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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We undertook to test the recent suggestion that measurement of immunoreactive carcinoembryonic antigen (CEA) in pancreatic secretion may be useful in diagnosis of pancreatic cancer. Using duodenal intubation and a perfusion method in 57 cases, we measured the rate of pancreatic CEA secretion into the duodenum under basal saline perfusion, alone and with continuous intravenous infusion of secretin (2 clinical units per kg per hr) and of cholecystokinin-pancreozymin (CCK, 15 Crick-Harper-Raper units per kg per hr); and we compared the CEA output with secretion of trypsin, lipase, and bicarbonate under the same conditions. Subsequent laparotomy revealed pancreatic carcinoma in 25 patients, pancreatitis in 7, other intraabdominal malignancies in 6, and benign nonpancreatic disorders in 19. CEA output rates did not differentiate all pancreatic-cancer patients from other patients in any test condition. However, pancreatic enzyme outputs were abnormal with almost 90% of cancers of the pancreatic head and with 75% of cancers of the pancreatic body and tail. For detection of pancreatic cancer, enzyme and bicarbonate outputs in response to CCK are more accurate than pancreatic CEA or bicarbonate outputs in response to secretin. Since CCK-stimulated enzyme outputs can be related accurately to malabsorption (not reported here), we prefer them to bicarbonate output for assessment of pancreatic function.
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PMID:Prospective evaluation of the pancreatic secretion of immunoreactive carcinoembryonic antigen, enzyme, and bicarbonate in patients suspected of having pancreatic cancer. 89 42

Specific points of physiology which are relevant for the understanding and management of chronic pancreatitis are focussed on. First, the regulatory factors of exocrine pancreatic secretion are described, discussing the role of the cholinergic system and of the classical gut hormones cholecystokinin and secretin. The association of upper gastrointestinal dysfunctions with a disturbed exocrine pancreatic response is also dealt with. Lastly, these changes are related to clinical consequences such as maldigestion or malabsorption.
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PMID:Relevant aspects of physiology in chronic pancreatitis. 147 84

How exocrine pancreatic secretion is regulated is only partly known. It is assumed that interaction of several neural and hormonal mechanisms is involved. In man, the intestinal component of these control mechanisms is very important while extra-intestinal mechanisms (such as the cephalic and the gastric phase) play lesser roles. Regulation of pancreatic secretion by the intestine is composed of three main mechanisms. 1. The proximal intestinal (duodenal) phase of the secretory response to a meal is elicited by nutrients within the proximal intestinal lumen. It is mediated mainly by interactions between cholinergic reflexes and release of the peptide hormone cholecystokinin (CCK). Recent data suggest that part of the action of CCK is not exerted directly on the acinar cellular level, but rather by modulation of cholinergic inputs. 2. The distal intestinal (ileal) phase is elicited by contact of the distal intestinal mucosa with nutrients that pass through the ileal lumen due to physiological malabsorption. The ileum (in contrast to the duodenum) induces net-inhibition of pancreatic secretion. The mediation is unknown, candidate mediators are PYY and GLP-1. 3. Intestinal feedback-regulation of pancreatic secretion in humans is controlled by intraluminal protease activity; this mechanism is not covered in the present paper.
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PMID:[Intestinal regulation of pancreatic enzyme secretion: stimulatory and inhibitory mechanisms]. 150 89

A 1.5-year-old girl was admitted with chronic diarrhea of 10 months duration and retarded physical and psychomotor development. Duodenal tryptic activity was absent on testing with secretin and cholecystokinin. With pancreatic enzyme replacement diarrhea ceased and growth recommenced. Duodenal tryptic activity returned to normal within 6 months. A 10-year follow-up revealed normal physical and mental growth. Secondary deficiency of trypsin is a rare cause of malabsorption in childhood; correct and timely treatment can avoid severe, irreversible developmental defects.
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PMID:[Malabsorption and developmental retardation due to secondary trypsin deficiency]. 168 66

This manuscript reviews the known satiety signals and the impact of antiobesity surgery on these physiological satiety mechanisms. Satiety signals originate from the stomach and small bowel to stop eating behavior. Stomach signals (gastric distension) produce early satiety by releasing hypothalamic cholecystokinin (CCK). The intermeal interval is probably mediated by peripheral CCK released by a threshold level of intraluminal calories. Anti-obesity operations probably rely little on these physiological satiety signals. Gastric balloons and gastroplasty produce nonphysiological gastric distension whereas intestinal bypass causes malabsorption. Gastric bypass combines supramaximal gastric distension with taste aversion from dumping. Future physiological manipulation of the satiety cascade will lead to improve obesity intervention.
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PMID:Physiological satiety implications of gastrointestinal antiobesity surgery. 173 29

