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

The levels of plasma carotenoids were markedly reduced in broiler cockerels infected with Eimeria acervulina or E. tenella. The mechanisms of this depigmentation differed between the two species, being primarily associated with interference of absorption of xanthophyll (carotenoids) from the intestinal lumen with E. acervulina infection and with leakage through the damaged wall of the cecum with E. tenella infection. Chicks reared on an essentially carotenoid-free diet and inoculated with E. acervulina showed no detectable levels of carotenoids in the blood 48 hours after being changed to a diet containing 30 mg of xanthophyll/kg. Conversely, uninoculated chicks and chicks inoculated with E. tenella showed significant and similar increases in plasma levels of carotenoids. Chicks reared on a diet containing xanthophyll and inoculated with E. tenella showed a more rapid decrease in plasma carotenoids than did uninoculated controls when changed to a xanthophyll-free diet. In chicks fed high xanthophyll diets containing chromic oxide, no indication of malabsorption was seen in chicks infected with E. tenella compared with uninoculated controls, whereas chicks inoculated with E. acervulina showed significantly less xanthophyll absorption. Conversely, a marked increase in the xanthophyll : Cr2O3 ratio was observed in the cecal contents of chicks inoculated with E. tenella compared with uninuoculated controls or those inoculated with E. acervulina. Studies of uninoculated chicks pair-fed with chicks inoculated with E. acervulina or E. tenella indicated that the decrease in plasma carotenoids and increases in intestinal pH are not associated with the reduced intake of feed associated with infection. The studies involving uninoculated birds with reciprocal chagnes between high and low xanthophyll diets indicated that plasma carotenoids are a more rapid and sensitive means of measuring changes in pigmentation levels than are visual skin scores carotenoid levels from the skin.
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PMID:Some mechanisms of reduction of carotenoid levels in chickens infected with Eimeria acervulina or E. tenella. 0 Apr 76

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

The intraluminal fate of orally administered radioactive vitamin B12 has been studied in control subjects with normal vitamin B12 absorption and those with vitamin B12 malabsorption due to tropical sprue. In control subjects 1 to 21% of the dose was bound to sedimentable material and 37 to 75% was bound to immunoreactive intrinsic factor. In subjects with vitamin B12 malabsorption due to tropical sprue, the results were identical with the control subjects. Bacteriological studies showed a statistically significant correlation between both the number of flora in the jejunum and the number of bacteroides in both the jejunum and ileum and vitamin B12 malabsorption. In patients with tropical sprue who have normal intrinsic factor secretion, the vitamin B12 absorptive defect is not due to binding of the vitamin to bacteria or to alteration to the intrinsic factor vitamin B12 complex in the intestinal lumen. The lesion appears to be one of the mucosal cell receptors or of the cells themselves, possibly caused by bacterial toxins.
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PMID:Vitamin B12 absorption--a study of intraluminal events in control subjects and patients with tropical sprue. 0 57

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

The pH of the stool and the amount of reducing substances present were observed in 51 normal neonates aged 5 to 8 days. A stool pH of 5 or less was found in 6, 4 of whom were exclusively breast fed. Reducing substances, 0-5% or more, were found in the stools of 16. Stool chromatography in 13 showed lactose, glucose, galactose, or a variable combination of these sugars--that is, a pattern consistent with lactose malabsorption. The stools of 3 infants contained oligosaccharides or maltose only. Chromatography of urine from 60 normal neonates showed detectable sugars in 11 but only 3 had levels above 50 mg/100 ml.
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PMID:Stool and urinary sugars in normal neonates. 0 29

1. Pteroylmonoglutamic acid (PteGlu) absorption has been measured by using the technique of small-intestinal perfusion with tritiated PteGlu in normal subjects and in patients with coeliac disease. 2. At similar intrajejunal pH, patients with untreated coeliac disease have significantly less PTEGlu than normal subjects and patients with treated coeliac disease. 3. The "resting" pH in the jejunum did not differ markedly between normal subjects and patients with coeliac disease. 4. Increasing pH decreased PteGlu absorption in patients with coeliac disease and in normal subjects. 5. These findings suggest that PteGlu malabsorption in coeliac disease is not due to abnormally high pH in the jejunum.
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PMID:The effect of pH on folic acid absorption in man. 0 22

