Helicobacter Pylori Infection Is Protective Against Development Of Complications Of Gastro Esophageal Reflux Disease (GERD): A Study Done In Central Gujarat.
H Pandya, N Singh, S Singh, P Salvi, J Patel, H Agravat, J Ruparelia
gastroesophageal reflux disease gerd, helicobacter pylori hp, prevalence, reflux esophagitis re
H Pandya, N Singh, S Singh, P Salvi, J Patel, H Agravat, J Ruparelia. Helicobacter Pylori Infection Is Protective Against Development Of Complications Of Gastro Esophageal Reflux Disease (GERD): A Study Done In Central Gujarat.. The Internet Journal of Gastroenterology. 2009 Volume 10 Number 1.
Gastroesophageal reflux disease (GERD) is a chronic, relapsing acid-peptic disorder characterized by recurrent troublesome reflux symptoms; esophageal injury, such as reflux esophagitis; a variety of extra esophageal complications, reduced salivary production, and altered esophageal mucosal resistance.1, 2
In Asia, GERD has been considered as an emerging digestive disease. 3
A variety of abnormality contribute to the development of GERD including transient lower esophageal sphincter relaxation, low esophageal sphincter pressure, presence of hiatus hernia and diminished esophageal clearance of reflux gastric content.4
Last few decades has witnessed a gradual decrease in the prevalence of
However there are no evidence based explanation of this phenomena and further investigations are needed.
In the light of this background information, we conducted study of 202 GERD patients in order to determine the prevalence of
Materials and Methods
Selection of Patients
Two hundred two patients out of total 462 dyspeptic patients (age 15-90 yrs) with a chief complaint of heartburn and primary diagnosis of GERD referred to the DEEP Surgical Hospital and endoscopy clinic, Anand, between January 2007 and December 2009, were prospectively enrolled in this study and their data were recorded.
The study was approved by the Local Ethical Committee of Pramukh Swami Medical College, Karamsad, Gujarat. Dully filled Consent form was obtained by all the patients participating in the study.
Inclusion criteria: All the patients with the symptoms of heartburn and acid reflux as their chief complaint, which improved on acid suppressive therapy or with persistent vomiting and abdominal pain, were enrolled.
Exclusion criteria were the following: 1) Previous therapy to eradicate HP. 2) Patients taking aspirin or non-steroidal anti inflammatory drugs (NSAIDS) in the past 4 weeks 3) Previous surgical procedure on digestive tract. 4) Patients were on proton pump inhibitors (PPI) 5) other severe accompanying diseases.
Demographics details of the GERD patients were recorded, including, Age, gender, smoking, alcohol, tobacco, presence of hiatus hernia. All recruited patients underwent EGD to assess the severity of reflux esophagitis and presence of hiatus hernia and to exclude coexisting peptic ulcers.
Esophagitis was graded by endoscopy according to the Los angeles Classification System for the endoscopic assessment of reflux esophagitis 10: Grade A: One or more mucosal breaks no longer than 5 mm, non of which extends between the tops of the mucosal folds. Grade B: One or more mucosal breaks more than 5 mm long, none of which extends between the tops of two mucosal folds. Grade C: Mucosal breaks that extend between the tops of two or more mucosal folds, but which involve less than 75% of the esophageal circumference Grade D: Mucosal breaks which involve at least 75% of the esophageal circumference
After endoscopy 5 ml of blood was collected from each patient and serum sample was processed for detection of
Definition of “gold standard”:
Subjects were classified as having current infection with
Slides for histopathology were stained by H&E, Giemsa and Warthin Starry, histological assessment was performed by an expert pathologist (Dr. Jignesh Brahmbhatt) independently and in a blind manner.
Control study was done on 100 healthy asymptomatic non reflux individuals
Risk factors that may affect the severity of GERD were evaluated using bivariate logistic regression analysis.
A total of 462 consecutive dyspeptic patients were included in this study, out of 462 patients, 202 were endoscopically diagnosed as GERD patients. Out of 202 patients, 118 were males and 84 were females with the mean age of 43± 16yrs (range 15-90yrs).
Out of 202 patients, 120 patients (59.4%) had a chief complain of abdominal pain with heart burn, 52 (25.7%) had the symptoms of persistent vomiting, 19 patients (9.4%) had Haemetemesis, 3 patients (1.4%) had Melena and 8 patients (3.9%) had Dysphagia.
Prevalence rate of GERD was found to be high 44%, may be due to low socioeconomic and educational level of these people. Yet it is comparatively low than the other gastro duodenal diseases (Table 1).
The patients were defined as HP positive according to our gold standard definition. On the basis of results all the patients were grouped as either HP positive or HP negative. We have already shown previously the assays sensitivity and specificity for a current, active infection (compare to RUT, and gram staining) has been 98.8% & 92.9% respectively. 13
Out of 202 GERD patients, HP infection were diagnosed in 89(44%) patients, 52 males (58%) and in 37 females (42%), while 113(56%) patients with 66 males (58%) and 47 females (42%) were HP negative.
