Atopic features in patients with ulcerative colitis

Abstract

SOFPAPERS 1153 ATOPIC FEATURES IN PATIENTS WITH ULCERATIVE COLITIS. R. V. Heatley, J. Rhodes, D. L. Roberts. Department of Gastroenterology, University Hospital of Wales, Cardiff, Great Britain. A questionnaire was used to establish the prevalence of atopic features in 250 patients with ulcerative colitis, 126 of whom had an ileostomy. Data was also collected from 260 matched controls. The spouses served as controls, giving matched pairs in 106 cases, while the other controls came from a dental outpatients' department. The questionnaire was completed by interview in 140 of the patients and 180 of the controls; the remainder were completed by post. Allergic rhinitis (20% compared with 11X), eczema (21% compared with 9%) and a family history of atopic manifestations (31% compared with 17%) were all more common in patients. There was no significant difference in the prevalence of asthma and hay fever between the two groups. The findings support previous suggestions that colitis is associated with atopic features and lends some support to the hypothesis that a reaginic reaction may be important at some stage in the pathogenesis of ulcerative colitis. LACTOFERRIN LEVELS IN BLOOD, DUODENAL JUICE AND PURE PANCREATIC JUICE IN THE DIAGNOSIS OF PANCREATIC DISEASES. S.S. Fedail, R.F. Harvey, P.R. Salmon and A.E. Read University Department of Medicine, Bristol Royal Infirmary, Bristol, England. A sensitive and specific radioirmnunoassay for lactoferrin has been developed (Fedail et al 1978). The assay was used to measure lactoferrin in plasma, duodenal juice in the basal state and following secretin stimulation, and in pure pancreatic juice obtained endoscopically. Plasma lactoferrin was measured in 12 control subjects and in 10 patients with chronic pancreatitis. Plasma levels in controls were (mean + 1SD) 1942 + 717 ng/ml, in patients with chronic pancreatiTis 6095 + 4742 ng/ml, the difference was statistically significant TP(O.05). Lactoferrin levels in duodenal juice were not significantly different in control subjects compared with patients with chronic pancreatitis. Patients with severe pancreatitis tended to have very high levels. Lactoferrin was also measured in pure pancreatic juice obtained from 23 patients with chronic pancreatitis; 16 control subjects and 10 patients with pancreatic cancer. The median lactoferrin level in controls was 73 ng/ml, range 16-390 ng/ml; in patients with chronic pancreatitis 2310 ng/ml, range 870-11400 nglml; in pancreatic cancer 105 ng/ml range lo-387 ng/ml. In a single patient with both cancer and pancreatitis lactoferrin was high 1300 ng/ ml. Pure pancreatic juice lactoferrin levels distinguish between those with chronic pancreatitis and those with either pancreatic cancer or normal pancreas. MOl-eOVer lactoferrin levels tend to correlate with the severity of pancreatitis as measured by pancreatography. Plasma and duodenal juice lactoferrin show a similar trend but there is considerable overlap between the different groups. Fedail, S.S., Harvey, R.F., Salmon, P.R., Read, A.E. (1978) Lancet I (in press) ROLE OF CELLULAR CALCIUM IN MODULATING THE INITIAL ACTION OF CHOLECYSTOKININ ON PANCREATIC ACINAR CELLS. R. Lopatin and J.D. Gardner. National Institutes of Health, Bethesda, Md. The initial steps in the action of CCK and carbachol on pancreatic acinar cells are to cause a 6-fold increase in the rate of release of membrane-bound calcium and a lofold increase in cellular cyclic GMP. In the present studies we have used dispersed acinar cells from guinea pig pancreas to examine the extent to which changes in cellular calcium can modify the actions of CCK n cellular cyclic GMP. In acinar cells preloaded @,;i ~~;e~,;;cubated with EDTA, membrane-bound t5: ring the first 15 minutes of incubation after which bound Ca decreased at a rate of 0.4% per minute. Under identical conditions the increase in cellular cyclic GMP caused Sy CCK was reduced by 50%. This decrease was maximal by 2 minutes of incubation without calcium and remained constant thereafter. In acinar cells preincubated without extracellular calcium, adding calcium caused a time-dependent increase in the action of CCK on cellular cyclic GMP and by 10 minutes the CCK-induced increase in cyclic GMP was equal to that in cells preincubated with calcium. Extracellular calcium concentrations of l.OmM or greater prevented the decrease in the action of CCK on cellular cyclic GMP. Magnesium, alone or in the presence of calcium, did not alter the increase in cellular cyclic GMP caused by CCK. Although removing extracellular calcium reduced the magnitude of the increase in cyclic GMP caused by CCK, there was no change in the maximally or minimally effective concen;t;$,ons of CCK. Increased cyclic Ge8was detected with M CCK, and was maximal at 3 x 10 M. These results indicate that the effect of removing extracellular calcium results from a decrease in cellular calcium, and that in pancreatic acinar cells there is a rapidly exchanging component of cellular calcium that functions to control the action of CCK on guanylate cyclase and by so doing influences cellular accumulation of cycle