The fractional absorption of vitamin B12 (FAB12) was measured by a double-isotope technique specially adapted for children. In six celiac children on a strict gluten-free diet and with a normal small intestinal biopsy, the FAB12 performed in the fasting patient averaged 30% (23-40%). After gluten challenge for a mean of 2 months (range 1-4), when mucosal damage was demonstrated by biopsy, the average fasting FAB12 in these patients decreased to 10% (0-17%) (p less than 0.05). However, when the FAB12 test was repeated by means of stimulation by a B12-free meal 1-3 weeks later, while the patients were still on a diet containing gluten, a significant increase was observed (mean 21%, range 14-27%) (p less than 0.05). In four of the six patients the B12 absorption was further evaluated by repeating the FAB12 test by means of intravenous cholecystokinin (CCK) stimulation (n = 3) or by administration of exocrine pancreas enzyme supplementation (EPES) (n = 2) or cobinamide (n = 1). These tests all showed FAB12 values within the range of the meal-stimulated FAB12. Moreover, in eight gluten-free celiac children with normal biopsies, no difference was found between fasting and meal-stimulated FAB12 values. Therefore, it is likely that the early-onset B12 malabsorption observed in the gluten-challenged celiac child with upper-small-intestinal mucosal damage is in part due to an insufficient stimulation of the exocrine pancreas when using the standard fasting B12 absorption test.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of the exocrine pancreas in early-onset vitamin B12 malabsorption in gluten-challenged celiac children. 191 49

Based upon the clinical finding that a Merck somatostatin-14 (S-14) analog induced steatorrhea in man, we sought to develop animal models to study the effects of S-14 and a series of synthetic analogs on absorption. Rats were trained to eat a diet (preweighed) containing 15% fat. Following the feeding period, the remaining diet was removed and the amount consumed recorded. This food conditioning of the rats was continued until the rats consumed approximately 15 g of the diet per day. Feces were collected and weighed prior to feeding periods. On test days, S-14 or analogs were administered sc to rats immediately prior to feeding. For each compound tested, fat absorption decreased in dose-dependent fashion. For example, S-14 at 0.5 mg/kg did not increase % of dietary fat in feces (% DFF). At 1.0 mg/kg, S-14 increased % DFF from 7.9 to 10.2 (p less than 0.01, pretest day vs test day), and at 10 mg/kg S-14, % DFF increased from 9.1 to 12.8 (p less than 0.001). For each analog, the subcutaneous dose required to decrease fat absorption in rats was several orders of magnitude higher than the intravenous dose required to inhibit insulin and glucagon. Moreover, the threshold for production of statistically significant increases in fecal fat differed among analogs when compared to their endocrine potencies. One analog administered in the model for 14 days was shown to produce consistent fat malabsorption throughout the entire test period; however, this lipid malabsorption was substantially more pronounced on the first three days of the treatment period. When the compound was not administered on day 15, the % DFF significantly decreased. In an attempt to develop a system more suitable for rapid screening, pancreatic secretagogues such as secretin or cholecystokinin, were administered intravenously to anesthetized rats whose duodena had been cannulated and perfused to enable collection of pancreatic secretions. Total amylase, lipase, and protein were determined in single animals in response to a secretagogue, both before and after iv pretreatment by S-14 or an analog. Pancreatic enzyme secretion in response to sequential secretagogue-stimulation was found to be reproducible for up to three injections and behaved in a dose-dependent fashion. In general, secretagogue-induced increases in amylase, lipase, and total protein were comparable. Pretreatment with the S-14 analogs substantially inhibited secretagogue-induced pancreatic exocrine secretion and was dose-dependent.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The effects of somatostatin and selected analogs on lipid absorption in animals. 286 42

