Comparison of fecal elastase-1 determination with the secretin-cholecystokinin test in patients with cystic fibrosis.

BACKGROUND: The secretin-cholecystokinin (CCK) test is the gold standard in the evaluation of exocrine pancreatic insufficiency. Because of its invasive character, it is of limited value in cystic fibrosis (CF) patients, especially in those with severe respiratory disease. The aim of the study was to evaluate the sensitivity of fecal elastase-1 in relation to the secretin-CCK test and quantitative fecal fat excretion in CF patients. METHODS: The study comprised 28 patients (11 females and 17 males) aged 4 to 20 years. In all patients the secretin-CCK test and determination of fecal elastase-1 concentration (with enzyme-linked immunosorbent assay) and fecal fat excretion were performed. RESULTS: The range of fecal elastase-1 was from undetectable to 485 microg/g (mean, 84.6+/-119.9 microg/g) and of fecal fat excretion from 1.0 to 55.1 g/day (mean, 15.0+/-12.2 g/day). On the basis of the results of the secretin-CCK test (and fecal fat analysis) exocrine pancreatic insufficiency was divided into three subgroups: mild (I), moderate (II), and severe (III). Four patients were classified in subgroup I, 4 in II and 20 in III. Fecal elastase (elastase-1) results were 332.0+/-124.9 microg/g in subgroup I, 96.9+/-45.7 microg/g in subgroup II, and 32.1+/-41.2 microg/g in subgroup III. The fecal elastase-1 sensitivity with a cut-off point of 200 microg/g was 89.3% for all patients, 100% for patients in subgroups II and III, but only 25.0% for patients in subgroup I; the specificity was 96.4%. Linear regression analysis showed a statistically significant correlation between fecal elastase (elastase-1) and duodenal volume, bicarbonate, amylase, lipase, and trypsin secretion (in all cases P < 0.001). CONCLUSIONS: Measurement of fecal elastase-1 is simple and very useful for assessing the exocrine pancreatic function in CF patients. Elastase is highly specific in severe and moderate exocrine pancreatic insufficiency, but it is rather unspecific for milder forms of pancreatic insufficiency.

Plasma concentrations of cholecystokinin and neurotensin in patients with cystic fibrosis.

BACKGROUND: Regulation of pancreatic exocrine secretion is controlled by vagovagal reflexes and hormones. A negative feedback control mechanism exists between the intraduodenal protease concentration and pancreatic enzyme secretion. In man cholecystokinin (CCK) is the major regulator of postprandial pancreatic enzyme secretion. There is a 50% reduction of meal-stimulated secretion by the specific CCK receptor antagonist loxiglumide, whereas atropine completely blocks postprandial secretion. Neurotensin is released postprandially by nerval reflexes and fat. It has been claimed that both hormones are increased in patients with pancreatic insufficiency. METHODS: We investigated CCK and neurotensin levels in patients with cystic fibrosis and pancreatic insufficiency. In 35 patients (2-24 years old) with cystic fibrosis with steatorrhea and in 15 patients (1.5-24 years old) with cystic fibrosis without pancreatic insufficiency pre- and post-prandial CCK and neurotensin plasma levels were measured 3 days after pancreatic enzyme therapy had been withdrawn. Nine patients (3-14 years old) who had no complaint of abdominal disease served as controls. RESULTS: Basal and postprandial CCK plasma levels did not differ statistically in the three groups, whereas basal and postprandial neurotensin levels were significantly increased in the cystic fibrosis groups. The severity of the disease had no effect on the neurotensin levels. CONCLUSIONS: Cystic fibrosis patients with severe pancreatic insufficiency did not have increased CCK plasma levels, suggesting that a CCK-mediated feedback mechanism of pancreatic enzyme secretion does not operate in our patients. In contrast, basal and postprandial neurotensin plasma levels were significantly increased in patients with cystic fibrosis but were independent of the severity of the pancreatic insufficiency.