Europe PMC

This website requires cookies, and the limited processing of your personal data in order to function. By using the site you are agreeing to this as outlined in our privacy notice and cookie policy.

Gastric pathology in patients with common variable immunodeficiency.

Author information

Affiliations

  • 1. Department of Clinical Medicine, Gastroenterology, "La Sapienza" University, Rome, Italy.
      Authors
    • Zullo A 1
    (1 author)

ORCIDs linked to this article

Gut, 01 Jul 1999, 45(1):77-81
https://doi.org/10.1136/gut.45.1.77 PMID: 10369708 PMCID: PMC1727591

Free full text in Europe PMC

Abstract 

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.

Free full text 

Logo of gutLink to Publisher's site
Gut. 1999 Jul; 45(1): 77–81.
PMCID: PMC1727591
PMID: 10369708

Gastric pathology in patients with common variable immunodeficiency

A Zullo, A Romiti, V Rinaldi, A Vecchione, S Tomao, F Aiuti, L Frati, and G Luzi
Author information Copyright and License information Disclaimer

Abstract

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.


Keywords: common variable immunodeficiency; Helicobacter pylori; p53; pathology; carcinogenesis; gastritis

Full Text

The Full Text of this article is available as a PDF (108K).

Selected References

These references are in PubMed. This may not be the complete list of references from this article.
  • Saxon A, Giorgi JV, Sherr EH, Kagan JM. Failure of B cells in common variable immunodeficiency to transit from proliferation to differentiation is associated with altered B cell surface-molecule display. J Allergy Clin Immunol. 1989 Jul;84(1):44–55. [Abstract] [Google Scholar]
  • Spickett GP, Farrant J, North ME, Zhang JG, Morgan L, Webster AD. Common variable immunodeficiency: how many diseases? Immunol Today. 1997 Jul;18(7):325–328. [Abstract] [Google Scholar]
  • Hermaszewski RA, Webster AD. Primary hypogammaglobulinaemia: a survey of clinical manifestations and complications. Q J Med. 1993 Jan;86(1):31–42. [Abstract] [Google Scholar]
  • Kinlen LJ, Webster AD, Bird AG, Haile R, Peto J, Soothill JF, Thompson RA. Prospective study of cancer in patients with hypogammaglobulinaemia. Lancet. 1985 Feb 2;1(8423):263–266. [Abstract] [Google Scholar]
  • Blaser MJ. Hypotheses on the pathogenesis and natural history of Helicobacter pylori-induced inflammation. Gastroenterology. 1992 Feb;102(2):720–727. [Abstract] [Google Scholar]
  • Craanen ME, Dekker W, Blok P, Ferwerda J, Tytgat GN. Intestinal metaplasia and Helicobacter pylori: an endoscopic bioptic study of the gastric antrum. Gut. 1992 Jan;33(1):16–20. [Europe PMC free article] [Abstract] [Google Scholar]
  • Eidt S, Stolte M. Prevalence of intestinal metaplasia in Helicobacter pylori gastritis. Scand J Gastroenterol. 1994 Jul;29(7):607–610. [Abstract] [Google Scholar]
  • Fontham ET, Ruiz B, Perez A, Hunter F, Correa P. Determinants of Helicobacter pylori infection and chronic gastritis. Am J Gastroenterol. 1995 Jul;90(7):1094–1101. [Abstract] [Google Scholar]
  • Kuipers EJ, Uyterlinde AM, Peña AS, Roosendaal R, Pals G, Nelis GF, Festen HP, Meuwissen SG. Long-term sequelae of Helicobacter pylori gastritis. Lancet. 1995 Jun 17;345(8964):1525–1528. [Abstract] [Google Scholar]
  • Rugge M, Cassaro M, Leandro G, Baffa R, Avellini C, Bufo P, Stracca V, Battaglia G, Fabiano A, Guerini A, et al. Helicobacter pylori in promotion of gastric carcinogenesis. Dig Dis Sci. 1996 May;41(5):950–955. [Abstract] [Google Scholar]
  • Correa P. Precursors of gastric and esophageal cancer. Cancer. 1982 Dec 1;50(11 Suppl):2554–2565. [Abstract] [Google Scholar]
  • Sipponen P, Kekki M, Haapakoski J, Ihamäki T, Siurala M. Gastric cancer risk in chronic atrophic gastritis: statistical calculations of cross-sectional data. Int J Cancer. 1985 Feb 15;35(2):173–177. [Abstract] [Google Scholar]
  • Uchino S, Tsuda H, Noguchi M, Yokota J, Terada M, Saito T, Kobayashi M, Sugimura T, Hirohashi S. Frequent loss of heterozygosity at the DCC locus in gastric cancer. Cancer Res. 1992 Jun 1;52(11):3099–3102. [Abstract] [Google Scholar]
  • Starzynska T, Bromley M, Ghosh A, Stern PL. Prognostic significance of p53 overexpression in gastric and colorectal carcinoma. Br J Cancer. 1992 Sep;66(3):558–562. [Europe PMC free article] [Abstract] [Google Scholar]
  • Shiao YH, Rugge M, Correa P, Lehmann HP, Scheer WD. p53 alteration in gastric precancerous lesions. Am J Pathol. 1994 Mar;144(3):511–517. [Europe PMC free article] [Abstract] [Google Scholar]
  • Teahon K, Webster AD, Price AB, Weston J, Bjarnason I. Studies on the enteropathy associated with primary hypogammaglobulinaemia. Gut. 1994 Sep;35(9):1244–1249. [Europe PMC free article] [Abstract] [Google Scholar]
