Positive Correlation between H,K-Adenosine Triphosphatase Autoantibodies and Helicobacter pylori Antibodies in Patients with Pernicious Anemia

Ma, Jie; Borch, Kurt; Sjöstrand, Sven Erik; Janzon, Lars; Mårdh, Sven

doi:10.3109/00365529409094870

Cited by 78 publications

(44 citation statements)

References 29 publications

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“…Moreover, it is known that H. pylori has the ability to trigger autoimmunity, possibly through mechanisms of molecular mimicry (24,25). Therefore, despite the absence of APCA, an autoimmune mechanism leading to the development of both CAG and HPTH cannot be entirely exluded, in the view of lack of detailed gastric and parathyroid autoantibody studies in our patients and those reported by others.…”

Section: Discussioncontrasting

confidence: 38%

The syndrome of gastric carcinoid and hyperparathyroidism: a family study and literature review

Christopoulos

Balatsos²,

Rotas³

et al. 2009

European Journal of Endocrinology

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Objective: To present evidence supporting the hypothesis that the coexistence of gastric carcinoids (GCs) and hyperparathyroidism may represent a distinct clinical entity, not related to multiple endocrine neoplasia type 1 (MEN1). Methods: We studied a cohort of five young siblings (age range 26-42 years), one of whom had been found to have GC and hyperparathyroidism. All siblings underwent serial gastroscopies for the assessment of gastric neuroendocrine cell proliferations over a mean follow-up period of 31.2 months. Imaging, biochemical and hormonal as well as molecular genetic investigations were performed in the direction of MEN1 syndrome. The literature was searched for cases with coexistence of GCs and hyperparathyroidism not associated with MEN1. Results: Four of the siblings, all male, were found to have GCs in a background of Helicobacter pyloriassociated chronic atrophic gastritis and pernicious anaemia, with no serological evidence of gastric autoimmunity. In two of them, asymptomatic hyperparathyroidism was also present. Screening for MEN1 gene mutations or large deletions was negative, and hormone and imaging investigations did not support a diagnosis of familial MEN1 syndrome. A literature search revealed sporadic reports of cases with GC and hyperparathyroidism not attributable to MEN1. Conclusions: The association of GCs and hyperparathyroidism appears to constitute a distinct syndrome that can be encountered in genetically predisposed individuals, and should not be regarded as 'atypical' or 'incomplete' expression of MEN1. Its prevalence and aetiology should be the subject of future studies. Screening for hyperparathyroidism seems to be justified in patients with GC of any type.

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Section: Discussioncontrasting

confidence: 38%

The syndrome of gastric carcinoid and hyperparathyroidism: a family study and literature review

Christopoulos

Balatsos²,

Rotas³

et al. 2009

European Journal of Endocrinology

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“…The presence of these autoantibodies in H. pylori infection was also significantly associated with higher fasting serum gastrin levels, a lower pepsinogen I to II ratio, and reduced secretion of gastric acid (8)(9)(10). In addition, pernicious anemia, which was earlier considered as an exclusive complication of autoimmune gastritis (11), was also shown to be accompanied by H. pylori infection (12)(13)(14). On the basis of these histologic and clinical similarities, the hypothesis has been raised that classic autoimmune gastritis may be triggered by H. pylori infection (15,16).…”

Section: Introductionmentioning

confidence: 86%

Gastric Parietal Cell Antibodies, Helicobacter Pylori Infection, and Chronic Atrophic Gastritis: Evidence from a Large Population-based Study in Germany

Zhang

Weck

Schöttker

et al. 2013

Cancer Epidemiology, Biomarkers &Amp; Prevention

106

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Background: Striking similarities between autoimmune gastritis and Helicobacter Pylori (H. pylori)-associated gastritis have suggested a potential link between these two pathologic conditions in the progression of chronic atrophic gastritis (CAG); however, evidence has remained conflicting.Methods: Serum pepsinogen I and II, and antibodies against H. pylori in general, the cytotoxin-associated gene A protein (CagA) and parietal cells were measured by ELISA in 9,684 subjects aged 50 to 74 years. Antigastric parietal cell antibody (APCA) prevalence was examined in the overall population and according to sex, age, and H. pylori serostatus. The association between APCA prevalence and CAG was assessed by logistic regression, overall and according to H. pylori status, controlling for potential confounding factors.Results: Overall APCA prevalence was 19.5%. APCA prevalence was strongly associated with CAG, and the association was increasing with increasing severity of CAG. Furthermore, the association between APCA and CAG was even stronger among H. pylori-negative subjects [odds ratio (OR) ¼ 11.3; 95% confidence interval (CI): 7.5-17.1)] than among H. pylori-positive subjects (OR ¼ 2.6; 95% CI: 2.1-3.3).Conclusions: APCA may play a role on the development of gastric atrophy, irrespective of H. pylori infection. Impact: Assessment of APCA might be a useful complement to established markers (such as pepsinogens and H. pylori antibodies) in screening for CAG. Cancer Epidemiol Biomarkers Prev; 22(5); 821-6. Ó2013 AACR.

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“…Parietal cell autoantibodies have been correlated with the occurance of atrophic gastritis in H. pylori infected humans (21,22). To screen for autoantibodies, sera from infected transgenic and normal mice were incubated with sections prepared (Fig.…”

Section: Lementioning

confidence: 99%

Epithelial attachment alters the outcome of Helicobacter pylori infection

Guruge

Falk

Lorenz

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

270

168

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Genetically defined in vivo models are needed to assess the importance of target cell attachment in bacterial pathogenesis. Gastric colonization by Helicobacter pylori in human populations is common and persistent, and has various outcomes including peptic ulcers and cancer. The impact of attachment on the course of infection was examined in transgenic mice expressing a human receptor for H. pylori in their gastric epithelium. Persistent infection by a clinical isolate occurred at comparable microbial densities in transgenic and nontransgenic littermates. However, microbial attachment in transgenic mice resulted in production of autoantibodies to Lewis x carbohydrate epitopes shared by bacteria and acid-secreting parietal cells, chronic gastritis, and parietal cell loss. This model should help identify bacterial and host genes that produce attachment-related pathology.

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Positive Correlation between H,K-Adenosine Triphosphatase Autoantibodies and Helicobacter pylori Antibodies in Patients with Pernicious Anemia

Abstract: There was a positive correlation and a high incidence of antibodies against H,K-ATPase and H. pylori in sera from patients with pernicious anemia. These antibodies recognized different epitopes.

Cited by 78 publications

References 29 publications

The syndrome of gastric carcinoid and hyperparathyroidism: a family study and literature review

The syndrome of gastric carcinoid and hyperparathyroidism: a family study and literature review

Gastric Parietal Cell Antibodies, Helicobacter Pylori Infection, and Chronic Atrophic Gastritis: Evidence from a Large Population-based Study in Germany

Epithelial attachment alters the outcome of Helicobacter pylori infection

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