New approaches in gastritis treatment

Abstract

Gastritis is an inflammation of the stomach lining, which is fairly common and could have different causes. Many kind of agents may lead the stomach into an inflamed statement; in first place, it could be due to non-steroidal anti-inflammatory drugs (NSAID) such as aspirin, ibuprofen, naproxen, etc. (Fig. 1), which are used in different treatments to calm down some specific illness, e.g. rheumatoid arthritis; in second place, inflamation could be due to abrasive compounds (alcohol, acids and others) or unbalanced diets where the stomach is damaged by its own gastric acid; in third place, long-term physical and/or mental stress that result in the production of excessive amounts of stomach acid; in last place, the infection caused by a well-known microorganism, Helicobacter (H) pylori. When stomach inflammation is not treated, mainly in the latter case, the illness could end in a gastric ulcer or in the worst case, in gastric cancer. The signs and symptoms of gastritis depend on how long the problem has existed. If it occurs suddenly is called acute gastritis. In acute phase, superficial inflammation of the stomach causes the classic nausea and pain or discomfort in the upper abdomen. If it develops gradually is called chronic gastritis, and the symptoms might vary from those of acute, with a dull pain in the upper abdomen and a feeling of fullness and loss of appetite after a few bites of food. However, in some cases, people with chronic gastritis could not feel any of these symptoms. Another type is the reactive or chemical gastritis, which is defined as a foveolar elongation, tortuosity, and hypercellularity of the gastric surface epithelium, together with edema, vasodilatation, congestion of gastric lamina propria, and a paucity of inflammatory cells. This type of gastritis has been thought to result from duodenogastric bile reflux or the use of NSAIDs (Voutilainen et. al., 2002). Nowadays, one of the most important cases of gastritis is the infection by H. pylori strains. This affection was the attention focus that led to many researchers in the last years to study different branches of the infection process (Chenoll et. al.; 2011; Cui et. al., 2010; Ko et. al., 2010; Wittschier et. al., 2009; Wolle & Malfertheiner, 2007). However, equal important is the gastritis associated to the consumption of NSAIDs since these drugs are widely used to treat some pains. The chronic use of NSAIDs is a common cause of gastroduodenal erosions and peptic ulcers resulting, in many cases, in fatal haemorrhage. Aspirin, a famous NSAID, is thought to cause gastric damage by both, topical irritant effects on the gastric epithelium and systemic effects related to suppression of mucosal prostaglandin synthesis (Fig. 1). Inhibition of prostaglandin synthesis reduces mucosal defenses, including mucus and bicarbonate secretion, blood flow, epithelial cell turnover and repair, and mucosal immunocyte function. NSAIDs can also interfere with the healing of preexisting lesions and cause a fast drop in pH within the mucus cap (Shiotani et. al., 2008). In clinical practice, a prostaglandin E1 derivative, misoprostol, and anti-acids, including proton pump inhibitors (PPIs) are routinely used for the treatment and prevention of NSAID enteropathy (Peura, 2004). The authors previously reported the usefulness of PPIs for healing the small intestinal mucosal injury in experimental animal models treated with NSAID; however, there are no clinical data on the usefulness of PPIs in such injuries. Some studies indicated the efficacy of misoprostol on NSAID-induced intestinal injuries (Kuroda et. al., 2006) whereas others reported no effectiveness (Davies et. al., 1993).