Evolution of gastric and duodenal ulcers at patients with helicobacter pylori infection, after treatment with proton pump inhibitors and an associated treatment

Evolution of gastric and duodenal ulcers at patients with helicobacter pylori infection, after treatment with proton pump inhibitors and an associated treatment

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Title: Evolution of gastric and duodenal ulcers at patients with helicobacter pylori infection, after treatment with proton pump inhibitors and an associated treatment
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Article_Title: Evolution of gastric and duodenal ulcers at patients with helicobacter pylori infection, after treatment with proton pump inhibitors and an associated treatment
Authors: Claudia Anca Dume, Ioan Puscas, Marcela Coltau
Affiliation: Regional Institute of Gastroenterology and Hepatology “Prof. Dr. O. Fodor”, Cluj-Napoca, Romania
Municipal Hospital “Prof. Dr. Ioan Puscas”, Simleu Silvaniei, Romania
Abstract: Modern antiulcer therapy consists in a combined treatment aims both to decrease gastric acid secretion and to eradicate Helicobacter pylori infection. In this paper we comparatively studied the clinical, the endoscopic, and the secretory evolution of two groups of patients with gastro-duodenal ulcers who were treated with Nexium (Esomeprazole) a single dose of 40 mg / day for 21 days, respectively with Nexium a single dose of 40 mg / day, associated with anti-H. pylori therapy (metronidazole 250 mg bid + amoxicillin 750 mg bid. The study results show that after associated treatment with PPIs and anti-H. pylori therapy, reduction of basal acid secretion is greater. The pain persists longer in patients who received treatment with PPIs alone without anti-H. pylori therapy. In case of 84% of patients with GU and 91% of those with DU, endoscopic healing of ulcer niche took place after 21 days of treatment with Nexium, respectively in case of 89% of patients with GU and 96% of those with DU after combination therapy.
Keywords: protons pump inhibitors, Helicobacter pylori, gastric ulcer, duodenal ulcer, basal acid secretion
References: Basu PP, Rayapudi K, Pacana T, Shah NJ, Krishnaswamy N, Flynn M. – A randomized study comparing levofloxacin, omeprazole, nitazoxanide and doxycycline versus triple terapy for the eradication of Helicobacter pylori. Am J Gastroenterol., 2011 Nov; 106(11): 1970-5.
Besancon M, Shin JM, Mercier F. Et al. – Membrane topology and omeprazole labelling of the gastric H+, K+- adenosinetriphosphatase, Biochemistry, 1993, 32: 2345-55.
Bretagne J.F., Traitement medical de la maladie ulcereuse gastrique en dehors de l’urgence. Gastroenterol Clin Biol, 1996; 20: S73-80.
Bytzer P., Eradication of Helicobacter pylori or longteam acid suppression in duodenal ulcer: a double-blind, randomized trial with a two year follow-up. Digestion, 1998; 59 (suppl. 3): A4
Buffet C., Helicobacter pylori update. Bull Acad Natl Med. 2003; 187(6): 1095-103.
Ghosh T., Lewis D.I., Axon A.T.R., Everett S.M., Methods of measuring gastric acid secretion, Alimentary Pharmacology and Therapeutics, 2011, (33), 7:768-781.
Hersey S.J., Sachs G., Gastric acid secretion, Physiological Reviews. 1995, 75,1:155-189
Hopkins RJ, Girardi LS, Turney EA., Relationship between Helicobacter pylori eradication and reduced duodenal and gastric ulcer recurrence: a review. Gastroenterology, 1996, 110: 1244-1252.
Jinda S., Nakatani K, Nishioka J., Yasuda K, Soya Y, Hayasi A, Wada H, Nobori T – Personalized treatment in the eradication therapy for Helicobacter pylori. Int J Mol Med, 2011 Feb.; 27(2): 255-61.
Keeling DJ, Fallowfield C, Underwood AH – The specificity of omeprazole as an (H++K+)-ATPase inhibitor depends upon the means of its activation. Biochem. Pharmacol. 1987, 36: 339-44.
