Correlation of Cag-A serological status with histological parameters of chronic gastritis among dyspeptic patients in south western Nigeria

Öz

Background: The aim of this study was to determine the sero-prevalence of Cag-A strains of Helicobacter pylori in both dyspeptic and non-dyspeptic individuals and also correlate the serological status of Cag-A strain of H. pylori with the various graded histological variables of chronic gastritis in the dyspeptic patients.

Methods: Using helicobacter p120 Cag-A enzyme linked immunosorbent assay, Cag-A serology test was carried out on 65 dyspeptic patients and 65 age and sex matched non-dyspeptic controls. The gastric biopsies of the patients were also histologically examined to ascertain the presence, nature and degree of the following histological variables of gastritis: colonisation by H. pylori; inflammation, intestinal metaplasia and mucosal atrophy. The CagA serological status was then correlated with the graded variables.

Results: A prevalence of 46.2% and 58.8% seropositivity for Cag-A strain of H. pylori was found among dyspeptic patients and control individuals respectively. Cag-A seropositive patients accounted for nine(81.8%) of the 11 cases with moderate to severe activity and 75% of both cases with mucosal atrophy and cases with intestinal metaplasia.

Conclusion: Infection with Cag-A positive Helicobacter pylori was equally prevalent among both dyspeptic patients and control subjects studied. CagA seropositivity, however, appeared to be associated with higher inflammatory activity in the mucosa of patients with chronic gastritis and may be associated with intestinal metaplasia and mucosal atrophy in H. pylori-induced chronic gastritis.

Keywords: CagA status H. pylori chronic gastritis Nigeria

Abstrait
Contexte: Le but de cette étude était de déterminer la séroprévalence des souches du Cag-A s de l’Helicobacter pylori tant chez les individus dyspeptiques que chez des non-dyspeptiques et aussi en corrélation avec le statut sérologique de Cag-A, une souche de H. pylori avec diverses variables histologiques graduées de la gastrite chronique chez les patients dyspeptiques.

Méthodes: L’utilisation d’Helicobacter p120 Cag-A, un dosage immunoenzymatique, le Cag-A, un test de sérologie sur 65 patients dyspeptiques âgés de 65 ans et sur les contrôles de sexe non-dyspeptiques correspondant a été fait. Les biopsies gastriques des patients ont également été histologiquement examinés pour déterminer la présence, la nature et le degré de suivantes variables histologiques de gastrite: la colonisation par H. pylori, l’inflammation, la métaplasie intestinale et l’atrophie de la muqueuse. Le statut sérologique du Cag-A a ensuite été corrélé avec les variables gradués.

Résultats: Une prévalence de 46,2% et 58,8% pour la séropositivité Cag-A, une souche de H. pylori a été retrouvée chez les patients dyspeptiques et contrôle les individus respectivement. CAG-A Les patients séropositifs du CAG-A représentaient neuf (81,8%) des 11 cas avec une activité modérée aux activités dure et 75% des cas avec à la fois de cas d’ atrophie de la muqueuse et des cas de métaplasie intestinale.

Conclusion: L’infection par le Cag-A Helicobacter pylori positif était également répandue à la fois chez les patients dyspeptiques et les sujets cotrolés étudiés. CagA séropositivité, cependant, semblait être associée à l’activité inflammatoire élevée dans la muqueuse des patients souffrant de gastrite chronique et peut être associé à une métaplasie intestinale et à l’atrophie de la muqueuse de H. pyloriinclus à la gastrite chronique.

Correspondence: Dr. A.O. Oluwasola, Department of Pathology, College of Medicine, University of Ibadan, PMB 5116, Ibadan, Nigeria. E-mail: oluwasol@yahoo.com.

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Referanslar

Blaser MJ and Atherton J. Helicobacter pylori persistence: biology and disease. J Clin Invest 2004; 113:321 – 33.

IARC Monographs on the evaluation of carcinogenic risks to humans. Volume 61 Schistosomes, liver flukes and Helicobacter pylori. Lyon, IARC (1994) pg. 220.

Jemilohun AC, Otegbayo JA, Ola SO, Oluwasola AO and Akere A. Prevalence of Helicobacter pylori among Nigerian patients with dyspepsia in Ibadan. Pan African medical Journal, 2010;6(18):

Oluwasola AO, Ola SO, Saliu L and Solanke TF. Helicobacter pylori infection in South Nigerians: a serological study of dyspeptic patients and healthy individuals. West Afr J Med. 2002; 21(2):138-141.

Ndububa DA, Agbakwuru AE, Adebayo RA, et al. Upper gastrointestinal findings and incidence of Helicobacter pylori infection among Nigerian patients with dyspepsia. West Afr J Med. 2001; 20(2):140-145.

Adesanya AA, Oluwatowoju IO, Oyedeji KS, da Rocha-Afodu JT, Coker AO and Afonja OA. Evaluation of a locally-made urease test for detecting Helicobacter pylori infection. Niger Postgrad Med J. 2002; 9(1):43-47.

