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

The failure of standard oral pancreatic enzyme replacement therapy to correct malabsorption in patients with advanced pancreatic insufficiency is likely due to acid-peptic inactivation of ingested enzymes. Theoretically, the use of cimetidine, an H2-receptor antagonist, in conjunction with oral enzymes, would permit greater transgastric passage of ingested enzymes with resulting improvement in intraluminal lipolysis. To test this hypothesis, we studied the effects of orally administered cimetidine in two groups of patients by utilizing a previously validated double-marker perfusion technique. Cimetidine, in varying doses, had no effect on postprandial exocrine pancreatic function in 16 duodenal ulcer patients without pancreatic disease. In six patients with pancreatic insufficiency, cimetidine produced a pronounced decrease in the output of gastric acid and secretory volume, resulting in reduction of postprandial acidity and intragastric volume. These actions of cimetidine should retard or prevent inactivation of ingested enzymes and also increase their intragastric concentration, with resulting enhancement of luminal duodenal enzyme activity. Supplemental cimetidine may thus be useful in the medical management of patients who fail to respond to routine pancreatic extract therapy alone.
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PMID:Rationale for the use of cimetidine in pancreatic insufficiency. 34 Aug 5

The Authors examined 515 children with abdominal pain in the outpatient clinics for a period of two years. The pain was frequently periumbilical or mid epigastric with a history of more than two months. Persistent lactose malabsorption was found in 252 children (48,9%), which justifies the use of Breath Hydrogen Test as a first diagnostic procedure for assessing recurrent abdominal pain. Putative pathogens were identified in the stool specimens of 21 patients. Oesophagitis was diagnosed in 18 children and duodenal ulcer in one. 91 patients (less than 6 years old) improved after successful treatment of the chronic upper respiratory inflammations. The authors did not find any causes in 18.1 per cent of the children examined and they think that the abdominal pain in these children may be psychogenic. The use of high-fiber diet is proposed for the later group.
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PMID:[Chronic recurrent abdominal pain and lactose malabsorption in childhood]. 226 51

The tests with lactose loading followed by the assay of blood sugar were conducted in 500 normal subjects, aged from 18 to 89 years, and 262 patients with gastro-intestinal diseases, aged from 25 to 55 years. When lactose malabsorption was detected, aspiration biopsy of the small intestine mucosa was performed followed by the study of the structure and the level of a number of disaccharidases (lactase, maltase, saccharase). Lactose malabsorption was detected in 72 (14.4%) out of 500 normal subjects (10.6%--aged 18-59, and 20%--aged 60-89 years), among them there were 12.5% of Russians, 13% of Byelorussians and 5.8% of Ukrainians (aged 25-55 years). The secondary lactose malabsorption was recorded in 44% of patients with ulcerative colitis, in 33% of patients with chronic enterocolitis, in 11.5% of patients with gastric ulcer, in 8% of those with duodenal ulcer, in 23.5% of patients with chronic gastritis attended by lowered secretory function, and in 8% of those with enhanced secretory function.
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PMID:[Current problems of lactase deficiency]. 296 77

In 16 consecutive patients with systemic mastocytosis, we prospectively evaluated a variety of gastrointestinal functions and examined how they relate to the occurrence of gastrointestinal symptoms. Nine patients had either a duodenal ulcer or duodenitis. Hypersecretion of gastric acid was present in 6 patients, and in these patients the mean basal acid output was 20.7 +/- 4.1 mEq/h (range 14-39 mEq/h). Impaired small intestinal absorption occurred in 5 patients, although this was usually mild. The mean fractional emptying rate of liquids for all patients (14.7% +/- 2.3% per minute) did not differ from that for controls (10.7% +/- 0.6% per minute). Mean mouth-to-cecum transit time measured by breath hydrogen testing was the same among patients (87.7 +/- 6.7 min) and controls (86.7 +/- 8.0 min). Plasma histamine concentrations were increased in all patients (mean 1886 pg/ml, range 480-7450) and correlated with the basal acid output (r = 0.64, p less than 0.02) but not maximal acid output or the presence or absence of pain or diarrhea. Mean fasting plasma concentrations of motilin, substance P, and neurotensin from 6 patients did not differ significantly from controls, whereas gastrin and vasoactive intestinal peptide were significantly less than in controls (p less than 0.01). Gastrointestinal symptoms, consisting of abdominal pain or diarrhea, occurred in 80% of patients. Abdominal pain classified as dyspeptic was usually associated with acid-peptic disease of the duodenum and hypersecretion of gastric acid, whereas abdominal pain of a nondyspeptic character was not. Only in those cases of diarrhea consisting of greater than 200 g stool/day was gastric acid hypersecretion frequently found. Neither fecal urgency nor nondyspeptic pain could be accounted for by alterations of gastrointestinal transit. These results demonstrate that gastrointestinal symptoms, peptic disease, and mild malabsorption are much more common than described previously in patients with systemic mastocytosis. Furthermore, the results provide no evidence for the contention that altered gastrointestinal transit is involved in the pathogenesis of these symptoms.
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PMID:Gastrointestinal dysfunction in systemic mastocytosis. A prospective study. 339 14