Kim H.S., Lee D.K., Suk K.T., Kim J.M., Baik S.K., Kwon S.O., Cho M.Y., Therapeutic effect of low- dose omeprazole vs. standard-dose ranitidine in mild to moderate reflux esophagitis. Korean J. Gastroenterol, 2004 Mar.; 43(3): 153-9.
Lindberg P, Nordberg P, Alimnger T, et al. – The mechanism of action of the gastric acid secretion inhibitor omeprazole. J.Med.Chem. 1986, 29:1327-29.
Lindberg P, Branstrom A, Wallmark B, et al. – Omeprazole: the first proton pump inhibitor. Med.Res.Rev., 1990, 10: 1-54.
Lorentzon P, Jackson R, Wallmark B, Sachs G. – Inhibition of (H++K+)-ATP-ase by omeprazole in isolated gastric vesicles requires proton transport. Biochim. Biophys. Acta, 1987, 897:41-51.
Penston GJ. – Review article: clinical aspects of H. pylori eradication therapy in peptic ulcer disease. Aliment Pharmacol Ther, 1996, 10: 469-486.
Sachs G, Carlsson E, Lindberg P, Wallmark B – Gastric HK-ATP-ase as therapeutic targert.Ann.Rev.Pharmacol.Toxicol., 1988, 28: 269-284.
Soll A.H., Peptic ulcer and its complications, In: Gastrointestinal and Liver Disease, Pathophysiology, Diagnosis, Management, Feldman M., Scharschmidt B.F., Sleisenger M.H. (eds.) ,W.B. Saunders Company, 1998, 620-678.
Wallmark B, Jaresten BM, Larsson H, et al. – Differentiation among inhibitory actions of omeprazole, cimetidine and SCN – on gastric acid secretion. Am.J.Physiol.1983, 245: G64-71.
Zimmerman, Donald W., A Note on Interpretation of the Paired-Samples t Test Journal of Educational and Behavioral Statistics, 1997, 22 (3): 349–360.
Read_full_article: pdf/23-2013/23-1-2013/SU23-1-2013-Dume.pdf
Correspondence: Claudia Anca Dume, Institutul Regional de Gastroenterologie si Hepatologie „Prof. Dr. O. Fodor” Cluj Napoca, Sectia Alergologie si Imunologie clinica, Tel. 0740169946, email: ancutadc@yahoo.com

Read full article
Article Title: Evolution of gastric and duodenal ulcers at patients with helicobacter pylori infection, after treatment with proton pump inhibitors and an associated treatment
Authors: Claudia Anca Dume, Ioan Puscas, Marcela Coltau
Affiliation: Regional Institute of Gastroenterology and Hepatology “Prof. Dr. O. Fodor”, Cluj-Napoca, Romania
Municipal Hospital “Prof. Dr. Ioan Puscas”, Simleu Silvaniei, Romania
Abstract: Modern antiulcer therapy consists in a combined treatment aims both to decrease gastric acid secretion and to eradicate Helicobacter pylori infection. In this paper we comparatively studied the clinical, the endoscopic, and the secretory evolution of two groups of patients with gastro-duodenal ulcers who were treated with Nexium (Esomeprazole) a single dose of 40 mg / day for 21 days, respectively with Nexium a single dose of 40 mg / day, associated with anti-H. pylori therapy (metronidazole 250 mg bid + amoxicillin 750 mg bid. The study results show that after associated treatment with PPIs and anti-H. pylori therapy, reduction of basal acid secretion is greater. The pain persists longer in patients who received treatment with PPIs alone without anti-H. pylori therapy. In case of 84% of patients with GU and 91% of those with DU, endoscopic healing of ulcer niche took place after 21 days of treatment with Nexium, respectively in case of 89% of patients with GU and 96% of those with DU after combination therapy.
Keywords: protons pump inhibitors, Helicobacter pylori, gastric ulcer, duodenal ulcer, basal acid secretion
References: Basu PP, Rayapudi K, Pacana T, Shah NJ, Krishnaswamy N, Flynn M. – A randomized study comparing levofloxacin, omeprazole, nitazoxanide and doxycycline versus triple terapy for the eradication of Helicobacter pylori. Am J Gastroenterol., 2011 Nov; 106(11): 1970-5.
