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 ~  Abstract
 ~  Materials and Me...
 ~  Results
 ~  Discussion
 ~  References

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Year : 2002  |  Volume : 20  |  Issue : 3  |  Page : 163-164
 

Helicobacter pylori in duodenal ulcer disease and its eradication


Department of Microbiology, Seth GS Medical College and KEM Hospital, Parel, Mumbai 400 012, India

Correspondence Address:
Department of Microbiology, Seth GS Medical College and KEM Hospital, Parel, Mumbai 400 012, India

 ~ Abstract 

Antral biopsy specimens were processed for Helicobacter pylori by Gram staining, rapid urease test (RUT) and culture from 25 patients with symptoms of duodenal ulcer, amongst whom the positivity rate was 84%. Follow up of 16 patients after appropriate therapy showed complete regression of the disease in 87.5% of cases whereas in 12.5% of cases a decrease in the extent of duodenal ulceration was noted.

How to cite this article:
Sengupta S, Saraswathi K, Varaiya A, De A, Gogate A. Helicobacter pylori in duodenal ulcer disease and its eradication. Indian J Med Microbiol 2002;20:163-4


How to cite this URL:
Sengupta S, Saraswathi K, Varaiya A, De A, Gogate A. Helicobacter pylori in duodenal ulcer disease and its eradication. Indian J Med Microbiol [serial online] 2002 [cited 2019 Dec 16];20:163-4. Available from: http://www.ijmm.org/text.asp?2002/20/3/163/6944


In recent years Helicobacter pylori has been increasingly regarded as the cause of duodenal ulcer and gastritis. The association of Helicobacter pylori has been reported in duodenal ulcer disease from different parts of the world including India.[1],[2] There have been limited reports evaluating the eradication of  H.pylori   after appropriate therapy.[3],[4] Hence, the present study was undertaken to study the incidence of H.pylori in patients with duodenal ulcer disease, determine antibiotic sensitivity pattern of H.pylori isolates and to assess the therapeutic response of the patients after appropriate antimicrobial agents.

 ~ Materials and Methods Top

A total of 25 patients attending the gastroenterology clinic of LTM General Hospital, Mumbai for endoscopic (diagnostic) evaluation of their symptoms were enrolled in our study. Amongst the patients aged between 17-58 years, 22 were males and 3 were females. 10 healthy controls without any endoscopic lesions were also included in the study. The patients underwent upper gastrointestinal (GI) endoscopy and all were diagnosed as duodenal ulcer disease. They were subjected to multiple biopsies at defined sites in the gastric antrum. Three antral biopsy specimens from all the patients were taken within 5 cm of the pylorus. One specimen was used for culture in  Brucella More Details broth,[5] second one was inoculated in Christensen's urea broth for rapid urease test (RUT)[6] and the third was processed for Gram staining and Giemsa staining.[7] All the specimens were processed within one hour of collection. A patient was defined as positive for H.pylori if the bacteria were identified by 2 out of 3 diagnostic methods used staining, RUT and culture.[7]
Antibiotic sensitivity tests were performed on  Brucella More Details blood agar plates by Kirby - Bauer disc diffusion method to ampicillin, tetracycline, erythromycin, amoxycillin and metronidazole (Hi-Media). Post treatment follow up of the duodenal ulcer patients was done 6 weeks after completion of appropriate therapy, based on antibiotic sensitivity. They were subjected to repeat endoscopic biopsies from gastric antrum and similar processing of the samples was done as above.

 ~ Results Top

Of the 25 patients studied, 24 were positive by RUT (96%), 21 by direct smear (84%) and 17 by culture (68%). Seventeen patients were positive by all three parameters and four were positive by Gram stain and RUT. Thus total number of true positives in patients with duodenal ulcer was 21 (positivity rate 84%) and all of them had associated antral gastritis (endoscopic findings). Three cases were false positive by RUT. Specimens from the control group were negative by all the three parameters.
Antibiotic sensitivity pattern of the 17 isolates of H.pylori revealed 95.8% sensitivity to tetracycline, followed by erythromycin (87.5%), metronidazole (83.3%), amoxycillin (75%) and ampicillin sensitivity was only 12.5%. All the isolates were sensitive to clarithromycin. Seventeen patients with duodenal ulcer disease who were positive by all the three parameters namely culture, direct smear and RUT, received triple therapy with amoxycillin, metronidazole along with omeprazole and/or bismuth compounds, as recommended by National Institute of Health in 1994.[8] Out of these 17 patients, 16 came for post treatment follow up of which only 2 patients showed direct Gram stain smear and RUT positivity for H.pylori six weeks after completion of the eradication therapy; however follow up cultures were negative in all cases. Clinically and endoscopically 14 patients showed complete regression (87.5%) in the follow up study. Two patients (12.5%) who showed decrease in the extent of duodenal ulceration, due to therapeutic response, however were lost to follow up.

