Sie sind auf Seite 1von 4

Journal of Medicinal Plants Research Vol. 5(16), pp.

3823-3826, 18 August, 2011


Available online at http://www.academicjournals.org/JMPR
ISSN 1996-0875 ©2011 Academic Journals

Full Length Research Paper

Prevalence of Helicobacter pylori in gastroenterological


disorders in Shifa Ul Mulk Memorial Hospital Karachi,
Pakistan
H. M. Asif1,2, Khan Usmanghani1, Naveed Akhtar2, M. Uzair3, Pervaiz Akhtar Shah4,
M. Akram1* and Zahoor-ul-Hasan1
1
Department of Clinical Sciences, Faculty of Eastern Medicine, Hamdard University, Karachi, Pakistan.
2
Faculty of Pharmacy and Alternative Medicine, The Islamia University of Bahawalpur, Pakistan.
3
Faculty of Pharmacy, Bahauddin Zakariya University Multan, Pakistan.
4
University college of Pharmacy, The University of Punjab Lahore, Pakistan.
Accepted 9 June, 2011

Prevalence of Helicobacter pylori (H. pylori) is very high and well documented in gastroenterological
disorders like gastritis, gastric carcinoma, peptic ulcer disease, and non ulcer dyspepsia and
gastroesophageal reflux disease. More than 50% of the world's population harbor H. pylori in their
upper gastrointestinal tract. Infection is more prevalent in developing countries, and incidence is
decreasing in Western countries. Our present study aims to review the recent H. pylori prevalence in
gastroenterological disorders in Shifa Ul Mulk Memorial Hospital Karachi, Pakistan. Over a 9-month
period, ninety seven patients of more than twelve years of age, with varied socioeconomic background,
presented to the out patent department (OPD) with dyspeptic symptoms suggestive of gastroduodenal
disease of more than two weeks duration were included in the study. All patients underwent endoscopy
for the diagnosis of gastroduodenal diseases and biopsies were taken for histopathology and rapid
urease test. Patient with history of intake of NSAIDs, steroids, alcohol, active bleeding, recent use of
antibiotics or proton pump inhibitors were excluded. Out of ninety seven patients; 54 (55.6%) had
chronic gastritis, 18 gastric ulcer (18.55%), 10 duodenal ulcer (10.3%) and 07 with combined gastric and
duodenal ulcers (7.21%), 01 (1%) adenocarcinoma and 07 (7.21%) had no pathology. Overall H. pylori
prevalence was 87.03% (47/54) in chronic gastritis, 66.66% (12/18) in gastric ulcer, 60.0% (6/10) in
duodenal ulcer, 71.42% (5/7) in combined gastric and duodenal ulcers, 100% (1/1) in adenocarcinoma
and 28.57% (2/5) with no pathology was recorded, respectively. The prevalence of H. pylori among our
chronic gastritis and peptic ulcer patients is slightly higher compared to overseas studies but when
compared indirectly to a previous local study, there was not much differences.

Key words: Helicobacter pylori, gastroenterological disorders, prevalence, Pakistan.

INTRODUCTION

Helicobacter pylori are a helix-shaped Gram-negative causes a chronic low-level inflammation of the stomach
bacterium, about 3 µm long with a diameter of about 0.5 lining and is strongly linked to the development of
µm. It is microaerophilic that can inhabit various areas of duodenal and gastric ulcers and stomach cancer
the stomach, particularly the antrum (Marshall and (Howden, 1996). Over 80% of individuals infected with
Warren, 1984). Prevalence of H. pylori is very high and the bacteria are asymptomatic. The cagA gene codes for
well documented in gastroenterological disorders like one of the major H. pylori virulence proteins. Bacterial
gastritis, gastric carcinoma, peptic ulcer disease, non strains that have the cagA gene are associated with an
ulcer dyspepsia and gastroesophageal reflux disease. It ability to cause ulcers (Baldwin et al., 2007). At least, half
the world's population is infected by the bacterium,
making it the most widespread infection in the world.
Rate of actual infection vary from nation to nation; the
*Corresponding author. E-mail: makram_0451@hotmail.com. people in developing countries has much higher infection
3824 J. Med. Plant. Res.

Table 1. Distribution of patients with gastro duodenal diseases.

