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

Alcohol and a number of drugs (e.g., neomycin, cholestyramine, antacids, laxatives, paraminosalicyclic acid, colchicine and oral hypoglycemic agents) can cause malabsorption due to drugs and alcohol is surveyed. Examined in detail are the mechanisms of malabsorption produced by neomycin and cholestyramine, and the factors responsible for malabsorption in the chronic alcoholic.
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PMID:Drugs, alcohol and malabsorption. 11 5

Effects of ethanol on the gastrointestinal tract are reviewed, and an overview of possible mechanisms of ethanol damage to the alimentary tract is presented. Ethanol toxicity most commonly results in metabsorption. Mechanisms contributing to ethanol-induced calcium malabsorption are considered in detail as a prototype for problems encountered in evaluating effects of toxicants on intestinal function. Effects at the local level in the intestine must be differentiated from systemic effects. The mechanism of suppression of calcium absorption by chronic ethanol ingestion differs from that produced by acute administration. Effects of acute administration appear to be due to local mucosal damage and are reversed in 18 hr. Such damage is not present with chronic administration, which affects only duodenal transport. Treatment with vitamin D and its metabolites does not reverse the inhibition of calcium transport. The overall findings suggest that ethanol inhibition of calcium transport is mediated at the intestinal level, probably affecting vitamid D independent mechanisms.
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PMID:Ethanol and development of disease and injury to tha alimentary tract. 59 53

Absorption of 57Co-labelled vitamin B12 - intrinsic factor (IF) complex and its binding to mucosal precipitate and brush border fractions of rat small intestine was studied in rats pair-fed with a liquid diet containing ethanol 5 g/100 ml, 35% of calories, or isocalorically substituted sucrose. IF was obtained from rats fasted for 18 h. and for each experiment the amount of vitamin B12 added was the minimum required to achieve maximum binding to IF. Rats fed alcohol exhibited hepatic steatosis, proliferation of smooth endoplasmic reticulum, and disordered mitochondria after 6 weeks on the diet, and absorption of vitamin B12, fed with IF by stomach tube, was reduced signficantly. In contrast, binding of 57Co-labelled vitamin B12 -IF complex to mucosal precipitate and brush border fractions was never less than that of fractions from control rats at 4, 8 and 12 weeks on the alcohol diet. Furthermore, binding to the brush border was significantly greater in alcohol-fed rats at 12 weeks whether expressed per unit of beta-naphthylamidase (EC 3.4.1.1) activity or per milligram of protein. Total mucosal sucrase (EC 5.2.1.26) and beta-naphthylamidase were unchanged or slightly increased (beta-naphthylamidase at 12 weeks) on the alcohol-containing diet indicating that total brush border membrane was not reduced. Total brush border binding activity was the same in alcohol-fed and control rats at each time period. These results indicate that malabsorption of vitamin B12 in rats fed alcohol cannot be due to decreased binding of the vitamin B12 - IF complex by brush border membrane receptors, or secondary to a net decrease in membrane receptors.
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PMID:Lack of effect of alcohol on small intestinal binding of the vitamin B12 - intrinsic factor complex. 97 75

Lactose-tolerance-test (LTT), ethanol-lactose-tolerance-test (ELTT), 14CO2 breath test and 14C-glucose determination were simultaneously performed in 27 healthy subjects, 16 patients with a Billroth II gastrectomy and 6 patients with a malabsorption syndrome. Intestinal mucosal lactase was absent or significant diminished in 5 of the B II cases and in all patients with malabsorption. In the lactase deficient patients a diminished serum glucose rise after ingestion of 50 g lactose was observed in LTT as well as in ELTT. False positive results in LTT could not be prevented by performing the ELTT. Furthermore the ELTT is not suitable for ambulant investigations because of the required high ethanol load of 0.5 g/kg. Most reliable results were obtained by determination of 14C-serum-glucose after oral application of about 15 muCi of 14C lactose. In respect to lactase level neither false positive nor false negative results were observed. For clinical investigations the procedure of isolation and measurement of 14C-glucose is too laborious however. 14CO2-exhalation test cannot be recommended because of many false positive and false negative results. Moreover 14CO2-exhalation seemed to be insensible and predominant depending on factors other than lactose absorption.
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PMID:[Diagnostics of lactose-malabsorption: value of tolerance tests and 14CO2 exhalation test in patients with and without lactase deficiency (author's transl)]. 99 41

Xylose absorption was measured, within ten days of being admitted to hospital, in 54 alcoholics with neurological abnormalities. Small-intestine malabsorption was demonstrated in 19. Classified according to the customary clinical diagnoses, 16 of 49 with alcohol polyneuropathy had abnormal values, with no correlation to nerve conduction velocity. There was also no difference among 14 in predelirium and eight in delirium. However, all four patients with Wernicke's encephalopathy had a malabsorption syndrome. These results are similar, also quantitatively, to those reported in the literature in alcoholics without neurological signs. Alcohol may be involved in the pathogenesis of alcoholic polyneuropathy both as a toxic factor and also via nutritional deficiency.
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PMID:[Alcohol and malabsorption in the pathogenesis of peripheral and central nerve damage (author's transl)]. 113 26

