Endoscopy 2009; 41(1): 51-54
DOI: 10.1055/s-2008-1077780
Endoscopy essentials

© Georg Thieme Verlag KG Stuttgart · New York

Ulcers and gastritis

H.  Kashiwagi1
  • 1Department of Surgery, Jikei University School of Medicine, Tokyo, Japan
Further Information

Publication History

Publication Date:
04 December 2008 (online)

Epidemiology of chronic atrophic gastritis: population-based study among 9444 older adults from Germany (Weck et al., Aliment Pharmacol Ther 2007 [1])

Chronic atrophic gastritis (CAG) plays a crucial role in the development of intestinal-type gastric carcinoma. Helicobacter pylori infection seems to be the main cause of CAG. Diagnosis of CAG is based mostly on gastroscopy and histological findings following gastric biopsy, which is difficult to apply in large-scale population-based studies. An approach more suitable for such studies is to obtain information on the gastric mucosal status by measuring pepsinogen (PG) concentrations in the blood, as has been developed by Miki et al. [2] and Samloff et al. [3]. The objectives of this study by Weck et al. were to estimate prevalence of CAG by using two diagnostic criteria and to examine the association between CAG and potential risk factors and clinical consequences in a large population-based study among elderly individuals in Germany. From the variety of cut-off points used to define CAG in previous epidemiological studies, the following two were chosen: (i) PG I < 25 ng/mL, which was used in the EUROGAST study by Webb et al. [4], the only large international comparative study to delineate severe forms of CAG; and (ii) PG I < 70 ng/mL and PG I/PG II < 3, as used in several studies from Japan to define any form of CAG. With the definition used in the EUROGAST study (PG I < 25 ng/mL), prevalence of CAG increased from 4.8 % in the age group 50 – 54 years to 8.7 % in the age group 70 – 74 years. The alternative definition of CAG (PG I < 70 ng/mL and PG I/PG II < 3) used in the Japanese studies, revealed a greater increase with age (from 2.7 % to 9.1 %) and a strong association with H. pylori infection. Prevalence of CAG was found to be at a low level in this large study of older adults in Germany, and strongly increased with age but was unrelated to sex, smoking, and alcohol consumption. A strong association with H. pylori infection emerged only when CAG was defined by both PG I and the PG I/PG II ratio. Therefore, the role of H. pylori infection may be underestimated in studies where CAG is defined only by PG I levels, supporting the use of the PG I/PG II ratio for the definition of CAG in epidemiological studies.

Patients with CAG, formerly known as type A gastritis, are frequently asymptomatic but may have an increased risk of developing gastric cancer. Therefore, it is important to make an early diagnosis in patients at risk and to find useful serum markers. Recently, Checchi et al. have reported that serum ghrelin levels are the most sensitive and specific markers for selecting those patients at high risk of gastric damage that needs to undergo further investigation, including gastric biopsy [5].

