cholecystokinin and Celiac-Disease

Topics: Celiac Disease; Cholecystokinin; Delayed Diagnosis; Gallbladder Diseases; Gallbladder Emptying; Humans

Coeliac disease is a chronic, small intestinal, immune-mediated enteropathy caused by a permanent intolerance to dietary gluten in genetically predisposed individuals. Clinical studies have found that intestinal cholecystokinin secretion and gallbladder emptying in response to a fatty meal are impaired before coeliac patients start the gluten-free diet (GFD).. However, it was never really appreciated whether coeliac disease is associated with gallstones because there were very few studies investigating the mechanism underlying the impact of coeliac disease on the pathogenesis of gallstones.. We summarize recent progress on the relationship between coeliac disease and gallstones and propose that coeliac disease is an important risk factor for gallstone formation because defective intestinal cholecystokinin secretion markedly increases susceptibility to cholesterol gallstones via a mechanism involving dysmotility of both the gallbladder and the small intestine. Because GFD can significantly improve the coeliac enteropathy, early diagnosis and therapy in coeliac patients is crucial for preventing the long-term impact of cholecystokinin deficiency on the biliary and intestinal consequences. When gluten is reintroduced, clinical and histologic relapse often occurs in coeliac patients. Moreover, some of the coeliac patients do not respond well to GFD.. It is imperative to routinely examine by ultrasonography whether gallbladder motility function is preserved in coeliac patients and monitor whether biliary sludge (a precursor of gallstones) appears in the gallbladder, regardless of whether they are under the GFD programme. To prevent gallstones in coeliac patients, it is urgently needed to investigate the prevalence and pathogenesis of gallstones in these patients.

Topics: Animals; Celiac Disease; Cholecystokinin; Disease Models, Animal; Forecasting; Gallbladder Emptying; Gallstones; Humans; Intestine, Small; Mice, Knockout; Receptors, Cholecystokinin; Risk Factors

Topics: Abdomen; Biopsy; Carcinoma, Intraductal, Noninfiltrating; Celiac Disease; Cholecystokinin; Diabetes Mellitus; Hepatomegaly; Humans; Jaundice; Laparotomy; Mental Disorders; Pain; Palliative Care; Pancreatectomy; Pancreatic Neoplasms; Prednisolone; Prognosis; Radioisotopes; Radionuclide Imaging; Secretin; Selenium

Topics: Bile; Binding Sites; Celiac Disease; Cholecystokinin; Cholestyramine Resin; Diarrhea; Diet Therapy; Digestion; Fatty Acids, Nonesterified; Humans; Hydrolysis; Malabsorption Syndromes; Neomycin; Phospholipids; Secretin; Triglycerides

Topics: Amylases; Celiac Disease; Cholecystokinin; Duodenum; Fasting; Food; Food Analysis; Humans; Intubation, Gastrointestinal; Liver Diseases; Pancreas; Pancreatic Diseases; Pancreatic Neoplasms; Secretin; Time; Trypsin

Topics: Celiac Disease; Cholecystokinin; Digestion; Gastrins; Gastrointestinal Hormones; Homeostasis; Humans; Postgastrectomy Syndromes; Secretin; Vagotomy; Zollinger-Ellison Syndrome

To further establish its role in the ileal brake mechanism, we determined the effect of the distal gut hormone peptide YY (PYY) on gallbladder motility and plasma gut hormones during the cephalic phase of meal stimulation.. Eight healthy volunteers were studied in a randomized crossover design, with or without intravenous infusion of a physiological dose of PYY. On each occasion, subjects underwent modified sham feeding followed by real feeding.. PYY reduced gallbladder emptying in response to modified sham feeding from 23 +/- 5% to 5 +/- 7% (P < 0.01) and integrated plasma pancreatic polypeptide from 2337 +/- 397 pmol/L x 90 min to 903 +/- 232 pmol/L x 90 min (P < 0.01). PYY enhanced plasma cholecystokinin in response to real feeding from 53 +/- 9 pmol/L x 90 min to 82 +/- 17 pmol/L x 90 min (P < 0.05), but did not significantly affect maximum gallbladder emptying and tended to decrease plasma pancreatic polypeptide.. Circulating PYY suppresses the cephalic phase of postprandial gallbladder emptying, but not meal stimulated maximum emptying. The results support the hypothesis that the effect of PYY on gallbladder emptying is mediated by vagal-dependent rather than cholecystokinin-dependent pathways.

Topics: Adult; Celiac Disease; Cholecystokinin; Cross-Over Studies; Fasting; Female; Food; Gallbladder Emptying; Humans; Injections, Intravenous; Male; Middle Aged; Pancreatic Polypeptide; Peptide YY; Vagus Nerve

Topics: Adult; Aged; Celiac Disease; Cholecystokinin; Chymotrypsin; Clinical Trials as Topic; Colonic Diseases, Functional; Feces; Female; Humans; Male; Middle Aged; Pancreas; Pancreatic Diseases; Secretin

Celiac disease is an autoimmune enteropathy caused by a permanent intolerance to dietary gluten in genetically predisposed individuals. Cholecystokinin (CCK) release from the proximal small intestine and gallbladder emptying in response to a fatty meal are greatly reduced in celiac patients before they start the gluten-free diet, showing a genetic predisposition to gallstones.. To elucidate the complex pathophysiological mechanisms determining the biliary characteristic of celiac disease, we investigated the effect of the absence of endogenous CCK on cholesterol crystallization and gallstone formation in mice fed a lithogenic diet for 28 days.. Fasting gallbladder volumes were increased and the response of gallbladder emptying to the high-fat diet was impaired in CCK knockout (KO) mice compared to wild-type mice. Because of the absence of CCK, small intestinal transit time was prolonged and intestinal cholesterol absorption was increased. During 28 days of feeding, elevated biliary cholesterol concentrations and gallbladder stasis promoted the growth and agglomeration of solid cholesterol crystals into microlithiasis and stones. Thus, cholesterol crystallization and gallstone formation were accelerated in CCK KO mice. In contrast, daily intraperitoneal administration of CCK-8 reduced gallstone formation in CCK KO mice even on the lithogenic diet.. The lack of endogenous CCK enhances susceptibility to gallstones by impairing gallbladder contractile function and small intestinal motility function. These findings show that celiac disease is an important risk factor for gallstone formation and the gallbladder motility function should be routinely examined by ultrasonography and gallbladder stasis should be prevented in celiac patients.

Topics: Animals; Bile; Celiac Disease; Cholecystokinin; Gallbladder Emptying; Gallstones; Gastrointestinal Transit; Mice; Mice, Inbred C57BL; Mice, Knockout; Real-Time Polymerase Chain Reaction

The aim of this study was to evaluate the concept that pancreatic dysfunction in patients having gluten sensitivity (celiac disease [CD]) or cow's milk protein enteropathy (CMPE) may result from the lack of pancreatic enzyme stimulation in the absence or decrease of cholecystokinin (CCK) secretion caused by villous atrophy.. The following parameters were measured: plasma CCK in response to a fatty meal and human pancreatic fecal elastase in 24 patients with CD while on gluten-free diet and after gluten provocation and in 12 patients with CMPE at diagnosis and after a 6-month period of cow's milk-free diet. Intestinal mucosa morphology was examined by small bowel biopsy. Sixty-three controls having no organic gastrointestinal problems were investigated once at the time of diagnostic evaluation.. Fasting CCK, obtained at a time when patients with CD or CMPE had normal intestinal mucosa, was significantly different from postprandial and comparable to that of the control group. Fasting CCK obtained from patients with villous atrophy was also statistically different, but not significantly, from the postprandial. Fasting and postprandial plasma CCK and fecal pancreatic elastase values from patients having normal intestinal mucosa were significantly higher than those obtained from patients with villous atrophy. Significant correlation of intestinal mucosa morphology and CCK with fecal elastase concentration was documented.. Exocrine pancreatic dysfunction in individuals having villous atrophy may be the consequence of decreased CCK secretion. Cholecystokinin and pancreatic secretion is restored to normal, with intestinal mucosa regeneration.

