Home About Us Contact Us

Official Journals By StatPerson Publication

Table of Content - Volume 12 Issue 3 - December 2019


 

Correlation of Barrett’s oesophagus, dysplasia in relation to H. pylori infection

 

Manonmani M H1, Raman M Hulinaykar2*

 

1,2Associate Professor, {1Department of General Surgery}, 2Associate Professor, {2Department of General Medicine}, Shridevi Institute of Medical Sciences and Research Hospital, NH-4, Bypass road, Tumkur- 572106

Email: hrbs2006@yahoo.co.in

 

Abstract               Background: H. Pylori infection leads to chronic gastritis, which can progress to intestinal metaplasia, dysplasia, and even gastric cancer. Chronic gastritis can also decrease production of gastric acid and possibly affect the spectrum of conditions related to gastro esophageal reflux, including Barrett esophagus. Methods: A total of 23 patients who underwent upper GI Endoscopy visiting tertiary care hospital in Tumkur were selected. All the cases were suspected for Barrett’s Oesophagus. Biopsy was taken in all the cases. Results: Barrett’s Oesophagus was seen in 13(56.5%) patients and absent in 10(43.5) patients. Dysplasia was present in 8(34.7%) patients and absent in 15(65.2%) patients, among the 8 patients 3(13%) had low grade dysplasia and 5(21.7) had mild dysplasia. Only 2(8.7%) patients were detected with H Pylori infection and both were male. Barrett’s Oesophagus, dysplasia were absent in both the cases of H Pylori infection. Conclusion: The prevalence of H. pylori infection in patients with Barrett’s oesophagus, dysplasia was nil, which indicates the possible protective role of this microorganism.

Key words: H. pylori, Barrett’s oesophagus, Dysplasia, Endoscopy.          

 

 

INTRODUCTION

In the mid-1990s, there were initial reports of patients developing either symptoms of gastro esophageal reflux disease (GERD) or endoscopic evidence of esophagitis following eradication of Helicobacter pylori. Since some patients with H pylori infection develop corpus atrophy with an associated decrease in gastric acid secretion, H pylori infection might protect against GERD and hence the development of Barrett’s esophagus and esophagea.l adenocarcinoma.1H. Pylori infection leads to chronic gastritis, which can progress to intestinal metaplasia, dysplasia, and even gastric cancer. Chronic gastritis can also decrease production of gastric acid and possibly affect the spectrum of conditions related to gastro esophageal reflux, including Barrett esophagus. H pylori infection, chronic gastritis, and intestinal metaplasia are each inversely associated with Barrett esophageal metaplasia.2 Helicobacter pylori, a bacterial infection that colonizes the human gastric mucosa, modulates gastric acid production, which may affect the development of reflux esophagitis, BE, and ultimately esophageal adenocarcinoma. H. pylori, which causes gastric inflammation and atrophy, may in some patient’s lower acid production in the stomach by damaging the acid-producing parietal cells in the corpus. Evidence from meta-analyses and systematic reviews examining the association between H. pylori and gastro esophageal reflux disease have tended to show an inverse association, although this association has been shown to be heterogeneous across studies. Similarly, meta-analyses examining the association between H. pylori and BE have shown heterogeneous findings across studies. There is a paucity of evidence evaluating source of this heterogeneity.3Helicobacter pylori infection (HPI) is well known to play a role in the carcinogenesis of gastric cancer, and has been associated with pancreatic and colon cancer. Barrett’s esophagus (BE) is associated with a 30 fold increase risk of esophageal adenocarcinoma. However, the association of BE with HPI is unclear.4 Therefore, this study aimed to correlate Barrett’s Oesophagus, dysplasia in relation to H Pylori infection.

 

METHODS

A total of 23 patients who underwent upper GI Endoscopy visiting tertiary care hospital in Tumkur were selected. All the cases were suspected for Barrett’s Oesophagus. Biopsy was taken in all the cases. The study was conducted from January 2019 to June 2019.All these patients were explained regarding the type of procedure and consent was taken. Diagnosis of infection with H. pylori was made by Rapid Urease test.

