Gastric endocrine cell hyperplasia and carcinoid tumors in pernicious anemia

Borch, Kurt; Renvall, H.; Liedberg, G

doi:10.1016/0016-5085(85)90131-3

Cited by 323 publications

(163 citation statements)

References 41 publications

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“…16,25 There is also indirect evidence that the same mechanisms act in humans, for instance in patients with endogenous hypergastrinaemia due to oxyntic mucosal atrophy and in the Zollinger±Ellison syndrome. 26,27 It is also of great interest in this context that long-term potent acid inhibition in humans induces hypergastrinaemia and ECL cell hyperplasia. 28 Upregulation of the gastrin receptor has been suggested to take part in this stimulatory process, 29 but the concept of ECL cell hyperplasia, increased histamine synthesis and release is not dependent on changes in gastrin receptor activity.…”

Section: Tolerance To Acid-inhibitory Drugsmentioning

confidence: 99%

“…A parallel to this situation is found in patients with the Zollinger±Ellison syndrome where ECL cell function is chronically upregulated and ECL cell hyperplasia and ECL cellderived tumours may be found. 27 In spite of sometimes extreme hypergastrinaemia these patients usually have their acid hypersecretion fully controlled with proton pump inhibitors in ordinary doses, 30 while histamine H 2 -receptor antagonists must be given in far higher doses than usually necessary for acid suppression. 31 An upregulation of the parietal cell histamine H 2 -receptors has been suggested to take part in this process.…”

Section: Tolerance To Acid-inhibitory Drugsmentioning

confidence: 99%

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Review article: the pharmacological inhibition of gastric acid secretion—tolerance and rebound

Sandvik

Brenna

Waldum

1997

Aliment Pharmacol Ther

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During the last decade our understanding of the regulation of gastric acid secretion has changed considerably. The recognition that gastrin acts mainly by releasing histamine from the enterochromaffin‐like (ECL) cell is of major importance. It is now necessary to review and seek new explanations for the development of tolerance and for the post‐treatment acid hypersecretion that may be observed when treatment with acid‐secretory inhibitors is discontinued. Tolerance and rebound related to H2‐receptor antagonists has previously been explained as upregulation of gastrin and/or histamine H2‐receptors, and/or an increased parietal cell mass. Experimental evidence for these theories is scarce. On the other hand, tolerance can now be explained by a gastrin‐induced increase in ECL cell‐derived histamine at the parietal cell H2‐receptor competing with the antagonist. The lack of tolerance to proton pump inhibitors may be explained by their mode of action, being non‐competitive and acting at the H+, K+‐ATPase rather than at stimulatory receptors. Post‐treatment rebound acid hypersecretion can be understood as gastrin upregulating and/or stimulating growth of the ECL cell, leading to increased amounts of releasable histamine post‐treatment. Novel experimental data strongly support this view of the development of tolerance and post‐treatment rebound acid hypersecretion.

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Section: Tolerance To Acid-inhibitory Drugsmentioning

confidence: 99%

Section: Tolerance To Acid-inhibitory Drugsmentioning

confidence: 99%

Review article: the pharmacological inhibition of gastric acid secretion—tolerance and rebound

Sandvik

Brenna

Waldum

1997

Aliment Pharmacol Ther

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“…Autoimmune gastritis is also a risk factor for gastric neuroendocrine tumors (carcinoids) and gastric cancer development (2). Gastric cancer incidence ranges from 1 to 3% for gastric carcinoma and from 2 to 12.5% for carcinoid tumors in patients with AIG with or without pernicious anemia (3)(4)(5)(6). Gastric carcinoid tumors that occur in patients with AIG are labeled as type I gastric carcinoids.…”

Section: Introductionmentioning

confidence: 99%

Factors associated with elevated serum chromogranin A levels in patients with autoimmune gastritis

Kalkan¹,

Karakaya²,

Soykan³

2016

Turk J Gastroenterol

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“…PCAs may also inhibit intrinsic factor secretion, leading to pernicious anemia, which is 10 times more common in type 1 diabetic than in nondiabetic subjects (15,16). Pernicious anemia and autoimmune gastritis may predispose to gastric tumors (17)(18)(19)(20)(21)(22), although this has not been consistently observed (23). Gastric adenocarcinomas develop in 1-10% of subjects with autoimmune gastritis through intestinal meta/dysplasia (17)(18)(19).…”

mentioning

confidence: 99%

“…Gastric adenocarcinomas develop in 1-10% of subjects with autoimmune gastritis through intestinal meta/dysplasia (17)(18)(19). Carcinoid tumors develop in 4 -7% of these subjects on a background of enterochromaffin-like (ECL) cell hyperplasia induced by sustained pronounced hypergastrinemia (20,21). Recently, Helicobacter pylori (HP) has been suggested to induce autoimmune gastritis (24 -26).…”

mentioning

confidence: 99%

Autoimmune Gastropathy in Type 1 Diabetic Patients With Parietal Cell Antibodies

et al. 2003

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OBJECTIVE -Approximately 15-20% of type 1 diabetic patients exhibit parietal cell antibodies (PCAs) targeting gastric H ϩ /K ϩ ATPase. We examined whether iron deficiency anemia, pernicious anemia, and autoimmune gastritis, which may predispose to gastric tumors, were more frequent in PCA ϩ than in PCA -patients. RESULTS -Autoimmune gastritis (AG) was present in 57% of PCA ϩ and 10% of PCA -cases (OR 12.5, P Ͻ 0.0001). PCA positivity (␤ ϭ 1.44; P ϭ 0.04) and hypergastrinemia (␤ ϭ 0.01; P ϭ 0.026), but not HP, age, diabetes duration, sex, and HLA-DQ type were risk factors for AG. Iron deficiency anemia (OR 3.9, P ϭ 0.015), pernicious anemia (OR ϭ 4.6, P ϭ 0.022), and hypochlorhydria (OR ϭ 20.0, P ϭ 0.0002) were more frequent in AG ϩ individuals. HP infection was present in 47 patients but did not influence corpus histology or gastrinemia. (Pre)malignant lesions were found in 26% of PCA ϩ subjects: ECL cell hyperplasia in 7 AG ϩ patients, comprising 1 with a gastric carcinoid tumor, and corpus intestinal metaplasia in 11 AG ϩ patients, including 1 with linitis plastica. RESEARCH DESIGN AND METHODS CONCLUSIONS -PCAϩ type 1 diabetic patients should be screened for autoimmune gastritis, iron deficiency, and pernicious anemia. Particularly hypergastrinemic PCA ϩ patients with autoimmune gastritis are at increased risk for (pre)malignant gastric lesions.

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Gastric endocrine cell hyperplasia and carcinoid tumors in pernicious anemia

Cited by 323 publications

References 41 publications

Review article: the pharmacological inhibition of gastric acid secretion—tolerance and rebound

Review article: the pharmacological inhibition of gastric acid secretion—tolerance and rebound

Factors associated with elevated serum chromogranin A levels in patients with autoimmune gastritis

Autoimmune Gastropathy in Type 1 Diabetic Patients With Parietal Cell Antibodies

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