Topics: Adolescent; Atrophy; Biopsy; Celiac Disease; Child; Child, Preschool; Cholecystokinin; Dietary Fats; Feces; Female; Humans; Infant; Intestinal Mucosa; Intestines; Male; Milk Hypersensitivity; Milk Proteins; Pancreas; Pancreatic Elastase; Sincalide

Cholecystokinin (CCK) release after a standard test meal is decreased in coeliac patients. The aim of the study was to determine the origin of the CCK deficiency and the relationship between the distinctive types of mucosal lesions observed in coeliac disease and the number of duodenal CCK cells and their peptide and mRNA content. Duodenal biopsies were obtained in ten controls and nineteen coeliac patients [seven with atrophic mucosa, six with increased numbers of intraepithelial lymphocytes (IELs) and six with fully normalized mucosa]. Immunocytochemistry was performed with a CCK C-terminal-specific polyclonal antiserum. The CCK cells were counted and related to the epithelial area using a semi-automated image analyser. CCK content in mucosal extracts was determined by radioimmunoassay. mRNA was measured with a semi-quantitative reverse transcriptase-PCR method using specific CCK and ribosomal protein L19 (RPL19) primers. CCK tissue concentration and CCK mRNA were significantly reduced in patients with atrophic mucosa [12.2 (range 6.9-17.5) pmol/g; CCK/RPL19 ratio 0.64 (0.30-0.99)] compared with patients with normal mucosa [40.5 (30.4-50.7) pmol/g; CCK/RPL19 ratio 1.40 (0.41-2.40)] or controls [42.7 (18.2-67.2) pmol/g; CCK/RPL19 ratio 1.35 (1.09-1.62)]. A similar decrease was observed in patients with an excess of IELs, 13.9 (3.8-31.8) pmol/g and 0.86 (0.57-1.15) pmol/g respectively. The number of CCK cells was, however, similar in all groups. Duodenal CCK concentration and mRNA are decreased not only in the mucosa presenting atrophic changes but also when disease activity is limited to infiltration by IELs. Reduced expression of the CCK gene could therefore be related to suppressive factors induced by the inflammatory infiltrate.

Topics: Adult; Case-Control Studies; Celiac Disease; Cell Count; Cholecystokinin; Duodenum; Female; Humans; Image Processing, Computer-Assisted; Intestinal Mucosa; Lymphocyte Count; Lymphocytes; Male; Radioimmunoassay; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger

Celiac disease is associated with impaired cholecystokinin (CCK) release. The mechanism by which CCK release is impaired is poorly understood and seems to be related to the mucosal atrophy or to decreased stimulation due to reduced intraduodenal nutrient hydrolysis. The aims of our study were to evaluate basal and postprandial CCK in celiac patients presenting with distinctive types of mucosal lesions (normal, infiltrative and atrophic), and to study the role of protein hydrolysis on CCK release. Plasma CCK was measured in 20 celiac patients (normal mucosa: n=6; infiltrative type: n=6; atrophic type=8) and 9 controls, before and after ingestion of a polymeric or a semi-elemental meal. Significant decreases in basal CCK plasma (B 0.6 [95% CI, 0.3-1.3] pmol/l; p<0.003) and postprandial CCK area under curve (AUC 34 [19-61] pmol/l x 120 min, p<0.0001) were observed in patients with an atrophic mucosa compared with treated patients (B 1.6 [1.0-2.4] pmol/l, AUC 267 [172-414] pmol/l x 120 min) or healthy volunteers (B 1.0 [0.7-1.4] pmol/l, AUC 186 [131-264] pmol/l x 120 min). A significant defective CCK release was also observed in patients with an infiltrative type: B 0.4 [0.2-0.7] pmol/l and AUC 56 [31-101] pmol/l x 120 min; p<0.0001. Administration of a semi-elemental diet did not correct the defective CCK release. In conclusion, the decreased CCK levels observed in celiac patients are not strictly related to the mucosal atrophy but rather to the lymphocytic infiltrate. Administration of a predigested meal did not correct the impaired CCK release. Some inhibitory mechanism could be involved in the CCK cell dysfunction observed in celiac patients presenting with lesser degrees of disease activity.

Topics: Adult; Area Under Curve; Atrophy; Celiac Disease; Cholecystokinin; Dietary Proteins; Female; Food, Formulated; Gallbladder; Glutens; Humans; Hydrolysis; Intestinal Mucosa; Lymphocytes; Male; Postprandial Period; Radioimmunoassay

The distal gut hormone peptide YY (PYY) mediates feedback inhibition of gastric acid secretion, gastrointestinal motility, and pancreatic enzyme output. To investigate the influence of maldigestion on PYY, we determined plasma PYY levels in patients with celiac disease under basal conditions and in response to intraduodenal fat. Basal PYY was increased in untreated celiac patients (N = 13) compared to patients on a gluten free diet (N = 9) [15.6 (11.8-27.0) pM vs 12.2 (10.1-13.1) pM; P < 0.05] and compared to control subjects (N = 15) [9.5 (8.3-10.4) pM; P < 0.001]. Integrated PYY in response to intraduodenally infused predigested fat (1071+/-293 pM 80 min) was significantly (P < 0.05) greater than in response to undigested fat (322+/-223 pM 80 min) in six untreated celiacs. Plasma concentrations of PYY and cholecystokinin were strongly correlated (r = 0.79; P < 0.001). We conclude that basal PYY levels in untreated celiac disease are elevated, that predigestion of fat enhances PYY release in these patients, and that PYY secretion is correlated with CCK release.

Topics: Case-Control Studies; Celiac Disease; Cholecystokinin; Corn Oil; Dietary Fats; Digestion; Female; Humans; Male; Middle Aged; Peptide YY

Gallbladder hypomotility in celiac disease has been attributed to decreased cholecystokinin secretion. The possible influence of somatostatin, which inhibits gallbladder motility, however, has never been evaluated. In this study gallbladder emptying and cholecystokinin and somatostatin plasma levels were evaluated in response to a fatty meal in patients with celiac disease at diagnosis and after long-term gluten-free diet and in controls.. Gallbladder volume and plasma levels of cholecystokinin and somatostatin were measured by ultrasonography and radioimmunoassay, respectively, at 0 time and 30, 60, 75, and 90 min after an oral fatty meal (227 kcal, 45% fat) in 10 celiac patients at diagnosis and after 18 months of successful gluten-free diet and in 10 healthy subjects. The pattern of gallbladder emptying was evaluated by mixed factorial analysis of variance and the curve fitting by multiple regression analysis.. Patients at diagnosis had significantly greater fasting gallbladder volume and higher somatostatin plasma levels than controls (25.7 +/- SD 9.7 ml vs 16.8 +/- 7.0 ml, p = 0.021 and 9.3 +/- 4.6 vs 4.8 +/- 3.4 pmol/L, p = 0.023, respectively), significantly lower fatty meal-induced gallbladder ejection fraction (55 +/- 11.2% vs 76 +/- 7.2%, p = 0.005), and cholecystokinin peak and smaller area under the cholecystokinin secretion curve (3.1 +/- 2.3 pmol/L vs 10.5 +/- 6.9 pmol/L, p = 0.028 and 157 +/- 142 pmol/L/90 min vs 453 +/- 229 pmol/L/90 min, p = 0.028, respectively). The two groups had a similar emptying pattern (p = 0.8913) expressed by a significant quadratic term of the emptying function (p = 0.0001). The mean overall emptying volume was significantly greater in patients than in controls (p = 0.0007). Gluten-free diet normalized these findings.. In patients at diagnosis, elevated somatostatin levels were associated with increased gallbladder fasting volume, whereas decreased cholecystokinin secretion was responsible for the reduced gallbladder emptying. Gluten-free diet reversed these abnormalities.

