gastrins and Dermatitis-Herpetiformis

Achlorhydric atrophic gastritis occurs in approximately 25% of patients with dermatitis herpetiformis (DH). The effect of gluten withdrawal on the gastric condition was studied in 35 patients, with a control group of 20 patients continuing their habitual diet. Gastrointestinal examinations were performed initially and repeated after about 1 3/4 years. Adherence to the diet was confirmed by dietary interviews, improvement of malabsorption test results and intestinal villous structure, and decreased dapsone requirement. Neither the non-restricted diet nor the gluten-free diet had any effect on gastric morphology, the ability to secrete gastric acid, serum gastrin levels, or the frequency or titres of circulating parietal cell antibodies. The findings indicate that gluten is not responsible for the perpetuation of the gastric affection in DH, in contrast to the enteropathy.

Topics: Adolescent; Adult; Aged; Antibodies; Dapsone; Dermatitis Herpetiformis; Female; Follow-Up Studies; Gastric Acid; Gastrins; Gastritis; Gastritis, Atrophic; Glutens; Humans; Intestinal Absorption; Intestine, Small; Male; Middle Aged; Parietal Cells, Gastric; Stomach

Gastric mucosal histology and function were evaluated in 57 Italian subjects with dermatitis herpetiformis (DH), by means of multiple endoscopic biopsies, gastrin and pepsinogen I (Pg I) serum levels, and parietal cell antibodies (PCA). One hundred and forty-nine patients with nonulcer dyspepsia served as reference population for the prevalence of atrophic gastritis of the body. Seventeen DH patients (30%) and 23 controls (15.4%) showed atrophic gastritis of the body mucosa (p less than 0.05). Nine of the DH patients with atrophic gastritis of the body also had atrophic changes in the antrum. Six patients, all with severe atrophic gastritis, had high gastrin levels and PCA; five of these six also had low Pg I levels. We found an increased prevalence of abnormal indirect function tests among patients with atrophic gastritis is due to the younger age of the patients in our series. Thus, atrophic gastritis can be detected early on a histologic basis, but functional impairment occurs later, as the mucosal damage increases in severity.

Topics: Adolescent; Adult; Age Factors; Aged; Autoantibodies; Dermatitis Herpetiformis; Female; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Italy; Male; Middle Aged; Parietal Cells, Gastric; Pepsinogens; Prevalence

The individual daily intake of gluten was calculated in 45 patients with dermatitis herpetiformis (DH) on the basis of a depth interview about food habits. Gastric and small intestinal morphology and function were studied concurrently. Mean daily gluten intake was estimated to be 15 g, a figure which corresponds well to the average gluten intake in Sweden. There was a significant correlation between the degree of morphological mucosal changes of the small intestine and the quantity of gluten ingested. All patients with jejunal villous atrophy consumed more than 10 g gluten daily and all but one patient with normal jejunal villous structure had a gluten intake of less than 10 g/d. The findings suggest a dose-dependent effect of gluten on the intestinal mucosa. Conversely, the daily gluten intake was not correlated to gastric morphology, gastric acid secretion, serum gastrin levels or serum parietal cell antibodies. Patients with reduced ability to secrete gastric acid did not differ from the remaining patients in this respect. Whereas the coeliac-like enteropathy in DH seems to be caused by ingested gluten, the frequently occurring achlorhydric atrophic gastritis must be assumed to be of different immunopathogenesis.

Topics: Achlorhydria; Adolescent; Adult; Aged; Celiac Disease; Dermatitis Herpetiformis; Duodenum; Feeding Behavior; Female; Gastric Acid; Gastric Mucosa; Gastrins; Glutens; Humans; Intestinal Mucosa; Jejunum; Male; Middle Aged

In order to study the development of atrophic gastritis, gastric secretory function was examined by a standard pentagastrin test 24 to 78 months after a previous examination (Ex I). The study included 12 patients with dermatitis herpetiformis (DH), 6 patients with functional signs of atrophic gastritis previously, and 8 healthy controls. The surrent examination (Ex II) also included microbiological culture of gastric juice and estimation of gastrin(s), parietal cell and thyroidal antibodies. Most of the controls had increased their maximum acidity and maximum acid output (MAO) between the examinations. This may indicate an altered potency of pentagastrin in recent years. Conversely, 5 of the 6 patients with atrophic gastritis showed a further reduction of maximum acidity and MAO, indicating progressive parietal cell atrophy. In the DH-group, two tendencies were observed: 6/12 patients had an increased MAO at Ex II. They had had lower mean age and higher mean MAO at Ex I, as compared with the remaining 6 patients who had a decreased MAO at Ex II. The latter group more often had parietal cell antibodies.

Topics: Adult; Aged; Dermatitis Herpetiformis; Female; Gastric Juice; Gastrins; Gastritis; Humans; Male; Middle Aged

Seventeen patients with dermatitis herpetiformis were tested for gastric hydrochloric acid secretion. Seven were found to be achlorhydric. Atrophic gastritis in these patients probably had an auto-immune pathogenesis, as judged by elevated serum gastrin level, high prevalence of antibodies against gastric parietal cells and antrum sparing of the gastric atrophy. This type of atrophic gastritis is considered to indicate a precursor state to pernicious anemia.

Topics: Adult; Aged; Autoantibodies; Autoimmune Diseases; Bile Acids and Salts; Dermatitis Herpetiformis; Female; Gastric Juice; Gastrins; Gastritis; Humans; Male; Middle Aged; Secretory Rate; Stomach