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\setlength{\parindent}{0pt}\raggedright \textcolor{GJMediumGrey}{\rule{\textwidth}{2pt}} \vskip16pt \textcolor{GJBlue}{\large\bfseries\abstractname\space} }{% \vskip8pt \textcolor{GJMediumGrey}{\rule{\textwidth}{2pt}} \vskip16pt } \usepackage[absolute,overlay]{textpos} \makeatother \usepackage{lineno} \linenumbers \begin{document} \author[1]{Eussera El-Magbri} \author[2]{Eussera El-Magbri} \affil[1]{ PINE} \renewcommand\Authands{ and } \date{\small \em Received: 15 December 2015 Accepted: 3 January 2016 Published: 15 January 2016} \maketitle \begin{abstract} UCHG) with upper gastrointestinal symptoms. The age range is 21-90 years with a median age of 52 years, 62% females, and 24% diabetics. They were divided into 3 groups 18-30 years, 31-60 years, and 61-90 years. The prevalence of H. pylori among the different spectrum of age is calculated using different methods of diagnosing H. pylori.Reliabilities of the diagnostic tests: The sensitivity, specificity, positive and negative predictive values for (i) Rapid urease test (RUT), (ii) ELISA, (iii) Histology and (iv) Culture. The rapid urease test was found to have a high sensitivity and specificity (89.5% and 96.8%), respectively. Although estimation of serum IgG H. pylori antibody by ELISA is relatively non-invasive procedure, unfortunately, it lacks sufficient sensitivity (63%) to be used as a sole diagnostic test for H. pylori infection. Histology on the other hand is widely available in most hospitals and has a relatively high sensitivity (77.4%) and specificity (75%). \end{abstract} \keywords{helicobacter pylori, sensitivity, specificity, rapid urease test, gastric cancer, ELISA test, IgG to H. pylori.} \begin{textblock*}{18cm}(1cm,1cm) % {block width} (coords) \textcolor{GJBlue}{\LARGE Global Journals \LaTeX\ JournalKaleidoscope\texttrademark} \end{textblock*} \begin{textblock*}{18cm}(1.4cm,1.5cm) % {block width} (coords) \textcolor{GJBlue}{\footnotesize \\ Artificial Intelligence formulated this projection for compatibility purposes from the original article published at Global Journals. However, this technology is currently in beta. \emph{Therefore, kindly ignore odd layouts, missed formulae, text, tables, or figures.}} \end{textblock*} \let\tabcellsep& \par Three hundred and thirty eight patients were included in the study. They presented to the endoscopy suite at University College Hospital Galway, Ireland (UCHG) with upper gastrointestinal symptoms. The age range is 21-90 years with a median age of 52 years, 62\% females, and 24\% diabetics. They were divided into 3 groups 18-30 years, 31-60 years, and 61-90 years. The prevalence of H. pylori among the different spectrum of age is calculated using different methods of diagnosing H. pylori.\par Reliabilities of the diagnostic tests: The sensitivity, specificity, positive and negative predictive values for (i) Rapid urease test (RUT), (ii) ELISA, (iii) Histology and (iv) Culture. The rapid urease test was found to have a high sensitivity and specificity (89.5\% and 96.8\%), respectively. Although estimation of serum IgG H. pylori antibody by ELISA is relatively non-invasive procedure, unfortunately, it lacks sufficient sensitivity (63\%) to be used as a sole diagnostic test for H. pylori infection. Histology on the other hand is widely available in most hospitals and has a relatively high sensitivity (77.4\%) and specificity (75\%). Culture of H. pylori was found to be highly specific (100\%) and sufficiently sensitive (86.2\%). \section[{Prevalence of H. pylori infection:}]{Prevalence of H. pylori infection:}\par The prevalence of H. pylori is assessed in the different age groups. There was a substantial increase in the prevalence of H. pylori infection with increasing age up to the age 61 years. In