References

  • 1 Weck M N, Stegmaier C, Rothenbacher D. et al . Epidemiology of chronic atrophic gastritis: population-based study among 9444 older adults from Germany.  Aliment Pharmacol Ther. 2007;  26 879-887
  • 2 Miki K, Ichinose M, Shimizu A. et al . Serum pepsinogens as a screening test of extensive chronic gastritis.  Gastroenterol Jpn. 1987;  22 133-141
  • 3 Samloff I M, Varis K, Ihamaki T. et al . Relationships among serum pepsinogen I, serum pepsinogen II, and gastric mucosal histology. A study in relatives of patients with pernicious anemia.  Gastroenterology. 1982;  83 204-209
  • 4 Webb P M, Hengels K J, Moller H. et al . The epidemiology of lower serum pepsinogen A levels and an international association with gastric cancer rates. EUROGAST Study Group.  Gastroenterology. 1994;  107 1335-1344
  • 5 Checchi S, Montanaro A, Pasqui L. et al . Serum ghrelin as a marker of atrophic body gastritis in patients with parietal cell antibodies.  J Clin Endocrinol Metab. 2007;  92 4346-4351
  • 6 Shiotani A, Uedo N, Iishi H. et al . Re-expression of sonic hedgehog and reduction of CDX2 after Helicobacter pylori eradication prior to incomplete intestinal metaplasia.  Int J Cancer. 2007;  121 1182-1189
  • 7 Zavros Y, Waghray M, Tessier A. et al . Reduced pepsin A processing of sonic hedgehog in parietal cells precedes gastric atrophy and transformation.  J Biol Chem. 2007;  282 33 265-33 274
  • 8 Shiotani A, Iishi H, Uedo N. et al . Helicobacter pylori-induced atrophic gastritis progressing to gastric cancer exhibits sonic hedgehog loss and aberrant CDX2 expression.  Aliment Pharmacol Ther. 2006;  24 (Suppl 4) 71-80
  • 9 Wong B C, Lam S K, Wong W M. et al . Helicobacter pylori eradication to prevent gastric cancer in high-risk region of China: a randomized controlled trial.  JAMA. 2004;  291 187-194
  • 10 Ravizza M. Does Helicobacter pylori eradication modify intestinal metaplasia evolution in the stomach?.  Minerva Gastroenterol Dietol. 2002;  48 165-167
  • 11 Koussoulas V, Tzivras M, Giamarellos-Bourboulis E J. et al . Can soluble triggering receptor expressed on myeloid cells (sTREM-1) be considered an anti-inflammatory mediator in the pathogenesis of peptic ulcer disease?.  Dig Dis Sci. 2007;  52 2166-2169
  • 12 Koussoulas V, Vassiliou S, Demonakou M. et al . Soluble triggering receptor expressed on myeloid cells (sTREM-1): a new mediator involved in the pathogenesis of peptic ulcer disease.  Eur J Gastroenterol Hepatol. 2005;  18 375-379
  • 13 Bodger K, Bromelow K, Wyatt J I. et al . Interleukin-10 in Helicobacter pylori associated gastritis: immunohistochemical localization and in vitro effects in cytokines secretions.  J Clin Pathol. 2001;  54 285-292
  • 14 Koussoulas V, Vassiliou S, Spyridaki E. et al . Evidence for the role of gastric mucosa at the secretion of soluble triggering receptor expressed on myeloid cells (strem-1) in peptic ulcer disease.  World J Gastroenterol. 2007;  13 4610-4614
  • 15 Ray W A, Chung C P, Stein C M. et al . Risk of peptic ulcer hospitalizations in users of NSAIDs with gastroprotective cotherapy versus coxibs.  Gastroenterology. 2007;  133 790-798
  • 16 Laine L. Nonsteroidal anti-inflammatory durg gastropathy.  Gastrointest Endsc Clin N Am. 1996;  6 489-501
  • 17 Laine L, Harper S, Simon T. et al . A randomized trial comparing the effect of rofecoxib, a COX-2 specific inhibitor, to ibuprofen on the gastroduodenal mucosa of osteoarthritis patients.  Gastroenterolgy. 1999;  117 776-783
  • 18 Rostom A, Muir K, Dube C. et al . Gastrointestinal safety of cyclooxygenase-2 inhibitors: a Cochrane Collaboration Systematic Review.  Clin Gastroenterol Hepatol. 2007;  5 818-828
  • 19 Laine L, Takeuchi K, Tarnawski A. Gastric mucosal defense and cytoprotection: bench to bedside.  Gastroenterology. 2008;  135 41-60
  • 20 Robson A J, Richards J M, Ohly N. et al . The effect of surgical subspecialization on outcomes in peptic ulcer disease complicated by perforation and bleeding.  World J Surg. 2008;  32 1456-1461
  • 21 Zaragoza A M, Tenias J M, Llorente M J. et al . Prognostic factors in gastrointestinal bleeding due to peptic ulcer: construction of a predictive model.  J Clin Gastroenterol. 2008;  42 786-790
  • 22 Larssen L, Moger T, Bjornbeth B A. et al . Transcatheter arterial embolization in the management of bleeding duodenal ulcers: a 5.5-year retrospective study of treatment and outcome.  Scand J Gastroenterol. 2008;  43 217-222
  • 23 Imhof M, Epstein S, Ohmann C. et al . Duration of survival after peptic ulcer perforation.  World J Surg. 2008;  32 408-412

H. KashiwagiMD 

Department of Surgery
Jikei University School of Medicine

3-25-8, Nishi-shinbashi
Minato-ku
Tokyo
Japan

Fax: +81-3-54724140

Email: hkashiwagi.surg@jikei.ac.jp

    >