The prevalence of pancreatic diseases as the cause for dyspepsia differs in clinical materials between 0 and 25-30%. In parallel, the incidence rate of chronic pancreatitis varies between 0.7 and 10 per 100,000 inhabitants per year. The correct figures are unsettled. The main reason for the great variability in figures for frequency of chronic pancreatitis is probably the different clinical awareness and variable practice for performing morphological and functional studies of the pancreas in patients with dyspepsia. Epidemiologic data indicate, but do not prove, an increasing frequency of chronic pancreatitis at least valid for the alcoholic chronic pancreatitis. Pancreatic function and pancreatic disease are probably connected to different gastro-intestinal diseases (duodenal ulcer, inflammatory bowel diseases, malabsorption syndromes, subtotal and total gastrectomy and to some extent in patients with hepatobiliary diseases). The prevalence of chronic pancreatitis can be calculated to around 70 per 100,000 inhabitants in the Western world. Around one-third of these present with exocrine pancreatic insufficiency. The demand for enzyme substitution based on marked exocrine pancreatic insufficiency in patients with chronic pancreatitis, pancreatic cancer and mucoviscidosis can be calculated to approximately 150 patients per 1 million inhabitants. The question concerning the analgetic effect of pancreatic enzyme substitution is still unsettled.
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PMID:Exocrine pancreatic function in dyspepsia. 349 32

An outline has been given of the major abnormalities of coagulation which can occur secondary to diseases in previously normal individuals. First, the disorders due to deficiency of the vitamin K-dependent clotting factors are described. Vitamin K deficiency can occur in the newborn, or at later stages in life when there is intestinal malabsorption. The malabsorption disorders, such as coeliac disease, together with major abdominal surgery or prolonged use of broad-spectrum antibiotics can give rise to vitamin K deficiency. Additionally, in obstructive jaundice the lack of secretion of bile salts into the upper intestine causes vitamin K malabsorption. The use of oral anticoagulants is associated with haemorrhage in a small proportion of patients. These patients usually have an excessively prolonged prothrombin time, due to overdosage with anticoagulants, but occasionally haemorrhage can occur from a localized bleeding site, such as a duodenal ulcer, in patients under good anticoagulant control. The large number of drugs which can interact with anticoagulants are listed, from which it can be seen that careful monitoring of all patients on oral anticoagulants must be carried out. The haemostatic defects associated with liver disease are then tabulated. In this situation abnormalities may be due to deficient synthesis of coagulation factors in hepatocellular failure, by failure of vitamin K absorption, and also by disseminated intravascular coagulation (DIC). DIC occurs in hepatocellular failure, because the liver cells are normally responsible for clearing activated products of the coagulation and fibrinolytic enzyme systems. The presence of clinical haemorrhage and haemostatic breakdown in hepatic disease usually indicates a serious prognosis, but appropriate replacement therapy is indicated in this situation. Disseminated intravascular coagulation embraces a large number of clinical haemorrhagic syndromes, where intravascular activation of the coagulation system takes place accompanied by compensatory fibrinolytic activity. DIC can be initiated by intravascular release of procoagulant substances, such as tissue thromboplastin, or by damage to vascular endothelium and platelets. The main clinical conditions associated with DIC comprise the severe infections and septicaemias, obstetric accidents, shock and trauma, neoplasia and snake-bite envenoming. In all instances, the pathophysiological disorder of haemostasis is managed by treating the underlying disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acquired coagulation disorders. 389 41