Fatty acid composition were determined by gas chromatography in serum triglycerides and cholesterol esters of 32 patients (aged 7-17 years) with cystic fibrosis. According to their exocrine pancreas function (determined with secretin-cholecystokinin test), patients were divided in 3 groups. In comparison with previously measured values in 30 metabolically healthy children, patients with cystic fibrosis showed a significantly increased level of palmitic, palmitoleic, stearic, oleic, and linolenic acid in the triglyceride fraction and a significantly increased level of myristic, myristoleic, palmitoleic, stearic, oleic, and triene acid in the cholesterol ester fraction. However, in both fractions, concentration of linoleic acid was significantly decreased. It seems unlikely that malabsorption of ingested fat is responsible for the abnormalities in fatty acid pattern, because no significant differences could be found between the 3 patient's groups.
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PMID:[Fatty acid pattern in children with mucoviscidosis in relation to the degree of exocrine pancreas insufficiency]. 366 28

Mouth-caecum transit time (M-CTT) of a lactulose labelled liquid test meal has been measured in 27 coeliac patients and 10 healthy controls using the breath hydrogen technique. Although all patients were urged to maintain a gluten free diet, not all did, and there was, therefore, a wide range in the severity of fat malabsorption within the patient group. Gastric emptying of a 113Indium DTPA-labelled liquid test meal was also assessed in separate studies on six healthy controls and 11 of the coeliac patients. Fasting breath hydrogen concentrations and the response to lactulose, as assessed both by the rate of rise, and the peak breath hydrogen concentration reached, showed no difference between coeliacs and controls, regardless of the presence or absence of steatorrhoea. Mouth-caecum transit time in the 16 coeliac patients with steatorrhea (faecal fat greater than 7 g/24 h) was, however, significantly prolonged being 158 +/- 18 minutes (mean +/- SEM), compared with 70 +/- 9 minutes for the controls (p less than 0.02), and 83 +/- 15 minutes for the 11 coeliacs without steatorrhoea (p less than 0.002). Mouth-caecum transit time in the coeliac patients was linearly related to the 24 hour faecal fat excretion, r = 0.55, n = 27, p less than 0.01. Slow mouth-caecum transit in the coeliacs with steatorrhoea was not caused by delayed gastric emptying as the t1/2 for coeliacs with steatorrhoea was within the normal range. Coeliacs with delayed mouth-caecum transit had impaired insulin release but the postprandial profiles of the other peptides measured (cholecystokinin, GIP, secretin, motilin, neurotensin, enteroglucagon, and peptide YY) were all within the normal range in this group of partially treated coeliac patients.
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PMID:Delayed mouth-caecum transit of a lactulose labelled liquid test meal in patients with steatorrhoea caused by partially treated coeliac disease. 367 57

We evaluated the bentiromide test by analyzing para-aminobenzoic acid (PABA) in plasma and urine (a) for the identification of patients with complete pancreatic insufficiency and (b) as an alternative to the secretin-cholecystokinin test. Nine control subjects, 18 patients with cystic fibrosis, and 4 patients with Shwachman's syndrome were studied. Based upon the secretin-cholecystokinin test, pancreatic function was judged to be less than 0.1% of normal in 7 patients with cystic fibrosis and malabsorption and between 0.7% and 90% of control values in 11 patients with cystic fibrosis and 4 patients with Shwachman's syndrome without malabsorption. The bentiromide test was performed in two stages: first with bentiromide alone, then with equimolar free PABA. After ingestion of free PABA, the plasma profile and urinary excretion of PABA were comparable in controls, patients with cystic fibrosis, and patients with Shwachman's syndrome. Thirty minutes after oral bentiromide, plasma PABA values in patients with and without malabsorption were significantly lower than in the control group. From 60 to 180 min after ingestion, plasma PABA levels in patients without malabsorption were no different from controls; whereas levels in patients with malabsorption were significantly lower than in controls and in those without malabsorption, reaching the highest significance at 90 min. Similar results were obtained when the urinary excretion of PABA was considered. Only the 90-min plasma test reliably detected cystic fibrosis patients with steatorrhea, however. Duodenal colipase output was highly correlated with both the 90-min plasma test and the urinary excretion of PABA, with similar results for lipase and trypsin output. Reliable detection of pancreatic dysfunction, nevertheless, was not obtained even with the plasma test, in cystic fibrosis patients with greater than 5%-10% of the mean normal enzyme output. In patients with Shwachman's syndrome, none of whom had malabsorption, the plasma and urinary test failed to detect pancreatic dysfunction even with enzyme output as low as 1% of normal.
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PMID:Bentiromide test for assessing pancreatic dysfunction using analysis of para-aminobenzoic acid in plasma and urine. Studies in cystic fibrosis and Shwachman's syndrome. 387 4


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