Study design: An observational clinical study. Chi-square/ Fisher Exact test has been used to find the significance of study parameters on categorical scale between two or more groups, Non-parametric setting for Qualitative data analysis. Fisher’s Exact test used when cell samples are very small. The Statistical software namely SPSS 18.0, and R environment ver.3.2.2 were used for the analysis of the data and Microsoft word and Excel have been used to generate graphs, tables etc.

 

RESULTS

There were total of 23 cases investigated for suspected Barrett’s oesophagus. 13(56.5%) were male and 10(43.5%) female. Highest number of cases were seen in age group 51-60 years which was 7(30.4%) cases followed by 61-70 age group which was 6(26.1%) cases. Barrett’s Oesophagus was seen in 13(56.5%) patients and absent in 10(43.5) patients. Dysplasia was present in 8(34.7%) patients and absent in 15(65.2%) patients, among the 8 patients 3(13%) had low grade dysplasia and 5(21.7) had mild dysplasia. Only 2(8.7%) patients were detected with H Pylori infection and both were male. Barrett’s Oesophagus, dysplasia were absent in both the cases of H Pylori infection.

Table 1: Age and gender distribution of patients studied

Age in years

Gender

Total

Female

Male

<30

0(0%)

1(7.7%)

1(4.3%)

30-40

1(10%)

1(7.7%)

2(8.7%)

41-50

1(10%)

1(7.7%)

2(8.7%)

51-60

4(40%)

3(23.1%)

7(30.4%)

61-70

2(20%)

4(30.8%)

6(26.1%)

>70

2(20%)

3(23.1%)

5(21.7%)

Total

10(100%)

13(100%)

23(100%)

P=0.976, Not Significant, Fisher Exact Test

 

Table 2: Barrets/Dysplasia/H Pylori distribution of patients studied

 

No. of patients (n=23)

%

Barrets

 

 

Absent

10

43.5

Present

13

56.5

Dysplasia

 

 

Nil

15

65.2

Low Grade

3

13.0

Mild dysplasia

5

21.7

Hpyloric

 

 

No

21

91.3

Yes

2

8.7

 

Table 3: Gender distribution of patients studied in relation to H Pyloric

Gender

Hpyloric

Total

No

Yes

Female

10(47.6%)

0(0%)

10(43.5%)

Male

11(52.4%)

2(100%)

13(56.5%)

Total

21(100%)

2(100%)

23(100%)

P=0.486, Not Significant, Fisher Exact test

 

Table 4: Correlation of Barrett’s Oesophagus and Dysplasia studied in relation to incidence H Pyloric

 

Hpyloric

Total

(n=23)

P value

No

(n=21)

Yes

(n=2)

 

 

Barrets

 

 

 

 

    Absent

8(38.1%)

2(100%)

10(43.5%)

0.178

    Present

13(61.9%)

0(0%)

13(56.5%)

Dysplasia

 

 

 

 

    Nil

13(61.9%)

2(100%)

15(65.2%)

1.000

    Low Grade

3(14.3%)

0(0%)

3(13%)

    Mild dysplasia

5(23.8%)

0(0%)

5(21.7%)

