MODIFICATIONS IN VALUES OF GASTRIN SERUM AND CARBONIC ANHYDRASE AFTER THERAPY TO ERADICATE THE HELICOBACTER PYLORI IN DUODENAL ULCER PATIENTS

This is an automatically generated default intro template – please do not edit.

	Read full article
Article Title:	MODIFICATIONS IN VALUES OF GASTRIN SERUM AND CARBONIC ANHYDRASE AFTER THERAPY TO ERADICATE THE HELICOBACTER PYLORI IN DUODENAL ULCER PATIENTS
Authors:	Claudia Anca DUME1*, Ioan PUSCAS2, Marcela COLTAU2
Affiliation:	1Regional Gastroenterology and Hepatology Institute “Prof. O. Fodor” Cluj Napoca; 2Municipal Hospital “Prof. Dr. Ioan Puscas” Simleu Silvaniei
Abstract:	Many researchers have suggested that measuring the levels of gastrin and pepsinogen during the treatment to eradicate H. pylori infection may be useful to assess whether the treatment is effective or not. The gastrin which is a key- enzyme in modulating gastric acid secretion is also a direct activator of carbonic anhydrase (CA). In our work we have studied the effect of treatment to eradicate H. pylori infection on the levels of serum gastrin and carbonic anhydrase IV in the gastric mucosa, in the case of two groups of patients with UD and positive H. pylori diagnostics who were treated by means of triple therapy, and respectively quadruple therapy for 10 days. Endoscopy with biopsy sampling was performed in the case of all patients. The study results prove the implication of isoenzyme CA IV of the gastric mucosa and the gastrin in the action of therapy mechanisms to eradicate H. pylori infection. Following the treatment to eradicate the H. pylori infection one reveals a decrease of CA IV gastric activity by 64% in the Group no. 1 patients, and 78% in the Group no. 2 patients, while the levels of serum in gastrin decrease by 58% in Group no. 1 and by 69% in group no.2, respectively.
Keywords:	Helicobacter pylori, Carbonic anhydrase, Duodenal (peptic) ulcer, Gastrin
References:	Calam J. Helicobacter pylori and hormones. Yale J. Biol. Med. 1997;69:39–49. Chen T. S., Tsay S. H., Chang F. Y., Lee S. D. Effect of eradication of Helicobacter pylori on serum pepsinogen I, gastrin, and insulin in duodenal ulcer patients: a 12-month follow-up study. Am. J. Gastroenterol. 1994;89:1511–1514. Frances Fischbach. Chemistry Studies. In A Manual of Laboratory and Diagnostic Tests. Lippincott Williams & Wilkins, USA, 8 Ed., 2009, 393-394. Harry LT Mobley, George L Mendz, and Stuart L Hazell (eds.) – Helicobacter pylori Physiology and Genetics, Washington (DC): ASM Press; 2001. Graham D. Y., Opekun A., Lew G. M., Evans, Jr D. J., Klein P. D., Evans D. G. Ablation of exaggerated meal-stimulated gastrin release in duodenal ulcer patients after clearance of Helicobacter (Campylobacter) pylori infection. Am. J. Gastroenterol.1990;85:394–398. Grossman M.I. – Control of gastric secretion. In: Gastrointestinal Disease, edited by M.H.Sleisenger and J.S.Fordtran, Saunders, Philadelphia, 1978, pp.640-659. Levi S., Beardshall K., Swift I., Foulkes W., Playford R., Ghosh P., Calam J. Antral Helicobacter pylori, hypergastrinaemia, and duodenal ulcers: effect of eradicating the organism. Br. Med. J. 1989;299:1504–1505. Logan RP, Walker MM – Epidemiology and diagnosis of Helicobacter pylori infection. BMJ 323 (7318): 920–2, 2001 Khalifah R.G. – The carbon dioxide hidration activity of carbonic anhydrase: stop-flow kinetic studies on the native human isozymes B and C. J.Biol.Chem., 1971, 246:2561-2573. Konturek JW – Discovery by Jaworski of Helicobacter pylori and its pathogenetic role in peptic ulcer, gastritis and gastric cancer. J. Physiol. Pharmacol. 54 Suppl 3: 23–41, 2003. Kusters JG, van Vliet AH, Kuipers EJ – Pathogenesis of Helicobacter pylori Infection. Clin Microbiol Rev 19 (3): 449–90, 2006. Maconi G., Lazzaroni M., Sangaletti O., Bargiggia S., Vagu L., Bianchi Porro G. Effect of Helicobacter pylori eradication on gastric histology, serum gastrin and pepsinogen I levels, and gastric emptying in patients with gastric ulcer. Am. J. Gastroenterol. 1997;92:1844–1848. Maren T.H., Wynns G.C., Wistrand P.J. – Chemical properies of carbonic anhydrase IV, the membrane-bound enzyme. Molec.Pharmacol., 1993, 44:901-905. Prewett E. J., Smith J. T., Nwokolo C. U., Hudson M., Sawyerr A. M., Pounder R. E. Eradication of Helicobacter pyloriabolishes 24-hour hypergastrinaemia: a prospective study in healthy subjects. Aliment. Pharmacol. Ther. 1991;5:283–290. Puscas I., Coltau M., Lazoc L. – Histamine, gastrin and acetylcholine activate CA IV from parietal cells and do not modify activity of the same isozyme from the kidneys. In: Carbonic Anhydrase and Modulation of Physiologic and Pathologic Processes in the Organism, I.Puscas (ed), Helicon Publ.House, Timisoara, Romania, 1994, 524-527. Puscas I. – Carbonic anhydrase is a modulator of vasculary and secretory processes in the organism. The pH theory. Digestion, 1998, 59 (suppl. 3), 671. Rotter J. L., Petersen G., Samloff I. M., McConnell R. B., Ellis A., Spence M. A., Rimoin D. L. Genetic heterogeneity of hyperpepsinogenemic I and normopepsinogenemic I duodenal ulcer disease. Ann. Intern. Med. 1979;91:372–377. Stenström B, Mendis A, Marshall B – Helicobacter pylori – The latest in diagnosis and treatment. Aust Fam Physician 37 (8): 608–12, 2008. Westblom T. U., Bhatt B. D. Diagnosis of Helicobacter pylori infection. Curr. Top. Microbiol. Immunol. 1999;241:215–235. Wilcox M. H., Dent T. H., Hunter J. O., Gray J. J., Brown D. F., Wight D. G., Wraight E. P. Accuracy of serology for the diagnosis of Helicobacter pylori infection—a comparison of eight kits. J. Clin. Pathol. 1996;49:373–376. Woo J. S., El-Zimaity H. M., Genta R. M., Yousfi M. M., Graham D. Y. The best gastric site for obtaining a positive rapid urease test. Helicobacter. 1996;1:256–259.
*Correspondence: