Gastritis

gastritis-endoscopyGastritis

Gastritis is a condition of inflammation of the stomach lining.  It is usually diagnosed by biopsy via upper GI endoscopy in which a tube is inserted through the oral cavity and through the esophagus and into the stomach and a tissue sample is removed and examined.  Sometimes it can be visualized through endoscopy and no tissue sample is needed.  Redness or swelling indicate inflammation or irritation of the stomach lining.   H. pylori infection is considered the most common cause of gastritis.  The second most common cause of gastritis is the use of PPI (proton-pump inhibitor) medications.  Another common cause of gastritis is the use of non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen and aspirin, which can irritate the stomach lining and lead to gastric ulcers and bleeding.[113]

h-pylori-and-ulcers“H. pylori infection causes chronic gastritis, which is asymptomatic in the majority of carriers but is considered a major risk factor for the development of gastric and duodenal ulcers and the two gastric malignancies (cancers).”[114]

“H. pylori is now accepted as the major cause for gastritis and gastric cancer. Numerous investigations for the pathogenesis of H. pylori have been done.  Antibiotic treatment for H. pylori has been such a controversial issue that it is still not well established as to who should be treated. The high ‘recurrence rate’, potential long term complications, and socioeconomic usefulness of the bactericidal treatment have been disputed.”[115]

nsaidsOther Causes of Gastritis: PPIs and NSAIDs

A recent large-scale study showed that over 20% of gastritis patients did not have H. pylori infection.  Among those patients, a majority of them (almost 70%) had a history of PPI medication use.[113]  Animal studies have suggested that long-term PPI use can lead to gastric inflammation, possibly through microbial overgrowth.[116]  Another common cause of gastritis is the use of non-steroidal anti-inflammatory drugs (NSAIDs). Almost half of the patients with H. pylori-negative gastritis were either past or current NSAID users.[113]  As we will learn in the section devoted to the small intestine, NSAID use causes damage not only to the stomach but to the intestines as well.  In fact, the damage is greater to the small intestines than to the stomach.[117]

nsaids-disrupt-gastric-mucosal-layer“…long-term administration of NSAIDs causes adverse gastrointestinal (GI) symptoms including mucosal lesions, bleeding, peptic ulcer, and inflammation in intestine leading to perforation, strictures in small and large intestines, leading to chronic problems. Some of the adverse effects of NSAIDs may be asymptotic, but in many cases there are reports of life-threatening incidents.”[118]

atrophic-gastritisAtrophic Gastritis

Atrophic gastritis (AG) is a stomach condition that is characterized by chronic inflammation of the gastric mucosa with loss of gastric glandular cells and replacement by intestinal-type epithelium and fibrous tissue. Atrophy of the gastric mucosa is the endpoint of chronic gastritis.  It has been associated with two primary causes: chronic Helicobacter pylori (H. pylori) infection and autoimmunity directed against gastric glandular cells, called autoimmune gastritis.[119] Patients with AG have a high risk for developing gastric cancer.  Since stomach acid production decreases with age, the prevalence of atrophic gastritis is increased in people over age 60. [120]

“Helicobacter pylori (H. pylori) infection is well known to be associated with the development of precancerous lesions such as chronic atrophic gastritis (AG), or gastric intestinal metaplasia (GIM), and cancer.”[121]

autoimmune-gastritisAutoimmune Gastritis

Autoimmune gastritis (AIG) is an organ-specific autoimmune disease, in which inflammation of the mucosa of the gastric body results in total loss of gastric glands and achlorhydria (non-acid production or severe hypochlorhydria). AIG patients typically have parietal cell antibodies which aid diagnosis. In many, but not all AIG patients, vitamin B12 absorption is deficient, which leads to pernicious anemia.[122]  Vitamin B12 deficiency is common in the elderly who often suffer from B12 malabsorption. Approximately 15%-20% of vitamin B12 malabsorption in elderly patients is due to pernicious anemia, which results from elevated antibodies against intrinsic factor (IF), which is necessary for vitamin B12 absorption.[123] As in atrophic gastritis, there is evidence of chronic H. pylori infection playing a role in the development of autoimmune gastritis.

h.pylori-2“Signs of H. pylori infection in autoimmune gastritis, and positive autoimmune serum markers in H. pylori gastritis suggest an etiological role for H. pylori in autoimmune gastritis.”[123]

In addition to gastric parietal cell antibodies, there is also evidence of a connection between H. pylori infection and TPO antibodies against the thyroid.

