VOLUME 14 | ISSUE 2 | MARCH 1994

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Helicobacter Pylori:Prevalence in 352 Consecutive Patients with Dyspepsia

Abdelrahman Elshiekh Mohamed, dtm&h, FRCP; Mohamed Ali Al-Karawi, FA(W. Germany); Abdelrahman Abdullah Al-Jumah, MBChB, DM(Lond), MRCP(I), ABIM(KSA); Abdul Mutaal Mohamed Ahmed, MRCP; Sohail Shariq, MRCP; Mohamed Ismail Yasawy, MD, DTM; Abdul Haleem, MPhil, FRCPath

From the Departments of Gastroenterology (Drs. Mohamed, Al-Karawi, Al-Jumah, Ahmed, Shariq, Yasawy) and Pathology (Dr. Haleem), Riyadh Armed Forces Hospital, Riyadh.

How to cite this article:

AE Mohamed, MA Al-Karawi, AA Al-Jumah, AMM Ahmed, S Shariq, MI Yasawy, A Haleem, Helicobacter Pylori: Prevalence in 352 Consecutive Patients with Dyspepsia. 1994; 14(2): 134-135

DOI: 10.5144/0256-4947.1994.134

Abstract

At the Riyadh Armed Forces Hospital (RAFH), 352 patients had gastroscopy and from each, antral gastric biopsies were taken for identification of Helicobacter pylori, by urease test and histopathology. In 217 (61.64%) of these 352 patients, the histology specimens showed Helicobacter pylori in 73.68% of patients with duodenal ulcer, 70% of patients with gastric ulcers and gastric erosions, 61% of patients with duodenitis and 52% of patients with gastritis. The urease test was positive at six hours in 164 (49.59%) of these 352 patients. The urease test was positive in 60% of each group of patients with endoscopic findings of gastric erosions, gastric ulcers and duodenal erosions.

Ann Saudi Med 1994;14(2):134-135.

Helicobacter pylori, previously known as Campylobacter, was first isolated in the human gastric mucosa by Warren and Marshall in 1983.¹Helicobacter pylori has an etiological role in peptic ulcer disease and nonulcer dyspepsia.^2-4Helicobacter pylori secrete substances that mediate inflammation, cause tissue damage, and affect gastric secretory function.⁵Helicobacter pylori infection is associated with alterations in surface mucous cells and with a marked inflammatory response consisting mainly of polymorphonuclear leukocyte infiltration.⁶

Helicobacter pylori colonization is now believed to be the major cause of type B gastritis.⁷Helicobacter pylori is strongly associated with duodenal ulcer and the association varies between 80% to 100% from published reports.⁸There are a few reports on Helicobacter pylori published from Saudi Arabia.^9-13 This study on the prevalence of Helicobacter pylori shows our experience at the Riyadh Armed Forces Hospital (RAFH), Riyadh.

Patients and Methods

A total of 352 consecutive patients with dyspepsia (excluding patients with bleeding, tumors and those taking nonsteroidal anti-inflammatory drugs) had gastroscopy at the Gastroenterology Department, Riyadh Armed Forces Hospital, between January and June 1991G. The age of these patients range between 17 and 69 years (mean 48.2 years). The endoscopic diagnosis of gastritis or duodenitis was made if the mucosa was hyperemic, erythematous, congested or friable. A gastric or duodenal ulcer was diagnosed when an ulcer crater was noted.

To determine the prevalence of Helicobacter pylori in these patients, three endoscopic biopsies (0.2 to 0.5 cm in size) were taken from the gastric antrum. One biopsy was placed immediately in the rapid urease test,¹⁴Campylobacter-like organism (CLO or gel test) and examined at 10 minute intervals for the next six hours. If a definite pink color developed in the urease test, a positive result was recorded. The other two biopsies were placed in a buffered formalin saline and sent for histology, where paraffin sections were stained with hematoxylin and eosin for grading gastritis and with a May-Grünwald Giemsa method for showing bacteria according to the method of Whitehead et al¹⁵ as modified by Marshall and Warren.¹⁶A positive Helicobacter pylori was recorded when a typical gram negative spiral bacteria was seen in the biopsy. In specimens where histology shows evidence of gastritis without Helicobacter, organisms are recorded as negative.