A 36 year old man with panarteriitis nodosa (PAN) presented over a certain period of time meinly with gastrointestinal symptoms. He was HBsAg positive and a "reactive" hepatitis with histologically demonstrated. Arterial microaneurysms and stenoses were detected by angiography in the liver, kidney and small intestine. These findings were confirmed by autopsy. Vascular occlusions had caused infarctions of the small intestine as well as necroses and ulcerations of the large bowel. Chronic ischemia is considered as cause of the patient's malabsorption-syndrome. It is suggested, that cachexia of PAN may be partly due to malabsorption.
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PMID:[Malabsorption caused by HBsAg-positive panareteritis nodosa]. 0 47

Folic acid is one of the 'younger' vitamins, yet it has attracted intensive study in the thirty years since the identification of pteroylglutamic acid and its polyglutamyl conjugates. The absorption and malabsorption of folates, natural, purified and synthetic, in disease has been studied more than any other vitamin and indeed folate absorption has become one clinical test of intestinal function. We know little about the release of folate from protein complexes, but we have learned, with the help of synthetic radiolabelled pteroylpolyglutamates that polyglutamyl folates are hydrolysed at or near the luminal border of the intestine and the released folate is efficiently absorbed. The rate limiting stage of folate absorption appears to be the transport of the monoglutamyl folate. In disease, and with drugs, folate malabsorption occurs primarily when monoglutamyl transport is depressed. The specific components of the folate transport system, listed in Table 4, are receiving increased attention. The mechanism of uptake is still a topic of controversy but a dual system including both a saturable and a diffusion component would explain most of the data. Reduction and methyl or formyl addition occur in the intestine but such metabolism is not obligatory for transport. The nature of folate binding within the cell and the function of specific folate binding proteins requires further study. At present we have little or no information about the mechanism of folate release from the epithelial cell to the circulation but this step also could influence the rate and specificity of overall process. The tools are now at hand to complete our understanding of the steps in folate absorption and metabolism. Such an understanding should facilitate the management of folate deficiency whenever it complicates gastrointestinal disease or drug therapy.
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PMID:Absorption and malabsorption of folates. 1 Jan 21

To determine the mechanism by which pancreatic extract (PE) corrects the malabsorption of vitamin B12 in chronic pancreatic insufficiency (CPI), the following hypotheses were investigated: Firstly, PE might stimulate the absorption of vitamin B12 by changing the intestinal pH, secondly PE might stimulate the intestinal uptake of unbound vitamin B12, thirdly PE might abolish the inhibitory effect of vitamin B12 binders on the intestinal uptake of vitamin B12 bound to intrinsic factor (IF). PE had no effect on the pH in the small intestine and did not stimulate the uptake of unbound 57CoB12 by perfused rat intestinal segments. Preincubation of 57CoB12-IF with a non-IF B12-binder from human saliva (R-binder) reduced the uptake of 57CoB12 from 18.5 pg per cm intestine +/- 3.4 S.E.M. to 7.8 +/- 1.6 (p less than 0.02). PE abolished this inhibitory effect (p less than 0.05). The results indicate that PE corrects the malabsorption of vitamin B12 in CPI by an effect on non-IF B12- binders.
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PMID:Pancreatic extract and the intestinal uptake of vitamin B12. III. Stimulatory effect in the presence of a non-intrinsic factor vitamin B12 binder. 1 12

Human beings today living in high industrialized areas suffer more frequently from fungal diseases than before. This is due to the management in animal production, but also to the use of cosmetics and contraceptives, smoking cigarettes, wearing clothes of synthetic polymers and application of new drugs, like antibiotics, cytostatics, immunosuppressives and others, which favours the growth of certain fungi in and on the skin and inside the human body. Some mechanisms are known from the macroorganism which are able to protect man from fungal invasion. Effective in this way are the normal flora of the skin, gut and the mucous membranes, the enzymes digestive and the natural low pH of the healthy skin. The fungal growths are favoured when primary diseases of not-infectious genesis due to disorders in metabolism or endocrinium, vitamin deficiency, malabsorption, maldigestion, false and malnutrition, and diseases of the haemopoetic system exist. But also viral and bacterial infections stimulate the development of secondary fungal diseases. The pathogens belong to three groups, dermatophytes, yeasts and molds, which can be differentiated according to their behaviour in culture and in tissue.
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PMID:[Mycoses. Pathogenicity and diagnosis of dermatophytes, yeasts and molds]. 1 35


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