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

A gas-solid chromatographic system using tandem silica gel and molecular sieve columns is described for the measurement of hydrogen, carbon dioxide, oxygen, and nitrogen in samples of respiratory gases. This system has a detection limit of 2 ppm of hydrogen in a 1 ml sample and can measure 120 ppm H2 and 5% CO2 with relative standard deviations of 1.3% and 1.7%, respectively. Improved sample storage and withdrawal techniques are described that give reproducible values for up to 6 weeks after collection. Finally we show that normalization of breath hydrogen values to an alveolar concentration, using the observed carbon dioxide concentrations, substantially reduces the range and variance of apparent H2 concentrations in human subjects. Normalization eliminates the need for rebreathing or end-expiratory collection techniques and substantially increases the reliability and clinical utility of hydrogen breath measurements in noninvasive tests of carbohydrate malabsorption.
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PMID:Improved gas chromatographic quantitation of breath hydrogen by normalization to respiratory carbon dioxide. 50 Dec 2

Sixteen male patients with stable chronic obstructive airways disease were separated into two groups of eight according to arterial carbon dioxide tensions. Hypercapnia was associated with lower arterial oxygen tensions, higher red cell volume, and increased weight, while normocapnic subjects were decidedly thin. The considerable difference in body weight between the two groups could not be explained by variation in caloric intake, and malabsorption was excluded as a cause of weight loss in the underweight subjects. Serum tri-iodothyronine, thyroxine, cortisol, and oestradiol concentrations were similar and normal in each group, but both groups had significantly low testosterone values as compared with controls, values in the hypercapnic being appreciably lower than in the normocapnic group. The adrenal androgen dehydroepiandrosterone was significantly high in the normocapnic group and low in the hypercapnic group compared with controls. Serum pituitary luteinising and follicle stimulating hormones were normal, but three hypercapnic individuals had high serum prolactin values. Early morning urinary aldosterone values were significantly higher in the hypercapnic than in the normocapnic group. Such hormone comparisons have not previously been made in subjects with chronic obstructive airways disease grouped according to arterial blood gas values, and it is concluded that major alterations in adrenal and testicular function may occur, possibly due to pituitary suppression from hypoxia. Such hormonal changes might in part account for the contrasting alterations in body habitus found in this condition.
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PMID:Diet, absorption, and hormone studies in relation to body weight in obstructive airways disease. 54 19

In summary, little progress has been made in the past several years with respect to the treatment of the baby with BPD. The conduct of convincing clinical research seems to be a casualty of budget cuts and a rush to learn the tools of molecular biology. To date, there are no clinical trials that have convincingly demonstrated that long-term diuretic, bronchodilator, vasodilator, or antioxidant therapy is effective in the treatment of chronic BPD. Short-term corticosteroid therapy hastens extubation, but long-term outcome is unaffected and serious questions remain about its safety. Multicenter clinical trials should be carefully designed and implemented to address the values of these therapies. In the design of these trials, care should be taken to stratify treatment groups for known risk factors for BPD. What are the future directions for the treatment of BPD? It is hoped that new BPD treatment strategies will be based on an improved understanding of mechanisms of lung repair and inflammation. Enzyme, gene, cytokine, antioxidant, and antiprotease therapies are being developed in animal models of lung injury. In addition, the use of lung transplantation has begun to be explored for severe cases of BPD. It is also possible, as has occurred in many chronic idiopathic diseases, that nonspecific treatment may prove beneficial. Perhaps it is only a matter of time before intravenous immunoglobulin, cyclosporine, methotrexate, or "biological response modifiers" will be administered to infants with severe BPD. For example, there is anecdotal evidence that recombinant human growth hormone may improve respiratory muscle function in adults with chronic obstructive pulmonary diseases. In the absence of convincing clinical trials, the clinician should reserve existing therapies for the ventilator-dependent infant or infants whose high oxygen requirement is prohibiting discharge or resulting in complex home care or frequent rehospitalizations. It should be emphasized that continuous oxygen therapy combined with avoidance of environmental inhalant and infectious hazards have the strongest rationale and widest margin of safety for treatment of the infant with BPD. Ironically, oxygen therapy is frequently underutilized and discontinued too rapidly. Early discontinuation of oxygen therapy with alveolar hypoxia results in feeding difficulty, slow growth, nutrient malabsorption, bronchoconstriction, and pulmonary hypertension. Oxygen therapy, although more cumbersome and certainly less glamorous than other pharmacologic agents, remains the essential element of BPD care.
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PMID:Current therapy of bronchopulmonary dysplasia. 152 72