Topics: Adult; Celiac Disease; Cholecystokinin; Dietary Fats; Fasting; Female; Gallbladder; Gallbladder Emptying; Humans; Male; Postprandial Period; Somatostatin; Ultrasonography

Cholecystokinin (CCK) response to a test meal should be increased in patients with pancreatic insufficiency, as trypsin is absent from the duodenum. If pancreatic enzymes are added, a restoration of the inhibitory feedback should result in lower levels of CCK. Ten patients with chronic pancreatitis and steatorrhea were studied. CCK basal and postprandial levels were evaluated the day before and 45 and 90 days after treatment with oral pancreatin. Twelve healthy volunteers were included as reference group. CCK basal levels did not vary. CCK response to a test meal was increased in patients before treatment and diminished when oral enzymes were maintained for months even after three days of therapy withdrawal. We conclude that long-term therapy with oral enzymes induces changes in CCK response that do not regress after three days of treatment suspension.

Topics: Adult; Case-Control Studies; Celiac Disease; Cholecystokinin; Chronic Disease; Female; Food; Gastrointestinal Agents; Humans; Male; Pancreatin; Pancreatitis; Postprandial Period; Time Factors

Impaired postprandial gallbladder emptying in celiac disease has been attributed to an absence of appropriate cholecystokinin release. To determine if a flat jejunal mucosa in celiac patients is related to a reduced cholecystokinin-secreting capacity, increasing doses of bombesin were infused into six patients with celiac disease and a flat jejunal mucosa (group A), in seven celiac patients with a normal jejunal mucosa while on a gluten-free diet (group B), and in seven healthy controls (group C). Bombesin induced significant (P < 0.05) increments of plasma CCK to a maximum value of 1.0 +/- 0.3 pM in group A, to 1.5 +/- 0.3 pM in group B, and to 1.2 +/- 0.3 pM in group C (NS between groups), that were accompanied by significant (P < 0.05) gallbladder emptying responses of 70 +/- 4% in group A, 47 +/- 10% in group B and 65 +/- 5% in group C. Dose-response relationships were not different between groups. We conclude that there is no major impairment of gallbladder responsiveness to bombesin or of cholecystokinin-secreting capacity in patients with a flat jejunal mucosa due to celiac disease.

Topics: Adult; Bombesin; Case-Control Studies; Celiac Disease; Cholecystokinin; Female; Gallbladder Emptying; Humans; Intestinal Mucosa; Jejunum; Male; Middle Aged

Cholecystokinin (CCK) release and gall bladder emptying in response to a fatty meal are completely abolished in coeliac disease. To determine the effect of lipid digestion on CCK release and gall bladder motility, six patients with untreated coeliac disease and a flat jejunal mucosa were studied on two separate days. After an overnight fast, the plasma CCK concentration and gall bladder volume were measured before and at regular intervals after the intraduodenal instillation of 60 ml corn oil (triglycerides) incubated with 40 ml saline or with 40 ml bile and pancreatic juice. The mean (SEM) concentration of free fatty acids in the aqueous phase of corn oil after incubation with bile and pancreatic juice (predigested corn oil) was 78 (35) mM compared with 0.1 (0.1) mM in the aqueous phase of corn oil incubated with saline (undigested corn oil). Integrated plasma CCK in response to predigested corn oil was significantly greater than that in response to undigested corn oil (101 (18) pM. 80 min v-2 (9) pM.80 min; p < 0.005). Similarly, integrated gall bladder contraction in response to predigested corn oil was significantly larger than that after undigested corn oil (817 (210) ml. 80 min v-225 (243) ml. 80 min; p < 0.05). In contrast to undigested corn oil, corn oil that has been predigested with bile and pancreatic juice induces plasma CCK secretion and gall bladder contraction in patients with untreated coeliac disease, presumably by generating and rendering soluble lipolytic products.

Topics: Adult; Bile; Celiac Disease; Cholecystokinin; Corn Oil; Digestion; Fatty Acids, Nonesterified; Female; Gallbladder Emptying; Humans; Kinetics; Lipolysis; Male; Middle Aged; Pancreatic Juice; Plant Oils

The present study was undertaken to determine whether alterations in the gallbladder sensitivity to cholecystokinin (CCK), apart from a reduced endogenous CCK secretion, contribute to the abnormally decreased postprandial gallbladder contraction in patients with coeliac disease. Gallbladder emptying, measured by cholescintigraphy, and plasma CCK levels, measured by radioimmunoassay, were studied during infusion of graded doses of the CCK analog cerulein in six coeliac patients with subtotal villous atrophy, six coeliac patients on a gluten-free diet with normal villous architecture, and nine control subjects. Both in the patients and in the controls infusion of stepwise increasing doses of cerulein, in the range of 1-16 ng.kg-1.h-1, induced dose-related changes in plasma CCK-like immunoreactivity (CCK-LI) (r = 0.99; p less than 0.001) and gallbladder emptying (r greater than 0.97; p less than 0.01-p less than 0.001). Plasma CCK-LI and gallbladder responses were not significantly different among untreated coeliac patients, treated coeliac patients, and controls. Gallbladder sensitivity to cerulein in untreated and treated coeliac patients was not significantly different from that in controls. It is concluded that the abnormally decreased gallbladder contraction in coeliac patients is the result of a reduced endogenous CCK secretion and not of a lack of end-organ responsiveness to CCK.

Topics: Celiac Disease; Ceruletide; Cholecystokinin; Female; Gallbladder; Humans; Male; Middle Aged; Muscle Contraction; Muscle, Smooth; Radioimmunoassay; Radionuclide Imaging

The aim of this study was to investigate simultaneously the endogenously stimulated exocrine pancreatic secretion and the cholecystokinin (CCK) response in patients suffering from coeliac sprue. A Lundh-test was performed in nine patients and twenty-six healthy volunteers. Basal plasma-CCK levels (3.4 +/- 0.5 pmol/l in sprue patients vs. 4.1 +/- 0.5 pmol/l in controls) and the integrated 120 min postprandial CCK values showed no differences in both groups. However, in controls the peak CCK value of 27.5 +/- 5.6 pmol/l appeared after 15 minutes whereas in sprue patients the peak of 18.9 +/- 4.5 pmol/l appeared after 60 minutes. CCK concentrations in duodenal biopsies of patients with coeliac sprue revealed significantly lower values compared to controls (123.4 +/- 37.4 versus 240.0 +/- 11.3 pmol/g wet weight). The stimulated lipase output was significantly lower throughout the whole sampling period in coeliac sprue patients whereas amylase output showed an inconstant reduction. The trypsin output was not altered. These results suggest that other mediators than CCK are responsible for the maintenance of trypsin output and for the reduction of lipase output in patients with coeliac sprue.

