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.

Bacterial transformation of bile acids is possibly involved in colorectal carcinogenesis. In several epidemiological studies, the secondary bile acid concentration in feces is related to the incidence of colonic cancer. However, data on fecal bile acids in case-control studies are conflicting. We investigated the influence of age, intestinal transit time, and dietary composition on fecal bile acid profiles in healthy subjects of three different age groups (mean ages 22, 48, and 67 years). Fecal bile acids were analyzed by gas-liquid chromatography. The concentration of the major secondary fecal bile acids increased with advancing age and was significantly higher in elderly subjects, compared to young adults. The concentration in middle-aged persons was intermediate. Analysis of dietary constituents showed that the fat intake in the three groups was comparable. The dietary fiber intake in elderly subjects was significantly lower than in the other two groups. The former group did excrete less dry fecal material compared to both other groups. Dietary fiber intake was negatively correlated with the total bile acid concentration. Probably, a decrease in dietary fiber intake results in higher fecal bile acid concentrations with advancing age. From the findings of this study, it is obvious that matching for age is important when case-control studies concerning the role of fecal bile acids in colorectal carcinogenesis are conducted.

Ten healthy subjects received 200 micrograms of human CRF (hCRF) and 200 micrograms of ovine CRF (oCRF) as an intravenous bolus injection on two different occasions. After hCRF plasma ACTH levels rose significantly (P less than 0.0005, by Friedman's nonparametric analysis of variance) from a basal value of 35 +/- 3 pg/ml (mean +/- SEM) to a peak value of 80 +/- 7 pg/ml 30 min after hCRF administration. This ACTH response was followed by a rise in plasma cortisol levels (P less than 0.0005, by Friedman's test) from a baseline value of 0.32 +/- 0.03 mumol/l to a peak value of 0.56 +/- 0.02 mumol/l 60 min after hCRF. Ovine CRF elicited similar rises in the plasma ACTH and cortisol levels. However, as derived from the faster rate of decline of ACTH and cortisol after hCRF than after oCRF, human CRF had a significantly shorter duration of action than ovine CRF in humans. Human CRF not only stimulated ACTH release by the human pituitary gland but also prolactin release. After hCRF administration prolactin levels rose significantly (P less than 0.005, by Friedman's test) from a basal value of 179 +/- 18 mU/l to a peak value of 288 +/- 34 mU/l at 10 min.

Shortly after intravenous injection of ""'Tech

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