Prevalence of Helicobactor pylori in patients with perforated duodenal ulcer.

It is believed that Helicobacter pylori (H. Pylori) plays an important role in the causation of peptic ulcer. However, its role in duodenal ulcer perforation (DUP) has not been investigated extensively and the results are conflicting. The aim of this study was to determine the prevalence of H. pylori in patients with DUP patients as compared to normal healthy volunteers (NHV). Eighty-six consecutives patients with DUP and 30 NHV were included in the study. The NHV, drawn from the Surgery outpatient, were subjected to upper gastrointestinal (UGI) endoscopy and multiple gastric mucosal biopsies. Gastric mucosal biopsies among patients with DUP were obtained during laparotomy by passing a biopsy forcep through the perforation site. Biopsy specimens were put in urea broth for the rapid urease test (RUT), brucella broth (used as a transport medium) for culture and 10% formalin for histopathology. The results were analysed as the percentage of positive cases. The mean (+/-SD) age of patients with DUP (39.4+/-15.5 years) and of the NHV (36.0+/-13.9 years) were comparable (p= 0.290). Sixty-one (70.9%)patients with DUP had used NSAIDs prior to perforation. Only 7 patients with DUP (8.14%) had a past history of symptoms of duodenal ulcer and had been treated for it. A positive history of smoking, alcoholism and tobacco use was present in 68 (78.9%), 59 (68.6%) and 41(47.7%) patient with DUP, respectively. No culture was positive. Histology was positive for H. pylori in 29 patients with DUP and in 2 (6.7%)NHV. RUT was positive for H. pylori in 43(50%) patients with DUP and 5 NHV (16.7%). The present study documented a markedly higher association of H. Pylori infection with perforated duodenal ulcer.

Helicobacter pylori infection delays ulcer healing in patients operated on for perforated duodenal ulcer.

BACKGROUND: A majority of duodenal ulcers are associated with Helicobacter pylori infection; eradication of the infection improves ulcer healing and reduces the ulcer recurrence rate. However, the frequency of H. pylori infection in patients with perforated duodenal ulcer is not clearly established. We studied the frequency of H. pylori infection in patients with perforated duodenal ulcer and its impact on their clinical presentation. METHODS: All patients presenting with perforated duodenal ulcer underwent emergency laparotomy and simple omental patch repair. Postoperatively they received standard antibiotics for 1-2 weeks along with ranitidine; ranitidine alone was continued thereafter till an endoscopy 4-6 weeks later. Positive rapid urease test along with identification of H. pylori on histology was taken as evidence of H. pylori infection. Patients who received anti-H. pylori therapy or nonsteroidal anti-inflammatory drugs (NSAIDs) postoperatively and/or proton pump inhibitors or antibiotics, during 4 weeks preceding the endoscopy, were excluded. RESULTS: 30 patients (27 men; mean [SD] age 32.9 [9.7 years]) presenting during the period June 1999 to October 2000 were studied. Upper gastrointestinal endoscopy was done 10.9 (6.3) weeks after surgery. Seventeen (56.6%) patients were infected with H. pylori; this group had significantly more men (17/17 versus 10/13 among uninfected) and fewer NSAID users (2/17 vs. 7/13). Median duration of epigastric pain before presentation was 18 weeks in the H. pylori-infected group as compared to one week in the non-infected group (p<0.001). Significantly more patients continued to have epigastric pain after surgery in the infected group (7/17 vs. 0/13). At endoscopy, active duodenal ulcer was present in 13 of 17 patients with evidence of H. pylori infection and none of the noninfected patients (p<0.001). Age, sex, duration between surgery and endoscopy, NSAID use, smoking and maintenance ranitidine use had no impact on ulcer healing after the surgery. CONCLUSIONS: In patients operated on for perforated duodenal ulcer, H. pylori infection was the only significant factor responsible for persistence of ulcer after surgery. We advocate H. pylori eradication therapy in patients operated on for perforated duodenal ulcer.