The discovery of Helicobacter pylori in 1982 was the starting point after which the management of peptic ulcer disease took a new turn. It has been recognized a pathogen not only for peptic ulcer disease but has been also found to be carcinogenic and known to cause gastric mucosa associated lymphoid tissue (MALT) lymphoma.1
There are various ways of the H-pylori causes damage to the gastric mucosa, as shown in this issue of the journal,2 and lead to ulcers. It produces many of the cytokines and various intercellular mechanisms are involved in ulceration and ultimately to dysplasia and neoplasia. Peptic ulcer disease has been the main focus of the H. pylori in many recent studies.3 Its diagnosis can be made by invasive means with biopsy of the gastric mucosa or by noninvasive means in which urea blood test, H. pylori stool antigen and serology.4 Culture and molecular diagnostic studies have been performed in research setting.
Mascerchit III has recommended indications for H. pylori eradication which include duodenal and gastric ulcer, MALT lymphoma with various other diagnoses which still are subject of controversy and include non-ulcer dyspepsia, atrophic gastritis, unexplained iron deficiency anemia and long term use of non-steroid inflammatory drugs.4 The first line treatment which is recommended by most authors is ten days treatment of twice a day Clarithromycin, amoxicillin and PPI.5 This has achieved nearly 80% of eradication,6 which must be documented with urea blood test and stool antigen examination. Failures do take place because of clarithromycin and amoxicillin resistance which has developed to high proportions in various developing countries. With this, second line regimens, which have included levofloxacin have emerged. Sequential therapy, in which five days treatment is followed by different drugs for next five days treatment has been recommended and salvage therapy have been used in failures. Yet newer regiments are under trial.
Helicobactor pylori, peptic ulcer disease, gastric lymphoma.