|Year : 2014 | Volume
| Issue : 2 | Page : 91-95
The prevalence of Helicobacter pylori in acid peptic disease
Arun Gupta, Darpan Bansal, Manan S Malhotra, Rana R Singh, Amrik S Bhatia, Kulwant S Ded
Department of Surgery, Sri Guru Ram Das Institute of Medical Sciences and Research, Amritsar, Punjab, India
|Date of Web Publication||16-Oct-2014|
Manan S Malhotra
H. No. 91/8, c/o Naveen Cloth Emporium, Bhut Nath Street, Mandi (H.P.) - 175001
Source of Support: None, Conflict of Interest: None
Background: Acid peptic disease is a common problem world over resulting from imbalance of acid and pepsin present in gastric secretions. It encompasses many conditions, including gastritis and peptic ulcer with dyspepsia being a common complaint. Prevalence of H. pylori is high in developing countries and low in developed countries. We study the prevalence of H. pylori and its association with age, sex, and dietary factors in patients with acid peptic disease.
Materials and Methods: The study was conducted on 200 patients >= 18 yrs visiting SGRD hospital with complaints of dyspepsia, in a period of 2 years. Patients who refused endoscopy, who were medically unstable, those with suspected perforation, those with deranged coagulation profile, patients with history of intake of PPIs, bismuth compounds, antibiotics (metronidazole, amoxicillin, clindamycin, clarithromycin) in previous 1 week, those suffering from cholecystitis, cholelithiasis, pancreatitis, were excluded from the study. Patients were advised to stop all anti-ulcer drugs, antibiotics and bismuth containing drugs at least 1 week prior to the study. Informed consent was taken from the patients. These patients were subjected to detailed history and physical examination. A detailed questionnaire which collected presenting complaints, sociodemographic characteristics, dietary habits, smoking and drinking habits, history of regular intake of NSAIDs, any other co-morbid condition present, and abdominal ultrasonography findings, was filled. On upper GI endoscopy, gastric antral biopsies were taken and subjected to rapid urease test using a commercially available test kit. The results were noted and analyzed statistically.
Results: Overall prevalence of H. pylori came out to be 80.5%. It was more in males than females. Prevalence increased with increasing age and was highest (90.9%) in age group >70 yrs. Most common dyspeptic symptom was fullness after meals. Prevalence was seen more in non-vegetarians (83.7%) than in vegetarians (78.1%) but statistically insignificant. Chronic gastritis was most common endoscopic finding with 96.1% prevalence of H. pylori associated with it and this was significant statistically (P < 0.05). Association with peptic ulcer did not come out to be statistically significant (P > 0.05).
Conclusions: Prevalence of H. pylori is very high in our part of the world and rapid urease test presents an easy, accurate, cost-effective method for its detection. No significant association seen with gender, dietary factors, NSAIDs, smoking and alcohol intake. Chronic gastritis shows a significant association, while both duodenal and gastric ulcer did not show any significant association with H. pylori. So, taking into account the high prevalence, and association with chronic gastritis, treatment should be offered to every patient with such complaints and findings on endoscopy.
Keywords: Endoscopy, H. pylori, dyspepsia, chronic gastritis
|How to cite this article:|
Gupta A, Bansal D, Malhotra MS, Singh RR, Bhatia AS, Ded KS. The prevalence of Helicobacter pylori in acid peptic disease
. Arch Int Surg 2014;4:91-5
|How to cite this URL:|
Gupta A, Bansal D, Malhotra MS, Singh RR, Bhatia AS, Ded KS. The prevalence of Helicobacter pylori in acid peptic disease
. Arch Int Surg [serial online] 2014 [cited 2022 Aug 8];4:91-5. Available from: https://www.archintsurg.org/text.asp?2014/4/2/91/143085
| Introduction|| |
"Acid peptic disease" is a collective term used to include many conditions such as esophageal ulcer, gastro-esophageal reflux disease (GERD), gastritis, gastric ulcer, duodenal ulcer, Zollinger Ellison Syndrome (ZES), and Meckel's diverticular ulcer. Dyspepsia, defined as pain centered in the upper abdomen or discomfort characterized by fullness, bloating, distention, early satiation, nausea or vomiting, is a common complaint of patients with acid peptic disease. 