Malnutrition is common among alcoholics because alcohol displaces protein-, vitamin-, and mineral-containing foods in the diet, and chronic alcohol consumption results in maldigestion and malabsorption of essential nutrients. In addition, alcohol exerts direct toxic effects on both the liver and gut, resulting in structural alterations in the intestine and the development of fatty liver, alcoholic hepatitis, and cirrhosis. Liver injury is preceded by an adaptive phase characterized by accelerated metabolism of drugs (including ethanol), and hyperlipemia, secondary to hypertrophy and hyperactivity of the smooth endoplasmic reticulum. Side effects include enhanced hepatotoxicity of CCI4 and possibly energy wastage. Alcoholics should not be led to beleive that correction or prevention of nutritional deficiency will prevent liver damage in the face of continued alcohol abuse.
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PMID:Alcohol and malnutrition in the pathogenesis of liver disease.. 117 54

In order to collect data on (1) the prevalence of lactose malabsorption and (2) the value of indirect diagnostic methods for hypolactasia in diabetics, we compared lactose tolerance tests using serum glucose, serum galactose (after oral ethanol intake) and breath hydrogen excretion as diagnostic cutoff in 144 nondiabetic and 46 diabetic subjects. A good rate of concordance was found for the hydrogen breath test and galactose-dependent lactose tolerance test. The glucose-dependent lactose tolerance test was found to be of satisfactory diagnostic value in nondiabetic subjects and was useless for diagnostic purposes in diabetics. Lactose malabsorption was no more frequent in diabetics than in controls and lactose intolerance was found to be less frequent in the diabetic group. A distinction between hypolactasia and other gastrointestinal disorders in diabetics is possible by ambulatory indirect tests.
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PMID:Concordance of indirect methods for the detection of lactose malabsorption in diabetic and nondiabetic subjects. 186 74

Abuse of alcohol is considered to be an important risk factor for fractures and osteoporosis. Alcohol abuse is associated with deleterious changes in bone structure detected by histomorphometry, and with a decrease in bone mineral density. These changes may also be produced by factors commonly associated with alcohol abuse, e.g., nutritional deficiencies, liver damage, and hypogonadism. Thus the etiology of alcohol-associated bone disease is multifactorial. Alcohol has, however, clear-cut direct effects on bone and mineral metabolism. Acute alcohol intoxication causes transitory hypoparathyroidism with resultant hypocalcemia and hypercalciuria. Prolonged moderate drinking elevates serum parathyroid hormone (PTH) levels, whereas chronic alcoholics are characterized by low serum levels of vitamin D metabolites with resultant malabsorption of calcium, hypocalcemia, and hypocalciuria. Independently of whether alcohol consumption is of short duration, social, or heavy and chronic, it seems to suppress the function of osteoblasts, as evidenced by low serum levels of osteocalcin. It has recently been reported, however, that alcohol can also have a beneficial effect on bone. Among postmenopausal women, moderate alcohol consumption correlates positively with central and peripheral bone mineral density, and with serum estradiol levels.
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PMID:Alcohol and bone. 193 4

Chronic consumption of substantial amounts of alcohol is not associated with the expected effect on body weight. Isocaloric substitution of carbohydrates by ethanol results in weight loss, and addition of ethanol to an otherwise normal diet does not produce the expected weight gain. This energy deficit cannot be explained by maldigestion or malabsorption but has been attributed to induction of the microsomal ethanol oxidizing system (a metabolic pathway that oxidizes ethanol without associated chemical energy production), increased sympathetic tone and associated thermogenesis, and/or enhanced ATP breakdown (with increased purine catabolism) secondary to the acetate produced from ethanol. All these hypotheses do not fully explain the lack of weight deficit when alcohol is consumed with a very-low-fat diet, which suggests that an alteration in the energy utilization derived from fat plays a major role, possibly through uncoupling of oxidation with phosphorylation in mitochondria damaged by chronic ethanol consumption.
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PMID:Perspectives: do alcohol calories count? 195 30

We used the miniature pig to evaluate the effect of ethanol ingestion on the hydrolysis of pteroylpolyglutamate and on the uptake of pteroylmonoglutamate (PteGlu) by the intestinal brush border membrane, processes that are required for folate absorption. After feeding ethanol or sucrose at 60% of calories for 11 mo, the uptake of PteGlu by jejunal brush-border-membrane vesicles was similar in both groups of animals. Jejunal brush border pteroylpolyglutamate hydrolase was decreased by one-half in the ethanol-fed group. Jejunal brush-border-membrane fluidity, measured by fluorescence polarization, was similar in both groups. Acute exposure of the jejunal vesicles to ethanol increased membrane fluidity and decreased hydrolase activity but had no effect on PteGlu transport. Inhibition of jejunal folate hydrolase by chronic exposure to ethanol may be an early effect in the pathogenesis of folate malabsorption and deficiency in chronic alcoholism.
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PMID:Folate absorption in alcoholic pigs: in vitro hydrolysis and transport at the intestinal brush border membrane. 259 33


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