this study the highest prevalence of infection was found in the age group 31-60 years. The overall prevalence of H. pylori infection in patients with upper gastrointestinal symptoms as assessed by histology (73\%), culture (53\%), serum IgG ELISA (56\%), and rapid urease test (65\%). \section[{Conclusion:}]{Conclusion:}\par The prevalent of Helicobacter pylori infection are worldwide and the infection rate is intimately related to age, ethnicity, and socio-economic factors. The sensitivity and specificity of the different methods used to detect H. pylori infection vary considerably and depends on the inherent characteristics of the test used. A test with high sensitivity and specificity is needed to capture the majority of patients with infection so they can be treated early and cured of the bacteria this will prevent the development of gastric and duodenal ulcer and the late consequences of gastric malignancy. \section[{I. Introduction}]{I. Introduction}\par tudies from Western Europe, New Zealand, Australia, and United States have shown that the prevalence of H. pylori infection in symptomatic patients undergoing endoscopy is very high. The rate of H. pylori infection in patients with upper gastro-intestinal symptoms ranges from 40-60\%. In benign gastric ulcer the organism is found in about 70\% \hyperref[b0]{(1)}. No the other hand, the rate of infection in duodenal ulcer patients is 85-95\% \hyperref[b1]{(2,}\hyperref[b2]{3)}. The rate of infection of H. pylori related to several factors, for example the rate of infection increases with age \hyperref[b0]{(1,}\hyperref[b3]{(4)}\hyperref[b4]{(5)}\hyperref[b5]{(6)}\hyperref[b6]{(7)}\hyperref[b7]{(8)}. The prevalence in children was found to range between 20-68\% \hyperref[b8]{(9)}\hyperref[b9]{(10)}\hyperref[b10]{(11)}\hyperref[b11]{(12)}\hyperref[b12]{(13)}\hyperref[b13]{(14)}\hyperref[b14]{(15)}. The rate of infection also correlate to underlying disease process; in duodenal ulcer and duodenitis the rate of H. pylori infection may be as high as 95\%, and in gastritis the rate of infection ranged from 62-97\% \hyperref[b15]{(16)}\hyperref[b16]{(17)}\hyperref[b17]{(18)}\hyperref[b18]{(19)}\hyperref[b19]{(20)}\hyperref[b20]{(21)}\hyperref[b21]{(22)}\hyperref[b22]{(23)}\hyperref[b23]{(24)}\hyperref[b24]{(25)}\hyperref[b25]{(26)}\hyperref[b26]{(27)}\hyperref[b27]{(28)}\hyperref[b28]{(29)}\hyperref[b29]{(30)}. The sensitivity and specificity of the various tests used to diagnose H. pylori infection have wide variation ranging from (63\% to 89.5\% for sensitivity) and (41.7\% to 100\% for specificity). The prevalence of H. pylori infection in different age groups was carried out in this study and was found to be highly variable in different age groups. The highest prevalence was found in the age group of 31-60 years. \section[{II. Subjects and Methods}]{II. Subjects and Methods}\par Three hundred and thirty eight patients were included in the study. They presented to the endoscopy suite at University College Hospital Galway, Ireland (UCHG) with upper gastrointestinal symptoms. The age range is 21-90 years with a median age of 52 years, 62\% females, and 24\% diabetics. They were divided into 3 groups 18-30 years, 31-60 years, and 61-90 years. The prevalence of H. pylori among the different spectrum of age is calculated using different methods of diagnosing H. pylori, table 3.2.\par Formal written consent was obtained and the procedure was explained to each patient included in the study.\par Blood was collected in a plain tube before endoscopy for estimation of serum IgG antibodies to H. pylori using ELISA test (Biometra, Germany). Specimens were taken from antrum and duodenum from each patient enrolled in the study, for histological examination and culture. They were forwarded to the bacteriology laboratory in a separate containers containing a transport medium (Nutrient Broth Code: CMI oxide) for direct smear and culture on Colombia blood agar base (code: CM331) containing cefoperazone selective supplement (code: SR125) mixed together into sterile Petri dishes prepared according to the specifications of the supplier (Oxide, Ireland).