Depending upon the clinical and endoscopic observation, the commonest cause of dyspepsia is said to be chronic gastritis. The diagnosis and management of dyspepsia has been revolutionized by the advent of fibreoptic upper GI endoscopy. Endoscopic biopsy of gastric mucosa has further solved the problem of diagnosis.
Recognition of the fact that chronic gastritis and peptic ulcers are due to a bacterial infection known as Helicobacter pylori, has revolutionized the approach to diagnosis of dyspeptic patients. Individuals infected with H. pylori have a 10-20% lifetime risk of developing peptic ulcers and 1-2% risk of acquiring stomach cancer.  Blaser postulated that the changes in gastric physiology caused by the loss of H. pylori accounted for the recent increase in incidence of several diseases, including type 2 diabetes, obesity, and asthma.  Lee Veen et al. and Xu JK et al., suggested that the pathogenicity of H. pylori is dependent on its urease production.  After the recognition of association between H. pylori and dyspeptic symptoms, various methods were used for detection of H. pylori. These include Gram staining, culture, histopathology, phase contrast microscopy, electron microscopy, serology, and urea breath testing. An easier method to detect H. pylori infection is by rapid urease test based on H. pylori's marked urease activity. Urease hydrolyzes urea to bicarbonate and ammonia thus raising the pH and changes the color of pH indicator. Sensitivity and specificity of biopsy urease tests is 80-95% and 95-100%, respectively.  Three type of rapid urease tests are being used at present. These are:
- Liquid urea broth, containing phenol red as indicator.
- Liquid urea broth, containing bromothymol blue as indicator, and
- CLO gel.
Out of the above, liquid urea broth test is simplest and results are available within minutes as suggested by D.K. Bhasin et al., in 1989. 
| Materials and Methods|| |
Our study was conducted on 200 cases presenting with dyspepsia in Sri Guru Ram Das Institute of Medical Sciences and Research, Vallah, Sri Amritsar after attaining approval from hospital ethics committee. This study was conducted over a span of 2 years from December 2011 to November 2013. Before performing endoscopy, informed consent was taken from the patients. These patients were subjected to detailed history and physical examination. A detailed questionnaire which collected presenting complaints, sociodemographic characteristics, dietary habits, smoking and drinking habits, history of regular intake of NSAIDs, any other comorbid condition present, and abdominal ultrasonography findings, was filled. These patients were advised to stop all anti-ulcer drugs, antibiotics, and bismuth-containing drugs at least 1 week prior to the study.
Endoscopy was performed and findings were recorded. Biopsy was taken from gastric antrum adjacent to the pylorus opening, avoiding areas of erosion and ulceration. The biopsy pieces were subjected to rapid urease test kit (PYLO DRY/ RUT DRY) containing phenol red as indicator. The change in color of the indicator was noted at ten- minute intervals for four hours. Observation was continued for a period of at least 24 hrs. The appearance of pink or red color of the indicator was taken as positive test and yellow color as negative.
All patients presenting with complaints of dyspepsia (viz., heart burn, epigastric pain, water brash, nausea, fullness after meals, etc.) above the age of 18 yrs.
- Patients who refuse endoscopy.
- Patients who are medically unstable.
- Patients with suspected perforation.
- Patients with deranged coagulation profile.
- Patients with intake of PPIs, bismuth compounds, antibiotics (metronidazole, amoxicillin, clindamycin, clarithromycin) in previous 1 week.
- Patients suffering from cholecystitis, cholelithiasis, pancreatitis.
| Results|| |
Out of 200 patients who were subjected to endoscopy and rapid urease test, 161 tested positive and 39 tested negative. So, overall prevalence of H. pylori in this study sample came out to be 80.5%.
Prevalence of H. pylori is high in all age groups, but highest prevalence of H. pylori infection is seen in those >70 years of age and is 90.9%. 51-60-year age group also presented with almost equally high prevalence of 90%. Lowest prevalence was 69.1% and was observed in 31-40-years age group. An increasing trend of prevalence was observed with advancing age. H. pylori infection was seen to be more in males as compared to females, but this difference was statistically insignificant (P > 0.05).
The most common presenting complaint was fullness after meals (83.5%), heart burn (80%), epigastric pain (35%), water brash (33%), and nausea/vomiting (26%). Prevalence of H. pylori infection was seen to be high in all patients who had these complaints, with highest being observed with the complaint of post-prandial fullness (82%), but none other less than 75% was noted. These observations were not significant statistically, so no specific association can be made between prevalence of H. pylori infection and any particular complaint of dyspepsia.