Besancon M, Shin JM, Mercier F. Et al. – Membrane topology and omeprazole labelling of the gastric H+, K+- adenosinetriphosphatase, Biochemistry, 1993, 32: 2345-55.
Bretagne J.F., Traitement medical de la maladie ulcereuse gastrique en dehors de l’urgence. Gastroenterol Clin Biol, 1996; 20: S73-80.
Bytzer P., Eradication of Helicobacter pylori or longteam acid suppression in duodenal ulcer: a double-blind, randomized trial with a two year follow-up. Digestion, 1998; 59 (suppl. 3): A4
Buffet C., Helicobacter pylori update. Bull Acad Natl Med. 2003; 187(6): 1095-103.
Ghosh T., Lewis D.I., Axon A.T.R., Everett S.M., Methods of measuring gastric acid secretion, Alimentary Pharmacology and Therapeutics, 2011, (33), 7:768-781.
Hersey S.J., Sachs G., Gastric acid secretion, Physiological Reviews. 1995, 75,1:155-189
Hopkins RJ, Girardi LS, Turney EA., Relationship between Helicobacter pylori eradication and reduced duodenal and gastric ulcer recurrence: a review. Gastroenterology, 1996, 110: 1244-1252.
Jinda S., Nakatani K, Nishioka J., Yasuda K, Soya Y, Hayasi A, Wada H, Nobori T – Personalized treatment in the eradication therapy for Helicobacter pylori. Int J Mol Med, 2011 Feb.; 27(2): 255-61.
Keeling DJ, Fallowfield C, Underwood AH – The specificity of omeprazole as an (H++K+)-ATPase inhibitor depends upon the means of its activation. Biochem. Pharmacol. 1987, 36: 339-44.
Kim H.S., Lee D.K., Suk K.T., Kim J.M., Baik S.K., Kwon S.O., Cho M.Y., Therapeutic effect of low- dose omeprazole vs. standard-dose ranitidine in mild to moderate reflux esophagitis. Korean J. Gastroenterol, 2004 Mar.; 43(3): 153-9.
Lindberg P, Nordberg P, Alimnger T, et al. – The mechanism of action of the gastric acid secretion inhibitor omeprazole. J.Med.Chem. 1986, 29:1327-29.
Lindberg P, Branstrom A, Wallmark B, et al. – Omeprazole: the first proton pump inhibitor. Med.Res.Rev., 1990, 10: 1-54.
Lorentzon P, Jackson R, Wallmark B, Sachs G. – Inhibition of (H++K+)-ATP-ase by omeprazole in isolated gastric vesicles requires proton transport. Biochim. Biophys. Acta, 1987, 897:41-51.
Penston GJ. – Review article: clinical aspects of H. pylori eradication therapy in peptic ulcer disease. Aliment Pharmacol Ther, 1996, 10: 469-486.
Sachs G, Carlsson E, Lindberg P, Wallmark B – Gastric HK-ATP-ase as therapeutic targert.Ann.Rev.Pharmacol.Toxicol., 1988, 28: 269-284.
Soll A.H., Peptic ulcer and its complications, In: Gastrointestinal and Liver Disease, Pathophysiology, Diagnosis, Management, Feldman M., Scharschmidt B.F., Sleisenger M.H. (eds.) ,W.B. Saunders Company, 1998, 620-678.
Wallmark B, Jaresten BM, Larsson H, et al. – Differentiation among inhibitory actions of omeprazole, cimetidine and SCN – on gastric acid secretion. Am.J.Physiol.1983, 245: G64-71.
Zimmerman, Donald W., A Note on Interpretation of the Paired-Samples t Test Journal of Educational and Behavioral Statistics, 1997, 22 (3): 349–360.
*Correspondence: Claudia Anca Dume, Institutul Regional de Gastroenterologie si Hepatologie „Prof. Dr. O. Fodor” Cluj Napoca, Sectia Alergologie si Imunologie clinica, Tel. 0740169946, email: ancutadc@yahoo.com