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INTRODUCTION

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The terms acid peptic diseases, peptic diseases, and acid-related disorders are used synonymously to describe digestive conditions that involve gastric acid and pepsin in their pathogenesis. These conditions include esophagitis, gastritis, peptic ulcer disease, and duodenitis. Inflammatory disorders of the stomach can be described more specifically as gastritis and peptic ulcer disease.

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Gastritis is strictly a histological condition that is diagnosed following the identification of inflammatory cells on tissue specimens (ie, endoscopic biopsies). Gastritis can be classified by the presence of atrophy (Sydney classification system), by endoscopic appearance (erosive vs nonerosive), or by risk of malignancy in adults (Operative Link for Gastritis Assessment [OLGA] Staging System).

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Gastropathy is a term used more generally to describe abnormalities in the stomach, irrespective of the histologic presence of inflammation. Although inflammation is absent in the majority of gastropathies, other abnormalities are common, including epithelial damage, regeneration, and vascular involvement. Various gastropathies are recognized endoscopically due to a characteristic appearance (eg, portal hypertensive gastropathy, prolapse gastropathy).

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Peptic ulcer disease can be defined as a break in the gastric mucosa or submucosa with a minimum diameter of 5 mm. Peptic ulcer disease is usually characterized as either primary (eg, caused by Helicobacter pylori) or secondary (eg, caused by Crohn disease), and is often accompanied by gastritis or a gastropathy.

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Although gastritis and peptic ulcer disease may occur as stand-alone entities, they are frequently part of a continuum of disease. An exception is H pylori, which is an important cause of gastritis and peptic ulcer disease and is discussed separately.

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PATHOGENESIS AND EPIDEMIOLOGY

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It was conventional wisdom that the stomach was a sterile organ in part because pH values less than 4 were able to sterilize the stomach, but in the past 30 years with the discovery of H pylori, we now know that the stomach supports a bacterial community with hundreds of phylotypes. While pH values less than 4 prevent bacterial overgrowth, the microbial density of the stomach is 101 to 103 colony-forming units (CFU) per gram. The stomach, along with the esophagus and the duodenum, are the least colonized regions of the gastrointestinal (GI) tract, in contrast to the high bacterial counts (1010 to 1012 CFU/g) observed in the colon. The low bacterial densities in the stomach are due to the effects of rapid peristalsis, low pH, and/or high bile concentration. However, as H pylori is directly implicated in several gastric diseases, including gastric atrophy and cancer, it is likely that there are important contributions made by other bacteria in gastric health and disease. The stomach secretes water, acid, bicarbonate, other electrolytes (K+, Cl, Na+), enzymes that are active at low pH (pepsin from chief cells and lipase from the gastric body epithelium), and intrinsic factor from parietal cells and mucins. The ...

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