Mustapha SK, Ajayi NA, Nggada HA, et al. Endoscopic findings and the frequency of Helicobacter pylori among dyspeptic patients in North-Eastern Nigeria. Highland Medical Research Journal. 2007; 5(1):78-81

Torres J, Perez-Perez G, Goodman KJ, et al. A comprehensive review of the natural history of Helicobacter pylori infection in children, Arch. Med. Res. 31 (2000) 431–469.

Atherton J.C. The Pathogenesis of Helicobacter pylori–Induced Gastro-Duodenal Diseases Annu. Rev. Pathol. Mech. Dis. 2006. 1:63–96

Suerbaum S and Michetti P. Helicobacter pylori infection. N Engl J Med 2002; 347:1175–86.

Ching CK, Wong BC, Kwok E, Ong L, Covacci A, and Lam SK. Prevalence of CagA-bearing Helicobacter pylori strains detected by the anti-CagA assay in patients with peptic ulcer disease and in controls. Am. J.Gastroenterol.1996; 91:949–953.

Kuipers EJ, Pérez-Pérez GI, Meuwissen SGM and Blaser MJ. Helicobacter pylori and Atrophic Gastritis: Importance of the CagA Status.J Natl Cancer Inst, 1995 87 (23): 1777-1780.

Amjad N, Osman HA, Razak NA, Kassian J, Din J and Abdullah N. Clinical significance of Helicobacter pylori CagA and iceA genotype status. World J Gastroenterol 2010; 16(35): 4443-4447

Paniagua GL, Monroy E, Rodríguez R, et al. Frequency of vacA, CagA and babA2 virulence markers in Helicobacter pylori strains isolated from Mexican patients with chronic gastritis. Ann Clin Microbiol Antimicrob. 2009;8:14

Erzin Y, Koksal V, Altun S, et al. Prevalence of Helicobacter pylori vacA, CagA, cagE, iceA, babA2 genotypes and correlation with clinical outcome in Turkish patients with dyspepsia. Helicobacter. 2006; 11(6):574-580.

Yakoob J, Jafri W, Abbas Z, Abid S, Khan R, Jafri N and Ahmad Z. Low prevalence of the intact Cag pathogenicity island in clinical isolates of Helicobacter pylori in Karachi, Pakistan. Br J Biomed Sci. 2009; 66(3):137-142.

Rocha AM, Rocha GA, de Magalhaes Queiroz DM, et al. Anti-CagA antibodies in Helicobacter pylori-positive patients and blood donors from Nigeria. Trop Doct. 2001 Jul;31(3):147-149.

Smith SI, Oyedeji KS, Arigbagbu AO, et al. Comparison of three PCR methods for detection of Helicobacter pylori DNA and detection of CagA gene in gastric biopsy specimens. World J Gastroenterol, 2004; 10 (13): 1958-1960.

Smith SI, Kirsch C, Oyedeji KS, et al. Prevalence of Helicobacter pylori vacA, CagA and iceA genotypes in Nigerian patients with duodenal ulcer disease. J. Med. Microbiol, 2002; 51: 851–854.

Huang JQ, Zheng GF, Sumanac K, et al. Meta-analysis of the relationship between CagA seropositivity and gastric cancer. Gastroenterology 2003; 125:1636 – 1644.

Parsonnet J, Friedman GD, Vandersteen D, et al. Helicobacter pylori infection and the risk for gastric carcinoma. N Engl J Med 1991;25: 1127 – 1131.

Cover TL, Y. Glupczynski AP, Lage A, et al. Serologic detection of infection with CagA+ Helicobacter pylori strains. J. Clin. Microbiol. 1995,33:1496-1500.

Sozzi M, Valentini M, Figura N, et al. Atrophic gastritis and intestinalmetaplasia in Helicobacter pylori infection: the role of CagA status. Am J Gastroenterol 1998; 93:375 –379.

Plummer M, van Door L, Franceshi S, et al. Helicobacter pylori cytotoxin associated genotype and gastric precancerous lesions. J Natl Cancer Inst 2007; 99:1328 – 1334.

Glocker E, Lange C, Covacci A, Bereswill S, Kist M and Pahl HL. Proteins Encoded by the cag Pathogenicity Island of Helicobacter pylori Are Required for NF-êB Activation. Infect Immun. 1998 May; 66(5): 2346–2348.

Van Doorn, L. J., C. Figueiredo, R. Sanna, M. J. Blaser, and W. G. Quint. Distinct variants of Helicobacter pylori CagA are associated with vacA subtypes. J. Clin. Microbiol. 1999; 37:2306–2311

Moorchung N, Srivastava AN, Gupta NK, Bandopadhyay S, Achyut BR and Mittal B : The Role of Helicobacter pylori And CagA Antibody Titers In The Pathology Of Chronic Gastritis . The Internet Journal of Tropical Medicine. 2006 Volume 3 Number 1

Rahman SHZ, Rahman MA, Arfin MS, Alam MM, Bhuiyan TM and Ahmed N. Helicobacter pylori Infection and Strain Types in Adult Dyspeptic Patients Undergoing Endoscopy in a Specialized Hospital of Dhaka City. Bangladesh J Med Microbiol 2009; 03 (01): 4-932.

