R. Stockbrügger

Gastric Morphology and Function in Dermatitis Herpetiformis and in Coeliac Disease

Gastric acid secretory capacity was evaluated in 116 patients with dermatitis herpetiformis by means of the pentagastrin test. Endoscopic gastric mucosal biopsy specimens were obtained from both the body and the antrum in 90 of them. Forty-eight patients (41%) had a maximal acid output less than 10 mmol/h, and 30 of them (26%) were achlorhydric. The frequency of achlorhydria increased with age, and 27 out of 58 patients (47%) more than 50 years old were achlorhydric. Antrum-sparing chronic atrophic gastritis was present in 92% of the achlorhydric patients, and hypergastrinaemia and serum parietal cell antibodies were found in most of them. The prevalence of chronic gastritis of the body and of the antrum increased with age. There was no correlation between atrophic gastritis or achlorhydria and small-intestinal villous atrophy, the results of the D-xylose test, and blood folate and serum zinc determinations. The transferrin saturation index was lower in patients with achlorhydria. The frequency of achlorhydria was significantly higher in patients with dermatitis herpetiformis than in 69 patients with coeliac disease.

Endoscopic Duodenal Biopsy Compared with Biopsy with the Watson Capsule from the Upper Jejunum in Patients with Dermatitis Herpetiformis

Forty-eight patients with dermatitis herpetiformis were investigated with duodenoscopy, endoscopic biopsy, and conventional upper jejunal biopsy. Three endoscopic biopsy specimens were obtained from the duodenal bulb, three to six specimens from the second part of the duodenum, and one suction biopsy from the upper jejunum. In 60%, 71%, and 65% of the patients subtotal or partial villous atrophy was found in biopsies from the three levels, respectively. In eight patients (17%) mucosal abnormalities were confined to the duodenal biopsies and in two patients to the jejunal biopsies. The technique of endoscopic biopsy is advocated because multiple visually selected duodenal specimens may be obtained and because this technique also enables a complete evaluation of the stomach.

Inhibition of Gastric Acid Secretion by Pirenzepine (LS 519) in Man

Pirenzepine is a new tricyclic drug used in the treatment of peptic ulcer disease. The effect of two doses of pirenzepine (25 mg twice daily and 50 mg thrice daily) was examined in ten healthy volunteers during basal acid secretion and under stimulation with two doses of pentagastrin (0.166 microgram/kg . h and 1 microgram/kg.h given as continuous intravenous infusion). Serum drug concentrations were determined by radioimmunoassay, and parallel studies of the salivary function were performed. Pirenzepine, 25 mg twice daily, reduced basal acid output by 50% and 55%, respectively, and inhibited stimulated acid output by 31% and 26%, respectively. The higher dose of pirenzepine, 50 mg thrice daily, augmented the effect insignificantly despite markedly increased serum drug levels. The recommended therapeutic dose of 25 mg twice daily gave no salivary inhibition. Pirenzepine may have an anticholinergic effect on the parietal cell, although systemic side effects were not seen. Pirenzepine does not competitively inhibit pentagastrin-stimulated acid secretion.

Influence of Gluten-Free Diet on the Gastric Condition in 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.

Enzyme Substitution in Chronic Pancreatitis: Effects on Clinical and Functional Parameters and on the Hydrogen (H2) Breath Test