Topics: Adult; Aged; Amylases; Biopsy; Celiac Disease; Cholecystokinin; Duodenum; Female; Humans; Intestinal Mucosa; Lipase; Male; Middle Aged; Prognosis; Trypsin

Coeliac patients are known to have an expanded bile salt pool which recirculates slowly due, at least in part, to impaired gall bladder contractility. We have investigated the possibility that delayed small bowel transit of chyme and bile may also contribute to this sluggish recycling. Plasma cholylglycine, total bile acids and cholecystokinin concentrations were measured after a lactulose-labelled test meal whose mouth-caecum transit time (M-C TT) was assessed by the breath hydrogen technique. Overall there were no significant differences in plasma bile acid profiles between seven healthy controls and a group of 25 coeliac patients. However, when subjects were divided according to their M-C TT, the 10 with the slowest transit were found to have significant elevation of fasting levels when compared with the 10 with the fastest transit, fasting total bile acids being 3.4 +/- 1.3 versus 0.7 +/- 0.6 mumol/l (P less than 0.02) and fasting cholylglycine being 0.43 +/- 0.17 versus 0.06 +/- 0.04 mumol/l (P less than 0.05) respectively. Peak bile acid levels did not differ significantly between subjects with fast or slow transit. However, subjects with slow transit were found to have a delay in the return of plasma bile acid levels to fasting levels so that the 4 h postprandial levels were significantly elevated when compared with those observed in the subjects with fast transit (total bile acids 3.6 +/- 1.2 versus 0.19 +/- 0.1 mumol/l and cholylglycine 0.70 +/- 0.13 versus 0.24 +/- 0.07 mumol/l respectively, both P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adolescent; Adult; Aged; Bile Acids and Salts; Cecum; Celiac Disease; Cholecystokinin; Food; Gastrointestinal Motility; Glycocholic Acid; Humans; Middle Aged; Mouth

The functional reserve capacity of the pancreas, as reflected by the absence of steatorrhea, was correlated with the results of a secretin-pancreozymin test (SPT) in 47 patients with exocrine pancreatic insufficiency due to chronic pancreatitis. The results indicate that a severe reduction in enzyme output (but not in bicarbonate concentration and output) is usually associated with steatorrhea. However, there were a number of patients with steatorrhea despite only moderate enzyme output impairment, while others had normal fat excretion but severely reduced enzyme secretion. Thus, the degree of impaired pancreatic function, as measured by the SPT, cannot be predicted by the presence of steatorrhea; vice versa, a moderately abnormal SPT does not exclude the presence of pancreatic steatorrhea. Therefore, for a sophisticated evaluation of the functional reserve capacity of the exocrine pancreas, both the SPT and fecal fat analysis are considered necessary. The correlation between impaired glucose tolerance and exocrine pancreatic function was poor.

Topics: Adolescent; Adult; Aged; Celiac Disease; Cholecystokinin; Enzymes; Feces; Female; Humans; Lipids; Male; Middle Aged; Pancreas; Pancreatic Function Tests; Pancreatitis; Secretin

Topics: Celiac Disease; Cholecystokinin; Gallbladder; Humans

In 93 patients with known exocrine pancreatic function (secretin-pancreozymin test), NMR spectrometry and chloroform-methanol extraction of quantitatively collected, homogenized and lyophilized stools provided significantly correlated results with respect to stool fat concentration (r = 0.872) and total stool fat excretion/day (r = 0.983). In 83% of 24 patients with total stool fat excretion/day of more than 15 g (chloroform-methanol extraction), the indication for enzyme replacement was also established by stool fat concentrations of more than 35% determined by NMR spectrometry, irrespective of whether stool fat was measured in total stools or in 3 consecutive unhomogenized samples. In the remaining (17%) patients total stool fat excretion/day was only slightly elevated (16-21 g). Interestingly, in only 58% of patients actually needing enzyme replacement, did the secretin-pancreozymin test reveal a reduction of stimulated enzyme secretion to below 15% of the lower normal limit. The results indicate that NMR spectrometry of lyophilized samples of 3 consecutive unhomogenized stools is suitable for stool fat quantitation and for establishing the indication for enzyme replacement in chronic pancreatitis.

Topics: Amylases; Celiac Disease; Cholecystokinin; Chymotrypsin; Dietary Fats; Feces; Humans; Magnetic Resonance Spectroscopy; Pancreas; Pancreatitis; Secretin; Trypsin

Pancreatic function was determined (using the secretin-pancreozymin test) before the use of gluten-free diet in 22 patients with endemic (celiac) sprue. Water and bicarbonate secretion were within normal limits, if anything there was a trend to high-normal values. Remarkable and apparently characteristic for celiac sprue was the only slight contraction of the gallbladder after intravenous injection of submaximal doses of cholecystokinin-pancreozymin (CCK). Secretion of the 3 enzymes amylase, lipase and trypsin was decreased in about one third of cases, the difference relating both to the concentrations and the amount secreted, compared with normal control values was significant (P greater than 0.01). But in no case was the reduced enzyme secretion so marked that one would expect maldigestion. Multivariate non-linear discriminance analysis demonstrated that pancreatic secretion in sprue is quite distinct from that in healthy subjects and those with chronic pancreatitis. It is assumed that there is a pattern of exocrine pancreatic secretion typical for sprue.

Topics: Adult; Aged; Amylases; Bile; Celiac Disease; Cholecystokinin; Female; Humans; Injections, Intravenous; Lipase; Male; Middle Aged; Pancreas; Secretin; Trypsin

Plasma concentrations of human pancreatic polypeptide (HPP) parallel exocrine pancreatic secretion in response to stimulation with cholecystokinin. We determined prospectively the relationships among fasting HPP level, integrated HPP response to infusion of cholecystokinin, and output of trypsin and also the sensitivity, specificity, and predictive values of the fasting HPP level in the diagnosis of exocrine pancreatic disease. Our study group consisted of 19 patients with acute pancreatitis, 17 with chronic pancreatitis, and 25 with ductal adenocarcinoma of the pancreas and 27 control subjects. In the control patients and those with chronic pancreatitis, significant correlations were detected between HPP level and output of trypsin (P less than 0.001) in response to infusion of cholecystokinin and between fasting HPP and integrated HPP levels (P less than 0.004); no correlation was detected between HPP level and steatorrhea. The sensitivity, specificity, and negative and positive predictive values of the fasting HPP level for detection of either chronic pancreatitis or pancreatic cancer were similar and approximated 0.88, 0.67, 0.88, and 0.66, respectively. The HPP concentration had no value in detecting acute pancreatitis. Because the fasting HPP level has a high degree of negative predictability and is simpler to measure than the integrated HPP level or the output of trypsin, it may be a useful test in patients suspected of having either chronic pancreatitis or pancreatic cancer. A fasting HPP level of 125 pg/ml or greater could be used to exclude chronic pancreatitis or pancreatic cancer, but the finding of a value of less than 125 pg/ml necessitates use of other diagnostic tests for reliable determination of the presence of these diseases.

