Medical Treatment

Diagnosis

Noninvasive diagnostic tests for H. pylori include urea breath tests, stool tests and blood tests consisting of whole blood and serological assays. Invasive tests include upper gastrointestinal (UGI) endoscopy with gastric biopsy.

Due to multiple factors, noninvasive tests may not be optimal for the pediatric population. Because the performance of the urea breath tests requires some level of oral-pharyngeal coordination and the ability to breathe into a straw, it may be difficult to produce accurate results from young children. Due to the persistence of immunoglobulin G (IgG) antibodies that may last for months and possibly years, the serologic assays cannot differentiate between active or past infection. Finally, stool antigen tests have not shown uniform results, reducing their positive predictive values. Due to the limitations of noninvasive tests, an UGI endoscopy with biopsy remains the recommended diagnostic test.

Direct visualization and biopsies of the affected areas of the mucosa can determine the organic etiology of ulcer disease and gastritis. A histologic study, rapid urease testing, or tissue culture on biopsy can identify H. pylori.

The differential diagnosis of dyspepsia in children with peptic ulcer disease includes esophagitis, cholecystitis, liver disease, pancreatitis and infectious gastroenteritis. For children presenting with hematemesis, the differential diagnosis should include peptic ulcer disease, esophagitis, Mallory-Weiss tear and esophageal or gastric varices.

Medical treatment is attempted first, with greater than 80% of patients responding within 8 weeks of therapy. The treatment of peptic ulcer disease in children is similar to that employed in adults. Antacids and H₂-receptor antagonists are the mainstays of medical therapy.

The dominant pathway of parietal cell activation is paracrine stimulation of the histamine-2 (H₂) receptor by histamine. H₂ receptor antagonists (i.e., cimetidine, ranitidine, famotidine) inhibit parietal cell responses to all secretagogues and are the main form of therapy for peptic ulcer disease. H₂ antagonists are effective agents against peptic ulcer disease, with relapse rates of less than 20%.

Other medical treatment options include omeprazole, sucralfate and prostaglandin therapies. Omeprazole inhibits gastric secretion at the final common pathway, the H+-K+ adenosine triphosphatase pump. It is effective in healing ulcers in 95% of patients within 4 weeks. Sucralfate forms a protective coat on the gastric mucosa. The negative charge of the sulfated disaccharide aluminum salt of sucralfate adheres to the positive protein charge of the injured gastric mucosa. Sucralfate also seems to enhance mucosal microvascular flow, mucus production and prostaglandin secretion.

Eradication of H. pylori requires a combination of gastric acid antisecretory agents plus an antimicrobial agent administered for 10 to 14 days (Table 4.5). Once treated and cured, children are at a low risk for recurrence. Children with persistent symptoms may require repeat endoscopy. Failure of treatment may be secondary to noncompliance or to H. pylori antimicrobial resistance to metronidazole or clarithromycin.

Table 4.5

Three Recommended Combination Eradication Therapies for H. pylori-Associated Disease in Children

(North American Society for Pediatric Gastroenterology, Hepatology and Nutrition position statement)

The effectiveness of H₂-receptor antagonists and proton-pump inhibitors for the prevention of stress ulcers is extremely effective.