The available data show that GIP is at present the strongest candidate for the insulin-secreting factor of the gut named incretin. Its release is triggered by the absorption of ingested nutrients. GIP acts on the B-cells of the pancreas by potentiating glucose-induced insulin secretion. The role of GIP as an enterogastrone is less well established. The release of GIP from the gut cells seems to be regulated by the composition and the amount of the ingested food, by the rate of absorption of nutrients by neural factors (vagal), and by feedback control mediated by insulin. In addition, the adaptation of the intestine to individual eating habits influences the response of the GIP cells. It is suggested that an overactive enteroinsular axis, i.e. enhanced GIP secretion, participates in the development of the hyperinsulinaemia of obesity and maturity onset diabetes mellitus. In gastrointestinal diseases accompanied by malabsorption the GIP response is diminished. In gastrointestinal disorders with rapid gastric emptying (duodenal ulcer) or with accelerated passage of the nutrients through the intestine, hypersecretion of GIP and insulin occurs. This may be significant for the reactive hypoglycaemia of these conditions.
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PMID:Gastric inhibitory polypeptide. 610 91

The effects of ranitidine, a new potent histamine H2-receptor antagonist, on gastric intrinsic factor (IF) secretion and protein-bound cobalamin absorption were evaluated in 6 patients with duodenal ulcer, before, during and after discontinuation of ranitidine therapy. Oral ranitidine (150 mg twice a day) resulted in a non significant decrease of IF concentration and IF output but was responsible for malabsorption of protein-bound cobalamin. This malabsorption was reversible upon discontinuation of ranitidine. These results indicate that occurrence of cobalamin deficiency cannot be excluded during long-term ranitidine treatment and emphasize the need for careful follow-up in these patients.
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PMID:[Effect of ranitidine on secretion of gastric intrinsic factor and absorption of vitamin B 12]. 613 42

The suppressive effects of cimetidine on acid, pepsin, and intrinsic factor secretion have been well documented; however, the effect of cimetidine on cobalamin absorption has not been assessed. The absorption of both unbound [57Co]cyanocobalamin and protein-bound [57Co]cyanocobalamin was evaluated in 12 patients with duodenal ulcer disease during and after discontinuation of cimetidine therapy. Cimetidine administration did not lead to malabsorption of unbound cobalamin but caused malabsorption of protein-bound cobalamin (0.22 +/- 0.08%, [mean +/- 1 SEM] versus 2.3 +/- 0.10% in control subjects, P less than 0.01). This malabsorption was reversible upon discontinuation of cimetidine. Patients on cimetidine therapy malabsorb protein-bound cobalamin and, during long-term treatment, are at risk for developing cobalamin deficiency. This malabsorption was reversible upon discontinuation of cimetidine. Patients on cimetidine therapy malabsorb protein-bound cobalamin and, during long-term treatment, are at risk for developing cobalamin deficiency. This malabsorption of protein-bound cobalamin is not detectable by the usual tests of cobalamin absorption which employ unbound cobalamin.
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PMID:Malabsorption of protein-bound cobalamin but not unbound cobalamin during cimetidine administration. 676 34

Over a 2.5-year period, 82 consecutive children complaining of recurrent abdominal pain underwent upper gastrointestinal endoscopy. Gastroscopy confirmed pathology in 48 of the children (58.5%). Four of the children, who also had undergone gastroscopy, had other diagnoses (lactose malabsorption, hydronephrosis, yersiniosis), and 30 of the children (36.6%) retained the initial diagnosis of recurrent abdominal pain syndrome. Gastritis was found in 48 of the children, 18 of whom (37.5%) had positive test results for Helicobacter pylori, based on histology and/or culture. Of 16 H. pylori-positive children tested, 12 (75%) also had an elevated concentration of IgG-class antibodies to H. pylori in their sera. Three of the children had duodenal ulcer disease, all of whom were H. pylori positive. Esophagitis was found in eight of the children with gastritis, all of whom were found to have gastroesophageal reflux. Our data suggest that among the children with recurrent abdominal pain syndrome, organic pathology is more common than was previously thought. Altogether 22% of the children with recurrent abdominal pain syndrome were infected with H. pylori.
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PMID:Upper gastrointestinal endoscopy in recurrent abdominal pain of childhood. 849 55


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