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| ORIGINAL ARTICLE |
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| Year : 2015 | Volume
: 4
| Issue : 3 | Page : 155-158 |
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In vitro effect of aspirin on Helicobacter pylori on upper gastrointestinal tract
Madhurima Kothapalli, Kolli Rama Lakshmi Surya Kirani
Department of Microbiology, Rangaraya Medical College, Kakinada, Andhra Pradesh, India
| Date of Web Publication | 15-Sep-2015 |
Correspondence Address:
Madhurima Kothapalli
Department of Microbiology,Rangaraya Medical College, Kakinada, Andhra Pradesh
India
 Source of Support: Nil., Conflict of Interest: There are no conflicts of interest.  | Check |
DOI: 10.4103/2277-8632.165409
The role of Helicobacter pylori in aspirin-associated gastroduodenal ulcer disease is a subject of controversy. Aspirin use is widespread, especially in elderly patients, leading to the increased incidence of gastrointestinal (GI) bleeding. Endoscopy-guided biopsy is diagnostic. H. pylori fecal antigen detection in stool samples by enzyme-linked immunosorbent assay (ELISA) is also an option.
Aim: The aims of this study were to assess the in vitro action of aspirin on H. pylori and to determine whether this effect has a role in different gastroduodenal lesions.
Materials and Methods: The study group consisted of 100 symptomatic cases with different upper GI tract disorders, the patients aged 20-60 years and of either sex. Ten (10) asymptomatic, apparently healthy individuals were also included as the control group, after their consent was obtained for endoscopy. Biopsy material obtained by endoscopy was subjected to rapid urease test and culture, and aspirin sensitivity was determined by incorporating 400 ug/mL of aspirin in the medium.
Results and Discussion: Out of the 41 culture-positive cases, 27 isolates were aspirin-sensitive. Among the various GI disorders analyzed, aspirin-sensitive H. pylori was found mostly in cases of gastritis (7) and duodenal ulcer (7). Two of five strains from duodenitis cases, one of four from esophagitis, all four from carcinoma, five isolated from symptomatic patients without visible lesions, and only one isolated from those asymptomatic with lesion were sensitive. The aspirin-sensitive organisms may or may not be associated with lesions, but the resistant strains were definitely associated with lesions. Although these findings do not change the current clinical approach, they do emphasize the need for screening. The Helicobacter pylori stool antigen (HpSA) test is sensitive and specific for planning eradication programs of H. pylori in colonized but presymptomatic cases. Keywords: Aspirin, Helicobacter pylori, H. pylori stool antigen test (HpSA)
How to cite this article:
Kothapalli M, Kirani KR. In vitro effect of aspirin on Helicobacter pylori on upper gastrointestinal tract. J NTR Univ Health Sci 2015;4:155-8 |
How to cite this URL:
Kothapalli M, Kirani KR. In vitro effect of aspirin on Helicobacter pylori on upper gastrointestinal tract. J NTR Univ Health Sci [serial online] 2015 [cited 2021 Jan 20];4:155-8. Available from: https://www.jdrntruhs.org/text.asp?2015/4/3/155/165409 |
| Introduction | |  |
In 1983, Warren (a biologist) and Marshall (a clinician) described Helicobacter pylori. The discovery of H. pylori revolutionized the concept of gastroduodenal pathology and diverted the worldwide attention from pH to "HP," that is, H. pylori. Over the past two decades, H. pylori as an etiologic agent in ulcer disease, gastric cancer, and dyspepsia has stimulated much research, but its role in aspirin-associated gastroduodenal ulcer disease is the subject of controversy.
Previous studies have reported that aspirin interferes with the growth of Gram-positive and Gram-negative bacteria. Graham and colleagues reported that H. pylori was not susceptible to aspirin,[1] but Caselli and colleagues observed an anti-H. pylori effect of aspirin [2]in vitro.
Endoscopy-guided biopsy is diagnostic. Nonendoscopic tests obviate the need for invasive procedures. The H. pylori stool antigen (HpSA) test is a rapid test based on monoclonal antibody enzyme-linked immunosorbent assay (ELISA) of stool samples. The test has been reported to be very specific (98%) and sensitive (94%).
| Aims | | |
- To assess the in vitro action of aspirin on H. pylori.
