* Corresponding Author
Vascular endothelial growth factor (VEGF) serum levelsof patients with Helicobacter pylori gastritis with cytotoxin-associated gene A positive (CagA+)status
https://doi.org/10.19106/JMedSci005104201907 Wira Prihatin Siregar(1*), Gontar Alamsyah Siregar(2), Taufik Sungkar(3)
(1) Gastroentero-hepatology Division of Internal Medicine Department, Medical Faculty of University of Sumatera Utara / Haji Adam Malik General Hospital
(2) Gastroentero-hepatology Division of Internal Medicine Department, Medical Faculty of University of Sumatera Utara / Haji Adam Malik General Hospital
(3) Gastroentero-hepatology Division of Internal Medicine Department, Medical Faculty of University of Sumatera Utara / Haji Adam Malik General Hospital
(*) Corresponding Author
Abstract
Helicobacter pylori (H.pylori) is an agent that causes gastritis and the ulcer of gaster, which are ultimately caused gastric tumors. The prevalence is about 80 % average in developing country and 20-50 % in developed countries. One of the virulence factor iscytotoxin-associated gene A (CagA) that plays a role in the inflammation process,cell proliferation and metaplasia in gastric mucosa. Vascular endothelial growth factor (VEGF)is one of angiogenic factors that plays a role in the process of making new mucosal tissue after the inflammation by H.pylori. The escalation of VEGF expression levels contribute to the beginning of gastric carcinogenesis. The studywas aimed to analyze of VEGF serum levels between CagA(+) and CagA(-) in patients with H.pylori gastritis. Cross sectional study was conducted on 30 patients with H.pylori gastritis after conducted gastroscopy,biopsy and CLO test, which were continued with VEGF serum examination using ELISA test and perfomed PCR test to determinethe CagA status.The data was analyzed with SPSS 22 version andp value <0.05 was considered significant.The results of this study were18 men (60 %) and 12 women (46%) from 30 total subjects, with a median age average was 53.5 years old.Majority ethnic was Batak with 16 subjects (53.3%). Helicobacterpylori gastritis with CagA(+) was about 21 subjects (70%) and H.pylori gastritis with CagA(-) was about 9 subjects (30%). We found that median VEGF serum levels of patients with H.pylori gastritis with CagA(+)[480.3 pg/dL (115.5-2185.2)] significantly higher compared to thatwith CagA(-) [291.1 pg/dL (158.4-556.7)] (p<0.05).In conclusion, the VEGF serum levels ofpatients withH.pylori gastritis with CagA(+) is higher compared to that withCagA(-).
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Site: http://www.repository.usu.ac.id.
11. Zhu Y, Zhou X, Wu J, Su J, Zhang G. Risk factors and prevalence of H.Pylori infection in persistent high incidence area of gastric carcinoma in Yangzhong city.Gastroenterol Res Pract2014; 2014:481365.
https://doi.org/10.1155/2014/481365
12. Betty, Lubis CP, Siregar GA. Infeksi Helicobacter pylori pada lesi gastritis yang didiagnosa dengan pewarnaan histokimia giemsa dan imunohistokimia Helicobacter pyloridi Laboratorium Patologi Anatomi Fakultas Kedokteran USU Medan.[Thesis].Fakultas Kedokteran USU,2012.
http://repository.usu.ac.id/handle/123456789/34694.
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https://doi.org/10.1083/jcb.200208039
14. Karayiannakis AJ, Syrigos KN, Polychronidis A, Zbar A, Kouraklis G, Simopoulos C, et al. Circulating VEGF levels in the serum of gastric cancer patients correlation with pathological variables, patient survival, and tumor surgery. Ann Surg2002; 236(1):37-42.
https://doi.org/10.1097/00000658-200207000-00007
15. Mangia A,Chiriatti A, Ranieri G, Abbate I, Coviello M, Simone G, etal.H.Pylori status and angiogenesis factor in human gastric carcinoma.World J Gastroenterol2006; 12(34):5465-72.
https://doi.org/10.3748/wjg.v12.i34.5465
1. Rugge M,Genta RM. Staging and grading of chronic gastritis. Hum pathol 2005;36(3):228-33.
https://doi.org/10.1016/j.humpath.2004.12.008
2. Fox JG, Megraud F. Helicobacter. In: Murray PR, editor. Manual of clinical microbiology. 9th ed. Pensylvania: Elsevier Mosby; 2007: 947-62.
