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In six patients suffering from severe early dumping and six patients with late dumping after peptic ulcer surgery, the effect of the somatostatin analogue SMS 201-995 was compared with placebo. In early dumpers subcutaneous administration of 50 micrograms SMS 201-995 prior to meal ingestion induced a strong improvement of dumping symptoms as reflected by a decrease of the Sigstad dumping score from 12 +/- 2 during placebo to 5 +/- 2 (p less than 0.05). Furthermore, the postprandial increase of pulse rate was abolished; maximum pulse rate decreased from 85 +/- 7 beats/min to 67 +/- 7 beats/min (p less than 0.05). SMS 201-995 did not significantly affect postprandial changes in packed cell volume. In late dumpers 50 micrograms SMS 201-995 reduced peak plasma insulin after oral glucose from 173 +/- 16 mU/L during placebo to 35 +/- 9 mU/L during SMS 201-995 (p less than 0.05) and increased individual plasma glucose nadirs from 1.9 +/- 0.3 mmol/L to 7.5 +/- 3.3 mmol/L (p less than 0.01). Both in early and late dumpers SMS 201-995 improved postprandial expiratory breath hydrogen excretion indicating slowing of gastrointestinal hurry. SMS 201-995 is a powerful therapeutic agent for the management of patients suffering from the dumping syndrome after gastric surgery.

Secondary bile acids have been implicated in colonic carcinogenesis. Transformation of primary into secondary bile acids (7 alpha-dehydroxylation) in the large bowel is a pH-dependent process. Inhibition of this reaction could be achieved by lowering colonic pH. We, therefore, studied the effects of lactulose (a non-absorbable disaccharide), which is capable of acidifying colonic contents, on secondary bile acid metabolism. Because this metabolism is age dependent, lactulose was given (0.3 g kg-1 twice daily for 12 weeks) to nine middle-aged (age 31-54 years; mean 45.7) and ten elderly subjects (age 56-81 years; mean 66.4). Twice before, and after 6 and 12 weeks' lactulose administration, biliary and faecal bile acids, whole gut transit time, faecal weight and dry weight, and faecal pH were recorded. The concentration of (iso)lithocholic and deoxycholic acid in faeces was higher in elderly subjects (P less than 0.05) but the excretion was comparable. After lactulose the concentration and excretion of the major secondary bile acids decreased. The primary bile acid fraction rose from 5% before, to more than 20% after, lactulose (P less than 0.05). Faecal weight increased and faecal dry weight decreased, resulting in a higher faecal water output during lactulose. Whole gut transit time did not change. The faecal pH dropped after 6 (P less than 0.05) and further after 12 weeks' lactulose (P less than 0.05). The percentage deoxycholic acid in bile was higher, and cholic acid lower, in elderly subjects (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Abstract. Class specific anti‐IgA (anti‐α) antibodies were found in seven out of sixteen patients in whom serum IgA was not demonstrable by the Mancini method (sensitivity down to 0.02 mg/ml). Allotype specific anti‐IgA [anti‐A2m(l)] antibodies were found in an eighth patient. The anti‐IgA antibodies proved to be of the IgG class. In the eight patients with anti‐IgA antibodies, the presence of these antibodies could not be ascribed to immunization by administration of blood products. Isoimmunization in pregnancy and absorption of colostral IgA or animal IgA were other possible causes of anti‐IgA antibodies.–Using a combined IgA/anti‐IgA radioimmunoassay very low IgA levels (0.00013‐0.020 mg/ml) were demonstrable in patients without anti‐IgA antibodies whose serum IgA levels could not be determined by the Mancini method.–IgA metabolism was studied in five IgA‐deficient patients. In two patients the rate of degradation of 132I‐IgA almost equalled that in individuals with a normal serum IgA level. In three patients, however, the rate of degradation was greatly increased. In their sera, in contrast to the first two, class specific anti‐a antibodies were demonstrated.–One of these patients showed an anaphylactic reaction immediately after intravenous injection of mI‐IgA. Only this patient showed complement fixation by the IgA/anti‐IgA complex and IgA stimulation of lymphocytes.–The presence of anti‐IgA antibodies has some important practical implications for those patients who need blood products.