- To determine whether this effect has an association with different gastroduodenal lesions.
| Materials and Methods | | |
One hundred (100) patients undergoing endoscopy for symptoms related to upper gastrointestinal (GI) tract lesions were taken as a study group. Ten (10) asymptomatic, apparently healthy individuals were also included as the control group, after taking their consent for endoscopy, and with the approval of the Institutional Ethical Committee.
Endoscopy-guided biopsy was taken from gastric antrum and the bits were inoculated immediately onto 10% urease slope and 20% glucose broth; a bit was crushed between two slides for staining and transported to the laboratory. The smears were stained with Grams and Giemsa stains, and the urease test was read after 2 h, 4 h, 6 h, and overnight incubation. The bit from the glucose broth was directly inoculated onto brain-heart infusion (BHI) agar with 5% sheep blood and vancomycin, colistin, nystatin, and trimethoprim (VCNT) supplement. The plates were incubated at 37°C for 4 days in an anaerobic jar under humidified microaerophilic conditions. The isolates showing Gram-negative, slender, curved or S-shaped [Figure 1] motile rods, which were urease-, oxidase-, and catalase-positive were identified as H. pylori. | Figure 1: Gram staining of the smear from antral mucosal material showing curved Gram-negative curved bacilli
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All the isolates were subcultured onto one plate of BHI agar containing pure aspirin (400 ug/mL) and one without aspirin and incubated at 37°C for 4 days. The isolates that were grown on both the plates were taken as aspirin-resistant organisms and those that had grown only on the plates without aspirin as sensitive strains.[3]
Stool samples were obtained simultaneously from all the cases and H. pylori antigen was detected in the stool sample by enzyme immuno assay (EIA) (Meridian Bioscience Inc. River Hills Drive, Cincinnati, Ohio, USA) as per manufacturer's instructions.
| Results | | |
A total of 110 samples (100 from symptomatic group and 10 from asymptomatic group) were processed by culture, urease test and HPSA test. Of the symptomatic group, 54 were HPSA positive [Table 1]. The effect of Aspirin on the isolates of H. pylori in association with various lesions is also analysed. Among the symptomatic group, more isolates were obtained from the cases with gastritis (n = 14; aspirin sensitive = 7) and duodenal ulcers (n = 8; aspirin sensitive = 7) [Table 2]. | Table 2: Effect of Aspirin on H. Pylori in Association with Various Lesions
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| Discussion | | |
Flagella and urease are very important for the colonization of the gastric mucosa by H. pylori. The adhesion of H. pylori to the gastric cells causes a direct decrease in mucosal levels of glutathione, a fundamental molecule in the maintenance of the cellular redox status and in the molecular regulation of host immune responses.[4]
Recent studies show that the ulcerogenic potential of different H. pylori strains differs in duodenal ulcer disease. It is generally recognized that H. pylori infection does not worsen mucosal injury with aspirin or nonsteroidal anti-inflammatory drug (NSAID) usage because H. pylori infection is associated with increased mucosal levels of prostaglandins.[5]
The results from some studies suggest that H. pylori infection increases the risk of complications in peptic ulcer disease, while others suggest that H. pylori plays a protective role.[6]
In one study, the number of endoscopic lesions in patients taking low-dose aspirin was higher in those with H. pylori infection than in those without H. pylori infection.[7]
In another study, more antral ulcers occurred in H. pylori-negative than in H. pylori-positive subjects taking low-dose aspirin.[6] Another study states that the association of H. pylori infection and NSAID use decreases the risk of bleeding from gastric ulcers, but not that from duodenal ulcers.[8]
It is now recognized that there is a two-way interaction between gastric acid secretion and H. pylori-associated gastritis. Gastric acid secretion influences the density of H. pylori colonization, its distribution within the stomach, and the severity of inflammatory response to infection. H. pylori gastritis also alters gastric acid secretion. In subjects with a predominant antral gastritis, it increases acid secretion, predisposing to duodenal ulcer.[9]
Culture of biopsy specimens is specific and cost-effective. It has disadvantages such as sampling errors, low sensitivity, and invasive nature. The HpSA test is sensitive (ELISA) and specific. Moreover, it is noninvasive. It is easy to perform. even by untrained personnel according to the manufacturer's instructions, and the result can be obtained within 2 h, marked by the visible color change. The only disadvantage is that it is expensive.
Of all the methods used to detect H. pylori, culture is taken as the gold standard. The sensitivity and specificity of the urease test are 95% and 73.33%, respectively.
The sensitivity and specificity of the HpSA test are 95% and 78.33%, respectively.