 ~ Discussion Top

Many methods for identification of H.pylori are now available, some of them being direct methods like smear examination, culture, histopathological sections and DNA probe technique; others are indirect methods like urease testing and serology. The plethora of diagnostic aids for the presence of H.pylori indicate that none of them are 100% accurate. The situation therefore demands a battery of tests to be applied for maximum possible positivity.
Our study was aimed to establish the incidence of H.pylori in duodenal ulcer patients and follow up of these patients after eradication therapy. Only the culture positive cases of duodenal ulcer were counselled for follow up study as institution of antimicrobial drugs was based on antibiotic sensitivity pattern of the H.pylori isolates.
Testing of biopsy specimen for urease is the single best indirect method for the identification of H.pylori.[6] The rapidity with which the test becomes positive is probably related to the number of H.pylori present in the specimen. In our study, majority of the positive biopsy specimens showed a detectable colour change within 10-30 minutes, though the tubes were observed for 24 hours. RUT was positive in 24 out of 25 patients with duodenal ulcer (96%). The overall positivity of RUT in our study correlated well with reports by Zaiton[9] while it was higher than that reported by Maimooma et al (65.8%)[6] and Sivaprakash et al (38.7%).[10] The direct Gram stained smear from biopsy specimens showed positivity in 21 patients (84%) in our study. Other reports show that it varies between 44-72%.[10],[11]
H.pylori was isolated in culture in only 17 out of 25 patients (68%). Isolation rate in our study was higher than that reported by Sivaprakash et al (43%)[10] and Maimomma et al (47%).[6]
In the present study out of 25 cases of duodenal ulcer disease, 21 were true positives, the positivity rate being 84%. In all 17 culture positive cases, Gram stain and RUT and Gram stain is very useful for diagnosis, as it is quick, cheap, sensitive and specific.[11]
In the post treatment follow up of duodenal ulcer patients, 14 out of 16 patients showed complete regression of duodenal ulcer endoscopically indicating that 87.5% of the patients with duodenal ulcer were cured by the eradication therapy for H.pylori. This correlates with the study of Marshall, where 90% of patients were permanently cured of duodenal ulcer with anti H.pylori therapy.[4] Hence, combination of appropriate antibiotic therapy with bismuth compounds and omeprazole along with endoscopic monitoring helps in eradication of H.pylori causing duodenal ulcer disease. 

 ~ References Top

1.Nanivadekar SA, Sawant PD, Saraswathi K. Association of Campylobacter pylori with gastritis, duodenal ulcer and gastric ulcer - a preliminary report of dyspeptic patients. Indian J Gastroentrol 1988;7:141-142.  Back to cited text no. 1    
2.Moss S, Calan J. H.pylori and peptic ulcer: the present position. GUT 1962; 33:289.  Back to cited text no. 2    
3.Borody TJ, Andrew P. H.pylori reinfection rate in patients with cured duodenal ulcer. Am J Gastroenterol 1994;89:529-532.  Back to cited text no. 3    
4.Marshall BJ. H.pylori - the etologic agent for peptic ulcer. J Am Med Assoc (JAMA) 1995;274:1064-1066.  Back to cited text no. 4    
5.Conti-Nibali S, Sferlazzas C. H.pylori infection: a simplified diagnostic approach. Am J Gastroenterol 1990;85:1573-1575.  Back to cited text no. 5    
6.Maimooma M, Habibulla CM, Nandan Singh, Hussan SI, Mahboobunissa. Evaluation of methods for detection of H.pylori from human antral mucosa. Indian J Med Microbiol 1994;12:39-43.  Back to cited text no. 6    
7.Forbes BA, Sahm DF, Weissfeld AS. Overview of conventional methods for bacterial identification. In: Bailey and Scott's Diagnostic Microbiology, 10th ed. (Mosby Inc., St. Louis) 1998;167-187.  Back to cited text no. 7    
8.NIH Consensus Development Panel on H.pylori in peptic ulcer disease. JAMA 1994;272:65-69.  Back to cited text no. 8    
9.Ziatoun AM, Histology compared with chemical testing of urease for rapid detection of H.pylori in gastric biopsy specimens. J Clin Pathol 1991;46:684-685.  Back to cited text no. 9    
10.Sivaprakash R, Rao UA. Indigenous, simple, sensitive and cost effective urease test in the diagnosis of H.pylori for the developing world. Indian J Med Microbiol 1994;12:111-115.  Back to cited text no. 10    
11.Montgomery E.A, Martin D F, Peure D A. Rapid diagnosis of C.Pylori by Gram's stain. Am J Clin Pathol 1990;90:606-609.  Back to cited text no. 11    
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