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

The authors have investigated intestinal absorption of folic acid by jejunal perfusion with a triple lumen tube in five subjects with regional enteritis. The subjects' intestinal disabilities ranged from terminal ileitis to short bowel syndrome. Two had steatorrhea and two had low serum folate levels. Absorption of pteroylglutamic acid was normal in all five. This suggests that folic acid deficiency, common in this disorder, is largely caused by malnutrition, not malabsorption.
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PMID:Folic acid absorption in regional enteritis. 0 8

To clarify the role of fat maldigestion in the pathogenesis of steatorrhea in patients with ileal resection the total and aqueous phase concentrations of bile acid and fatty acid were characterized in 8 such patients (5 patients with small ileal resection, bile acid diarrhea, and steatorrhea less than 20 g per day; 3 patients with large ileal resection, fatty acid diarrhea, and steatorrhea greater than 20 g per day) as well as 4 healthy control subjects after a morning and an afternoon liquid test meal. The study was then repeated with cholestyramine, 4 g being administered before each meal to induce fat maldigestion. After a conventional test meal, patients with large resections and severe steatorrhea had significantly lower aqueous phase concentrations of bile acids (and fatty acids) than patients with smaller resections or control subjects, explained in part by intraluminal precipitation of about one-half of the bile acids during digestion. When cholestyramine was administered before the meal, aqueous phase bile acid concentrations decreased in all patients, including the normal control subjects; the degree of fat maldigestion induced in the patients with small resections (and the control subjects) became similar to that present after the conventional test meal in the patients with large resections. Because steatorrhea increased little in the patients with small resections when cholestyramine was administered continuously, the data suggest that fat maldigestion per se does not induce severe fat malabsorption in patients with sufficient anatomical reserve, because such patients can absorb fat efficiently by utilizing the distal small intestine. In patients with large ileal resections, severe steatorrhea is explained in part by the combination of fat maldigestion and decreased surface area. It is also speculated that the steatorrhea occurring in patients with small resections and relatively normal fat digestion during two test meals may be explained by impaired fat digestion which occurs during the final meal of the day, which is often the largest meal.
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PMID:Role of fat maldigestion in pathogenesis of steatorrhea in ileal resection. Fat digestion after two sequential test meals with and without cholestyramine. 0 60

To assess the fate and efficacy of orally ingested enzymes in pancreatic insufficiency, we administered pancreatin to six patients by two schedules--eight tablets with a standard meal or two tablets hourly--and in six normal controls, quantified duodenal enzyme activity and related inactiviation of ingested enzymes to gastric and duodenal pH; in the six patients we measured malabsorption by fecal balance studies. Postprandially, gastric pH was similar in health and pancreatic insufficiency, and below 4 after 40 minutes. Duodenal pH in pancreatic insufficiency declined to approximately 4 beyond 100 minutes--lower than in health (P less than 0.05). Approximately 22 per cent and 8 per cent of trypsin and lipase activity ingested with either schedule was delivered to the ligament of Treitz. Prandial was as effective as hourly administration in decreasing steatorrhea and perhaps more effective in abolishing azotorrhea, and since it is also more convenient, we recommend it.
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PMID:Fate of orally ingested enzymes in pancreatic insufficiency. Comparison of two dosage schedules. 1 13

The incidence rate of complications in patients, who underwent stomach resection as surgical treatment procedure is rather high (20%). Postprandial syndromes (dumping syndrome, lactose-intolerance, afferent loop-syndrome), malabsorption syndromes (anemia, osteopathia, steatorrhea, protein deficiency) and late organic manifestations (anastomotic and suture ulcers, retrograde intussusception, gastric-stump carcinoma) were usually summarized as "postgastrectomy syndrome". A review of pathogenesis, symptoms and therapeutic approach for the various postoperative disorders is given. Selective proximal vagotomy as the surgical treatment procedure of choice is emphasized.
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PMID:[Pathogenesis, clinical manifestations and treatment of the "postgastrectomy-syndrome" (author's transl)]. 3 63

Phosphorylcholine and homocysteine have an important choleretic action and also potentiate exocrine pancreatic secretion by way of stimulation and a more effective preparation of the substrate against attack by lipolytic enzymes. The protection offered by pancreatic enzymes in the correction of the digestive insufficiency in the endoluminal stage is also known. An analysis was therefore made of the action of an association of phosphorylcholine homocysteine and digestive enzymes in cases of exocrine pancreatic insufficiency and primary or secondary malabsorption. This action was evaluated on the basis of the reduction of elimination of steatorrhoea. For this purpose, faecal lipids were determined with the method proposed by van de Kramer et al. The most significant results were obtained in cases where digestive insufficiency was most marked, where correction of the pancreatic enzyme deficiency and improved biliary function were particularly required.
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PMID:[Therapeutic effect of a pharmacologic combination of choleretics and digestive enzymes in exocrine pancreatic insufficiency]. 4 15

