
Recent progress in the area of ulcer and gastritis is still dominated by findings and reports on Helicobacter pylori and nonsteroidal anti-inflammatory drugs, which in turn are the two major causes of peptic ulcers. Although the prevalence of H. pylori is declining in most developed countries, it is still contributing to a significant proportion of peptic ulcers globally. The interrelationship of H. pylori gastritis in patients with gastroesophageal reflux has become more apparent. H. pylori-induced gastric body gastritis is associated with reduced acid production, and thus with reduced reflux and esophagitis. The controversies regarding the interactions between H. pylori and NSAIDs have still not been settled. With the availability of the new COX-2-specific inhibitors, the current scenario of NSAID-related gastroduodenal complications will certainly change. Short-term usage of these agents has significantly reduced the incidence of endoscopic ulcers, but the benefits in terms of clinical outcomes, such as bleeding or perforation, remain to be determined. This review summarizes the recent literature on peptic ulcer and gastritis.
Peptic Ulcer, Helicobacter pylori, 610, Gastritis - Diagnosis - Pathology, Peptic Ulcer - Diagnosis - Pathology, Gastric Mucosa - Pathology, Helicobacter Pylori, Helicobacter Infections, Gastric Mucosa, Risk Factors, Gastritis, Helicobacter Infections - Diagnosis - Pathology, Humans, Precancerous Conditions - Diagnosis - Pathology, Precancerous Conditions
Peptic Ulcer, Helicobacter pylori, 610, Gastritis - Diagnosis - Pathology, Peptic Ulcer - Diagnosis - Pathology, Gastric Mucosa - Pathology, Helicobacter Pylori, Helicobacter Infections, Gastric Mucosa, Risk Factors, Gastritis, Helicobacter Infections - Diagnosis - Pathology, Humans, Precancerous Conditions - Diagnosis - Pathology, Precancerous Conditions
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