Out of 200 patients, 114 (57.0%) were vegetarians and 86 (43.0%) were non-vegetarians. Sixty-nine out of 200 patients i.e., 34.5% had a history of excessive intake of spicy food, while the rest i.e., 131 (65.5%) had no such history. Prevalence of H. pylori infection is more in non- vegetarians and in those who regularly eat spicy food, but statistically, these findings are not significant (P > 0.05) to establish an association between dietary factors and H. pylori infection.
H. pylori prevalence was seen to be more in those who smoke [Table 1] and are alcoholic, but not significant enough statistically (P > 0.05) to establish an association between alcohol/smoking and prevalence of H. pylori infection [Table 2] and [Table 3].
This finding of such a high prevalence of H. pylori infection in patients of chronic gastritis was very significant statistically (P < 0.05) and as such a strong association could be established between H. pylori infection and chronic gastritis [Table 4], [Table 5], [Table 6], [Table 7].
| Discussion|| |
H. pylori infection is considered the most common bacterial infection in the world with an estimated 75% of population in developing country being infected with organism even at an early age  and lower in the developed country (typically less than 40%) with a declining pattern worldwide. ,
Overall prevalence of these bacteria in our study population came out to be 80.5%, which is quite high. This has been supported by many studies done in past and in recent times. A recent report by Poddar U and Yachha SK from India indicated that almost 80% of the population is infected with H. pylori 109. In another recent report by Ahmed KS et al., the overall prevalence of H. pylori was detected to be 80%. 
Our study showed more prevalence of H. pylori infection in smokers than in non-smokers (100% vs 80.3%) but it was not significant statistically. Many studies as of Shi R et al., showed no association between H. pylori prevalence and smoking.  Contrary to this, Murray LJ et al., observed that infection was significantly more common in current smokers and ex- smokers than in subjects who had never smoked and that smoking was identified as a possible risk factor for H. pylori infection.  Work by Thjodleifsson B et al., also showed a positive association between H. pylori infection and smoking. 
Our study has not shown any association between H. pylori and esophagitis. But there is a good amount of literature available which shows an inverse association between H. pylori infection and reflux esophagitis.
Upper GI endoscopy showed gastritis [Figure 1], and that too chronic gastritis to be the most common finding in patients with acid peptic disease. Prevalence of H. pylori infection in these patients was very high (96.1%) and which was quite significant statistically. So, our study showed a strong and significant association between chronic gastritis and H. pylori positivity. This has been supported by many reports in literature. Works by Hopkins RJ, Morris JG and Veldhuyzen van Zanten SJO, Sherman PM clearly show that H. pylori is undeniably the cause of chronic 'nonspecific' gastritis, , a condition located predominantly in the gastric antrum.
There is neither any association between gastric ulcer and H. pylori positivity, nor between duodenal ulcer and H. pylori positivity. This is in contrast to what has been evident from literature which gives a strong evidence of causality for H. pylori in peptic ulcer disease. ,, The correlation between H. pylori infection and duodenal ulcer (du) is exceedingly strong, whereas the correlation with gastric ulcer (gu) is impressive, but not nearly as compelling. Approximately 95% of du that are not caused by non-steroidal anti-inflammatory drugs (NSAIDs), are associated with H. pylori infection. The evidence linking H. pylori to peptic ulcer disease is so compelling that even the staid United States National Institutes of Health (NIH) has acknowledged this association and recommends concomitant anti-microbial therapy for patients with du in association with H. pylori infection.  The reasons for such a finding in our study may be attributed to decreasing prevalence of peptic ulcer disease due to widespread use of proton pump inhibitors (PPIs), H-2 receptor antagonists and mucosal protective agents as over-the-counter first line drugs for the treatment of peptic ulcer disease; a small sample size and also due to the fact that subjects under study need not have a single specific finding at the time of examination.
Our study showed a very high prevalence of H. pylori in subjects who had hiatus hernia on UGI endoscopy as compared to those without (100% vs 79.1%), but even this difference was statistically insignificant. We did not come across any literature which showed any correlation between H. pylori positivity and hiatus hernia and this remains an area for further research.