Disease Male [n (%)] Female [n (%)] Total [n (%)]


Chronic gastritis 32 (59.25) 22 (40.74) 54 (55.6)
Gastric ulcer 10 (55.55) 8 (44.44) 18 (18.55)
Duodenal ulcer 07 (70) 03 (30) 10 (10.3)
Combined GU and DU 05 (71.42) 02 (28.57) 07 (7.2)
Adenocarcinoma 01 (100) 00 (0) 01 (100)
No pathology 03 (42.85) 04 (57.14) 07 (7.21)
Total 58 (59.79) 39 (40.20) 97

rates than the developed countries where infection rates examination of the biopsy specimen after staining with Toluidine
are documented to be around 25%. Infections are usually blue. Variables recorded included age, gender, socioeconomic
status, presenting complaints, history of medication or alcohol
acquired in early childhood in all countries. However, the intake, clinical and biochemical data suggestive of chronic liver
infection rate of children in developing countries is higher disease and chronic renal failure.
than in developed countries, probably due to poor
sanitary conditions. In developed nations, it is currently
uncommon to find infected children, but the percentage of Statistical analysis
infected people increases with age, with about 50%
Fisher exact test (2-tailed test) was used to assess the independent
infected for those over the age of 60 compared with effect of age, sex and NSAID use on H. pylori prevalence.
around 10% between 18 and 30 years (Malaty, 2007). Statistical analysis was performed using Statistical Package for
In Pakistan, H. pylori infection is strongly associated Social Sciences (SPSS) Version 17.0. Statistical significance is
with peptic ulcer disease and gastritis. H pylori infection taken at 0.05.
rate increases with advancement of age and lowering of
socioeconomic status in Pakistan (Qureshi et al., 1999).
Previous data shows overall exposure rate to H. pylori in RESULTS
children was 33% while in adults 85% cases of duodenal
ulcer were due to H. pylori infection (Qureshi et al., 1999; 109 patients with dyspeptic symptoms were eligible for
Kazi et al., 1990). Peptic ulcer disease occurred the study during the nine-month period. 5 patients were
predominantly between 30 to 50 years of age with a excluded because of a past history of peptic ulcer and 4
male-female ratio of 6:1. History of NSAID intake was patients because of recent antibiotic use. Of the 100
present in only 5% of these cases (Ahmed et al., 1990). patients selected, 3 patients were further excluded due to
The aim of our study was to determine the prevalence of missing data on H. pylori status (H. pylori status was
H. pylori in gastroenterological disorders in Shifa Ul Mulk either not documented or not established). Data analysis
Memorial Hospital Karachi, Pakistan. was then carried out on the remaining 97 patients.
Among these patients studied, 54 (55.6%) had chronic
gastritis, 18 gastric ulcer (18.55%), 10 duodenal ulcer
MATERIAL AND METHODS (10.3%) and 07 with combined gastric and duodenal
ulcers (7.21%), 01 (1%) adenocarcinoma and 07 (7.21%)
From February 2009 to December 2009, consecutive patients who had no pathology as shown in Table 1 and Graph 1.
underwent oesophagogastroduodenoscopy (OGD) and diagnosed
with positive H. pylori at Shifa Ul Mulk Memorial Hospital for
Eastern Medicine, Hamdard University Karachi, Pakistan were
considered for inclusion into the study. Ninety seven patients more DISCUSSION
than twelve years of age, with varied socioeconomic background,
presenting to the OPD with dyspeptic symptoms suggestive of Prevalence
gastroduodenal disease of more than two weeks duration were
included in the study. Symptoms included pain, burning in
epigastrium and retrosternal area, vomiting, bloating, water brash Overall H. pylori prevalence was 87.03% (47/54) in
and anorexia. chronic gastritis, 66.66% (12/18) in gastric ulcer, 60.0%
Those patients with less than 6 weeks history of intake of (6/10) in duodenal ulcer and 100% (1/1) in
NSAIDs, steroids, alcohol, antibiotic and antisecretory drugs, active adenocarcinoma respectively as shown in Table 2. The
bleeding, hypertensive, diabetic patients and with chronic liver local H. pylori prevalence rate was higher than some
disease and chronic renal failure were excluded from the study. All
overseas prevalence studies. Low H. pylori prevalence in
the patients were subjected to oesophagogastroduodenoscopy.
Biopsies were taken from abnormal sites. Specimens were some geographical regions had been described
examined for histopathology, culture of H. pylori and rapid urease (Schubert et al., 1999). Apart from genetic and socio-
test. Diagnosis of H. pylori was confirmed by microscopic economic factors, several other possibilities may account
Asif et al. 3825

35

30

25 Male

Female
20

15

10

0
Ch. gastritis

G. ulcer

D. ulcer

Combined

Carcinoma

No Pathology
Graph 1. Distribution of patients with gastroduodenal diseases

Table 2. Prevalence of H. pylori in gastroenterological disorders.