Table: Incidence of Helicobacter pylori in 352 patients.

Endoscopic Findings	No. of Patients	Positive Urease Test	Positive Histology
Gastritis	84 (23.86%)	36 (42.85%)	44 (52.38%)
Gastric erosions	46 (13.06%)	28 (60.86%)	32 (69.56%)
Gastric ulcer	10 ( 2.84%)	6 (60%)	7 (70%)
Duodenal ulcer	57 (16.19%)	32 (56.14%)	42 (73.68%)
Duodenitis	36 (10.22%)	20 (55.55%)	22 (61.11%)
Duodenal erosions	10 ( 2.84%)	6 (60.00%)	5 (50.00%)
Esophagitis	28 ( 7.95%)	10 (35.71%)	16 (57.14%)
Normal	81 (23.01%)	26 (32.09%)	49 (60.49%)
Total	352	164 (49.59%)	217 (61.64%)

Results

The table shows the number of patients who have a positive urease test or positive histology according to the endoscopic findings. In about 40% of these 352 patients, there were abnormal endoscopic findings in the stomach (gastritis, gastric erosions or gastric ulcer), while in the remaining 60% of the patients, the stomach was normal.

From the 352 patients, in 217 patients (61.64%) the histology specimens showed the presence of typical gram negative spiral bacteria. The urease test was positive in 164 (49.59%) patients from these 352 patients. The remainder of the patients had a negative histology or urease test at six hours.

The highest incidence of Helicobacter pylori was found in histological specimens in 73.68% of patients with duodenal ulcer, followed by 70% in patients with gastric ulcer and duodenal erosions. The urease test was positive in 60% of each group of patients with gastric erosions, gastric ulcer, and duodenal erosions. In 81 patients with normal endoscopic findings, the urease test was positive in 32%, while histology was positive in 60% of these 81 patients.

Discussion

There is an etiological link between Helicobacter pylori and peptic ulcer disease and nonulcer dyspepsia.^3-8Information on the pathogenesis and natural history of Helicobacter pylori infection is limited.⁵ Histological examination of gastric biopsies has shown that Helicobacter pylori is strongly associated with active chronic gastritis when polymorphonuclear leucocytes are present.^8,17 Active chronic gastritis can be one cause of gastric ulcer and gastric ulcers are commonly found in inflamed antral mucosa.^18,19 The type and grade of gastritis strongly predicts the risk of co-existing gastric or duodenal ulcer.²⁰

The endoscopic findings of the stomach were abnormal in about 40% of our patients and in whom it showed either gastritis, gastric erosions or gastric ulcer and in these patients, Helicobacter-like organisms were histologically identified in 52% to 70% of their gastric biopsies. These findings were consistent with previous studies.^17-19 In 73.68% of our patients with duodenal ulcer, gastric biopsies showed Helicobacter-like organisms and this is consistent with other studies.^8,19

The urease test findings were recorded only up to six hours in our patients and it was positive in a range of 42.85% to 60.86% in patients with abnormal endoscopic findings in the stomach or duodenum.

Several studies from Saudi Arabia showed the incidence of Helicobacter pylori.^9-13 The incidence of Helicobacter pylori in histological specimens of our patients with gastritis is less than those reported by Mahmood,¹¹ who reported an incidence of 96.5% colonization of the gastric mucosa with Helicobacter-like organisms in their patients.

However, a similar incidence in our patients was reported by Satti et al¹² who reported an incidence of 76% in their patients with gastritis. Darwish⁹ reported an incidence of 74% positive CLO test in 69 patients.

Our study shows that Helicobacter pylori may play a role in peptic ulcer disease in Saudis and the identification of Helicobacter pylori by histological techniques is better than using urease tests. This finding was consistent with other studies.^21,22

References

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