Incidence of Helicobacter pylori in Perforated Duodenal Ulcers: A Prospective Study

ABSTRACT

Introduction: It was found that duodenal ulcer patients tend to have an elevated maximal acid output (MAO), in response to histamine or pentagastrin, reflecting a greater parietal cell mass (Blair et al., 1987). In addition, the physiology control of acid secretion is abnormal. Basal acid is increased to greater extent than would be predicted from the increase in MAO. A work on hormonal control focused on the antral acid-stimulating hormone gastrin. Research showed that the inhibition of gastrin release by intragastric acid is decreased in duodenal ulcer patients (Moss and Calam, 1992). Somatostatin is an important mediator of gastric inhibition, and both the number of immunoreactive somatostatin cells and the amount of somatostatin peptide in gastric antral mucosa are diminished in duodenal ulcer patients (Mc Henry Jr et al., 1993). Helicobacter pylori decreases the reflex inhibition of peptone-stimulated gastrin release by luminal acid. This reflex is known to be mediated through the release of somatostatin. Eradication of H. pylori from duodenal ulcer patients elevates somatostatin RNA by about 2 times in antral and duodenal mucosa but not in corpus biopsies, reflecting the typical distribution of mucosal involvement in duodenal ulcer patients (Sipponen, 1992). Materials and Methods: A total of 25 patients who underwent surgery for perforated duodenal ulcer on emergency basis in the Department of General Surgery in S.V.S. Medical College between October 2012 and September 2014 were included in this study. Inclusion Criteria (1) Patients between 18 and 70 years of age and (2) patients having perforated duodenal ulcers were included in the study. Exclusion Criteria (1) Patients below 18 years and above 70 years of age, (2) patients on nonsteroidal anti-inflammatory drugs (NSAIDs) for more than 1 month duration, (3) patients who have received anti-H. pylori treatment, and (4) patients with gastric ulcers or ulceroproliferative growth were excluded from the study. The study population consisted of 150 patients between the age group of 18 and 55 years. Exploratory laparotomy was performed in all cases. Two mucosal biopsies were taken through the perforation. One specimen is immediately put into a preformed H. pylori detection kit for rapid urease test (RUT), which shows the presence of urease-producing bacteria by a change in the color of the medium within a time frame which is read as follows. Results: The mean age of the patient is 43.6 years. All the patients are males. 80% are smokers (21 of 25 patients). Three were addicted to pan chewing and 4 were in the habit of gutka chewing. 14 of 25 patients had a history of pain abdomen more in the epigastrium relived by taking antacids/H2 blockers. 15 of 25 patients had a history of NSAID abuse. None of the patients ever used steroids. 49% of patients whose mucosal biopsy was subjected to RUT tested positive for urease (10 strongly positive and 4 moderately positive). 11 of 25 tested negative for RUT. 16 of the 20 patients (80%) whose mucosal biopsy was, especially, investigated for H. pylori by Genta tested positive for the bacteria. Conclusions: This study has demonstrated that H. pylori is present both at the ulcer edge and antrum in a large percentage of perforated ulcers, and ulcer relapse in the form of perforation is probably correlated with pre-existing H. pylori infection. What remains to be evaluated is the relationship between the presence/absence of infection and future relapse and perhaps also H. pylori eradication and relapse, in perforated peptic ulcer patients treated with simple repair only. However, our study showed 50% association of H. pylori with duodenal ulcer perforation, and the extensive usage of antibiotics and liberal utility of proton pump with or without combination of H2 receptor blockers shows 50% positivity and 50% negativity with the incidence of H. pylori