Disease Total patient H. pylori positive Prevalence (%)


Chronic gastritis 54 47 87.03
Gastric ulcer 18 12 66.66
Duodenal ulcer 10 06 60.0
Combined GU and DU 07 05 71.42
Adenocarcinoma 01 01 100
No pathology 07 02 28.57
Total 97 73 75.25

for the variations in prevalence in different studies (Xia et none of our patients was critically ill or from intensive
al., 1999). Our study demonstrated that gender had an care units. This can be explained by H pylori, host and
influence on H. pylori infection rate in gastroenterological environmental factors all having a role in
disorders and it appeared that females were less likely to gastroenterological diseases especially peptic ulcer
be infected with H. pylori than males. The discrepancy of disease. Prevalence of lymphoma, gastric carcinoma and
male dominance and younger age was probably because ulcer was low as compared to gastritis and duodenal
of society being male dominant with social norms giving ulcer as most of our patients were young with duration of
less chance to the females to be investigated by symptoms not long enough to develop these
specialists. Results of our study are comparable to some complications. Age-related increase in H. pylori
local studies (Kazi et al., 1990) but no much difference in prevalence is due to the fact that infection is usually
prevalence has been recorded. Also, some cases of H. acquired in childhood and carried for life, rather than a
pylori infection might have been missed on both rapid higher risk of H. pylori associated with peptic ulcer
urease test and histopathology. It is also known that in disease in the older generation.
some of the critically ill patients with co-morbid We did not find any association between risk factors
conditions, stress related ulcers may occur. However, such as smoking and alcohol intake with peptic ulcer
3826 J. Med. Plant. Res.

disease in any group. Abdominal pain and retrograde Howden CW (1996). Clinical expressions of Helicobacter pylori
infection. Am. J. Med., 100: S27-34.
burning sensation were frequent in all groups. In early
Kazi JI, Jafarey NA, Alam SM, Zuberi SJ, Kazi AM, Qureshi H, Ahmed
diagnosed cases, H. pylori can be eradicated and may W (1990). Association of Helicobacter pylori with acid peptic disease
lead to decrease mortality, morbidity of peptic ulcer in Karachi. J. Pak. Med. Assoc., 40: 240-241.
disease and gastric carcinoma. Some studies suggest Malaty HM (2007). "Epidemiology of Helicobacter pylori infection". Best
that triple therapy (2 antibiotic agents and at least 1 Pract. Res. Clin. Gastroenterol., 21(2): 205-214.
Marshall BJ, Warren JR (1984). Unidentified curved bacilli in the
adjunctive agent for 14 days) or quadruple therapies (2 stomach of patients with gastritis and peptic ulceration. Lancet, 1:
antibiotics, 2 adjunctive agents for 07 days) are the drug 1311-1315.
of choices in the emerging therapies can significantly Megraud F, Marshall BJ (2000). How to treat Helicobacter pylori. First-
line, second-line, and future therapies. Gastroenterol. Clin. North
reduce ulcer recurrence and its completions especially in
Am., 29: 759-773.
patients present with ulcer complications (Megraud and Qureshi H, Hafiz S, Medhi I (1999). H pylori IgG antibodies in children.
Marshall, 2000). In conclusion, we found H. pylori J. Pak. Med. Assoc., 49: 143-144.
prevalence was 87.03% in chronic gastritis, 66.66% in Schubert M, DeWitt JM, Taylor CA (1999). Prospective evaluation of the
prevalence of Helicobacter pylori in duodenal and gastric ulcer: Is its
gastric ulcer, 60.0% in duodenal ulcer and 100% in
role overstated? Digestive Diseases Week, A244: 1361.
adenocarcinoma, respectively. Xia HHX, Phung N, Kalandar J, Talley NJ (1999). Characteristic of
Helicobacter pylori positive and negative peptic ulcer disease.
Digestive Diseases Week, A245: 1365.
REFERENCES

Ahmed W, Quereshi H, Alam SE, Zuberi SJ (1990). Patterns of


duodenal ulcer in Karachi. J. Pak. Med. Assoc., 40: 212-215.
Baldwin DN, Shepherd B, Kraemer P (2007). "Identification of
Helicobacter pylori genes that contribute to stomach colonization".
Infect. Immun., 75(2): 1005-1016.