Duodenogastric reflux in patients with gastric ulcer disease.

We studied reflux of duodenal contents into the stomach in patients with gastric ulcers, patients with duodenal ulcers, and normal subjects. Duodenogastric reflux was assessed in the fasting state and after cholecystokinin octapeptide administration (0.02 micrograms/kg intravenously). Slight reflux was observed in the fasting state in all three groups. However, after cholecystokinin octapeptide administration, reflux was significantly greater in gastric ulcer patients than in control patients for pancreatic phospholipase A2 (p less than 0.01) and lysophosphatidylcholine (p less than 0.001). Also in gastric ulcer patients, the gastric contents were significantly more alkaline (pH 5.26 +/- 0.58, p less than 0.001) during duodenogastric reflux than in normal subjects (pH 3.65 +/- 0.50) or duodenal ulcer patients (pH 2.67 +/- 0.63). Our results suggest that reflux of both pancreatic and biliary secretions might contribute to the gastric mucosal injury in gastric ulcer patients and we postulate that pancreatic phospholipase A2 might have a greater role in this process than has been previously acknowledged.

Transient pure red-cell aplasia: cell-mediated suppression of erythropoiesis associated with hepatitis.

Transient pure red-cell aplasia is a rare complication of persistent acute hepatitis. We have investigated possible mechanisms for marrow suppression in one such patient who developed erythroid aplasia in the course of transfusion-related hepatitis. The patient's lymphocytes, obtained during the acute illness, markedly inhibited erythroid colony formation by donor marrow. After the patient recovered, remission lymphocytes in co-culture did not inhibit colony formation. No reversible suppression was demonstrable by addition of patient serum. These observations suggest that hematocytopenias associated with hepatitis may result from cell-mediated suppression induced by hepatic injury.

Factors influencing small bowel changes in dermatitis herpetiformis.

Factors influencing small bowel morphology in dermatitis herpetiformis (DH) were investigated by comparing patients with DH and normal small bowel biopsies to patients with DH and abnormal small bowel biopsies. The mean age of 18 patients with morphological changes in small bowel (38 years) was significantly lower (P less than 0-001) than the mean age of nine patients with normal bowel mucosa (60 years). HLA typing confirmed the high frequency of HLA-B8 in DH (64%) but HLA-B8 was unrelated to the presence or severity of small bowel lesions. Four patients had diarrhoea with progressive weight loss or abdominal cramps subsequently responsive to gluten withdrawal. In this subgroup serum levels of IgG and IgM were significantly lower than in patients with normal small bowel mucosa. Small bowel involvement appeared to be independent of the duration and severity of skin disease, and the deposition of immunoglobulin and complement (C3) in the dermal papillae of skin adjacent to skin lesions.