\par The specimens for the histological examination were labeled with reference numbers, and were formalin fixed and prepared according to the standard methods. Sections 5 µm thin and stained with haematoxylin and eosin (H\&E) or modified Giemsa stain and read by an experienced pathologist (RS) without previous knowledge of clinical or microbiological information.\par A biopsy specimen was examined by commercially available rapid urease test kindly provided by (Jatrox HP-Test, Rohm Pharma Waterston, Germany).\par The performance of the different tests used to diagnose H. pylori was outlined in table 3.1. \section[{III. Results}]{III. Results}\par Reliabilities of the diagnostic tests: The sensitivity, specificity, positive and negative predictive values for (i) Rapid urease test, (ii) ELISA, (iii) Histology and (iv) Culture are shown in table 3.1.\par The rapid urease test (RUT) was found to have a high sensitivity and specificity (89.5\% and 96.8\%) respectively. However, it needs an endoscopic procedure to obtain an antral biopsy for the assay which is not available in all hospitals. Endoscopy is an invasive and expensive procedure.\par Although estimation of serum IgG H. pylori antibody by ELISA is relatively non-invasive procedure, unfortunately, it lacks sufficient sensitivity (63\%) to be used as a sole diagnostic test for H. pylori infection, table -3.1.\par Histology on the other hand is widely available in most hospitals and has a relatively high sensitivity (77.4\%) and specificity (75\%), table 3.1. It is relatively quick, cheap and easy to perform but is requires endoscopic examination which is an invasive technique and needs a well trained histological expertise and therefore, it cannot be utilized as a screening test for H. pylori diagnosis.\par Culture of H. pylori was found to be highly specific (100\%) and sufficiently sensitive (86.2\%), table -3.1. However, it takes a few days for the results to come through and it cannot be used for quick diagnosis of H. pylori infection. Culture of H. pylori is, however, needed to determine the sensitivity of the bacterium to the antimicrobial agents, especially to metronidazole. Obtaining the biopsy for culture is an invasive procedure.\par Prevalence of H. pylori infection: The prevalence of H. pylori is assessed in the different age groups, table -3.2. There was a substantial increase in the prevalence of H. pylori infection with increasing age up to the age 61 years. This result agrees with the results of previous workers. However, in the age group 18-30 years the prevalence of H. pylori infection in patients with dyspepsia ranges from 45-53\% depending on the mode used for diagnosis.\par In this study the highest prevalence of infection was found in the age group 31-60 years, table-3.2. Usually the colonization of the bacteria is most prevalent in the elderly. The reason for this finding is not entirely clear. However, the frequent use of drugs like NSAIDS, and corticosteroids could contribute to the relatively low prevalence in this age group.