Etiology

PUD is the progressive loss of the mucosal integrity up to the formation of a crater (ulcer). This is the final process of different etiological factors, which produce lesions by different mechanisms. These factors and mechanisms are not mutually exclusive and may co-operate to bring about their damage. The classical pathogenic theory was that an ulcer develops when the equilibrium is lost between defensive factors and aggressive factors. Defensive factors are the mucus layer, constituted by glycoproteins, bicarbonate and prostaglandins; and the gastric mucosa barrier, constituted by the epithelial layer, submucosal tissue and microcirculation. The best known aggressive factors are gastric acid, pepsins, gastrolesional substances, such as alcohol, drugs, non-steroidal anti-inflammatory drugs (NSAIDs) and, last to be identified, H. pylori infection). In primary ulcers (deep erosive lesions not secondary to other known causes) the most important factor was considered to be the acid output of the stomach. Both research and therapeutic interven-tional studies were directed towards evaluating and suppressing acid secretion (according to the theory 'no acid, no ulcer') until the discovery of H. pylori. The demonstration that duodenal ulcer is almost invariably associated with H. pylori infection, and recurrence depends on its persistence, established the importance of H. pylori as the main etiological factor in PUD.3,29 Indeed, H. pylori infection has been demonstrated in 92% (33-100%) of children with duodenal ulcer in 14 studies, and in 25% (11-75%) of children with gastric ulcer in four studies.30 Recurrence of ulcer after healing has been reported in 47% of children where Helicobacter was not eradicated, but it is rare, if not exceptional, in patients in whom eradication was achieved.31 H. pylori is the main known etiological factor in chronic gastritis in adults as well as in children.30

H. pylori is a Gram-negative, unipolar flagellated bacterium with a spiral appearance (Figure 6.1). It was the first recognized bacterium of a new genus whose different species colonize the gastrointestinal tract of the human (H. pylori and H. heilman-nii) and animals (all remaining species) (Table 6.1).2

Figure 6.1 Electron micrograph of Helicobacter pylori attached to the cell membrane of gastric epithelial cells with evident cytoplasmic vacuolization.

H. pylori colonizes only the gastric mucosa, wherever it may be present: in the stomach or in heterotopic areas, as in Barrett's esophagus or in gastric metaplasia of the duodenum.2 H. heilmannii is a rare (0.5% prevalence in humans) cause of dyspeptic symptoms and inflammation in adults, and its pathogenic role in children seems limited.32

The H. pylori genome (1.65 million bp) codes for about 1500 proteins and shows an extraordinary heterogeneity,33 which could in part explain the wide spectrum of clinical pictures. Multiple strains may be present in the same patient, particularly in developing countries. Recombination and mutation between strains produces continuous changes of the genome during long-term gastric colonization in the same host.34

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