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Lancet 1996;347:975. 10. Salmeron M, Desplaces N, Lavergne A, Houdart R. Campylobacter-like organisms and acute purulent gastritis. Lancet 1986;2:975-6. 11. Mitchell JD, Mitchell HM, Tobias V. Acute Helicobacter infection in an infant, associated with gastric ulceration and serological evidence of intra-familial transmission. Am J Gastroenterol 1992;87:382-6. 12. Frommer DJ, Carrick J, Lee A, Hazell S. Acute presentation of Campylobacter pylori gastritis. Am J Gastroenterol 1988; 83:1168-71. 13. Rocha GA, Queiroz DMM, Mendes EN, Barbosa AJA, Lima GF Jr, Oliveira CA. Helicobacter pylori acute gastritis: histological, endoscopical, clinical, and therapeutic features. Am J Gastroentrol 1991;86:1592-5. 14. Xiang Z, Censini S, Bayeli PF, Telford JL, Figura N, Rappuoli R, et al. Analysis of expression of CagA and VacA virulence factors in 43 strains of Helicobacter pylori reveals that clinical isolates can be divided into two major types and that CagA is not necessary for expression of the vacuolating cytotoxin. Infect Immun 1995;63:94-8. 15. Tummuru MKR, Cover TL, Blaser MJ. Cloning and expression of a high-molecular-mass major antigens of Helicobacter pylori: evidence of linkage to cytotoxin production. Infect Immun 1993;61:1799-809. 16. Fujimoto S, Marshall B, Blaser M. PCR-based restriction fragment length polymorphism typing of Helicobacter pylori. J Clin Microbiol 1994;32:331-4. 17. Katz D, Siegal HI. Erosive gastritis and acute gastrointestinal mucosal lesions. In: Glass GBJ, editor. Progress in gastroenterology. Vol 1. New York: Grune and Siralton; 1968. p. 67-96. 18. Laine L, Cominelli F, Sloane R, Casini-Raggi V, MarinSorensen M, Weinstein WM. Interaction of NSAIDs and Helicobacter pylori on gastrointestinal injury and prostaglandin production: a controlled double-blind trial. Aliment Pharmacol Ther 1995;9:127-35. 19. Graham DY, Alpert LC, Smith JL, Yoshimura HH. Iatrogenic Campylobacter pylori infection is a cause of epidemic achlorhydia. Am J Gastroenterol 1988;83:974-80. 20. Langenberg W, Rauws EAJ, Oudbier JH, Tytgat GNJ. Patient-to-patient transmission of Campylobacter pylori infection by fiberoptic gastroduodenoscopy and biopsy. J Infect Dis 1990;161:507-11. 21. Sugiyama T, Naka H, Yabana T, Awakawa T, Furuyama S, Kawauchi H, et al. Is Helicobacter pylori infection responsible for postendoscopic acute gastric mucosal lesions? Eur J Gastroenterol Hepatol 1992;4(Suppl 1):S93-6. 22. Miyaji H, Kohli Y, Azuma T, Ito S, Hirai M, Ito Y, et al. Endoscopic cross-infection with Helicobacter pylori [letter]. Lancet 1995;345:464. 23. Matysiak-Budnik T, Briet F, Heyman M, Megraud F. Laboratory-acquired Helicobacter pylori infection. Lancet 1995;346:1489-90. 24. Ghiara P, Marchetti M, Blaser MJ, Tummuru MKR, Cover TL, Segal ED, et al. Role of the Helicobacter pylori virulence factors vacuolating cytotoxin, CagA, and urease in a mouse model of disease. Infect Immun 1995;63:4154-60.

Background: Endoscopic variceal banding ligation (EVL) and sclerotherapy (EVS) have been used to prevent variceal hemorrhage. However, the rate of recurrence of esophageal varices after EVL or EVS is considerably high. Argon plasma coagulation (APC) is a new modality of electrosurgery to apply high frequency electric current into tissue to cause defined thermal effects. This study was conducted to determine whether APC is beneficial for eradication of residual esophageal varices after EVL or EIS. Methods: Cirrhotic patients with endoscopically assessed high-risk esophageal varices but no history of bleeding underwent EVL or EIS to reduce the risk of hemorrhage. When the size of varices was reduced 1 week later, the entire esophageal mucosae 4-5 cm proximal to the esophagogastric junction was coagulated with one session of APC in a total of 15 patients.APC was performed with the use of argon source APC300 and high frequency generator ICC 200 (ERBE, Germany). Follow-up endoscopy was performed 7 days and 1 month after the initial procedure and thereafter every 3 months, to check for recurrent/residual esophageal varices and its complications. Results: Ten to 14 days after APC, ulcerations with white coating were noted in all cases, whereas varices were completely eradicated. One month after APC, while the varices remained eradicated, coagulated esophageal mucosae became whitish and the ulcerations were nearly completely healed. During the course, no patients complained of dysphagia or retrosternal pain. Furthermore, neither development of gastric varices nor aggravation of portal hypertensive gastropathy was observed endoscopically. No serious complication such as bleeding necessitating endoscopic therapy and perforation or stricture of the esophagus was encountered. Over a maximum follow-up period of 5 months, neither recurrence of nor hemorrhage from esophageal varices was observed. Conclusions: APC ablation of residual esophageal varices in patients who have undergone prior EVL or EIS is safe and may be a novel approach to eradicate esophageal varices. It requires a long term follow-up of the eradicated varices to further evaluate its efficacy.