\par The overall prevalence of H. pylori infection in patients with upper gastrointestinal symptoms as assessed by histology (73\%), culture (53\%), serum IgG ELISA (56\%), and rapid urease test (65\%) table-3.2 agree with the previous studies from the developed countries \hyperref[b30]{(31)}\hyperref[b31]{(32)}\hyperref[b32]{(33)}. \section[{IV. Discussion}]{IV. Discussion}\par Infection with H. pylori is rampant and worldwide. The rate of infection is influenced by age, race, geographical and socio-economic factors, as well as dietary practices \hyperref[b33]{(34)}\hyperref[b34]{(35)}\hyperref[b35]{(36)}\hyperref[b36]{(37)}\hyperref[b37]{(38)}\hyperref[b38]{(39)}\hyperref[b39]{(40)}\hyperref[b40]{(41)}\hyperref[b41]{(42)}\hyperref[b42]{(43)} {\ref (44)}. The rate of infection is found to be higher in China and India than in North America. On the other hand, the infection rate is similar in Mexico and the United States \hyperref[b36]{(37,} {\ref 45)}. It has been revealed that the rate of infection of H. pylori in the United States is influenced by many factors like socialeconomic, ethnicity, age, and gender. These findings suggest that the rate of H. pylori infection is modified by geographical and host factors. The type and severity of gastritis associated with H. pylori colonization are also influenced the rate of infection.\par The epidemiology of H. pylori infection has been extensively studied and was found to be closely correlated with superficial type-B gastritis. Infection with H. pylori is associated with active and chronic inflammation of gastric mucosa \hyperref[b31]{(32,} {\ref 46)}. The density of the bacteria in the tissue is also correlated to the severity of inflammation and the local and systemic immune response mounted against the bacteria \hyperref[b31]{(32,} {\ref (46)} {\ref (47)} {\ref (48)}.\par H. pylori infection can be detected with various methods e. g histological examination and culture of the gastric biopsy specimens which takes several days, serology, rapid urease test etc. Serum IgG/IgA ELISA and Rapid Urease test were compared to the gold standard tests (histology and culture) and evaluated in this study. The organism was detected in 76 of 107 dyspeptic patients attending GI unit at UCHG. We found a relatively good correlation between serology and histological findings in the antral biopsies despite the \hyperref[b14]{(15,} {\ref (49)} {\ref (50)} {\ref (51)} {\ref (52)} {\ref (53)} {\ref (54)} {\ref (55)} {\ref (56)}), but disagreed with the results of Nichols and others \hyperref[b22]{(23,} {\ref 57)}. The advantages of quick test e.g. RUT is that treatment can be given to the patients within one hour of their endoscopic procedures. In the Amsterdam study \hyperref[b14]{(15)} the results of culture and histology were analogous to ours.\par We found that, histological examination, culture, ELISA and RUT revealed an increased prevalence of H. pylori infection and the rate of infection are rising with increasing age up to the age of 61 years. This is in parallel with the findings that the prevalence of infection is related to the prevalence of gastritis \hyperref[b5]{(6,}\hyperref[b30]{(31)}\hyperref[b31]{(32)}\hyperref[b32]{(33)}. However, the prevalence of H. pylori in the elderly age group is lower than the reported prevalence from Western countries, table-3.2. We noted that the prevalence of H. pylori infection in the age group 61-90 years was below that of 30-60 years. This agreed with the findings of Newell et al (57).\par Previously, it has been suggested that the age discrepancy is due to progressive atrophic gastritis with hypochlorhydria in the body and fundus of the stomach of the elderly patients. This environment is hostile to the existence of the organism. Another possible explanation to the low infection rate in the elderly could be related to the increased use of the antibiotics in this age group which may clear the organism. The histological sections from the mucosa of the 25 patients from the group 61-90 years old were reviews, none were taken NSAIDs concurrently. We found 14(56\%) of these patients had either normal or mild inflammation and of them 6(43\%) were H. pylori positive. Moderate inflammation was present in 9(36\%) all were