In our study, no correlation between H. pylori positivity and esophageal varices could be elucidated. Similarly, no association can be made between prevalence of H. pylori infection and portal gastropathy. The reason for these occasional findings may be attributed to the heavy drinking in our part of country, resulting in alcoholic liver disease which manifests as these findings. Literature, as well which we came across, did not show any comparison between H. pylori positivity and these findings and so, this area still needs further research in future. [Figure 2], [Figure 3], [Figure 4] show normal endoscopic views of fundus and body of stomach, the second part of duodenum and gastro esophageal junction respectively.
| Conclusion|| |
- H. pylori is highly prevalent in the population studied.
- Overall prevalence of H. pylori in patients with acid peptic disease is quite high.
- Rapid urease test has a great role in testing for the presence of H. pylori. It is cost effective, easy to perform, easy to interpret, and results are obtained within minutes (usually). So, it has emerged as one of the best methods to detect the presence of H. pylori.
- Gastritis has emerged as the single-most common abnormal finding on upper GI endoscopy. Chronic gastritis has shown a strong association with H. pylori positivity, whereas acute gastritis is not associated with H. pylori.
- Esophagitis has not shown any association with H. pylori positivity. Small sample size and the fact that one patient had more than one finding, may be the reason for such an observation. But to say with certainty, it demands further research.
- Peptic ulcer disease is quite rare in the population studied. This may be attributed to the increasing use of proton pump inhibitors, H-2 receptor antagonists and mucosal protective agents as over-the-counter first-line drugs for the treatment of peptic ulcer.
| References|| |
Talley NJ. American Gastroenterological Association: American Gastroenterological Association medical position statement: Evaluation of dyspepsia. Gastroenterol 2005;129:1753-5.
Kusters JG, van Vliet AH, Kuipers EJ. Pathogenesis of Helicobacter pylori infection. Clin Microbiol Rev 2006;19:449-90.
Blaser MJ. An endangered species in the stomach. Sci Am 2005;292:38-45.
Xu JK, Goodwin CS, Cooper M, Robinson J. Intracellular vacuolization caused by the urease of Helicobacter pylori. J Infect Dis 1990;161:1302-4.
Valle JD. Peptic ulcer disease and related disorders. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, editors. Harrison's Principles of Internal Medicine. 18 th
ed. New York: McGraw Hill; 2011. p. 2447.
Bhasin DK, Gupta MM, Ayyagari A, Singh V, Roy P, Malik AK, et al. Relative merits of various rapid biopsy urease tests for diagnosis of Helicobacter pylori (Campylobacter pylori). J Assoc Physicians India 1990;38:689-91.
Smith JG, Li W, Rosson RS. Prevalence, clinical and endoscopic predictors of Helicobacter pylori infection in an urban population. Conn Med 2009;73:133-7.
Akçam M. Helicobacter pylori and micronutrients. Indian Pediatr 2010;47:119-26.
Pandeya N, Whiteman DC. Australian Cancer Study. Prevalence and determinants of Helicobacter pylori sero-positivity in the Australian adult community. J Gastroenterol Hepatol 2011;26:1283-9.
Ahmed KS, Khan AA, Ahmed I, Tiwari SK, Habeeb A, Ahi JD, et al. Impact of household hygiene and water source on the prevalence and transmission of Helicobacter pylori: A South Indian perspective. Singapore Med J 2007;48:543-9.
Shi R, Xu S, Zhang H, Ding Y, Sun G, Huang X, et al. Prevalence and risk factors for Helicobacter pylori infection in Chinese populations. Helicobacter 2008;13:157-65.
Murray LJ, McCrum EE, Evans AE, Bamford KB. Epidemiology of Helicobacter pylori infection among 4742 randomly selected subjects from Northern Ireland. Int J Epidemiol 1997;26:880-7.
Thjodleifsson B, Asbjörnsdottir H, Sigurjonsdottir RB, Gíslason D, Olafsson I, Cook E, et al. Seroprevalence of Helicobacter pylori and cagA antibodies in Iceland, Estonia and Sweden. Scand J Infect Dis 2007;39:683-9.
Hopkins RJ, Morris JG. Helicobacter pylori: The missing link in perspective. Am J Med 1994;97:265-77.
Veldhuyzen van Zanten SJ, Sherman PM. Helicobacter pylori infection as a cause of gastritis, duodenal ulcer, gastric cancer and nonulcer dyspepsia: A systematic overview. CMAJ 1994;150:177-85.
NIH Consensus Development Panel. Helicobacter pylori in peptic ulcer disease. JAMA 1994;272:65-71.
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]