Intrinsic-Factor Antibody, Parietal-Cell Antibody, and Latent Pernicious Anæmia in Diabetes Mellitus

Ungar, Berta; Stocks, A.E.; Martin, F. I. R.; Whittingham, Senga; Mackay, I. R.

doi:10.1016/s0140-6736(68)90462-5

Cited by 119 publications

(32 citation statements)

References 28 publications

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“…Gastritis develops in diabetic patients possibly because of: 1) parietal cell destruction resulting from autoimmunity involving an antibody to the parietal cell which diabetic patients possess (Unger et al 1968); 2) vascular diseases (Kihara et al 1983) which give rise to gastric mucosal lesion (Angervall et al 1961); 3) nutritional disorder of the parietal cell due to vagal neuropathy; 4) metabolic derangements due to diabetes or nutritional disturbance inducedby the effects of insulin on the gastric mucosa; and 5) Helicobacter pylori infection. Helicobacter pylori is now accepted as a cause of chronic active gastritis (Graham 1988).…”

Section: Discussionmentioning

confidence: 99%

Decreased Gastric Secretory Functions in Diabetic Patients with Autonomic Neuropathy.

Nakamura

Takebe

Imamura

et al. 1994

Tohoku J. Exp. Med.

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Section: Discussionmentioning

confidence: 99%

Decreased Gastric Secretory Functions in Diabetic Patients with Autonomic Neuropathy.

Nakamura

Takebe

Imamura

et al. 1994

Tohoku J. Exp. Med.

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“…One-third of PCA ϩ type 1 diabetic patients may develop autoimmune gastritis (9). PCAs may also inhibit intrinsic factor secretion, leading to pernicious anemia, which is 10 times more common in type 1 diabetic than nondiabetic subjects (10,11). Gastric carcinoid tumors, evolving from enterochromaffin-like (ECL) cell hyperplasia induced by chronic hypergastrinemia, may develop in 4 -9% of patients with autoimmune gastritis/pernicious anemia and are 13 times less frequent in control subjects (12)(13)(14)(15)(16).…”

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confidence: 99%

Neuroendocrine Tumor Markers and Enterochromaffin-Like Cell Hyper/Dysplasia in Type 1 Diabetes

et al. 2004

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OBJECTIVE -Parietal cell antibodies (PCAs) are found in 20% of type 1 diabetic patients, denoting autoimmune gastritis and pernicious anemia, which may predispose to enterochromaffin-like (ECL) cell hyper/dysplasia and gastric carcinoid tumors. We evaluated whether chromogranin A (CgA), 5-hydroxyindole acetic acid (5-HIAA), and neuron-specific enolase (NSE) contribute to screening for ECL cell hyper/dysplasia. RESEARCH DESIGN AND METHODS-Sera from 93 type 1 diabetic patients (53 men and 40 women, 31 PCA ϩ and 62 PCA Ϫ , aged 45 Ϯ 13 years) were analyzed for PCAs by indirect immunofluorescence and for CgA, NSE, and gastrin by radioimmunoassay. Urinary 5-HIAA was tested by high-performance liquid chromatography. Corpus atrophy and ECL cell proliferation were assessed in gastric biopsies. RESULTS -PCAϩ patients had higher gastrin (P Ͻ 0.0001) and CgA levels (P ϭ 0.003) and were more prone to autoimmune gastritis (odds ratio [OR] 17, P Ͻ 0.0001) and ECL cell hyper/dysplasia (OR ϭ 23, P ϭ 0.005) than PCA Ϫ subjects. ECL cell hyper/dysplasia was present in seven PCA ϩ patients who showed higher CgA levels (P Ͻ 0.0001) than subjects without ECL cell hyper/dysplasia, but NSE and 5-HIAA levels were similar. CgA levels correlated with gastrinemia (r ϭ 0.50, P Ͻ 0.0001), PCA titer (r ϭ 0.42, P ϭ 0.001), and 5-HIAA levels (r ϭ 0.38, P ϭ 0.012). Logistic regression identified the CgA level (␤ ϭ 0.01, P ϭ 0.027) as an independent risk factor for ECL cell hyper/dysplasia when PCA, CgA, 5-HIAA, NSE, gastrin, sex, and age were tested. Multivariate linear regression demonstrated that CgA level was determined by ECL cell density (r ϭ 0.59, P Ͻ 0.0001) and gastrin level (r ϭ 0.67, P ϭ 0.02). One PCA ϩ patient with elevated gastrin, CgA, and 5-HIAA levels had a gastric carcinoid tumor. CONCLUSIONS -PCAϩ patients, particularly those with high gastrin and CgA levels, risk developing ECL cell hyper/dysplasia. The determination of CgA, but not NSE and 5-HIAA, may complement histology in evaluating ECL cell mass.

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“…Chronic autoaggression to the proton pump may result in hypo/ achlorhydria, hypergastrinemia, and iron deficiency anemia (11)(12)(13)(14). 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).…”

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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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Intrinsic-Factor Antibody, Parietal-Cell Antibody, and Latent Pernicious Anæmia in Diabetes Mellitus

Cited by 119 publications

References 28 publications

Decreased Gastric Secretory Functions in Diabetic Patients with Autonomic Neuropathy.

Decreased Gastric Secretory Functions in Diabetic Patients with Autonomic Neuropathy.

Neuroendocrine Tumor Markers and Enterochromaffin-Like Cell Hyper/Dysplasia in Type 1 Diabetes

Autoimmune Gastropathy in Type 1 Diabetic Patients With Parietal Cell Antibodies

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