H. pylori positive. Only 2(8\%) had severe inflammation and both were H. pylori positive. Atrophy of specialized cells in the fundus and body of the stomach cannot be inferred from examination of antral biopsies. Thus in this study we have no evidence to support the notion that atrophic gastritis is associated with a decreased prevalence of H. pylori in the elderly. We concluded that the majority if the elderly (>61 years) had a prevalence of H. pylori ranging from (45-64\%), table-3.2, depending on the mode used for detection of H. pylori infection. More than 50\% of them had only mild inflammation; in these group H. pylori was isolated in 43\%. However, moderate to severe degree of inflammation was present in 44\% of them and H. pylori were always associated with gastritis. \section[{V. Conclusion}]{V. Conclusion}\par The prevalent of Helicobacter pylori infection are worldwide and the infection rate is intimately related to age, ethnicity, and socio-economic factors. The sensitivity and specificity of the different methods used to detect H. pylori infection vary considerably and depends on the inherent characteristics of the test used. A test with high sensitivity and specificity is needed to capture the majority of patients with infection so they can be treated early and cured of the bacteria this will prevent the development of gastric and duodenal ulcer and the late consequences of gastric malignancy. \section[{Volume XVI Issue}]{Volume XVI Issue}\begin{figure}[htbp] \noindent\textbf{}\includegraphics[]{image-2.png} \caption{\label{fig_0}}\end{figure} \begin{figure}[htbp] \noindent\textbf{} \par \begin{longtable}{P{0.85\textwidth}} low sensitivity (\\ Year 2016\\ D D D D ) F\\ (\end{longtable} \par \caption{\label{tab_0}}\end{figure} \begin{figure}[htbp] \noindent\textbf{} \par \begin{longtable}{P{0.020992544268406337\textwidth}P{0.5735321528424977\textwidth}P{0.011090400745573159\textwidth}P{0.20715284249767008\textwidth}P{0.013863000931966447\textwidth}P{0.014259086672879775\textwidth}P{0.009109972041006524\textwidth}} \tabcellsep \multicolumn{2}{l}{44. The Gastrointestinal Physiology Working Group.}\tabcellsep \multicolumn{3}{l}{51. Ching CK, Buxton C, Holgate C, et al. Cytological}\\ \tabcellsep \multicolumn{2}{l}{Helicobacter pylori and Gastritis in Peruvian}\tabcellsep \multicolumn{3}{l}{brushing urea broth test: a highly sensitive and}\\ \tabcellsep \multicolumn{2}{l}{Patients: Relationship to Socioeconomic Level, Age,}\tabcellsep \multicolumn{3}{l}{specific test for Helicobacter pylori infection.}\\ \tabcellsep \multicolumn{2}{l}{and Sex. The Am J Gastroenterol. 1990; 85(7):}\tabcellsep \multicolumn{3}{l}{Gastrointestinal Endoscopy. 1991: 550-551}\\ \tabcellsep 819-23\tabcellsep \tabcellsep \multicolumn{3}{l}{52. McNulty CAM, Dent JC, Uff JS, et al. Detection of}\\ \tabcellsep \multicolumn{2}{l}{45. Bertram TA, Murray PD, Morgan DR, et al. Gastritis}\tabcellsep \multicolumn{3}{l}{Camploybacter pylori by the biopsy urease test: an}\\ \tabcellsep \multicolumn{2}{l}{associated with infection by Helicobacter pylori in}\tabcellsep \multicolumn{3}{l}{assessment in 1445 patients. Gut. 1989; 30: 1058-}\\ \tabcellsep \multicolumn{2}{l}{humans: Geographical differences. Scand J.}\tabcellsep 1062\tabcellsep \\ \tabcellsep \multicolumn{2}{l}{Gastroenterol. 1991; 26 (suppl. 181): 1-8}\tabcellsep \multicolumn{3}{l}{53. Thillainayagam AV, Arvind AS, Cook RS, et al.}\\ \tabcellsep \multicolumn{2}{l}{46. Karttunen T, Niemela S, Lehtola J. Helicobacter}\tabcellsep \multicolumn{3}{l}{Diagnostic efficiency of an ultrarapid endoscopy}\\ \tabcellsep \multicolumn{2}{l}{pylori in dyspeptic patients: quantitative association}\tabcellsep \multicolumn{3}{l}{room test for Helicobacter pylori. Gut. 1991; 32:}\\ \tabcellsep \multicolumn{2}{l}{with severity of gastritis, intragastric pH, and serum}\tabcellsep \multicolumn{2}{l}{467-69}\\ Volume XVI Issue IV Version I Year 2016 ( D D D D ) F\tabcellsep \multicolumn{3}{l}{gastrin concentrations. Scand J Gastroenterol. 