Correlation of serum antibody titres with invasive methods for rapid detection of Helicobacter pylori infections in symptomatic children

Abstract

Helicobacter pylori (H. pylori) is causally associated with peptic ulcer disease and gastric carcinoma. Typically, children get infected during the first decade of life, but diseases associated with H. pylori are seen mainly in adults. Multiple diagnostic methods are available for the detection of H. pylori infection. The aim of this study was to evaluate the correlation and diagnostic accuracy of three invasive methods [rapid urease test (RUT), histology and bacterial culture] and one non-invasive method (IgG serology) for diagnosis of H. pylori infection in a prospective cohort study conducted on 50 symptomatic children between two and eighteen years of age. Endoscopies with gastric biopsies were performed for RUT, culture and histopathological examination, respectively. IgG antibodies were measured in patient sera using a commercially available enzyme-linked immunosorbent assay (ELISA). RUT and positive H. pylori IgG antibodies were concordant in 88% (44/50) of patients. Both tests were negative in 32% (16/50), and both were positive in 56% (28/50). Disagreement occurred in 12% (6/50) of the patients: three of them (6%) had positive RUT and negative H. pylori IgG, and another three (6%) had negative RUT and positive H. pylori IgG. A combination of RUT with non-invasive serology constituted the optimum approach to the diagnosis of H. pylori infection in symptomatic children. The non-invasive serological test (ELISA) could not be used alone as the gold standard because it cannot distinguish between active and recently treated infection; and bacterial culture could not be used alone because of its low sensitivity.

Figure 1

A section of stomach antrum in a Helicobacter pylori-infected patient showing (1-a) rod-shaped organism (arrow) stained blue along the luminal surface and in the luminal mucosa (Giemsa ×1000). (1-b) Chronic inflammatory cells (C) infiltrate the foveolar epithelium and superficial lamina propria and lymph follicle with germinal cap (F) present in the lower portion of mucosa (H&E ×100). (1-c) Heavy infiltration of full thickness of mucosa with chronic inflammatory cells (C) and the glands (G) are compressed (H&E ×400).

Figure 2

A section of stomach antrum in a Helicobacter pylori-infected patient showing (2-a) atrophy of the gastric mucosa (arrow) (H&E ×200). (2-b) Intestinal type of columnar epithelium with goblet cells (arrow) replaced atrophic gastric mucosa and with mild infiltration of the lamina propria by chronic inflammatory cells (C) (H&E ×200). (2-c) Intestinal type of columnar epithelium with goblet cells (arrow) stained blue with alcian blue replaced atrophic gastric epithelial cells and glands and with mild infiltration of lamina propria by chronic inflammatory cells (C) (Genta ×200).

Figure 3

Scanning electron micrograph of a section of stomach antrum in Helicobacter pylori-infected patient showing (3-a) pili and ruffle formation of Helicobacter pylori (arrow) on the gastric epithelial cells (×800). (3-b) Degeneration and necrosis of gastric epithelial cells (×600).

Figure 4

Transmission electron micrograph of a section of stomach antrum in Helicobacter pylori-infected patient showing (4-a) gastric lumen (L) and spiral bacteria (S) adherent by filament-like structure (arrow) to gastric epithelial cells and its cytoplasm contain numerous electron dense secretory granules (E) (×20,000). (4-b) Intestinal metaplastic columnar absorptive cells with surface microvilli (M) and intracytoplasmic Helicobacter pylori (arrow) (×17,000).