A clinical study of prevalence of helicobacter pylori in patients with gastritis
DOI:
https://doi.org/10.18203/2349-2902.isj20163564Keywords:
Gastritis, Retrosternal- burn, Helicobacter Pylori, UreaseAbstract
Background: Stomach infections with Helicobacter pylori mainly occur during childhood. If persistent, these may cause chronic gastritis often leading to peptic ulcer disease, later on in life. Ulcer is a sore or hole in the lining of the stomach or duodenum (the first part of the small intestine). Objective was to detect the prevalence of H. Pylori in patients with gastritis.
Methods: This study involved 90 patients with gastritis who attended surgical outpatient as well as inpatient department of ESIC Medical college hospital from April 2014 to March 2016.
Results: Endoscopy was carried for all patients to diagnose gastritis. Urease and Serum IgG anti H. Pylori antibodies used to detect the presence of H. Pylori in these patients. Ninety patients; 60 males (66.67%) and 30 females (36.33%) were infected with gastritis. The results showed that 53.33% of the patients gave positive results on urease test. The results showed that for screening and determining the clinical features of gastritis, at least one method for H. Pylori are required to give positive result in order to identify an infected patient with H. Pylori.
Conclusions: There is an additional aspect to treatment of gastric ulcers, the one of health care providers and patient’s awareness of the cause and most efficient treatments for this medical condition. Ulcers that presented until recently a life-long disease with only symptomatic relieve available, became an easily curable condition, when the right pathway of treatment is chosen.
References
Fauci AS, Braunwald E, Isselbacher KJ. Harrison’s Principles of Internal Medicine, 14th edition (New York, NY: McGraw-Hill); 1998.
Kaptan K, Beyan C, Ural AU, Cetin T, Avcu F, Gülşen M. Helicobacter pylori-is it a novel causative agent in Vitamin B12 deficiency? Archives of Internal Medicine. 2002;160(9):1349-53.
Laurila A, Cole SP, Merat S, Obonyo M, Palinski W, Fierer J. High-fat, high-cholesterol diet increases the incidence of gastritis in LDL receptor-negative mice. Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21(6):991-6.
Qasim A, Morain CA. Review article: treatment of Helicobacter pylori infection and factors influencing eradication. Alimentary Pharmacology and Therapeutics. 2002;16(Suppl 1):24-30.
Dohil R, Hassall E. Peptic ulcer disease in children. Balliere's Clin Gastroenterol. 2002;1:53-73.
Letley DP, Rhead JL, Twells RJ, Dove B, Atherton JC. Determinants of non-toxicity in the gastric pathogen Helicobacter pylori. J Bio Chemist. 2003;278(29):26734-41.
Schenk BE, Kuipers EJ, Klinkenberg-Knol EC, Eskes SA, Meuwissen SG. Helicobacter pylori and the efficacy of omeprazole therapy for gastroesophageal reflux disease. American J Gastroenterol. 1999;94(4):884-7.
Ally R, Mitchell H, Segal H. Cag a positive H.pylori aplenty in South Africa: the first systemic study of H.pylori infection in systemic children in Soweto. Gut. 1999;45:97-8.
Drumm B, Koletzko S, Oderda G. Helicobacter pylori infection in children: a consensus statement, medical position paper: a report of the European Pediatric Task Force on Helicobacter pylori on a consensus conference, Budapest, Hungary, September 1998. J Pediat Gastroenterol Nutr. 2003;30:207-13.
Shuker WS. Immune response in patients infected with Helicobacter pylori, Entamoebahistolytica and Giardia lamblia, Ph. D. Thesis. University of Baghdad; 2007.
Twaij A. Invasive and non-invasive methods for detection of H. pylori with some molecular aspects of its pathogenesis. PhD Thesis, College of Medicine, Al-Nahrain University; 2006.