1991; (suppl. 186): 124-34 47. Mollenkopf C, Steinger H, Weineck G, Meyer M. Gastritis: Immunohistochemical detection of specific and nonspecific immune response to Helicobacter pylori. Zeitschrift Fur Gastroenterol. 1990; 28 (7): 327-34 48. Crabtree JE, Shallcross TM, Wyatt JI, et al. Mucosal humoral immune response to Helicobacter pylori in patients with Duodenitis. Dig Dis Scien. 1991; 36 (9): 1266-73 49. Carvalho AS, Queiroz DM, Mendes EN, et al. Diagnosis and distribution of Helicobacter pylori in the gastric mucosa of symptomatic children. Brazilian J Med \& Biolog Resea. 1991; 24(2): 163-66 50. Borromeo M, Lambert JR, Pinkard KJ. Technical Methods; Evaluation of "CLO-test" to detect Campylobacter pyloridis in gastric mucosa. J. Clin. Pathology. 1987; 40: 462-468 54. Test Sensitivity Specificity}\tabcellsep PP value\tabcellsep NP value\tabcellsep Year 2016 ( D D D D ) F\\ \tabcellsep Histology\tabcellsep 77.4\%\tabcellsep 75\%\tabcellsep 83.7\%\tabcellsep 66.7\%\\ \tabcellsep Culture\tabcellsep 86.2\%\tabcellsep 100\%\tabcellsep 100\%\tabcellsep 76.5\%\\ \tabcellsep Serum IgG\tabcellsep 63\%\tabcellsep 97\%\tabcellsep 98\%\tabcellsep 51\%\\ \tabcellsep Local IgA\tabcellsep 79.2\%\tabcellsep 41.7\%\tabcellsep 57.6\%\tabcellsep 66.7\%\\ \tabcellsep Urease test\tabcellsep 89.5\%\tabcellsep 96.8\%\tabcellsep 98.6\%\tabcellsep 78.9\%\end{longtable} \par \caption{\label{tab_1}}\end{figure} \begin{figure}[htbp] \noindent\textbf{3} \par \begin{longtable}{P{0.19112426035502958\textwidth}P{0.18106508875739644\textwidth}P{0.1760355029585799\textwidth}P{0.1559171597633136\textwidth}P{0.14585798816568046\textwidth}} \tabcellsep 18-30 years\tabcellsep 31-60 years\tabcellsep 61-90 years\tabcellsep Overall\\ Histology\tabcellsep 52.9\%\tabcellsep 85.3\%\tabcellsep 56\%\tabcellsep 72.8\%\\ Culture\tabcellsep 47.1\%\tabcellsep 57.4\%\tabcellsep 45.5\%\tabcellsep 53\%\\ ELISA\tabcellsep 45.8\%\tabcellsep 61.2\%\tabcellsep 52.6\%\tabcellsep 55.8\%\\ Rapid Urease test\tabcellsep 47.06\%\tabcellsep 69.8\%\tabcellsep 64\%\tabcellsep 64.8\%\end{longtable} \par \caption{\label{tab_2}Table 3 .}\end{figure} \footnote{© 2016 Global Journals Inc. (US)} \footnote{Prevalence of Helicobacter Pylori Infection among the Whole Spectrum of Age and the Performance of the Different Diagnostic Tests} \backmatter \begin{bibitemlist}{1} \bibitem[Kosunen et al. ()]{b39}\label{b39} ‘Agedependent increase of Campylobacter pylori antibodies in blood donors’. T U Kosunen , J Hook , H I Rautelin . \textit{Scad J Gastroenterol} 1989. 24 p. . \bibitem[Drumm et al. ()]{b8}\label{b8} ‘Association of Campylobacter pylori on the Gastric Mucosa with Antral Gastritis in Children’. B Drumm , P Sherman , E Cutz . \textit{N Eng J Med} 1987. 316 p. . \bibitem[Hill et al. ()]{b11}\label{b11} ‘Campylobacter pylori and gastritis in children’. R Hill , J Pearman , P Worthy . \textit{Lancet} 1986. i p. 387. \bibitem[Price et al. ()]{b25}\label{b25} ‘Campylobacter pylori in peptic ulcer disease: microbiology, pathology, and scanning electron microscopy’. A B Price , J Levi , J M Dolby . \textit{Gut} 1985. 26 p. . \bibitem[Wyatt et al. ()]{b29}\label{b29} ‘Campylobacter pyloridis and acid induced gastric metaplasia in the pathogenesis of duodenitis’. J I Wyatt , B J Rahthbone , M F Dixon , R V Heatley . \textit{J Clin Pathol} 1987. 40 p. . \bibitem[Cadranel et al. ()]{b12}\label{b12} ‘Campylobacter pyloridis in children’. S Cadranel , H Goossens , M Boek De . \textit{Lancet} 1986. p. . \bibitem[Eastham and Elliott ()]{b13}\label{b13} ‘Campylobacter pyloridis in children’. E J Eastham , Tsm Elliott . \textit{Arch Dis Child} 1987. 