DISCUSSION

A total of 23 cases were investigated for suspected Barrett’s oesophagus. 13(56.5%) were male and 10(43.5%) female. Highest number of cases were seen in age group 51-60 years which was 7(30.4%) cases followed by 61-70 age group which was 6(26.1%) cases. Mean age was 59.2 ± 15.45 years. In a study by Asadulla et al the average age of patients in Barrett’s oesophagus was 52.4 ± 10.8 years with men (78.0%) representing more than women which is similar to our study.5Barrett’s Oesophagus was seen in 13(56.5%) patients and absent in 10(43.5) patients. The study conducted by A Meining et al on diagnosis of Barrett’s oesophagus by endoscopy and biopsy showed that 76.4% of patients showed negative on histology while only 23.6% were positive for Barrett’s oesophagus.6 This difference is probably due to the less number of cases in the present study which is 23 when compared to 110 cases by A Meining. Study by Yeong et al showed only 43.75% (7/16) of the patients suspected to have Barrett’s esophagus on endoscopy fulfilled the histological criteria of Barrett’s esophagus.7Study by K Egger et ala total of 168 cm of BO mucosa were screened and a total of 530 biopsies were taken, 345 of which (65%) demonstrated Barrett’s epithelium.8In the present study dysplasia was present in 8(34.7%) patients and absent in 15(65.2%) patients, among the 8 patients 3(13%) had low grade dysplasia and 5(21.7) had mild dysplasia. Study by K Egger et al showed that among 35 patients studied 9 (25.7%) were diagnosed for dysplasia. 8(22.8%) had low grade dysplasia and 1(2.8%) had high grade dysplasia which is similar to our study.8 In the present study only 2(8.7%) patients were detected with H Pylori infection and both were male. Barrett’s Oesophagus, dysplasia were absent in both the cases of H Pylori infection. There was an inverse association between H Pylori infection and Barrett’s oesophagus, dysplasia. Augustine Salami et al concluded that H Pylori infection is not associated with an increased risk of Barrett ’oesophagus, and may actually confer decrease.4Study by Asadulla Baig et al showed that in Barrett’s oesophagus group, H. pylori infection was present in 16.0% of patients. The prevalence of H. pylori infection in patients with Barrett’s oesophagus was lower in comparison with patients with GERD (p<0.01). They concluded that prevalence of H. pylori infection in patients with Barrett’s oesophagus, especially those with Lower Segment BE was very low, which indicates the possible protective role of this microorganism.5 Safatle-Ribeiro AV et al observed that there was no H. pylori infection detected in regions showing dysplasia. H. pylori colonization was associated with degree of inflammation (P = 0.00001) and cell proliferation (P = 0.0001). In conclusion, H. pylori is commonly seen many years after gastrectomy, it is associated with an increased epithelial cell proliferation, and it is not present in areas of histologic markers of premalignancy.9

 

CONCLUSION

The prevalence of H. pylori infection in patients with Barrett’s oesophagus, dysplasia was nil, which indicatesthe possible protective role of thismicroorganismas supported by other studies.H. pylori and Barrett’s oesophagus, dysplasia have tended to show an inverse association, although this association has been shown to be heterogeneous across studies. Further prospective studies need to be done with a larger sample size.

 

REFERENCES

    • RubensteinJH, Inadomi JM, Scheiman J, Schoenfeld P,Appelman H, Zhang M,Metko V, Kao JY. Association between Helicobacter pylori and Barrett’s Esophagus, Erosive Esophagitis, and Gastroesophageal Reflux Symptoms. ClinGastroenterolHepatol. 2014 Feb; 12(2): 239–245.
    • Bjorkman DJ, Sonnenberg A et al. Helicobacter pylori Infection and Barrett Esophagus. Gastroenterology. 2010 Dec.
    • Fischbach LA, Graham DY, Kramer JR et al Association between Helicobacter pylori and Barrett's esophagus: a case‐control study. Am J Gastroenterol 2014; 109: 357-368.
    • Salami A, Njei BM, DitahShow More IC. Helicobacter pylori and the risk of Barrett's esophagus: A meta-analysis. Journal of Clinical Oncology. 2012 Feb; 30: 35-35.
    • Asadulla Baig, Pavan BK, Bhaskaran A, Akarsh YG. Role of H pylori in GERD- A prospective study. International Journal of Surgery Science. 2019; 3(1): 207-209
    • A Meining, R Ott, I Becker, S Hahn, J Muhlen, M Werner, H Hofler et al. The Munich Barrett follow up study: suspicion of Barrett’soesophagus based on either endoscopy or histology only- what is the clinical significance. Gut 2004; 53:1402–1407.
    • Lee YY, Sharif SET, Syed Hassan Syed Abd Aziz SHSA, Mahendra Raj S. Barrett's Esophagus in an Area with an Exceptionally Low Prevalence of Helicobacter pylori Infection. ISRN Gastroenterology. Volume 2011, Article ID 394734, 4 pages http://dx.doi.org/10.5402/2011/394734.
    • K Egger, M Werner, A Meining, R Ott, H-D Allescher, H Hofler et al. Biopsy surveillance is still necessary in patients with Barrett’s oesophagus despite new endoscopic imaging techniques. Gut 2003; 52:18–23.
    • Safatle-Ribeiro AV, Riberio U , Clarke MR, Sakai P, Ishioka S,Garrido AB et al. Relationship between persistence of Helicobacter pylori and dysplasia, intestinal metaplasia, atrophy, inflammation, and cell proliferation following partial gastrectomy.Dig Dis Sci. 1999 Feb; 44(2):243-52.