3. Cesar ACG, Cury PM, Payao SLM, Liberatore PR, Silva AE. Comparison of histological and molecular diagnosis of Helicobacter pylori in benign lesions and gastric adenocarcinoma. Braz J Microbiol 2005;36(1):12-16.
https://doi.org/10.1590/S1517-83822005000100003
4. Banerjee A, Mukhopadhyay AK, Paul S, Bhattacharyya A, Swarnakar S. Unveiling the intricacies of Helicobacter pylori-induced gastric inflammation: T helper cells and matrix metalloproteinases at a crossroad. In Mozsik G, editor. Current Topics in Gastritis. Croatia: InTech Publishers; 2013.Chapter 7.
https://doi.org/10.5772/54193
5. Maciorkowska E, Marcinkiewicz S, Kaczmarski M, Kemona A. Inflammatory changes of the gastric mucosa and serum concentration of chosen growth factors in children. Adv Med Sci 2010; 55(1):59-66.
https://dx.doi.org/10.2478/v10039-010-0007-6
6. Aziz F,Chen X,Yang X, Yan Q.Prevalence and correlation with clinical diseases of helicobacter pylori caga and vaca genotype among gastric patients from northeast China.BioMed Research International 2014; 2014:1-7.
https:/doi.org/10.1155/2014/142980
7. Tahara T, Arisawa T, Shibata T, Nakamura M, Yamashita H, Yoshioka D, et al. Effect of polymorphisms in the 3’-untranslated region (3’-UTR) of VEGF gene on gastric premalignant condition. Anticancer Res 2009; 29(2):485-9.
8. Matsukura N, Yamada S, Kato S, Tomtitchong P, Tajiri T, Miki M, et al. Genetic differences in interleukin-1 betapolymorphisms among four Asian populations: an analysis of the Asian paradox between H. pylori infection and gastric cancer incidence. J Exp Clin Cancer Res 2003; 22 (1):47-55.
9. Caputo R, Tuccillo C, Manzo BA, Zarrilli R, Tortora G, Blanco CV, et al. Helicobacter pylori VacA toxin up-regulates vascular endothelial growth factor expression in MKN 28 gastric cells through an epidermal growth factor receptor-, cyclooxygenase-2-dependent mechanism. Clin Cancer Res 2003;9(6):2015-21.
10.Jamaludin,Siregar GA. Perbandingan kadar serum VEGF dan MMP 9 pada pasien gastritis H.Pylori dan Non-H.Pylori.[Thesis], Magister Program Studi Ilmu Penyakit Dalam Fakultas Kedokteran USU.2015.
Site: http://www.repository.usu.ac.id.
11.Zhu Y, Zhou X, Wu J, Su J, Zhang G. Risk factors and prevalence of H.Pylori infection in persistent high incidence area of gastric carcinoma in Yangzhong city.Gastroenterol Res Pract2014; 2014:481365.
https://doi.org/10.1155/2014/481365
12.Betty, Lubis CP, Siregar GA. Infeksi Helicobacter pylori pada lesi gastritis yang didiagnosa dengan pewarnaan histokimia giemsa dan imunohistokimia Helicobacter pyloridi Laboratorium Patologi Anatomi Fakultas Kedokteran USU Medan.[Thesis].Fakultas Kedokteran USU,2012.
http://repository.usu.ac.id/handle/123456789/34694.
13.Churin Y, Laila AG, Oliver K, Thomas FM, Walter B, Michael N.Helicobacter pylori Cag A protein targets the c-Met receptor and enhances the motogenic response. JCell Biol2003;161(2):249-55.
https://doi.org/10.1083/jcb.200208039
14.Karayiannakis AJ, Syrigos KN, Polychronidis A, Zbar A, Kouraklis G, Simopoulos C, et al. Circulating VEGF levels in the serum of gastric cancer patients correlation with pathological variables, patient survival, and tumor surgery. Ann Surg2002; 236(1):37-42.
https://doi.org/10.1097/00000658-200207000-00007
15.Mangia A,Chiriatti A, Ranieri G, Abbate I, Coviello M, Simone G, etal.H.Pylori status and angiogenesis factor in human gastric carcinoma.World J Gastroenterol2006; 12(34):5465-72.
https://doi.org/10.3748/wjg.v12.i34.5465
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DOI: https://doi.org/10.19106/JMedSci005104201907
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