The relationship between Hp
infection and GER(D) remains a matter of controversy. There are data suggesting a protective role of Hp infection in GERD, related to the hypochlorhydria and atrophic gastritis caused by the H.
Other data suggest an aggravating role, while many studies support a mere co-existance of the two conditions.3,14
Awad et al.15
studied 37 adult patients with GERD, of whom 75.6% were Hp-positive, using endoscopy, ambulatory 24-hour esophageal pH-metry and manometry: there was no difference in the severity of esophagitis, and acid exposure as well as manometric findings between Hp-positive and Hp-negative groups. We reported similar results in our study.
Manes et al.16
came to the same conclusions by studying 50 adults with GERD, of whom 24 Hp-positive and 26 Hp-negative. The authors concluded that the presence of Hp has no impact on esophageal motility, LESP, or GER.
There are many studies in adults about the impact of Hp eradication on GERD. Most of them include patients with dyspepsia, peptic ulcer and asymptomatic Hp-positive patients. Labenz et al.17
found an exacerbation of GER after eradication of Hp in patients with peptic ulcer disease. More recent studies came to the same conclusion.18–20
On the other hand, many adult studies support that Hp eradication results in a decreased GER symptomatology. Loren and Sugg included 8 prospective trials in a meta- analysis and showed that Hp eradication improved GER symptoms.21
Others report that Hp eradication has no impact on GER symptoms, suggesting a co-existance of the two conditions.22,23
We eradicated H. Pylori
in 40 patients with GERD symptoms and re-evaluated them in 6 months. We found just a slight improvement of clinical symptomatology that was not statistically significant ().
There are only very few published studies on the relationship between Hp status, esophageal motility and acid exposure in patients with GERD. Verma et al.
found no significant correlation between the motility indexes and esophageal acid exposure in patients with GERD after eradication. Guliter and Kandilci studied 18 adult patients with GERD and Hp-gastritis using 24-hour pH-metry and static esophageal manometry.25
After successful eradication of Hp, no difference was found in the pH and manometric findings and only a slight improvement of clinical symptomatology.
In East-Asian patients, where Hp-gastritis is primarily located in the corpus, the eradication of Hp leads sometimes to an increase in esophageal acid exposure and a worsening of the symptoms. Wu et al.
studied esophageal acid exposure in 14 adult patients with GERD and Hp-gastritis. Twenty-six weeks after eradication of Hp, three of patients presented with worsening of the heartburn.
Levine et al.27
evaluated the effect of eradication of Hp on GER symptoms in a pediatric cohort of 95 children and adolescent with GER symptoms. They concluded that eradication of Hp did not increased symptoms of GER.
The relation between Hp infection and GERD was studied in 43 neurologically impaired pediatric patients, showing esophagitis in 14/43 patients.28
Four to 6 weeks after Hp eradication, a second endoscopy was performed: Hp infection was eradicated in all 14 patients with esophagitis but in only 19 of 29 (66%) of those without (P=0.01). In 29 patients with a normal esophagus at the first endoscopy, only one case of esophagitis was observed after H. pylori
eradication. In our study, in patients with Hp and GERD, a significant increase of the LESP and a decrease of the RI were found after Hp eradication. Normalization of hypergastrinemia after eradication of Hp (not measured in our study) could explain the findings, given that gastrin decreases LESP.29,30 The increase of LESP, in combination with the decrease of acid volume due to the healing of gastritis may lead to the decrease of esophageal acid exposure. The beneficial results of Hp eradication in this study are most likely due to the type of gastritis of our patients (antral predominant active), the most common type in children and young adults.31
In case of atrophic corpus gastritis which is associated with decreased gastric acid production the results may be different.32
The type and the localization of the gastritis may have great importance and may be the result of the age of contamination with the Hp If Hp-infection occurs in teenagers and young adults, the gastritis is limited to the antrum, and antral gastritis is associated with an increase in gastric acid production. The severity of GERD is related to the esophageal acid load, which in turn is affected by acid production in the stomach. Thus, patients with antral gastritis have an increased risk, not only of peptic ulceration, but also of GERD. Eradication of Hp in this population reduces acid production and may improve reflux and ulcer-related symptoms.32