section: Discussionsupporting

confidence: 93%

Endocrine cell growths in atrophic body gastritis. Critical evaluation of a histological classification

et al. 1997

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“…In contrast to a previous report by Bordi et al [1], 57.1% of our patients were male, and these showed an earlier manifestation (mean age: 64.1_10.0 years) than the female patients (mean age: 67.7_+18.1 years); this may be due to the small number. All our patients suffered from type A gastritis.…”

Section: Referencescontrasting

confidence: 99%

“…In autoimmune gastritis the advanced parietal cell atrophy first results in hyperplasia of the antr_al G cells with consequent hypergastrinaemia, which leads to proliferation of ECL (enterochromaffin-like) cells in the body of the stomach as a secondary effect [1,5]. An histopathological classification for these nonantral endo- crine cells was recently proposed by Solcia et al [13], distinguishing hyperplasia, dysplasia (precarcinoid lesion) and neoplasia (see Fig.…”

Section: Introductionmentioning

confidence: 99%

Pattern of gastric endocrine cells in microcarcinoidosis ? an immunohistochemical study of 14 gastric biopsies

Reinecke

Borchard

1996

Vichows Archiv A Pathol Anat

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A total of 14 gastric biopsy specimens from patients with microcarcinoidosis were analysed by immunohistochemical methods to evaluate the pattern of endocrine cell hyperplasia and dysplasia. All the patients had type A gastritis (autoimmune gastritis). Nonantral proliferations of gastric endocrine cells were classified according to Solcia et al. All 14 cases had hyperplasia and 13 (92.9%) of them, dysplasia of gastric endocrine cells; 9 (64.3%) of the 14 were found to have showed a coexisting invasive gastric carcinoid at the time of diagnosis of microcarcinoidosis. The patients with invasive carcinoids had higher degrees and more complex forms of endocrine dysplasia (precarcinoid lesions). The average size of the foci of the microcarcinoidosis in gastric biopsies was 0.14 +/- 0.09 cm in the patients without invasive carcinoid, as against to 0.5 +/- 0.24 cm in the group of patients with associated invasive carcinoid. Microcarcinoid gastric biopsies about 0.5 cm in size, are suggestive of adjacent invasive carcinoid. However, even frankly invasive ECL carcinoids seem to be clinically less dangerous than was thought until recently.

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“…There are two main categories of human hypergastrinaemic states: physiological responses due to acid hyposecretion/achlorhydria in such disorders as pernicious anemia/atrophic gastritis (table 3), and hypergastrinaemia associated with hypersecretion of gastric acid (Jensen 1996) (table 3). Chronic hypergastrinaemia in both of these categories can be of clinical significance because it can result in gastric ECL cell hyperplasia and the development of gastric carcinoid tumours (Bordi et al 1974, 1986 & 1995; Solcia et al 1993; Håkanson et al 1994; Peghini et al 2002). This will be discussed.…”

Section: Clinically Important Disorders Involving Gastrin or Cckb Recmentioning

confidence: 99%

Involvement of Cholecystokinin/Gastrin‐Related Peptides and their Receptors in Clinical Gastrointestinal Disorders

Jensen

2002

Pharmacology & Toxicology

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In this paper the possible roles of cholecystokinin (CCK), gastrin, or gastrin-related peptides and their receptors in human gastrointestinal diseases are reviewed. For CCK/CCK A receptors (CCK A -R), the evidence for their proposed involvement in diseases caused by impaired CCK release or CCK A -R mutations, pancreatic disorders (acute/chronic pancreatitis), gastrointestinal motility disorders (gallbladder disease, irritable bowel syndrome), pancreatic tumor growth and satiety disorders, is briefly reviewed. The evidence that has established the involvement of gastrin/CCK B -R in mediating the action of hypergastrinaemic disorders, mediating hypergastrinaemic effects on the gastric mucosa (ECL hyperplasia, carcinoids, parietal cell mass), and acid-peptic diseases, is reviewed. The evidence for their possible involvement in mediating growth of gastric and pancreatic tumours and possible involvement of gastrin-related peptides in colon cancers, is reviewed briefly.Since the discovery of cholecystokinin (CCK) in 1928 by Ivy & Oldberg of its action on the gallbladder and structural characterization by Mutt & Jorpes (1968), similar to the closely-related peptide, gastrin, whose acid-releasing activity was described in 1905 by Edkins and structural characterization by Gregory & Tracy in 1964, there have been many studies to attempt to define their roles in both physiological and pathological gastrointestinal processes (Jorpes & Mutt 1973;Lamers et al. 1990; Liddle 1994;Walsh 1994;Baldwin 1995;Guo & Townsend, Jr. 2000;Otsuki 2000;Dockray et al. 2001) . Despite recent insights elucidating the structure of the two G-protein-coupled receptors that mediate their cellular actions (i.e., the CCK A and CCK B receptor) (Wank 1995), characterization of receptor location, peptide and receptor genes, development of receptor antagonists and receptor and peptide knockout animals (Liddle 1994;Jensen 1994;Walsh 1994;Langhans et al. 1997; Hinkle & Samuelson 1999;Lacourse et al. 1999;Miyasaka et al. 1999;deTullio et al. 2000), especially the role of CCK and to a lesser extent, gastrin, in normal gastrointestinal physiology as well as in clinically important gastrointestinal pathologic states, remains largely unclear and in many cases, controversial. In this review the latter aspect will be primarily dealt with, which is their role in clinically important processes rather than their role in normal physiology. By this it is meant their role in disease states which cause clinical symptoms in man.In this review these disorders will be divided into those involving primarily CCK A and those involving primarily CCK B receptors. Because only sulfated CCK analogues have a high affinity for CCK A Liddle 1994), CCK A -R disorders involve the potential role of CCK in disease states. Gastrin and CCK can interact with CCK B receptors Liddle 1994); however, much more information is available on the role of gastrin causing CCK B receptor-mediated disorders than CCK. Clinically important gastrointestinal disorders involving CCK or CCK A r...

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Argyrophil Cell Hyperplasia of Fundic Mucosa in Patients with Chronic Atrophic Gastritis

Cited by 47 publications

References 8 publications

Endocrine cell growths in atrophic body gastritis. Critical evaluation of a histological classification

Endocrine cell growths in atrophic body gastritis. Critical evaluation of a histological classification

Pattern of gastric endocrine cells in microcarcinoidosis ? an immunohistochemical study of 14 gastric biopsies

Involvement of Cholecystokinin/Gastrin‐Related Peptides and their Receptors in Clinical Gastrointestinal Disorders

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