IgG subclass response to Helicobacter pylori in patients with chronic active gastritis and duodenal ulcer.

The IgG subclass response is determined by the type of bacteria producing the infection and by genetic factors of the host. Patients with a Helicobacter pylori infection develop a specific immune response that is mainly of the IgA and IgG class. We measured the IgG subclass response in 20 patients with chronic active gastritis without a history of duodenal ulcer and 20 patients with chronic active gastritis and duodenal ulcer diagnosed by endoscopy and histology. A control group included 20 H. pylori-negative patients and 60 H. pylori-positive blood transfusion donors. Systemic IgG subclass response was measured with a modified enzyme-linked immunosorbent assay technique, using as antigen a sonicate of six different H. pylori strains. Mouse monoclonal antibodies against each of the four human IgG subclasses (IgG1, IgG2, IgG3, and IgG4) were used. The total IgG anti-H. pylori antibody titres were equal in all three H. pylori-positive groups and significantly different from that of the negative control group (p less than 0.01). The IgG subclass response in persons infected with H. pylori involved all four subclasses but was predominantly of the IgG1 and IgG2 subclasses. All of the groups with H. pylori infection had significantly higher levels of IgG1 than the negative control group, but no differences were detected among the three groups. However, the duodenal ulcer group had a significantly higher IgG2 response than the gastritis group (mean optical density +/- SEM, 0.382 +/- 0.047 versus 0.200 +/- 0.025, respectively; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Alpha-1-antitrypsin phenotypes and serum concentrations in duodenal ulcer patients in The Netherlands.

Hereditary alpha 1-antitrypsin (alpha 1-AT) deficiency has been suggested to be associated with peptic ulcer disease. Since the serum concentration of the enzyme is the result of both hereditary and nonhereditary factors, we have studied not only the serum levels but also the alpha 1-AT electrophoretic variants in 177 Dutch patients with duodenal ulcer disease and compared with 357 healthy blood donors. No relation was found between any of the alpha 1-antitrypsin phenotypes and duodenal ulcer disease. Serum levels of alpha 1-AT were significantly higher than in the controls in the patients. This study does not support an association between hereditary alpha 1-AT deficiency and duodenal ulcer disease, and makes therefore a possible role of such a deficiency in the etiology of peptic ulcer disease highly unlikely.

Serum pepsinogen I levels: assessment of gastric acid secretion?

We measured serum PG I levels by an Elisa technique before and after stimulation with pentagastrin in 260 patients (161 males and 99 females). The serum levels were correlated to basic acid output (BAO), maximum acid output (MAO) and peak acid output (PAO). The correlation coefficient between serum PG I and PAO varied between -0.482 and 0.744 depending on the diagnosis. This indicates that a simple measurement of PG I cannot replace the pentagastrin test in estimating gastric acid secreting capacity. However, since all patients who were achlorhydric had a serum PG I level of less than 50 micrograms/l the measurement of serum PG I can be recommended as a screening test for achlorhydria.

HLA and duodenal ulcer in The Netherlands.

Eighty-one Dutch patients with a duodenal ulcer (DU) were tested with respect to 24 HLA antigens. There was no significant difference in the distribution of HLA antigens between the DU patients and the controls. However, none of the 22 patients younger than thirty years at the onset of symptoms had HLA-Bw35, whereas among the 59 patients aged between thirty and eighty at the onset of symptoms, twelve had this antigen.