  • Misbah SA, Chapel HM, Johnston BJ, Ali MH, Reed PI, O'Sullivan D. Attempt to reverse atrophic gastritis associated with common variable immunodeficiency. J Clin Gastroenterol. 1992 Dec;15(4):354–355. [Abstract] [Google Scholar]
  • Dixon MF, Genta RM, Yardley JH, Correa P. Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994. Am J Surg Pathol. 1996 Oct;20(10):1161–1181. [Abstract] [Google Scholar]
  • Filipe MI, Potet F, Bogomoletz WV, Dawson PA, Fabiani B, Chauveinc P, Fenzy A, Gazzard B, Goldfain D, Zeegen R. Incomplete sulphomucin-secreting intestinal metaplasia for gastric cancer. Preliminary data from a prospective study from three centres. Gut. 1985 Dec;26(12):1319–1326. [Europe PMC free article] [Abstract] [Google Scholar]
  • Faigel DO, Furth EE, Childs M, Goin J, Metz DC. Histological predictors of active Helicobacter pylori infection. Dig Dis Sci. 1996 May;41(5):937–943. [Abstract] [Google Scholar]
  • den Hartog G, Jansen JB, van der Meer JW, Lamers CB. Gastric abnormalities in humoral immune deficiency syndromes. Scand J Gastroenterol Suppl. 1992;194:38–40. [Abstract] [Google Scholar]
  • Figura N. Progress in defining the inflammatory cascade. Eur J Gastroenterol Hepatol. 1995 Apr;7(4):296–302. [Abstract] [Google Scholar]
  • Negrini R, Savio A, Poiesi C, Appelmelk BJ, Buffoli F, Paterlini A, Cesari P, Graffeo M, Vaira D, Franzin G. Antigenic mimicry between Helicobacter pylori and gastric mucosa in the pathogenesis of body atrophic gastritis. Gastroenterology. 1996 Sep;111(3):655–665. [Abstract] [Google Scholar]
  • Filipe MI, Barbatis C, Sandey A, Ma J. Expression of intestinal mucin antigens in the gastric epithelium and its relationship with malignancy. Hum Pathol. 1988 Jan;19(1):19–26. [Abstract] [Google Scholar]
  • Correa P. Human gastric carcinogenesis: a multistep and multifactorial process--First American Cancer Society Award Lecture on Cancer Epidemiology and Prevention. Cancer Res. 1992 Dec 15;52(24):6735–6740. [Abstract] [Google Scholar]
  • Correa P. Chronic gastritis: a clinico-pathological classification. Am J Gastroenterol. 1988 May;83(5):504–509. [Abstract] [Google Scholar]
  • Correa P, Fox J, Fontham E, Ruiz B, Lin YP, Zavala D, Taylor N, Mackinley D, de Lima E, Portilla H, et al. Helicobacter pylori and gastric carcinoma. Serum antibody prevalence in populations with contrasting cancer risks. Cancer. 1990 Dec 15;66(12):2569–2574. [Abstract] [Google Scholar]
  • Hollstein M, Sidransky D, Vogelstein B, Harris CC. p53 mutations in human cancers. Science. 1991 Jul 5;253(5015):49–53. [Abstract] [Google Scholar]
  • Wynford-Thomas D. P53 in tumour pathology: can we trust immunocytochemistry? J Pathol. 1992 Apr;166(4):329–330. [Abstract] [Google Scholar]
  • Romiti A, Moretti A, Vecchione A, Muraro R, Feudi ML, Rinaldi V, Mancini R, Valli C, Mozzicafreddo A, Frati L, et al. Analysis of p53 expression in precancerous and malignant gastric mucosa. Oncol Rep. 1998 Jan-Feb;5(1):109–113. [Abstract] [Google Scholar]
  • Brito MJ, Williams GT, Thompson H, Filipe MI. Expression of p53 in early (T1) gastric carcinoma and precancerous adjacent mucosa. Gut. 1994 Dec;35(12):1697–1700. [Europe PMC free article] [Abstract] [Google Scholar]
  • Saito T, Ootaka T, Sato H, Furuta T, Sato T, Soma J, Abe K, Yoshinaga K. Participation of macrophages in segmental endocapillary proliferation preceding focal glomerular sclerosis. J Pathol. 1993 Jun;170(2):179–185. [Abstract] [Google Scholar]
  • Vorechovský I, Scott D, Haeney MR, Webster DA. Chromosomal radiosensitivity in common variable immune deficiency. Mutat Res. 1993 Dec;290(2):255–264. [Abstract] [Google Scholar]
  • Fox JG, Li X, Cahill RJ, Andrutis K, Rustgi AK, Odze R, Wang TC. Hypertrophic gastropathy in Helicobacter felis-infected wild-type C57BL/6 mice and p53 hemizygous transgenic mice. Gastroenterology. 1996 Jan;110(1):155–166. [Abstract] [Google Scholar]

Figures and Tables

An external file that holds a picture, illustration, etc. Object name is 98357.f1.jpg

p53 expression in a Helicobacter pylori negative patient (14 year old girl) with normal gastric mucosa at endoscopy and with mild chronic inactive gastritis at histological assessment. Original magnification, ×200.

Articles from Gut are provided here courtesy of BMJ Publishing Group

Full text links 

Read article at publisher's site: https://doi.org/10.1136/gut.45.1.77

Read article for free, from open access legal sources, via Unpaywall: https://gut.bmj.com/content/gutjnl/45/1/77.full.pdfUnpaywall

Citations & impact 

Impact metrics

62
Citations
Jump to Citations

Citations of article over time

Article citations

Go to all (62) article citations

Similar Articles 

To arrive at the top five similar articles we use a word-weighted algorithm to compare words from the Title and Abstract of each citation.