Topics: Acute Disease; Adult; Aged; Carcinoma, Intraductal, Noninfiltrating; Celiac Disease; Cholecystokinin; Chronic Disease; Fasting; Humans; Middle Aged; Pancreas; Pancreatic Diseases; Pancreatic Neoplasms; Pancreatic Polypeptide; Pancreatitis; Prospective Studies; Trypsin

Normal volunteers (n = 6), patients with untreated celiac disease and subtotal villous atrophy (n = 6), patients with nonresponsive celiac disease (n = 2), and patients with celiac disease on a gluten-free diet with a virtually normal biopsy specimen (n = 6) drank a liquid fat meal after an overnight fast. Gallbladder emptying was monitored by using 99mTc-eHIDA, and blood samples were taken for cholecystokinin estimation by radioimmunoassay after high-performance liquid chromatography. The half-times of gallbladder emptying were 20.4 +/- 2.9 min (mean +/- SEM) for normals and 22.1 +/- 2.8 min in treated patients with celiac disease (NS). In patients with untreated celiac disease half-times were 154.3 +/- 10.3 min (p less than 0.02 vs. normals and treated patients with celiac disease), and in 2 nonresponsive patients, half-times were 40.7 and 37.3 min. Integrated plasma cholecystokinin responses were 473 +/- 87 and 436 +/- 137 pmol X L-1 X 30 min-1 in normals and treated patients with celiac disease (NS). In untreated patients with celiac disease values were 16 +/- 9 pmol X L-1 X 30 min-1 (p less than 0.001 vs. normals and treated patients with celiac disease), and in nonresponsive patients values were 442 and 322 pmol X L-1 X 30 min-1. In 2 patients studied before and during gluten-free diet half-times for gallbladder emptying changed from 168.9 and 302.4 min to 20.1 and 23.4 min, and cholecystokinin responses changed from 0 and 45 to 623 and 298 pmol X L-1 X 30 min-1. Cholecystokinin immunoreactivity cochromatographing with cholecystokinin-octapeptide was responsible for 50%-60% of circulating cholecystokinin in normals and in treated patients but the small amount of cholecystokinin that was released in untreated patients with celiac disease cochromatographed with cholecystokinin-33/39. We conclude that there is a reversible defect of gallbladder emptying and cholecystokinin release in celiac disease.

Topics: Adult; Aged; Celiac Disease; Cholecystokinin; Dietary Fats; Female; Gallbladder; Glutens; Humans; Middle Aged

Using a sensitive and specific radioimmunoassay for cholecystokinin (CCK) we have measured plasma CCK levels in patients with and without chronic pancreatitis. All patients suffered from steatorrhea. The basal plasma values in patients with chronic pancreatitis (n = 10) were significantly higher compared with a control group of 40 normal subjects. After ingestion of a test meal peak plasma levels of CCK were significantly higher than in controls, but the integrated CCK release did not differ from the normal subjects. The findings indicate a close relationship between plasma CCK concentration and exocrine pancreatic function.

Topics: Adult; Celiac Disease; Cholecystokinin; Chronic Disease; Female; Food; Humans; Male; Middle Aged; Pancreatitis; Radioimmunoassay; Time Factors

A quantitative morphological investigation of eight endocrine cell types in mucosal biopsies from adults with untreated celiac sprue was undertaken. The quantitative data expressed as cells per millimeter of epithelium most accurately reflected the changes seen in celiac disease, as it takes into account changes in mucosal thickness due to the absence of villi in celiac biopsies. The results showed significant increases in the number of cholecystokinin and enterochromaffin cells, a significant decrease in somatostatin, gastric inhibitory polypeptide and secretin cells, and no change in the motilin, gastrin, and glicentin cells. Significant changes in cell size (cross-sectional area) were also demonstrated in the somatostatin and gastrin cells which were smaller in the celiac biopsies.

Topics: Adult; Aged; Celiac Disease; Cell Count; Cholecystokinin; Duodenum; Enterochromaffin Cells; Female; Gastric Inhibitory Polypeptide; Gastrointestinal Hormones; Glucagon; Humans; Intestinal Mucosa; Male; Middle Aged; Motilin; Proglucagon; Protein Precursors; Secretin; Somatostatin

Gallbladder emptying was evaluated in 15 adult celiac disease patients by oral cholecystography or ultrasonography, after fatty meal or cholecystokinin stimulation. Gallbladder inertia was found in 13 cases. Our study agrees with previously reported results; however it is the first one in which this abnormality was demonstrated by ultrasonography. Our findings may suggest that gallbladder inertia is due to duodenal release of an inactive endogenous cholecystokinin. Control studies demonstrates that gallbladder inertia is reversible after gluten-free diet, recurs with relapse, and thus represents a true celiac disease sign, and not an associated condition. Finally, our cases suggest that gallbladder inertia may be radiologically evident before clinical features of malabsorption become apparent. Awareness of this possibility may persuade the radiologist to research in this condition an occult celiac disease.

Topics: Adult; Aged; Biliary Dyskinesia; Celiac Disease; Cholecystography; Cholecystokinin; Female; Gallbladder; Gallbladder Diseases; Humans; Male; Middle Aged; Ultrasonography

Two boys with idiopathic hypoparathyroidism had extensive studies of gastrointestinal function during hypocalcemia accompanied by steatorrhea. No evidence of generalized gastrointestinal moniliasis or abnormal mucosal structure or function was observed. Studies of pancreatic function and bile salt metabolism during hypocalcemia demonstrated deficient meal-stimulated intraluminal pancreatic enzyme concentrations in both subjects and reduced bile salt concentrations in one subject. However, following stimulation with exogenous octapeptide of cholecystokinin, intraluminal pancreatic enzyme and bile salt concentrations were normal in both. Cholic acid pool sizes were markedly increased in both subjects during hypocalcemia (9 and 12 times larger than during normocalcemia) and cholic acid turnover was reduced during hypocalcemia in one subject. Our findings suggest that during hypocalcemia, insufficient endogenous cholecystokinin is released by the duodenal mucosa during a meal stimulus to stimulate normal gallbladder contraction and pancreatic enzyme secretion.

Topics: Adolescent; Bile Acids and Salts; Celiac Disease; Child; Cholecystokinin; Cholic Acid; Cholic Acids; Digestion; Humans; Hypocalcemia; Hypoparathyroidism; Male; Pancreatin; Peptide Fragments; Sincalide

Topics: Adolescent; Adult; Celiac Disease; Cholecystokinin; Chronic Disease; Female; Humans; Lipase; Male; Middle Aged; Pancreas; Pancreatic Polypeptide; Pancreatitis; Pentagastrin; Peptide Fragments; Secretin; Sincalide; Trypsin

The amount and type of cholecystokinin (CCK) in duodenal extracts and plasma of celiac patients and normal subjects was studied by radioimmunoassay and gel filtration. In both groups there were similar patterns of molecular forms in extracts of duodenal biopsies, but concentrations in celiac disease were significantly depressed. In boiling water extracts of duodenal mucosa from both groups a factor with the properties of the COOH-terminal octapeptide of cholecystokinin predominated, but there were also significant amounts of a larger molecular weight form. In acid extracts of mucosa a factor with the properties of the 33 or 39 residue form was identified in amounts that were approximately 25% those of CCK8; there were also similar amounts of an acid-soluble form that had an apparent molecular weight higher than CCK39. Plasma immunoreactive cholecystokinin was studied after concentration by immunoaffinity adsorption and fractionation by gel filtration. In normal subjects fasting CCK-like immunoreactivity was less than 0.8 pmol/liter, and after a light breakfast increased to 2.0 +/- 0.7 (range 1.0 to 4.8) pmol/liter; CCK8-like activity accounted for all the increased immunoreactivity. In five of six celiac patients the concentrations of both fasting and postprandial CCK-like immunoreactivity in plasma were undetectable (less than 0.8 pmol/liter). We conclude that diminished production and release of CCK could account for the impaired pancreatic and gall bladder responses to intraluminal stimuli in celiac disease.

