Autoimmune gastritis in children with autoimmune diseases

The results of inspection of 70 children for autoimmune gastritis are represented. Children with blood serum antibodies to stomach parietal cells were selected for more profound investigation. It was shown, that autoimmune gastritis in the childhood is one of the components of multiorgan autoimmune pathology in 0-33 % of patients and is characterized by minimum clinical, morphological and endoscopic data, combination with Helicobacter pylori.

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Induction of Follicular Gastritis following Postthymectomy Autoimmune Gastritis in Helicobacter pylori-Infected BALB/c Mice

Infection and Immunity ◽

10.1128/iai.68.1.100-106.2000 ◽

2000 ◽

Vol 68 (1) ◽

pp. 100-106 ◽

Cited By ~ 21

Author(s):

Chikashi Oshima ◽

Kazuichi Okazaki ◽

Yumi Matsushima ◽

Mitsutaka Sawada ◽

Tsutomu Chiba ◽

...

Keyword(s):

Helicobacter Pylori ◽

Early Stage ◽

Parietal Cells ◽

Antibody Responses ◽

Autoimmune Gastritis ◽

Interleukin 4 ◽

Fundic Gland ◽

H Pylori ◽

Gland Atrophy ◽

Follicular Gastritis

ABSTRACT Helicobacter pylori is the major causative agent of chronic antral gastritis and is thought to be involved in the pathogenesis of mucosa-associated lymphoid tissue lymphoma (MALToma) developing in the human stomach. The aim of this study was to clarify whether corporal autoimmune gastritis (AIG), which is known to decrease acidity due to destruction of parietal cells, predisposes mice toH. pylori infection, thereby leading to MALToma-like pathology. BALB/c mice in which AIG had been induced by thymectomy 3 days after birth (AIG mice) were used. The AIG mice were orally administered mouse-adapted H. pylori at the age of 6 weeks and were examined histologically and serologically after 2 to 12 months. The results were compared with those obtained from uninfected AIG mice and infected normal mice. Germinal centers were induced in the corpus in 57% of the H. pylori-infected AIG mice, which elicited anti-H. pylori antibody responses in association with upregulation of interleukin-4 (IL-4) mRNA. In these mice, parietal cells remained in the corpus mucosa. These findings were in contrast to those with the uninfected AIG mice: fundic gland atrophy due to disappearance of parietal cells associated with upregulation of gamma interferon, but not IL-4, mRNA and no germinal center formation in the corpus. These observations suggest that AIG alters the infectivity ofH. pylori, leading to MALToma-like follicular gastritis, at an early stage after H. pylori infection.

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Autoimmune gastritis: comorbid pathology in type 1 diabetes

Diabetes Mellitus ◽

10.14341/dm9465 ◽

2018 ◽

Vol 21 (5) ◽

pp. 404-408

Author(s):

Olga S. Derevyanko ◽

Liudmila I. Ibragimova ◽

Magomedkerim R. Ragimov ◽

Tatiana V. Nikonova

Keyword(s):

Type 1 Diabetes ◽

Early Diagnosis ◽

Autoimmune Diseases ◽

Mucous Membrane ◽

The Body ◽

Autoimmune Gastritis ◽

Main Role ◽

Autoimmune Pathology ◽

Number Of Patients

In recent years noted an increased number of patients with autoimmune diseases (AID), and the special attention deserves combination of several autoimmune pathologies collected in one patient, because such patients requires special tactics of management. Autoimmune diseases of the gastrointestinal tract are less researched and, nevertheless, prognostically unfavorable. Autoimmune gastritis (AIG) has a special place in other stomach diseases, which develops in the aggregate with type 1 diabetes. AIG is a chronic inflammation of the mucous membrane of the body of the stomach, leading to the appearance of atrophy and hypoxecretion. AIG is found in 510% of individuals in general population, with a higher incidence of AIG in patients with diabetes and other established autoimmune pathology. AIG is asymptomatic at the early stage of the disease and clinical manifestations appear after the atrophic changes in the mucous membrane of the stomach develop. Since autoimmune gastritis does not have pathognomonic signs, it can manifest itself in hematological and oncological complications at later stages. This is why screening, early diagnosis, prevention and treatment are very important. Early diagnosis and prevention of AIG and its complications play the main role. This article provides an overview of the worldwide data dedicated to this issue.

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Evidence for high Helicobacter pylori mucosal specific IgG secretion in autoimmune gastritis

Gastroenterology ◽

10.1016/s0016-5085(01)83525-3 ◽

2001 ◽

Vol 120 (5) ◽

pp. A708-A708

Author(s):

G DORTA ◽

D ANTOS ◽

J RADKE ◽

S MIEHLKE ◽

J MARTINEK ◽

...

Keyword(s):

Helicobacter Pylori ◽

Autoimmune Gastritis ◽

Specific Igg ◽

Igg Secretion

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Hyperstimulation of the immune system as a cause of autoimmune diseases

Annals of the Russian academy of medical sciences ◽

10.15690/vramn1276 ◽

2020 ◽

Vol 75 (3) ◽

pp. 204-213

Author(s):

Varvara A. Ryabkova ◽

Leonid P. Churilov ◽

Yehuda Shoenfeld

Keyword(s):

Immune System ◽

Autoimmune Diseases ◽

Genetic Basis ◽

Threshold Model ◽

Subsequent Development ◽

Threshold Effect ◽

Successful Management ◽

Polygenic Inheritance ◽

Autoimmune Pathology ◽

The Common

The pathogenesis of autoimmune diseases is very complex and multi-factorial. The concept of Mosaics of Autoimmunity was introduced to the scientific community 30 years ago by Y. Shoenfeld and D.A. Isenberg, and since then new tiles to the puzzle are continuously added. This concept specifies general pathological ideas about the multifactorial threshold model for polygenic inheritance with a threshold effect by the action of a number of external causal factors as applied to the field of autoimmunology. Among the external factors that can excessively stimulate the immune system, contributing to the development of autoimmune reactions, researchers are particularly interested in chemical substances, which are widely used in pharmacology and medicine. In this review we highlight the autoimmune dynamics i.e. a multistep pathogenesis of autoimmune diseases and the subsequent development of lymphoma in some cases. In this context several issues are addressed namely, genetic basis of autoimmunity; environmental immunostimulatory risk factors; gene/environmental interaction; pre-clinical autoimmunity with the presence of autoantibodies; and the mechanisms, underlying lymphomagenesis in autoimmune pathology. We believe that understanding the common model of the pathogenesis of autoimmune diseases is the first step to their successful management.

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