H. Pylori and the relationship with gastritis, peptic ulcers & symptoms

When normal stomach acid kills most of the bacteria, H. Pylori or helicobacter pylori can survive against stomach acid as well as develop resistance against antibiotics. In our earlier article we wrote about how weak stomach acid leads to acidity, heartburn and natural remedies. We also wrote about why actually antacid or other acid suppressor actually killing you. As I promise here I am continuing with the next part of stomach problem i.e. H. Pylori and the relationship with gastritis, peptic ulcers & symptoms.

What is H. Pylori?

In simple word H. Pylori is a bacteria that is found in considerable percentage of people with gastritis, ulcer and stomach cancer. Earlier the root cause of peptic ulcer from helicobacter pylori was unknown. In 1982 Australian scientists Barry Marshall and Robin Warren identified H. Pylori’s causative  rule in connection with chronic gastritis and gastric ulcers, challenging decades of medical doctrine holding that ulcers were caused primarily by stress, spicy foods, and too much acid. Their discovery was not accepted earlier, later it has been well established and it led to them sharing the 2005 Nobel Prize in Physiology or Medicine.

H. Pylori and the relationship with gastritis, peptic ulcers & symptoms

Stomach infection, gastritis, peptic ulcers, cancer

Helical shape of H. pylori allows it to burrow inside the mucus layer of stomach, which is less acidic environment. H. pylori releases large amount of a compound called ureases that converts to ammonia and carbon di-oxide. And these further neutralize the nearby acid environment in stomach i.e. raises stomach ph. (1)Earlier we mentioned that higher ph means weak acid and on the other hand low ph indicates strong acid. And in that way it can create a hospitable environment for bacteria as well as create infection in stomach lining. Also H. pylori develop antibiotic resistance.

Helicobacter pylori infection induces Atrophic gastritis which is a process of chronic inflammation in internal stomach mucous membrane or stomach mucosa.(2)

It damages gastric mucosa or internal mucous membrane layer of stomach and changes the pattern of hormone release. And thereby affects gastric physiology. In general body’s immune responses identify and kill harmful bacteria and other pathogens. By producing and utilizing various molecule or compound H. Pylori targets different cellular proteins and interfere with local immune system of stomach and modulate immune system. H. pylori damages gastric mucosa in multiple way which results chronic gastritis and peptic ulcer. And in long term, H. Pylori infection is associated to two forms of stomach cancer, gastric cancer (GC) and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. As such International Agency for Research on Cancer recognize H. pylori as class I carcinogen.(3,4)

Disease mechanism

H. pylori infection is well established. But researches are still going on for the mechanism of H.pylori infection and diseases. Some mechanism demonstrates as under.

Colonization of h. pylori enhance production of free radicals and other toxins.

When H. Pylori causes infection and inflammation in antrum of the stomach, the condition stimulates the uninflamed tissues to produce more acids and further predisposes to duodenum ulcers. Duodenum is the connecting part of the stomach and small intestine and is not designed to take too much acid load.

On the other hand when H. Pylori find its home at the corpus(body) of the stomach, the results go in a different way. The resulting infection as well as inflammation or atrophic gastritis inhibits normal acid production and causes hypochlorhydria. Further localized infection can lead to gastric ulcer even in low acid condition. And prolonged such condition can make a way to gastric cancer or stomach caner. From data around 15% of those colonized can develop disease.(5)

H pylori deliver bacterial products that modulate body’s inflammatory responses. Complex interfere of h. Pylori with celluar proteins as well as local immune system may lead to Gastric mucosa-associated lymphoid tissue lymphoma.

Statistics

Data of h. pylori infections varies worldwide. H. pylori infects and colonizes the human stomach in 50% of the world’s population. H. pylori causes over 60% of all stomach cancers, which corresponds to more than 5.5% of all cancers in the world.(6)An infected individual has an estimated lifetime risk of 10-20% for the development of peptic ulcer disease. H. pylori infection can be diagnosed in 90-100% of duodenal ulcer patients and in 60-100% of gastric ulcer patients. (7)

H. Pylori and acid suppressing drug

It is very possible that acid suppressing medicine can create more hospitable environment to bacteria. Study has indicated that H. pylori–infected patients with the highest serum levels of gastrin before application of proton pump acid suppression medicine  showed the most marked progression in atrophic gastritis during the period of application of the medicine.(8)Long term use of over the counter antacid or acid suppressing medicine can create health hazard in such condition. And hence individual should use such drug only under prescribed condition not as over the counter drug.

Symptoms:

Common symptoms of h. Pylori infection induced peptic ulcer includes abdominal pain/discomfort, burping, nausea, bloating, heartburn, dark or tarry stools, bad breadth, anemia as well as fatigue and some other.

Botttom line:

Helicobacter pylori stay in the stomach of most of the people in more or lesser percentage. However hospitable environment like weak stomach acid can help in growth and colonization in stomach. Stool sample testing, breath sample testing, tissue testing are some better way to detect H. Pylori colonization. I hope above information will give some idea about H. Pylori and the relationship with gastritis, peptic ulcers & symptoms along with cancer in stomach. You can also read about best natural treatment to eradicate h. Pylori bacteria from stomach and natural way to heal ulcer in stomach. 

Disclaimer: Information provided here are generalized information for  
informational and entertainment purpose only,  not intended to provide one  
to one health consultation or replace practice of a qualified practitioner.  
Different people may have different health condition and may have different  
reaction to the same food. Hence it has been advised to consult with health  
care provider before application of any of above information

Source & references:
 1.Helicobacter pylori: Physiology and Genetics,Harry L. T. Mobley,Chapter 
16Urease, Department of Microbiology and Immunology, University of Maryland 
School of Medicine, Baltimore, MD, 21201 
2.Host factors are important in determining clinical outcomes of 
Helicobacter pylori infection, Tsutomu Chiba,Hiroshi Seno,Hiroyuki 
Marusawa,Yoshio Wakatsuki,Kazuichi Okazaki, Journal of 
Gastroenterology,January 2006, Volume 41, Issue 1,  pp 1–9 
3.Pathogenesis of Helicobacter pylori infection,Kusters JG1, van Vliet AH, 
Kuipers EJ., Clin Microbiol Rev. 2006 Jul;19(3):449-90 
4.Helicobacter pylori-induced gastric inflammation and gastric 
cancer,FeiWang,WenboMeng, BingyuanWang,LiangQiao, Cancer Letters,Volume 
345, Issue 2, 10 April 2014, Pages 196-202 
5.Atherton JC. The pathogenesis of Helicobacter pylori-induced gastro-
duodenal diseases. Annu Rev Pathol. 2006;1:63–96. 
doi:10.1146/annurev.pathol.1.110304.100125
6.Role of Bacteria in Oncogenesis,Alicia H. Chang, Julie Parsonnet,ASM 
Journals, 10.1128/CMR.00012-10 
7.The prevalence of Helicobacter pylori in peptic ulcer disease,Kuipers EJ, 
Thijs JC, Festen HP.,Aliment Pharmacol Ther. 1995;9 Suppl 2:59-69 
8.Gastric mucosa during treatment with lansoprazole: Helicobacter pylori is 
a risk factor for argyrophil cell hyperplasia, Eissele R, Brunner G, Simon 
B, Solcia E, Arnold R., Gastroenterology. 1997 Mar;112(3):707-17.

Author: Bikramjit Konwar