Association of CagA-positive infection with Helicobacter pylori antibodies of IgA class.

cagA gene, the best known virulence factor of Helicobacter pylori, codes for an immunodominant CagA protein. In this study, CagA antibodies of the IgG class were measured by immunoblot or enzyme immunoassay in subjects with positive H. pylori serology, and the presence of CagA antibodies was compared with that of H. pylori antibodies of IgA and IgG classes. Serum samples were available for a total of 1,481 subjects, including gastroscopied patients with biopsy-verified H. pylori infection, smoking men with a normal or low serum pepsinogen I level indicating atrophic corpus gastritis, and subjects who later developed gastric cancer and their matched controls. CagA antibodies were significantly more prevalent among individuals with elevated H. pylori antibody titres of the IgA class than in those with IgG antibodies only, with the exception of a small subgroup of individuals who later developed gastric cancer. CagA-positive H. pylori strains seem to induce an immune response with a markedly higher frequency of IgA than what is found in inflammation caused by CagA-negative strains. The presence of serum IgA antibodies to H. pylori seems to indicate a higher risk for CagA-positive H. pylori infection and possibly more severe late sequelae of the disease.

Spontaneous rupture and functional state of the esophagus.

Esophageal function was investigated after 1 to 8 years in five consecutive patients surviving spontaneous esophageal rupture (Boerhaave's syndrome) and treated by suturation. Only one patient was symptom free and had almost normal esophageal function as judged by manometry, 24-hour pH monitoring, endoscopy, and barium swallow. In the other four patients reflux symptoms and a severe functional disturbance of the esophagus were observed. In four patients the manometry revealed a lack of propulsive peristaltic movements and esophageal muscular incoordination (particularly in the upper part of the esophagus) closely mimicking those seen in the nonspecific esophageal motility disorder. In 24-hour intraesophageal pH monitoring a pathologic gastroesophageal reflux with long-lasting single reflux periods was observed, suggesting poor esophageal clearance. Also endoscopic and histologic signs of reflux esophagitis were seen in the same four patients. In contrast, lower esophageal sphincter pressure was normal in all five survivors. It is concluded that patients with spontaneous esophageal rupture have a severe disturbance of esophageal motility. The concomitant reflux esophagitis may be caused primarily by the esophageal motility disturbance, which may also contribute to the origin of the rupture.