“Results of this study support the idea of a connection between infection of H. pylori and the occurrence of anti-TPO autoantibodies representing thyroid autoimmunity and gastric parietal cells autoantibodies representing the thyrogastric syndrome.”[124]

Related Articles

Hypochlorhydria (Low Stomach Acid)

Gastroesophageal Reflux Disease (GERD)

Adverse Effects of PPIs

Gastric (Peptic) Ulcer and Duodenal Ulcer Disease

Intestinal Permeability/Leaky Gut

NSAID-Induced Enteropathy

Irritable Bowel Syndrome (IBS)

Small Intestinal Bacterial Overgrowth

The Neuroendocrine System of the Gut and the Brain-Gut Axis

References

113. Helena Nordenstedt, David Y. Graham, et al.  Helicobacter pylori-Negative Gastritis: Prevalence and Risk Factors. Am J Gastroenterol. Author manuscript; available in PMC 2014 April 12.

114. Salama NR, Hartung ML, Müller A. Life in the human stomach: persistence strategies of the bacterial pathogen Helicobacter pylori.  Nat Rev Microbiol. 2013 Jun; 11(6):385-99.

115. Inchul Lee. Critical pathogenic steps to high risk Helicobacter pylori gastritis and gastric carcinogenesis. World J Gastroenterol. 2014 June 7; 20(21): 6412–6419. Published online 2014 June 7. doi: 10.3748/wjg.v20.i21.6412

113. Helena Nordenstedt, David Y. Graham, et al.  Helicobacter pylori-Negative Gastritis: Prevalence and Risk Factors. Am J Gastroenterol. Author manuscript; available in PMC 2014 April 12.

116. Zavros Y, Rieder G, Ferguson A, et al. Genetic or chemical hypochlorhydria is associated with inflammation that modulates parietal and G-cell populations in mice. Gastroenterol. 2002;122:119–33.

113. Helena Nordenstedt, David Y. Graham, et al.  Helicobacter pylori-Negative Gastritis: Prevalence and Risk Factors. Am J Gastroenterol. Author manuscript; available in PMC 2014 April 12.

117. John L Wallace. Mechanisms, prevention and clinical implications of nonsteroidal anti-inflammatory drug-enteropathy. World J Gastroenterol. 2013 March 28; 19(12): 1861–1876. Published online 2013 March 28. doi: 10.3748/wjg.v19.i12.1861

118. Mau Sinha, Lovely Gautam, et al. Current Perspectives in NSAID-Induced Gastropathy Mediators Inflamm. 2013; 2013: 258209. Published online 2013 March 12. doi: 10.1155/2013/258209

119. Yan-Cheng Dai, Zhi-Peng Tang, Ya-Li Zhang. How to assess the severity of atrophic gastritis. World J Gastroenterol. 2011 April 7; 17(13): 1690–1693. Published online 2011 April 7. doi: 10.3748/wjg.v17.i13.1690

120. Saltzman JR, Russell RM.  The aging gut: nutritional issues. Gastroenterol Clin North Am. 1998;27:309-324.

121. Jiro Watari, Nancy Chen, et al. Helicobacter pylori associated chronic gastritis, clinical syndromes, precancerous lesions, and pathogenesis of gastric cancer development. World J Gastroenterol. 2014 May 14; 20(18): 5461–5473. Published online 2014 May 14. doi: 10.3748/wjg.v20.i18.5461

122. Aino Mirjam Oksanen, Katri Eerika Haimila, Hilpi Iris Kaarina Rautelin, Jukka Antero Partanen. Immunogenetic characteristics of patients with autoimmune gastritis. World J Gastroenterol. 2010 January 21; 16(3): 354–358. Published online 2010 January 21. doi: 10.3748/wjg.v16.i3.354

123. Lea Irene Veijola, Aino Mirjam Oksanen, Pentti Ilmari Sipponen, Hilpi Iris Kaarina Rautelin. Association of autoimmune type atrophic corpus gastritis with Helicobacter pylori infection. World J Gastroenterol. 2010 January 7; 16(1): 83–88. Published online 2010 January 7. doi: 10.3748/wjg.v16.i1.83

123. Lea Irene Veijola, Aino Mirjam Oksanen, Pentti Ilmari Sipponen, Hilpi Iris Kaarina Rautelin. Association of autoimmune type atrophic corpus gastritis with Helicobacter pylori infection. World J Gastroenterol. 2010 January 7; 16(1): 83–88. Published online 2010 January 7. doi: 10.3748/wjg.v16.i1.83

124. Sterzl I1Hrdá PMatucha PCerovská JZamrazil V. Anti-Helicobacter Pylori, anti-thyroid peroxidase, anti-thyroglobulin and anti-gastric parietal cells antibodies in Czech population. Physiol Res. 2008;57 Suppl 1:S135-41. Epub 2008 Feb 13.