Topics: Adult; Amino Acid Sequence; Celiac Disease; Cholecystokinin; Duodenum; Female; Humans; Immunologic Techniques; Intestinal Mucosa; Male

Human pancreatic lipase in duodenal secretions was studied under conditions of maximal activation by porcine colipase and maximal inhibition by sodium taurodeoxycholate. In almost all samples, total lipase activity in 4 mM sodium taurodeoxycholate was activated by the addition of porcine colipase. Activation was linear until saturation by cofactor was reached, and maximum activity was greater than that obtained in the absence of bile salts. At pH 8.0 in 4 mM sodium taurodeoxycholate, lipase activity was due to pancreatic lipase in samples from normal and steatorrheic individuals and was proportional to the concentration of endogenous colipase in samples that could be activated by exogenous colipase. In these samples, therefore, colipase activity could be conveniently assayed as the lipase activity at pH 0.8 in 4 mM sodium taurodeoxycholate. Colipase to total pancreatic lipase ratios varied widely from individual to individual and on average were significantly lower in steatorrheic patients. In individual samples, colipase secretion was stimulated by pancreozymin and secretin roughly in parallel with total pancreatic lipase, but some variation in the ratio of the two was often seen in successive collection periods. Because pancreatic lipase is usually unsaturated with respect to cofactor, lipolytic activity in duodenal secretions may be finely controlled by modulation of colipase secretion.

Topics: Animals; Celiac Disease; Cholecystokinin; Colipases; Dose-Response Relationship, Drug; Duodenum; Humans; Hydrogen-Ion Concentration; Intestinal Secretions; Lipase; Micelles; Pancreas; Proteins; Secretin; Swine; Taurodeoxycholic Acid

Topics: Avitaminosis; Celiac Disease; Child; Child, Preschool; Cholecystokinin; Diagnosis, Differential; Humans; Infant; Intestinal Absorption; Secretin

The diagnostic value of the fecal chymotrypsin test (FCT) was reevaluated with regard to (a) proved pancreatic hypofunction of different severity (183 pancreozymin-secretin tests); (b) the final clinical diagnosis, and (c) fecal fat excretion (208 patients with chronic pancreatitis; CP). Progressive pancreatic disease (cancer, CP) was mainly associated with moderate or severe pancreatic hypofunction (119/138; 86.2%) and a low incidence of false-normal FCT values (14/138; 10.1%). Miscellaneous disorders (mainly reversible pancreatic hypofunction) were mainly associated with slight pancreatic hypofunction and a high incidence of false-normal FCT values (17/45; 37.8%). Pancreatic steatorrhea (greater than 10 g/day) was found only in patients with markedly depressed FCT values. Progressive deterioration of pancreatic function was demonstrated by repeated FCT in CP (n = 220).

Topics: Celiac Disease; Cholecystokinin; Chronic Disease; Chymotrypsin; Exocrine Pancreatic Insufficiency; False Negative Reactions; Feces; Humans; Lipids; Pancreatic Function Tests; Pancreatitis; Secretin

Cholesterol gallstones occur 600-1000 times more frequent in adults than in children. Seeking a possibility to explain this discrepancy, the molar concentrations of cholesterol, lecithin and bile acids as well as the bile acid pattern have been determined in duodenal juice, after an injection of 2 U/kg pancreocymin, of 33 children aged between 4 months and 14 years who were gastroenterologically healthy. The absolute values as well as the percentage composition were calculated. The lithoindices have been determined to be Li1=0.54 +/- 0.25 and Li2=1.06 +/- 0.50 according to the formulas of Thomas and Hofmann. Dependence on age in infancy and during childhood could be excluded. The main reason for the fact that hardly any gallstones occur among children, compared to the occurrence in adults seems to be the small concentration of cholesterol in the bile. Whereas there had been no deviations either of lithoindices or in the bile acid pattern in 10 patients with coeliac disease, 2 out of 6 children with mucoviscidosis and 3 out of 4 children with small bowel syndrome showed apparently increased lithoindices. Only in the last group a bile acid pattern was found which could reduce the higher risk of getting cholelithiasis.

Topics: Adolescent; Age Factors; Bile Acids and Salts; Celiac Disease; Child; Child, Preschool; Cholecystokinin; Cholelithiasis; Cholesterol; Cystic Fibrosis; Germany, West; Humans; Infant; Intestinal Secretions; Intestine, Small; Phosphatidylcholines

The coexistence of nontropical sprue and advanced pancreatic insufficiency is uncommon. The purposes of this report are to: (a) describe 3 patients with non-tropical spruc and severe pancreatic insufficiency, (b) determine the frequency, magnitude, and clinical importance of diminished pancreatic secretion in nontropical sprue, and (c) assess whether patients with pancreatic insufficency secondary to chronic pancreatitis or pancreatic cancer have jejunal mucosal histologic abnormalities. In each of 3 patients with nontropical sprue and associated severe exocrine pancreatic insufficiency, an optimal clinical response required the appropriate treatment of both causes of malabsorption. Of 31 subjects with proved nontropical sprue, cholecystokinin-stimulated duodenal tryptic activity or lipolytic activity (or both) was reduced in 13 (42%) but severely reduced in only the three case reports (10%). The morphologic structure of the small bowel was normal in 21 patients with primary pancreatic insufficiency secondary to chronic pancreatitis or pancreatic cancer. Mild-to-moderate exocrine pancreatic insufficiency is a frequent finding in untreated nontropical sprue, is presumably reversible, and rarely contributes to the development of steatorrhea. However, if patients with nontropical sprue fail to respond to a gluten-free diet, coexistent severe pancreatic insufficiency is a possible cause for treatment failure.

Topics: Aged; Celiac Disease; Cholecystokinin; Chronic Disease; Female; Humans; Jejunum; Lipase; Middle Aged; Pancreas; Pancreatic Diseases; Pancreatic Juice; Pancreatic Neoplasms; Pancreatitis; Trypsin

A secretin-pancreozymin test was conducted with 43 gastroenterologically healthy children and 12 patients with subtotal atrophy of intestinal mucosa. While the pancreas enzymes were normal, the patients with coeliac disease reacted to the injection of the peptide hormones by producing a larger volume of secretion than did the control group. Despite the increased secretion there was at the same time a significantly higher concentration of bile acids in the duodenal juice. Analysis of the bile acid distribution indicated no deviation from the norm. There was, however, a striking discrepancy between the bile acid and the bilirubin excretion in the children with subtotal atrophy, whose bilirubin secretion, compared to that of the control group, was greatly reduced.

Topics: Adolescent; Atrophy; Bile Acids and Salts; Celiac Disease; Child; Child, Preschool; Cholecystokinin; Giardiasis; Humans; Ichthyosis; Infant; Intestinal Diseases; Intestinal Mucosa; Intestine, Small; Psoriasis; Secretin

Topics: Celiac Disease; Cholecystokinin; Chymotrypsin; Clinical Enzyme Tests; Fats; Feces; Humans; Lipid Metabolism; Lipids; Lymphatic System; Secretin; Vitamin A

Eleven patients with celiac sprue were studied. Biliary function in the basal state and gallbladder response to perfusion of the small intestinal mucosa with magnesium sulfate was assessed. It was shown that bilirubin output in basal conditions is decreased in these patients and that magnesium sulfate does not stimulate gallbladder contraction. In addition it was shown that in 4 of the 11 cases studied there was a complete lack of bile reaching the duodenum in the basal state as well as in 7 of 11 cases in the digestive period. That gallbladder function was intact was shown by the normal response to intravenous CCK-PZ administration, and the patency of the common bile duct was demonstrated by intravenous cholangiography. Thus the already impaired fat absorption in celiac sprue is magnified by the lack of bile delivery, and this is probably due to an alteration in the synthesis or release of endogenous CCK-PZ.