The H. pylori eradication rate with standard triple eradication regimen has been shown to be significantly higher among long-term aspirin users than in controls.[10] The combination of the omeprazole-amoxicillin-clarithromycin (OAC) regimen and aspirin was not significantly superior to the standard OAC regimen, but it was well tolerated in a group of patients with peptic ulcer disease. Its potential for clinical use to augment the efficacy of H. pylori eradication may warrant further investigation.[11]
The major causes of peptic ulcers are Helicobacter pylori infection and NSAIDs. Some data suggest that the clinical course may differ with the etiology of the ulcer. Ulcers in H. pylori-positive patients are more likely to be duodenal and less likely to be multiple.
H. pylori was associated mostly with the symptomatic group in our study. The only isolate from the asymptomatic group with endoscopically visible lesions and all the isolates from symptomatic group without lesions were sensitive to aspirin. However, only 21 out of 35 isolates from the symptomatic group with lesions were aspirin-sensitive [Table 3].
The present study shows that some strains (N = 27) of H. pylori were aspirin-sensitive, while others (N = 14) were resistant. An interesting observation is that sensitive organisms may or may not be associated with lesions, but resistant strains are definitely associated with lesions [Table 4].
Peptic ulcer bleeding in aspirin users occurs predominantly in people infected with the ulcerogenic bacterium, H. pylori. The hypothesis is that low doses of aspirin do not cause ulcers in the way that high doses do. Instead, H. pylori causes the ulcer and it is the aspirin, by thinning the blood, that makes it bleed. If the bacterium is eradicated, the patient will not get an ulcer; therefore, there is no increased bleeding risk with aspirin.[12]
Although these findings do not change the clinical approach, they do emphasize the need for screening and eradication programs of H. pylori in colonized but presymptomatic cases.[12]
| References | | |
| 1. | Graham DY, Lidsky MD, Cox AM, Evans DJ Jr, Evans DG, Alpert L, et al. Long-term nonsteroidal antiinflammatory drug use and Helicobacter pylori infection. Gastroenterology 1991;100:1653-7.  |
| 2. | Caselli M, Pazzi P, LaCorte R, Aleotti A, Trevisani L, Stabellini G. Campylobacter-like organisms, nonsteroidal anti-inflammatory drugs and gastric lesions in patients with rheumatoid arthritis. Digestion 1989;44:101-4. |
| 3. | Wang WH, Wong WM, Dailidiene D, Berg DE, Gu Q, Lai KC, et al. Aspirin inhibits the growth of H.pylori and enhances its susceptibility to antimicrobial agents. Gut 2003;52:490-5. |
| 4. | |
| 5. | Cryer B, Feldman M. Effects of very low dose daily, long-term aspirin therapy on gastric, duodenal, and rectal prostaglandin levels and on mucosal injury in healthy humans. Gastroenterology 1999;117:17-25. |
| 6. | Bjorkman DJ. Helicobacter pylori and low dose aspirin'. Journal watch Gastroenterology 15, 2001. |
| 7. | Kordecki H, Kurowski M, Kosik R, Pilecka D. Is Helicobacter pylori infection a risk or protective factor for mucosal lesions development in patients chronically treated with acetyl salicylic acid? J Physiol Pharmacol 1997;48(Suppl 4):85-91. |
| 8. | Santolaria S, Lanas A, Benito R, Pérez-Aisa MF, Montoro M, Sainz R. Helicobactor pylori infection is a protective factor for bleeding gastric ulcers but not for bleeding duodenal ulcers in NSAID users. Aliment Pharmacol Ther 1999;13:1511-8. |
| 9. | McColl KE, el-Omar E, Gillen D. Interaction between H.pylori infection, gastric acid secretion and antisecretory therapy. In: Patchet FM, editor. Helicobacter Infection. 8 th ed. London, UK: The Royal Society of Medicine Press Limited; 1998. p. 121-38. |
| 10. | Babu V, Ananthakrishnan N, Kate VN. Current concepts in diagnosis and management. In: Gupta RL, editor. Recent Advances in Surgery. 10 th ed. New Delhi: Jaypee Publishers; 2006. p. 227. |
| 11. | Park SH, Park DI, Kim SH, Kim HJ, Cho YK, Sung IK, et al. Effect of high-dose aspirin on Helicobacter pylori eradication. Dig Dis Sci 2005;50:626-9. |
| 12. | |
[Figure 1]
[Table 1], [Table 2], [Table 3], [Table 4]
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