Have H Pylori Again but No Acid Reflux
September 18, 2020
3 min read
What Is the Role of Helicobacter pylori in GERD?
Nosotros were unable to process your asking. Delight try again later. If y'all continue to take this issue please contact customerservice@slackinc.com.
Helicobacter pylori is a gram-negative, screw, flagellated organism that infects the gastric mucosa, leading to chronic gastritis. It has been causally related to duodenal and gastric ulcers, gastric cancer, and gastric mucosa associated lymphoid tissue (MALT) lymphoma. Information technology has been linked to the increased chance for development of ulcer affliction in patients on nonsteroidal anti-inflammatory drugs and as a potential contributor to functional or nonulcer dyspepsia.
At that place are three patterns of infections. Chronic active antral gastritis results in an increment in gastric acid secretion and duodenal ulcer gamble. Chronic agile corpus gastritis results in a decrease in acid secretion and an increment in gastric ulcer. The bug tin event in chronic pangastritis, which is associated with atrophy, gastric intestinal metaplasia, and the perceived and documented increase in gastric cancer.
The relationship of H. pylori and gastroesophageal reflux disease has been one of controversy. Some early on studies suggested that eradication of H. pylori infection in the setting of duodenal ulcer disease would result in an increase in erosive esophagitis and GERD symptoms. Although in that location are several studies to support this, the weight of the testify suggests strongly that eradication of H. pylori has no effect on the development of heartburn and in fact does not exacerbate GERD symptoms when they are nowadays at baseline. There are also several studies that suggest that in the setting of chronic corpus gastritis and/or panatrophic gastritis, the prevalence of erosive esophagitis, and, in fact, the frequency of Barrett's esophagus, is less than in matched groups who do non have infection. This has led to some authorities proposing that H. pylori infection might be protective against severe cease organ damage in patients with GERD. Bluntly, this paradox of H. pylori infection being detrimental to the gastric mucosa and at the same time protective of the esophageal mucosa is difficult to reconcile.
When i attempts to work their way through the data, I am comfortable with the post-obit clinical caveats. H. pylori infection itself clearly does not crusade GERD nor, in fact, have any dramatic effect on symptoms. Eradication of H. pylori does not, in my practice, appear to bear upon the natural history of or the treatment of GERD at all (Figure 36-ane). It is, therefore, my recommendation that if the clinical presentation mandates investigation for Helicobacter (suspicion of gastric ulcer, duodenal ulcer, or in certain situations functional dyspepsia), testing for H. pylori is warranted. In the GERD patient, I find no role in my clinical practice for testing. Should testing be needed, active testing with either a stool antigen examination or ureal breath test is preferred to serum immunoglobulin G (IgG) antibody testing as the increased sensitivity and specificity of the old outweigh the upfront cost advantages of the latter. Rapid urease testing of gastric biopsies should be performed if the patient is undergoing endoscopy and testing is indicated. I do not advocate routine biopsy of the gastric mucosa when endoscoping a patient with suspected gastroesophageal reflux disease. If H. pylori infection is present for whatever reason, I follow the standard recommendation that the organism be treated and employ traditional proton pump inhibitor–based triple therapy for eradication.
Figure 36-i. Heartburn later on H. pylori treatment. Well-done study showing no divergence in reflux symptoms one and 6 months after H. pylori eradication. (Reprinted from Vakil North, Hahn B, McSorley D. Recurrent symptoms and gastrooesophageal reflux disease in patients with duodenal ulcer treated for Helicobacter pylori infection. Aliment Pharmacol Ther. 2000;14(1):45-51, with permission from Blackwell Scientific Publications.)
The patient seen in the emergency room with noncardiac chest pain is not a candidate for H. pylori testing, as the potential etiologies for her hurting do non include gastric ulcer and/or duodenal ulcer in my opinion. It is highly unusual in my practice to recollect any patient who experienced an improvement in their chronic breast pain with eradication of infection. The question as posed assumes that the noncardiac chest pain is due to reflux, which information technology may not be. Regardless, there is no reason to suspect that H. pylori eradication would make chest hurting worse. It is worth commenting that using serology to document infection in this type of patient creates "more than trouble than information technology is worth" every bit there is no mode to determine without a careful history whether or not this represents active or sometime infection. Ultimately, the best course of action for Ms. Smith would be to evaluate and treat her for noncardiac chest pain with suspected esophageal etiology and non exam for H. pylori at all.
Source: https://www.healio.com/news/gastroenterology/20200929/what-is-the-role-of-helicobacter-pylori-in-gerd
0 Response to "Have H Pylori Again but No Acid Reflux"
Post a Comment