Topics: Adult; Atrophy; Bile; Bile Ducts; Bilirubin; Celiac Disease; Cholecystokinin; Female; Gallbladder; Humans; Intestine, Small; Magnesium Sulfate; Male; Middle Aged; Stimulation, Chemical

Topics: Celiac Disease; Cholecystokinin; Gastrointestinal Diseases; Humans; Pancreatic Diseases

Present knowledge about gastrointestinal peptide hormones is discussed from three points of view: (a) diagnostic significance of these hormones; (b) states characterized by over-production or deficiency of peptide hormones; (c) clinical application and perspectives of gastrointestinal hormones. The data in the literature are subjected to a critical analysis; in addition, the author's own experiments are discussed.

Topics: Anemia, Pernicious; Celiac Disease; Cholecystokinin; Duodenal Ulcer; Duodenum; Esophageal Diseases; Gastrins; Gastrointestinal Hormones; Humans; Peristalsis; Pyloric Stenosis; Secretin; Spasm; Zollinger-Ellison Syndrome

Topics: Adult; Aged; Alcoholism; Calcinosis; Celiac Disease; Cholecystokinin; Chronic Disease; Creatinine; Diabetes Complications; Feces; Female; Humans; Lipase; Male; Middle Aged; Pancreas; Pancreatitis; Secretory Rate; Stimulation, Chemical; Time Factors; Trypsin

Digestive enzymatic activities (disaccharidases, alkaline phosphatase, peptide hydrolases) have been determined in the mucosa of 14 patients with chronic pancreatitis. All had an abnormal secretin-pancreozymin test. Four patients had insulin-dependent diabetes mellitus, four a pathological glucose tolerance test. Nine patients had steatorrhoea. Maltase, sucrase, and alkaline phosphatase activity was significantly elevated in patients with exocrine pancreatic insufficiency, whereas those of lactase, trehalase, and peptide hydrolase were normal. Patients with steatorrhoea had higher maltase and sucrase activity than those without steatorrhoea, whereas decreased glucose tolerance had no effect on brush border enzymatic activity. It is suggested thatdecreased exocrine rather than decreased endocrine pancreatic function is responsible for the increase in intestinal disaccharidase and alkaline phosphatase activity, possible by the influence of pacreatic enzymes on the turnover of brush border enzymes from the luminal side of the mucosal membranes or by direct hormonal stimulation though cholecystokinin.

Topics: Adult; Alkaline Phosphatase; Biopsy; Celiac Disease; Cholecystokinin; Diabetes Complications; Disaccharidases; Galactosidases; Glucose Tolerance Test; Glucosidases; Humans; Intestinal Mucosa; Islets of Langerhans; Pancreas; Pancreatitis; Peptide Hydrolases; Secretin; Sucrase; Trehalase

Topics: Celiac Disease; Cholecystokinin; Dietary Fats; Fasting; Female; Gallbladder; Humans; Iodine Radioisotopes; Male; Middle Aged

Topics: Celiac Disease; Cholecystokinin; Gallbladder; Humans; Pancreas

Idiopathic late-onset immunoglobulin deficiency in a young man was associated with achlorhydria and a severe intestinal malabsorption syndrome that did not respond to conventional therapy. Combined therapy with high doses of prednisone and tetracycline hydrochloride resulted in weight gain, cessation of diarrhea, improved absorption of water, fat, and vitamin B12, and production of gastric acid after stimulation with histamine. Serum immunoglobulin levels, however, did not increase.

Topics: Achlorhydria; Adult; Age Factors; Body Weight; Celiac Disease; Cholecystokinin; Diarrhea; Drug Therapy, Combination; Humans; Immunoglobulin M; Immunologic Deficiency Syndromes; Malabsorption Syndromes; Male; Prednisone; Tetracycline; Vitamin B 12

The vitamin A absorption test and its interaction with the secretin-pancreozymin test, the d-xylose absorption test, fecal fat content and the small intestine biopsy are estimated on their significance in the diagnosis and course of sprue and pancreatic insufficiency. The investigation includes 39 patients with different stages of pancreatic insufficiency and 10 patients with sprue. First it results relatively wide spread normal values in a control collective with sometimes unexplained low values, the significance of the vitamin A absorption test as screening test therefore is limited. Secondly the absent rise after vitamin A ingestion in serum after 3 and 6 hours favours the diagnosis of sprue, correlates with the histological findings of the mucosa and appears more reliable than the d-xylose test. Thirdly this test seems to allow the differentiation between malabsorption and maldigestion when steathorroe is proved: In contrast to sprue-syndromes pancreatic insufficiency shows significant reduced 3 hour values at subnormal 6 hour values after vitamin A ingestion.

Topics: Adult; Celiac Disease; Cholecystokinin; Diagnosis, Differential; Feces; Humans; Lipids; Malabsorption Syndromes; Pancreatic Diseases; Secretin; Time Factors; Vitamin A; Xylose

Topics: Celiac Disease; Cholecystokinin; Clinical Laboratory Techniques; Diarrhea; Feces; Gastric Juice; Gastric Mucosa; Hormones; Humans; Hydrogen-Ion Concentration; Intestine, Small; Jejunum; Pancreas; Peptic Ulcer; Secretin; Time Factors

Topics: Adolescent; Bile Acids and Salts; Celiac Disease; Child; Child, Preschool; Cholecystokinin; Clinical Enzyme Tests; Cystic Fibrosis; Duodenum; Female; Gallbladder; Humans; Infant; Male; Pancreas; Pancreatic Diseases; Pancreatic Juice; Secretin; Stimulation, Chemical

Topics: Adult; Celiac Disease; Cholecystokinin; Gallbladder; Humans; Radioimmunoassay; Time Factors

The uptake of (75)Se Selenomethionine by the pancreas has been evaluated in 102 patients and compared with the secretin-pancreozymin test of pancreatic function. In groups of patients with chronic pancreatitis and cancer of the pancreas abnormal scans closely parallel the diminished exocrine secretion, especially bicarbonate output, following a submaximal dose of secretin. Thirty per cent of the group with no pancreatic abnormality have abnormal scans, though the secretinpancreozymin test is normal. Though a normal scan excludes the presence of chronic pancreatitis and cancer of the pancreas with a probability greater than 90%, an abnormal scan is found so frequently in normal subjects that it does not provide a reliable index of impaired pancreatic function.