Ten patients with chronic pancreatitis (with abdominal pain and/or diarrhoea) were treated in a double-blind multiple cross-over trial with Pankreon granules 20 g per day or placebo during three periods of one month each. Pain and bowel habits were recorded. Faecal fat and breath hydrogen (H2) excretion were analyzed during the last days of each treatment period. The pain score was initially low in all patients and was not affected by enzymes. The number of daily bowel movements was reduced from 3.16 to 2.32 (n.s.). Faecal fat excretion per 72 hrs was reduced from 357 +/- 158 mmol free fatty acid to 226 +/- 98 mmol (p less than 0.05). With placebo treatment H2 excretion (from 60 and 180 min after a standard breakfast) was significantly increased compared with 19 healthy volunteers (p less than 0.05). It was not significantly reduced by enzymes. In 28 comparisons the H2 output between 60 and 180 min was correlated to faecal fat. In eight patients the oro-coecal transit-time could be determined by the H2 breath test. The transit-time did not differ from that of ten healthy volunteers and remained unchanged by enzymes. Carbohydrate maldigestion occurs parallel to fat maldigestion in chronic pancreatitis, and is not sufficiently reduced by 20 g of pancreatic enzymes.

The effect of pirenzepine on basal, pentagastrin- and insulin-stimulated gastric acid secretion in patients with peptic ulcer disease.

The effect of pirenzepine on basal and stimulated acid secretion was tested in five patients with peptic ulcer disease and gastric hypersecretion. Two types of stimulation were compared, namely pentagastrin by intravenous infusion (1 microgram/kg/h) and hypoglycaemia induced by insulin given subcutaneously (0.125 IU/kg). Basal acid output/30 min was reduced by 44% and 69%, respectively. Pentagastrin-stimulated acid output was reduced by 30%/120 min, and insulin-stimulated acid output by 47%. The reduction was similar during the first and second hour of stimulation in both series. These results strengthen our previous impression that pirenzepine may interfere with cholinergic receptors at the parietal cell level. As the inhibition of gastric acid secretion by pirenzepine is similar to that produced by oral doses of cimetidine, pirenzepine may be useful in the treatment of peptic ulcer disease.

Clinical results of parietal cell vagotomy and selective vagotomy with pyloroplasty in the treatment of duodenal ulcer. Two-year follow-up of a prospective randomized study.

Fifty patients were randomized in a consecutive series of parietal cell vagotomy (PCV) and selective vagotomy with pyloroplasty (SV +P) in the treatment of duodenal ulcer. There were no operative deaths, and the length of the hospital stay and time off from work were the same in both groups. The clinical results were evaluated at 1 and 2 years after operation. Within the first 3 years there were two recurrences after PCV and three after SV +P. The overall clinical result 2 years after surgery did not significantly differ between the two groups; 16/24 after PCV and 17/23 after SV +P classified as excellent results (Visick I). Significantly fewer patients had dumping after PCV (3/23) than after SV +P (13/22). No patient had diarrhoea postoperatively. It is concluded that parietal cell vagotomy gives less dumping than selective vagotomy with pyloroplasty. It is, however, too early to say whether the overall clinical result in a long-term follow-up favours PCV rather than SV +P.

Hydrogen (H2) Breath Excretion in Peptic Disease before and during Treatment with Ranitidine

Gastric juice pH, bacterial flora, and the H2 breath excretion were studied in patients treated with 150 mg ranitidine twice daily. The intragastric pH and bacterial contents rose during therapy. Before treatment upper respiratory tract bacteria were found in 4 of 23 patients and after 4 weeks of medication in 15 of 23. The median bacterial concentration was increased (p less than 0.01) and in five patients included bacteria normally found in the colon. Prolonged therapy for up to 12 weeks (n = 8) did not further change the bacteriologic pattern. Prophylactic treatment for 1 year (n = 3) showed gastric bacteria in high concentration, including Pseudomonas, in one patient. Postprandial H2 production remained unchanged after 4 (n = 23) and 12 (n = 7) weeks of therapy. In two of three patients treated prophylactically H2 excretion was increased after 1 year of medication. We conclude that acid reduction with ranitidine causes changes of the intragastric bacterial flora similar to those with other acid-reducing drugs in equipotent doses. The unchanged H2 breath test result after 4 and 12 weeks of treatment contradicts small-intestinal bacterial overgrowth. The elevated H2 excretion in two of the three patients after 1 year of treatment suggests the importance of a time factor in small-intestinal bacterial colonization.