Diagnosis of ulcer is based on the endoscopic examination of the stomach and the duodenal

Figure 6.3 Endoscopic appearance of a Helicobacter pylori-associated peptic ulcer of the posterior wall of the duodenal bulb in an 11-year-old girl.
Figure 6.4 Endoscopic appearance of Helicobacter pylori-associated multiple peptic ulcers of the gastric body and hyperplastic regeneration of the surrounding mucosa in a 12-year-old girl.

bulb. Primary ulcers are often single and localized at the duodenal bulb (Figure 6.3) or in the distal part of the stomach (Figure 6.4) (antrum, lesser curvature); while secondary ulcers (NSAIDs, stress ulcer) can be located in all parts of the stomach and can be multiple. Endoscopy may show changes of the gastroduodenal mucosa typical of gastropathy. Dohil et al90 have suggested an easy and quite useful endoscopic classification of gastropathies in erosive and non-erosive forms (Table 6.5). Even if some disorders may show both erosive and nonerosive lesions, each is classified by its most common clinical manifestation. The endoscopic picture of H. pylori-associated gastritis is characterized by the presence of micronodularity of the antral mucosa in more than 50% of cases (Figure

Some endoscopic pictures might be suggestive of inflammation and/or be specific for a given etiology, but confirmation of the initial impression and definitive diagnosis is dependent on histo-logical examination. For this reason, each endoscopic examination must be completed by biopsy sampling of both endoscopically abnormal and normal mucosa. At least two biopsies for H. pylori detection must be taken at the antral site. Further sampling from the fundus may be useful, especially after treatment, because of the tendency of the bacterial colonization to migrate proximally. Biopsies for other procedures (culture, urease test) should be considered after sampling for routine histology.

H. pylori-associated gastritis is the most frequent microscopic finding. It is predominantly an antral gastritis, but in some patients, and particularly in adults, inflammation may involve the entire stomach (pangastritis). In children, its severity is usually less, and features of activity (presence of polymorphonuclear leukocytes) are reported in 40% of cases.69,90 The presence of lymphoid follicle hyperplasia (follicular gastritis) (Figure 6.6), suspected of being the histological counterpart of the nodular appearance of the gastric mucosa at endoscopy, has been reported in 20% of patients.69,90 In adults, pangastritis may show gastric atrophy and/or focal intestinal metaplasia, particularly in association with gastric ulcers. In children, these findings are rarely reported (Figure 6.7).

Table 6.5 Classification of gastritis and gastropathy in children*90

Erosive and/or hemorrhagic gastritis or gastropathy 'Stress' gastropathy Neonatal gastropathies Traumatic gastropathy

Aspirin and other non-steroidal anti-inflammatory drugs Other drugs

Portal hypertensive gastropathy Uremic gastropathy Chronic varioliform gastritis Bile gastropathy Henoch-Schonlein gastropathy Corrosive gastropathy Exercise-induced gastropathy or gastritis Radiation gastropathy

Non-erosive gastritis or gastropathy 'Non-specific' gastritis Helicobacter pylori gastritis Crohn's gastritis Allergic gastritis

Proton pump inhibitor gastropathy Celiac gastritis

Gastritis of chronic granulomatous disease

Cytomegalovirus gastritis

Eosinophilic gastritis

Collagenous gastritis

Graft-versus-host disease

Menetrier's disease

Pernicious anemia

Gastritis with autoimmune disease

Other granulomatous gastritides

Phlegmonous and emphysematous gastritis

Other infectious gastritides

*Although some disorders can present as either erosive or non-erosive, each is classified by its most common manifestation

In recent years, the importance of the histological diagnosis of gastritis, on the basis of routinely obtained antral and body biopsies, has increased enormously, particularly because of the discovery of H. pylori. The introduction of the Sydney system made it possible, for the first time, to grade histological parameters, to identify topographic distribution and, finally, to make a statement about

Antral Nodular Helicobacter

Figure 6.5 Endoscopic appearance of antral nodularity associated with Helicobacter pylori infection (a). After biopsy, mucosal bleeding enhances the evidence of the picture (b).

Figure 6.6 Immunohistochemical staining for B lymphocytes of a mucosa-associated lymphoid follicle in a child with Helicobacter pylori-associated antral nodularity.

Figure 6.7 Giemsa-stained antral specimen showing, on the left side, typical intestinal metaplasia and, on the right side, Helicobacter pylori-associated chronic gastritis.

Figure 6.6 Immunohistochemical staining for B lymphocytes of a mucosa-associated lymphoid follicle in a child with Helicobacter pylori-associated antral nodularity.

Figure 6.7 Giemsa-stained antral specimen showing, on the left side, typical intestinal metaplasia and, on the right side, Helicobacter pylori-associated chronic gastritis.

the etiopathogenesis of the gastritis in H. pylori- or non-H. pylori-associated gastritis.91

Multiple samplings from the antrum, the body and the fundus of the stomach allow further subdivision of the group of H. pylori-associated gastritis into forms of gastritis whose morphological distribution patterns usually identify them as sequelae of H. pylori infection. Moreover, the group of gastritis not associated with H. pylori can be differentiated into autoimmune, chemically induced reactive gastritis, ex-H. pylori gastritis, H. heilmannii gastritis, Crohn's gastritis and a number of special forms of gastritis (see Table 6.5).

Diagnosis of H. pylori infection is based on the demonstration of H. pylori by either direct (invasive) or indirect (non-invasive) methods. H. pylori can be demonstrated on the gastric mucosa specimen by staining with Warthin-Starry, Giemsa (Figure 6.7) or orange acridine stain, or it can grow in culture of gastric biopsies on specific media and in microaerophilic conditions.2 Culture may be particularly useful for specific antibiotic sensitivity testing. An easy, diffuse and rapid test is the urease test, which is based on the color reaction induced by the presence of urease in the gastric specimen within 1 h.92

Indirect tests are based on the demonstration of an elevated titer of IgG or IgA antibodies against H. pylori in serum22 or in saliva,93 or the presence of a positive immunoassay for H. pylori in the stools.94 For research purposes, H. pylori may be detected by PCR in some human samples, such as dental plaque or feces.25,28 Results obtained using these diagnostic methods are variable, but among invasive tests, histology and culture are superior. If indirect tests are considered, the 13C-urea breath test (UBT) and fecal antigen tests show the best accuracy. In a recent study comparing more tests on 53 children,1 all the diagnostic tests except serology were excellent methods of diagnosing H. pylori infection. The diagnostic accuracy was 96.2% for the stool antigen test, 96.2% for the biopsy urease test, 98.1% for histology, 94.3% for PCR, 98.1% for culture, 100% for the 13C-UBT and 84.9% for serology.95

The North American Society of Pediatric Gastroenterology, Hepatology and Nutrition (NASPGHAN) clinical practice guidelines (Table 6.6),96 as well as the European (EPTFHP) (Table 6.6)97 and Canadian98 pediatric consensus conferences on H. pylori infection, recommend making a definitive diagnosis of H. pylori infection through endoscopy with multiple biopsies of the stomach. The role of non-invasive methods has to be reserved to the demonstration of eradication and for follow-up. For this purpose, the 13C-UBT is the best validated method,99 even though some problems may exist in patients younger than 6 years of age.

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