Topics: Bicarbonates; Celiac Disease; Cholecystokinin; Chronic Disease; Humans; Jaundice; Liver Cirrhosis; Liver Cirrhosis, Biliary; Methionine; Pancreas; Pancreatic Neoplasms; Pancreatitis; Radionuclide Imaging; Secretin; Selenium

Topics: Adult; Aged; Celiac Disease; Cholecystokinin; Duodenum; Electromyography; Female; Gastrointestinal Hormones; Gastrointestinal Motility; Humans; Male; Manometry; Middle Aged; Muscle, Smooth; Pentagastrin; Physical Stimulation; Pressure; Scleroderma, Systemic; Secretin; Stimulation, Chemical; Water

Topics: Acute Disease; Adolescent; Adult; Aged; Alcoholism; Calcinosis; Celiac Disease; Child; Cholecystokinin; Chronic Disease; Diabetes Complications; Female; Follow-Up Studies; Humans; Male; Middle Aged; Pancreas; Pancreatitis; Recurrence; Secretin; Switzerland; Time Factors

Topics: Bicarbonates; Celiac Disease; Cholecystokinin; Feces; Gastrectomy; Humans; Lipid Metabolism; Lipids; Male; Pancreas; Pentagastrin; Postgastrectomy Syndromes; Secretin; Stomach Ulcer; Trypsin

Topics: ABO Blood-Group System; Adult; Alcohol Drinking; Blood Protein Disorders; Calcinosis; Celiac Disease; Cholecystokinin; Chronic Disease; Female; Glucose Tolerance Test; Humans; Male; Middle Aged; Pancreas; Pancreatitis; Radiography; Secretin; Sodium; Sweat

Topics: Amylases; Bicarbonates; Celiac Disease; Cholecystokinin; Diet; Folic Acid Deficiency; Humans; Intestinal Diseases; Intestine, Small; Malabsorption Syndromes; Nutrition Disorders; Pancreas; Protein Deficiency; Secretin; Serum Albumin

Topics: Adolescent; Bile Acids and Salts; Bile Ducts; Bile Ducts, Intrahepatic; Body Weight; Celiac Disease; Child; Child, Preschool; Cholecystokinin; Cholestyramine Resin; Chronic Disease; Diet Therapy; Dietary Fats; Duodenum; Female; Humans; Infant; Intestinal Secretions; Liver Cirrhosis; Liver Diseases; Liver Function Tests; Male; Triglycerides

Topics: Celiac Disease; Cholecystokinin; Dietary Fats; Humans; Intestinal Absorption; Intestine, Small; Lipase; Lipid Metabolism; Pancreas

Topics: Adult; Aged; Amino Acids; Bile Acids and Salts; Celiac Disease; Cholecystokinin; Digestion; Female; Gallbladder; Humans; Intestinal Absorption; Intestinal Mucosa; Lipase; Lipid Metabolism; Male; Middle Aged; Pancreas

Topics: Adult; Aged; Ampulla of Vater; Bile Acids and Salts; Biliary Tract Diseases; Carbon Isotopes; Celiac Disease; Cholecystography; Cholecystokinin; Dietary Fats; Female; Gallbladder; Humans; Intestinal Mucosa; Intestine, Small; Male; Methods; Middle Aged; Muscle Contraction; Pancreas; Time Factors

Topics: Adult; Celiac Disease; Cholecystokinin; Gallbladder; Humans

Topics: Adolescent; Adult; Age Factors; Celiac Disease; Child; Cholecystokinin; Chronic Disease; Clinical Enzyme Tests; Diabetes Mellitus; Feces; Female; Follow-Up Studies; Humans; Male; Middle Aged; Pain; Pancreas; Pancreatitis; Time Factors

Topics: Adolescent; Adult; Aged; Bile Acids and Salts; Celiac Disease; Child; Cholecystokinin; Cholesterol; Crohn Disease; Duodenum; Fats; Feces; Female; Humans; Ileitis; Ileostomy; Intestinal Absorption; Liver; Male; Middle Aged

Topics: Barium Sulfate; Celiac Disease; Cholecystokinin; Colectomy; Colitis, Ulcerative; Enteritis; Gastrointestinal Motility; Humans; Ileostomy; Intestinal Diseases; Intestine, Small; Radiography

Topics: Bicarbonates; Bile Pigments; Body Weight; Celiac Disease; Chlorides; Cholecystokinin; Duodenal Ulcer; Duodenum; Humans; Hydrochloric Acid; Intestinal Secretions; Jejunum; Secretin; Trypsin

Topics: Bile Acids and Salts; Celiac Disease; Cholecystography; Cholecystokinin; Gallbladder; Humans

Topics: Adolescent; Adult; Aged; Amylases; Bicarbonates; Bile Duct Neoplasms; Biliary Tract Diseases; Bilirubin; Celiac Disease; Cholecystokinin; Diagnosis, Differential; Duodenum; Female; Hemochromatosis; Humans; Hydrogen-Ion Concentration; Intestinal Secretions; Male; Middle Aged; Pancreas; Pancreatic Neoplasms; Pancreatitis; Protein-Losing Enteropathies; Secretin

Topics: Acute Disease; Calcium; Celiac Disease; Cholecystography; Cholecystokinin; Chronic Disease; Clinical Enzyme Tests; Exocrine Glands; Glucose Tolerance Test; Humans; Hypocalcemia; Hypoparathyroidism; Male; Middle Aged; Pancreatitis; Radionuclide Imaging; Secretin; Triglycerides

Topics: Adult; Aged; Amylases; Bicarbonates; Celiac Disease; Cholecystokinin; Chronic Disease; Duodenum; Fats; Feces; Female; Humans; Intestinal Secretions; Male; Middle Aged; Pancreatic Juice; Pancreatitis; Secretin

Topics: Adult; Aged; Amylases; Celiac Disease; Cholecystitis; Cholecystokinin; Cholelithiasis; Gastrointestinal Diseases; Humans; Infusions, Parenteral; Middle Aged; Pancreas; Pancreatitis; Proteins; Secretin; Secretory Rate

Topics: Amylases; Celiac Disease; Cholecystokinin; Diarrhea; Humans; Lipase; Pancreas; Pylorus; Secretin; Vagotomy

Topics: Adult; Amylases; Bicarbonates; Calcinosis; Celiac Disease; Cholecystokinin; Diabetes Mellitus; Diagnosis, Differential; Female; Humans; Intubation, Gastrointestinal; Male; Middle Aged; Pancreatic Juice; Pancreatitis; Secretin

Topics: Bile Acids and Salts; Blood Chemical Analysis; Celiac Disease; Cholecystokinin; Feces; Gastrectomy; Gastrointestinal Hormones; Intestinal Absorption; Intestinal Diseases; Iodine Isotopes; Lipid Metabolism; Pancreatectomy; Pancreatic Juice; Pancreatitis; Pharmacology; Physiology; Salts; Sprue, Tropical; Triolein

A series of 53 cases of chronic pancreatic disease is described and attention drawn to the frequency with which symptoms are persistent rather than intermittent. A plea is made for the use of the term ;progressive' rather than ;relapsing' in describing many of these cases. Alcohol was an unimportant factor in the aetiology. The possibility of achieving an accurate and early diagnosis using the serum secretin/pancreozymin test is emphasized. The frequent relief of symptoms and the prevention of progress of the disease by surgery, especially sphincterotomy, is recorded.

Topics: Aged; Amylases; Celiac Disease; Cholecystokinin; Clinical Enzyme Tests; Clinical Laboratory Techniques; Gastrointestinal Hormones; Humans; Pancreas; Pancreatic Diseases; Pancreatitis; Pancreatitis, Chronic; Prognosis; Secretin; Statistics as Topic; Surgical Procedures, Operative

Topics: Celiac Disease; Cholecystokinin; Gangrene; Gastrectomy; Gastrointestinal Hormones; Humans; Ileum; Intestine, Small; Intestines; Mesenteric Vascular Occlusion; Pancreatic Extracts; Pancreatic Juice; Postgastrectomy Syndromes; Proteins; Secretin; Sprue, Tropical; Surgical Procedures, Operative; Trypsin