62 p. 652. \bibitem[Rauws et al. ()]{b26}\label{b26} ‘Campylobacter pyloridis-associated chronic active antral gastritis’. Eaj Rauws , W Langenberg , H J Houthoff . \textit{Gastroenterology} 1988. 94 p. . \bibitem[Burnett et al. ()]{b16}\label{b16} ‘Campylobacter-like organisms in the stomach of patients and healthy individuals’. R A Burnett , Jah Forrest , Rwa Girdwood . \textit{Lancet} 1984. p. 1349. \bibitem[Langenberg et al. ()]{b21}\label{b21} ‘Campylobacter-like organisms in the stomach of patients and healthy individuals’. M L Langenberg , Gnj Tytgat , Mei Schipper . \textit{Lancet} 1984. p. . \bibitem[Jones et al. ()]{b20}\label{b20} ‘Campylobacterlike organisms on the gastric mucosa: culture, histological, and serological studies’. D M Jones , A M Lessells , J Eldridge . \textit{J Clin Pathol} 1984. 37 p. . \bibitem[Mendall et al. ()]{b41}\label{b41} ‘Childhood living conditions and Helicobacter pylori seropositivity in adult life’. M A Mendall , P M Goggin , N Molineaux . \textit{Lancet} 1992. (8798) p. 339. \bibitem[Siurala et al. ()]{b5}\label{b5} ‘Chronic gastritis: dynamic and clinical aspects’. M Siurala , P Sipponen , M Kekki . \textit{Scand J Gastroenterol} 1985. 20 (109) p. . (suppl) \bibitem[Booth et al. ()]{b15}\label{b15} ‘Clinical importance of Campylobacter pyloridis and associated serum IgG and IgA antibody responses in patients undergoing upper gastrointestinal endoscopy’. L Booth , G Holdstock , Macbride . \textit{J Clin Pathol} 1986. 39 p. . \bibitem[Wulffen et al. ()]{b28}\label{b28} ‘Detection of Campylobacter pylori in patients with antrum gastritis and peptic ulcer by culture, complement fixation test, and immunoblot’. Von Wulffen , H Heesemann , J Butzow , GH . \textit{J Clin Microbiol} 1986. 24 p. . \bibitem[Graham et al. ()]{b35}\label{b35} ‘Effect of Age on the Frequency of Active Campylobacter pylori Infection Diagnosed by the (C13) Urea Breath Test in Normal Subjects and Patients with Peptic Ulcer Disease’. D Y Graham , P D Klein , A R Opekun . \textit{J Infect Disease} 1988. 157 p. . \bibitem[O'connor et al. ()]{b17}\label{b17} ‘Effect of duodenal ulcer surgery and enterogastric reflux on Campylobacter pyloridis’. H J O'connor , M F Dixon , J I Wyatt . \textit{Lancet} 1986. ii p. . \bibitem[Kang et al. ()]{b38}\label{b38} ‘Helicobacter pylori and gastritis in patients with peptic ulcer and nonulcer dyspepsia: ethnic differences in Singapore’. J Y Kang , A Wee , M V Math . \textit{Gut} 1990. 31 p. . \bibitem[Dixon ()]{b1}\label{b1} ‘Helicobacter pylori and peptic ulceration: histopathological aspects’. M F Dixon . \textit{J Gastroenterol Hepatol} 1991. 6 p. . \bibitem[Malaty et al. ()]{b40}\label{b40} ‘Helicobacter pylori in Hispanics: Comparison with blacks and whites of similar age and socioeconomic class’. H M Malaty , D G Evans , D J Evans . \textit{Gastroenterology} 1992. 103 p. . \bibitem[Heatley ()]{b2}\label{b2} ‘Helicobacter pylori Infection and Inflammation’. R V Heatley . \textit{Scand J Gastroenterol} 1991. 26 p. . (suppl. 187) \bibitem[Parsonnet et al. ()]{b14}\label{b14} ‘Helicobacter pylori infection and the risk of gastric carcinoma’. J Parsonnet , G D Friedman , D P Vandersteen . \textit{N Eng J Med} 1991. 325 p. . \bibitem[Haruma et al. ()]{b19}\label{b19} ‘Helicobacter pylori infection causes low antral somatostatin content: pathogenesis of inappropriate hypergastrinemia’. K Haruma , K Sumii , S Okamoto . \textit{Gastroenterology} 1992. 102 (2) p. A80. \bibitem[Prieto et al. ()]{b31}\label{b31} ‘Helicobacter pylori infection in children: clinical, endoscopic, and histological correlations’. G Prieto , I Polanco , J Larrauri . \textit{J Ped Gastroenterol \& Nutrit} 1992. 14 (4) p. . \bibitem[Tytgat et al. ()]{b42}\label{b42} ‘Helicobacter pylori: Causal agent in peptic ulcer disease?’