As shown in table 1, out of total 462 consecutive dyspeptic patients included in this study, 220were HP positive and 242 were HP negative, out of 220 HP positive 89 had GERD (40%) and out of 242 HP negative 113 had GERD (47%). This shows the low prevalence of GERD in HP infected than in HP non infected patients.
Further more we found no statistical difference regarding the severity of symptoms complain by the patients between HP positive and HP negative group (Table 2).
High prevalence of GERD was seen in age -group 31-40 yrs (29%) than in 41-50 yrs (22%), followed by 51-60 yrs (15%), 61-70 yrs (11%) and least was found in the older age group 71-80(4%).
Table 3 shows that smoking (
Out of 202 GERD patients, only 64 (32%) patients showed habits of either smoking, drinking or chewing tobacco. Out of these 64 patients, 25 were HP positive (40%), and 38 were HP negative (60%). One hundred and thirty eight (69%) GERD patients did not show any habits. Out of these 139 patients, 64 were HP positive (46%), 75 were HP negative (54%).
Sliding Hiatus hernia was found in only 14 cases out of 462 patients (3%), and all the 14 patients had GERD
Logistic regression coefficient shows that patients having hiatus hernia have approximately 22 times risk of getting GERD (Table 4). Chi square analysis shows that presence of hernia does not affect the severity of GERD, (
Reflux oesophagitis was evidenced by endoscopy in 202 patients (44%), according to the Los-angeles classification, out of 202 patients, 183 were graded A (84 HP positive and 99 HP negative); 13 patients were graded (B&C), 4 HP positive and 9 HP negative, finally 6 patients were graded D (1 HP+ positive, 5 HP negative). All the patients with grade D esophagitis had an esophageal ulcer but none of them had Barrett epithelium.
Eighty nine GERD patients were confirmed to have HP infection, of these 84(94.3%) had mild (Grade A) esophagitis whereas 4 had Grade B&C esophagitis (4.4%) and only 1 had esophageal ulcer (1%). Amongst those with esophagitis,
One hundred age and sex matched non-reflux; healthy volunteers were studied as a control. Prevalence of
GERD is a common condition affecting nearly 30% of the population. 14, 15 The relationship between
Different studies have evaluated the prevalence of HP infection in the patients with GERD. 15 Absence of control group is the major short coming in several studies 16
It was suggested that HP could contribute to GERD through different mechanisms: cardia inflammation causing lower esophageal sphincter weakness; increased acid secretion due to antral gastritis; delayed gastric emptying and cytotoxin production causing esophageal epithelium injury. 17
Several protective mechanism have been postulated to explain the protective effect of
At epidemiological level a decrease in the incidence of gastro duodenal ulcer diseases in western countries has been observed in last few decades, probably due to reduction in
Our study shows 44% overall prevalence of HP infection in GERD patients, this percentage confirms the result of other epidemiological studies which shows prevalence of 40% in most of the cases 20.
Young age group 31-40 yrs showed highest prevalence amongst the all, the plausible explanation for this may be due to their dependency on abusive habits.
Studies suggest that smoking reduces LES muscle function, increases acid secretion, impairs muscle reflexes in the throat, and damages protective mucus membranes. Smoking reduces salivation, which helps neutralize acid.21, 22
Alcohol has mixed effects on GERD. It relaxes the LES muscles and, in high amounts, may irritate the mucus membrane of the esophagus. Small amounts of alcohol, however, may actually protect the mucosal layer. A combination of heavy alcohol use and smoking increases the risk for esophageal cancer. 23
Univariate statistical analysis showed a moderately strong, dose-dependent relationship between increased duration of daily tobacco smoking and risk of reflux symptoms (
We found no significant correlation or outcome between habits and development of GERD (Table 3). This conflicting report was may be as majority of our patients were not chronic smokers or alcoholics. This result may be contradictory to the other authors who had shown the influence of smoking on GERD 24
The presence of a hiatal hernia increases the number of reflux episodes by mechanically weakening esophagogastric junction (EGJ) and impairs esophageal clearance 25.
In our study we found significant correlation of hiatus hernia with GERD (
To avoid inter-observer variation and bias in assessing the severity of esophagitis, our study was designed so that all cases were assessed by a single endoscopist who viewed video tape of the endoscopic examination without knowing the
As a whole, out of 89 HP positive 82 patients had mildest form of GERD, correlates with the fact of protective mechanism of HP on complications of GERD.
CagA positive strains are considered to be more virulent and induce more severe corpus gastritis . It has been postulated that not only the presence of
We found positivity for anti CagA antibody in 51% of Grade A&B and 40% of Grade C&D patients. This difference in prevalence did not show statistically significant difference by chi- square test (χ2>0.05).
Our study correlate with the study of Vicari
Our control study results correlates with the study of Haruma et al  2000, Koike
In Conclusion, Prevalence of
However, this is an evolving area with ongoing research; still relationship between HP and GERD needs to be clarify, and better designed, large scale prospective studies and trials are required.