Holcombe C, Kaluba J and Lucas SB. Helicobacter pylori infection and gastritis in healthy Nigerians. Eur J. Epidemiol. 1994 April; 10(2): 223-235.

Otegbayo, J. A., Oluwasola A.O., Yakubu, A., Odaibo G. N. and Olaleye, O. D. Helicobacter pylori serology and evaluation of gastroduodenal disease in Nigerians with dyspepsia. African Journal of Clinical and Experimental Microbiology. 2004; Vol. 5 No 4: 126-133.

Enroth H, Kraaz W, Engstrand L, Nyren O and Rohan T. Helicobacter pylori strain types and risk of gastric cancer: a case control study. Cancer Epidemiol Biomarkers Prev 2000; 9: 981-985.

Dixon MF, Genta RM, Yardley JH, et al. Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994. Am J Surg Pathol 1996; 20:1161–1181.

Gologan A, Graham DY and Sepulveda AR. Molecular markers in Helicobacter pylori -associated gastric carcinogenesis. Clin LabMed 2005; 25: 197 – 222.

Smith MG, Hold GL, Tahara E, et al. Cellular and molecular aspectsof gastric cancer. World J Gastroenterol 2006; 12: 2979 – 2990.

El-Omar EM, Rabkin CS, Gammon MD, et al. Increased risk of noncardia gastric cancer associated with proinûammatory cytokine gene polymorphisms. Gastroenterology 2003; 124: 1193– 1201.

Smith MG, Hold GL, Rabkin CS, et al. The IL-8-251 promoter polymorphism is associated with high IL-8 production, severe inûammation and increased risk of pre-malignant changes in H. pylori positive subjects. Gastroenterology 2004; 124 (Suppl 2):A23.

Huang JQ, Zheng GF, Sumanac K, et al. Meta-analysis of the relationship between CagA seropositivity and gastric cancer. Gastroenterology 2003; 125: 1636 – 1644.

Brenner H, Arndt V, Stegmaier C, et al. Is Helicobacter pylori infection a necessary condition for noncardia gastric cancer? Am J Epidemiol 2004; 159: 252–258.

Peek RM Jr, Miller GG, Tham KT, et al. Heightened inûammatory response and cytokine expression in vivo to CagA_ Helicobacter pylori strains. Lab Invest 1995; 73(6):760-770.

Peek RM Jr, Moss SF, Tham KT, et al. Helicobacter pylori CagA strains and dissociation of gastric epithelial cell proliferation from apoptosis. J Natl Cancer Inst 1997; 89:863–868.

Figura N, Vindigni C, Covacci A, et al. CagA positive and negative Helicobacter pylori strains are simultaneously present in the stomach of most patients with non-ulcer dyspepsia: relevance to histological damage. Gut 1998; 42: 772–778.

Amieva MR and El-Omar EM. Host-bacterial interactions in Helicobacter pylori infection. Gastroenterology. 2008; 134 (1): 306-323

Yamaoka Y, Kita M, Kodama T, Sawai N and Imanishi J. Helicobacter pylori CagA gene and expression of cytokine messenger RNA in gastric mucosa. Gastroenterology. 1996 Jun; 110(6):1744-1752.

Bhat N, Gaensbauer J, Peek RM, Bloch K, et al. Local and Systemic Immune and Inflammatory Responses to Helicobacter pylori Strains. Clinical and Diagnostic Laboratory Immunology, 2005; 12 (12):1393-1400.

Soltermann A, Koetzer S, Eigenmann F and Komminoth P. Correlation of Helicobacter pylori virulence genotypes vacA and CagA with histological parameters of gastritis and patient’s age. Modern Pathology, 2007; 20: 878–883.

Loh JT, Friedman DB, Piazuelo MB et al, Analysis of Helicobacter pylori cagA promoter elements required for salt-induced upregulation of CagA expression. Infect. Immun. 2012; 80(7): doi:10.1128/IAI.00232-002312

Chen VW, Abu-Elyazeed RR, Zavala DE et al,. Risk factors of gastric precancerous lesions in a high-risk Colombian population. II. Nitrate and nitrite. Nutr. Cancer, 1990; 13:67-72.

Howson CP, Hiyama T, Wynder EL. et al. 1986. The decline in gastric cancer: epidemiology, 1986; 582

You WC, Blot WJ and Chang YS, Diet and high risk of stomach cancer in Shandong, 650 China. Cancer Res. 1988; 48:3518-3523.

Olubodun JO, Akingbade OA and Abiola OO. Salt intake and blood pressure in Nigerian hypertensive patients.Int J Cardiol. 1997 Apr 18;59(2):185-188.