. G N Tytgat , Atr Axon , M F Dixon . \textit{Working Party Reports} 1990. p. . \bibitem[Fiocca et al. ()]{b18}\label{b18} ‘High incidence of Campylobacter-like organisms in endoscopic biopsies from patients with gastritis, with or without peptic ulcer’. R Fiocca , L Villani , F Turpini . \textit{Digestion} 1987. 38 p. . \bibitem[Craanen et al. ()]{b33}\label{b33} ‘Intestinal metaplasia and Helicobacter pylori: an endoscopic bioptic study of the gastric antrum’. M E Craanen , W Dekker , P Blok . \textit{Gut} 1992. 33 p. . \bibitem[Ihamki et al. ()]{b30}\label{b30} ‘Longterm observation of subjects with normal mucosa and with superficial gastritis. Results of 23-27 years follow up examination’. T Ihamki , M Saukkonen , M Siurala . \textit{Scand J Gastroenterology} 1979. 13 p. . \bibitem[Siurala et al. ()]{b6}\label{b6} ‘New aspects on epidemiology, genetics, and dynamics of chronic gastritis’. M Siurala , K Varis , M Kekki . \textit{Front Gastrointest Res} 1980. 6 p. . \bibitem[Oderda et al. ()]{b10}\label{b10} ‘Non-specific abdominal pain in childhood: Can serology detect those with Campylobacter associated gastritis?’. G Oderda , D Vaira , J Holton . 29: A 1475. \textit{Gut} 1988. \bibitem[Dooley et al. ()]{b34}\label{b34} ‘Prevalence of H pylori infection and histological gastritis in asymptomatic persons’. C P Dooley , H Cohen , P L Fitzgibbons . \textit{N Eng J Med} 1989. 321 (23) p. . \bibitem[Marshall et al. ()]{b23}\label{b23} ‘Pyloric Campylobacter infection and gastrodudodenal disease’. B J Marshall , D B Mcgechie , P A Rogers . \textit{Med J Austr} 1985. 142 p. . \bibitem[Czinn and Carr ()]{b9}\label{b9} ‘Rapid diagnosis of Campylobacter pylori associated gastritis’. S J Czinn , H Carr . \textit{J Ped} 1987. 110 p. . \bibitem[Sipponen and Hyvarinen ()]{b7}\label{b7} ‘role of Helicobacter pylori in the pathogenesis of gastritis, peptic ulcer, and gastric cancer’. P Sipponen , H Hyvarinen . \textit{Scand J Gastroenterol} 1993. 28 p. . (suppl) \bibitem[Graham et al. ()]{b36}\label{b36} ‘Seroepidemiology of Helicobacter pylori infection in India. Comparison of developing and developed countries’. D Y Graham , E Adam , G T Reddy . \textit{Dig Dis Scien} 1991. 36 (8) p. . \bibitem[Hopkins et al. ()]{b37}\label{b37} ‘Seroprevalence of Helicobacter pylori in Seventh-Day Adventists and Other Groups in Maryland’. R J Hopkins , R G Russell , J M O'donnoghue . \textit{Arch Int Med} 1990. 150 p. . \bibitem[Perez-Perez et al. ()]{b3}\label{b3} ‘Seroprevalence of Helicobacter pylori infection in Thailand’. G I Perez-Perez , D N Taylor , L Bodhidatta . \textit{J Infect Dise} 1990. 161 p. . \bibitem[Siurala et al. ()]{b32}\label{b32} M Siurala , K Varis , Gastritis . \textit{Scientific foundations of gastroenterology}, W Sircus, A N Smith (ed.) 1980. p. . \bibitem[Mcnulty and Watson ()]{b24}\label{b24} ‘Spiral bacteria of gastric antrum’. Cam Mcnulty , D M Watson . \textit{Lancet} 1984. p. . \bibitem[Rathbone et al. ()]{b27}\label{b27} ‘Systemic and local antibody responses to gastric Campylobacter pylori in non-ulcer dyspepsia’. B J Rathbone , J I Wyatt , B W Worseley . \textit{Gut} 1986. 27 p. . \bibitem[Dwyer et al. ()]{b0}\label{b0} ‘The prevalence of Campylobacter pylori in human populations’. B Dwyer , J Kaldor , W Tee . \textit{Blackwell Science Publ} Rathbone BJ \& Heatley RV (ed.) 1989. p. . (Campylobacter pylori and Gastroduodenal Disease) \bibitem[Przyklend et al. ()]{b4}\label{b4} ‘The role of Campylobacter (Helicobacter) pylori in disorders of the gastrointestinal tract’. B Przyklend , A Bauernfeind , W Bornschein . \textit{Infection} 1990. 18 (1) p. . \bibitem[Bj and Warren ()]{b22}\label{b22} ‘Unidentified curved bacillus in the stomach of patients with gastritis and peptic ulcerations’. Marshall Bj , J R Warren . \textit{Lancet} 1984. p. . \end{bibitemlist} \end{document}