100 g of spinach a day was added to the hospital diet of fifty-four patients with suspected malabsorption. Hyperoxaluria was found in thirty-eight patients; all of them had steatorrhoea. No patient with steatorrhoea had a urinary oxalate excretion of less than 40 mg a day. Ten other patients had hyperoxaluria, but the faecal fat determinations were regarded as unreliable in almost all and malabsorption could not be confirmed. It is suggested that in clinical practice determination of urinary oxalate after an oral load of oxalate could replace faecal fat determination in most patients with suspected malabsorption.
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PMID:Urinary oxalate on a high-oxalate diet as a clinical test of malabsorption. 7 94

We have studied 5 infants with persistent severe diarrhea from birth and marked abnormalities of absorption associated with failure to thrive leading to death in 4 infants. Three had siblings who died and a sibling of a 4th is ill at present, all with a similar illness; 2 were the products of consanguinous marriages. Exhaustive investigation failed to identify a recognized disease entity in any patient. Steatorrhea, sugar malabsorption, dehydration, and acidosis were severe in all patients, whatever the diet fed. Total parenteral nutrition was used, but excessive stool water and electrolyte losses persisted even when nothing was fed by mouth. There was no evidence of a hematological or consistent immunological defect in any infant and no abnormalities of intestinal hormones were noted. In the duodenal mucosa of all infants we saw similar abnormalities characterized by villus atrophy, crypt hypoplasia without an increase in mitoses or inflammatory cell infiltrate in the lamina propria and in villus enterocytes absence of a brush border, increase in lysosome-like inclusions, and autophagocytosis. In 3 infants studied by marker perfusion of the proximal jejunum we found abnormal glucose absorption and a blunted response of Na+ absorption to actively transported nonelectrolytes; in 2 there was net secretion of Na+ and H2O in the basal state. Our patients evidently suffered from a congenital enteropathy which caused profound defects in their capacity to assimilate nutrients. The similar structural lesion seen in the small intestinal epithelium of all of our cases undoubtedly contributed to their compromised intestinal function, but the pathogenesis of this disorder, if indeed it is a single disease, remains obscure.
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PMID:Familial enteropathy: a syndrome of protracted diarrhea from birth, failure to thrive, and hypoplastic villus atrophy. 10 Mar 67

Fourteen patients with ileal dysfunction due to resection or bypass were encountered over an 18-month period. Symptoms had been present for a mean period of 1.8 years. Diarrhoea was a universal symptom, and varied from mild to incapacitating. Weight loss, due in part to malabsorption and in part to the patients' fear of eating, occurred in 10 of 14 patients. The chief metabolic abnormalities were steatorrhoea and hypokalaemia. Vitamin B12 deficiency, folate deficiency, anaemia, hypoalbuminaemia, hypocalcaemia, hypomagnesaemia, hyperoxaluria, and an abnormal prothrombin ratio were less frequently seen. Treatment with cholestyramine and/or long-chain fat restriction effectively reduced diarrhoea in every case, and this was supplemented by replacement of specific deficiencies. There was little added benefit from non-specific antidiarrhoeal agents. It was found that the major symptoms of ileal dysfunction are readily treated, but that attention should also be given to a number of nutritional deficiencies.
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PMID:Consequences of ileal dysfunction: an approach to management. 10 34

A 63-year-old man with Waldenstrom's macroglobulinemia had severe steatorrhea, marked protein-losing enteropathy, and excessive endogenous fecal calcium clearance. The malabsorption and protein loss resulted in weight loss and hypoalbuminemia. In contrast, the striking enteric calcium loss was completely compensated by an increase in calcium absorption resulting in a positive calcium balance.
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PMID:Case report: intestinal clearance of calcium and protein in Waldenstrom's macroglobulinemia. 10 40

Before reviewing the consequences of extensive exeresis of the small intestine, the physiology of the entero-hepatic circulation of bile salts, the absorption of triglycerides and the varying sites of absorption of foodstuffs at intestinal level are discussed. It has been found that massive (i.e. at least 2/3) removal of the small intestine is incompatible with life owing to the onset of serious metabolic disturbances due to the increase in the speed of transit of foodstuffs from stomach to colon. Malabsorption of lipides causes steatorrhoea and is often associated with choleriform diarrhoea owing to the massive losses of water and electrolytes (Na, Cl, Ca, Mg). Some surgical techniques are illustrated and the local compensation mechanisms (anatomical adaptation of the intestinal mucosa, functional adaptation) designed to prolong transit time are described. Feeding must be parenteral for the first 2--3 months and oral during the alimentary adaptation phase.
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PMID:[Problems of alimentation in massive intestinal resections]. 12 96


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