Gastric Abnormalities in Humoral Immune Deficiency Syndromes

Hartog, G. den; Jansen, Josephine; Meer, J.W.M. van der; Lamers, C. B. H. W.

doi:10.3109/00365529209096024

Cited by 6 publications

(4 citation statements)

References 46 publications

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“…It should also be pointed out that both of the H pylori negative patients harbouring MAG had notable neutrophil and lymphocyte infiltration of the gastric mucosa, suggesting that H pylori infection cannot be excluded in these two patients 2226 27Indeed, the negative results obtained with both the rapid urease test and on histological assessment could simply depend on a low bacterial load resulting from the previous use of antibiotics (both clarithromycin six and seven weeks before) for unrelated infection.…”

Section: Discussionmentioning

confidence: 99%

Gastric pathology in patients with common variable immunodeficiency

Zullo¹,

Romiti

Rinaldi

et al. 1999

Gut

112

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Background/Aims-Common variable immunodeficiency (CVID) is an immunological disorder characterised by defective antibody production. Patients with CVID have a high risk of gastric cancer. It has been suggested that gastric cancer results from an interaction between environmental factors and a genetic predisposition. The role of Helicobacter pylori as an environmental factor in gastric carcinogenesis is of current interest. Moreover, p53 gene mutations have been reported in gastric cancer. This study focuses on the gastric pathology of patients with CVID and correlation with H pylori infection. Methods-Thirty four consecutive dyspeptic patients with CVID (mean age 49.6 years, range 14-72; 17 men) were included in the study. An upper gastrointestinal endoscopy was performed and biopsy specimens were taken from the antrum, incisura angularis, and gastric body. Biopsies were used for histological assessment, to identify the presence of H pylori, and to evaluate p53 overexpression. Results-H pylori infection was detected in 14/34 (41%) patients. Chronic active gastritis involving both antrum and body was observed more frequently in H pylori positive (79%) than H pylori negative (20%) patients (p = 0.001). Similarly, a histological feature of multifocal atrophic gastritis was found more frequently in infected (50%) than uninfected patients (10%) (p = 0.012). In addition, one case of gastric adenocarcinoma and another of notable dysplasia were observed in the H pylori positive group. Overexpression of p53 was found in six (18%) patients, including one with normal gastric mucosa. Conclusions-It can be hypothesised that both H pylori and p53 alterations play a role in the gastric carcinogenesis of patients with CVID. (Gut 1999;45:77-81)

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Section: Discussionmentioning

confidence: 99%

Gastric pathology in patients with common variable immunodeficiency

Zullo¹,

Romiti

Rinaldi

et al. 1999

Gut

112

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“…Mucosal biopsies of the antrum typically show low gastrin content. Impairment in gastrin secretion is unique to CVID and is not seen in XLA or other conditions with hypogammaglobulinemia [24,25].…”

Section: Stomachmentioning

confidence: 92%

Common variable immunodeficiency and the gastrointestinal tract

Kalha

Sellin

2004

Curr Gastroenterol Rep

103

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Common variable immunodeficiency (CVID) is the second most prevalent primary immunodeficiency disorder but clinically the most important. It causes a wide spectrum of symptoms and signs affecting many systems of the body. CVID is a combination of humoral and cell-mediated deficiency, which explains not only why so many systems are affected but also why standard therapy in the form of intravenous immunoglobulin is not always effective. The gastrointestinal tract is the largest immune organ in the body, and it is therefore expected that this immunodeficiency will affect it in some way. The gastrointestinal manifestations of CVID are variable and tend to mimic known diseases, such as celiac sprue, pernicious anemia, and inflammatory bowel disease, but show significant differences on the microscopic level. Many studies continue to confirm a high prevalence of inflammatory, malignant, and infectious gastrointestinal disorders in patients with CVID. The T-cell-mediated defects of this immunodeficiency disorder are thought to be the cause of the majority of the gastrointestinal disorders in CVID and not the antibody deficiency. Therefore, intravenous immunoglobulin alone may be ineffective. Combination therapy with immunomodulators, such as azathioprine and 6-mercaptopurine, may be needed to treat these gastrointestinal manifestations of CVID.

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“…1,4,7,15 This is theorized to relate to a background of altered immune surveillance and chronic atrophic gastritis rather than Helicobacter infection. 7 Conley et al 4 described multifocal gastric adenocarcinoma arising in a background of hemorrhagic atrophic gastritis and achlorhydria in an 11-year-old girl with common variable immunodeficiency. The gastritis was apparently responsive to corticosteroid therapy, but relapsed with tapering of the steroid dose.…”

Section: Discussionmentioning

confidence: 97%

Atrophic Autoimmune Pangastritis: A Distinctive Form of Antral and Fundic Gastritis Associated With Systemic Autoimmune Disease

Jevremović¹,

Torbenson

Murray

et al. 2006

American Journal of Surgical Pathology

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The 2 major recognized forms of atrophic gastritis are autoimmune and environmental atrophic gastritis. These differ in their topographical distribution in the stomach, histologic features, and etiology. Autoimmune atrophic gastritis results from immune-mediated destruction of specialized oxyntic glands, is restricted to the body and fundus, and shows characteristic neuroendocrine hyperplasia. Environmental atrophic gastritis is associated with long-standing Helicobacter pylori infection and preferentially involves antrum and transition zone mucosa. In this study, we describe a distinctive form of atrophic gastritis that differs markedly from both of these classic variants. This gastritis is characterized by: (1) intense mucosal inflammatory infiltrates, persisting even into the phase of severe glandular atrophy, (2) pangastric distribution with diffuse involvement of both body and antrum, (3) lack of association with H. pylori, and (4) lack of neuroendocrine hyperplasia. The 8 patients presented ranged from 1 to 75 years and showed a slight female predominance (5F:3M). All had systemic autoimmune and/or connective tissue diseases including autoimmune enterocolitis (4 cases), systemic lupus erythematosus, refractory sprue, autoimmune hemolytic anemia, and disabling fibromyalgia. Positive serum autoimmune markers were documented in 7 of 8 (87%) patients, but serologies for antiparietal cell and anti-intrinsic factor antibodies were undertaken in only 1 patient each and were negative. We propose that the distinctive histology of this form of atrophic pangastritis and its association with systemic autoimmune disease suggests an autoimmune process directed against multiple cell lineages in the stomach. The development of multifocal low-grade dysplasia in 1 patient, a 19-year-old woman, suggests that this condition might have neoplastic potential.

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Gastric Abnormalities in Humoral Immune Deficiency Syndromes

Cited by 6 publications

References 46 publications

Gastric pathology in patients with common variable immunodeficiency

Gastric pathology in patients with common variable immunodeficiency

Common variable immunodeficiency and the gastrointestinal tract

Atrophic Autoimmune Pangastritis: A Distinctive Form of Antral and Fundic Gastritis Associated With Systemic Autoimmune Disease

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