Phosphorus is the sixth most abundant element in the body after oxygen, hydrogen, carbon, nitrogen, and calcium. It comprises about 1% of the total body weight of humans. Eighty-five percent of it is stored in the bone in the form of hydroxyapatite crystal; 14% is in the soft tissues in the form of energy-storing bonds with nucleotides (ATP, GTP), nucleic acids in chromosomes and ribosomes, 2,3-DPG in the red blood cells, and phospholipids in the cells' membranes. Less than 1% is in the extracellular fluids. Phosphate balance is maintained by multiple systems. The gut is responsible for the absorption of two thirds of the 4-30 mg/kg/day of phosphate intake. Absorption sites are all along the gut; in humans the most active site is the jejunum. The kidney filters 90% of the plasma phosphate and reabsorbs it in the tubuli. In states of hypophosphatemia the kidney can reabsorb the filtered phosphates very efficiently, reducing the amount excreted in the urine virtually to zero. The healthy kidney can excrete high loads of phosphate and rid the body of phosphate overload. Through the vitamin D-PTH axis the endocrine system regulates the phosphate balance by influencing the kidney, gut, and bone. Other hormones, including thyroid, insulin, glucagon, glucocorticosteroid, and thyrocalcitonin, play a lesser role in regulation of phosphate metabolism. Because of the complex control of phosphate homeostasis, various clinical conditions may lead to hypophosphatemia. These include nutritional repletion, gastrointestinal malabsorption, use of phosphate binders, starvation, diabetes mellitus, and increased urinary losses due to tubular dysfunction. The clinical picture of phosphate depletion is manifested in different organs and is due mainly to the fall in intracellular levels of ATP and decreased availability of oxygen to the tissues, secondary to 2,3-DPG depletion. The various manifestations of phosphate depletion are listed in Table 2. The treatment of hypophosphatemia consists of administering enteral or parenteral phosphate salts. An important aspect of dealing with the potentially serious effects of phosphate depletion is to prevent the depletion from happening in the first place. Hyperphosphatemia can occur in renal failure, hemolysis, tumor lysis syndrome, and rhabdomyolysis. The treatment of hyperphosphatemia usually consists of fluid administration (in the absence of kidney failure). In chronic hyperphosphatemia, phosphate binders such as aluminum and magnesium salts can reduce the phosphate load. The use of these phosphate binders is limited by their potential side effects.
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PMID:Consequences of phosphate imbalance. 306 Jan 61

Infants are born with low tissue stores of tocopherol and accumulate this vitamin from feedings after birth. If prolonged malabsorption of tocopherol occurs, a recognized hemolytic anemia and spinocerebellar degeneration develops after a period of months to years. This is preventable with tocopherol supplementation. However, a benefit of tocopherol supplementation in premature infants who are transiently unable to feed after birth has been harder to prove. Pharmacologic doses have not definitively been shown to be beneficial in any of the putative oxygen toxicity syndromes, with the possible exception of PV/IVH. It is exciting that tocopherol appears to reduce significantly the incidence and severity of IVH, and this potential application underscores the urgent need for pharmacologic studies of this lipid nutrient. In order to administer the drug safely, we must establish the best means of assessing sufficiency and toxicity in premature infants. Measures of tissue capacity to resist oxidative stress appear to be the most promising of these tests at this time. In the interim, a working proposition is to provide sufficient tocopherol to these infants to raise the plasma levels into the range considered normal for term, breastfed infants.
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PMID:The role of vitamin E therapy in high-risk neonates. 306 10

In order to study arterial concentrations and splanchnic exchange of substrates and hormones in patients with chronic inflammatory bowel disease three patients with Crohn's disease and four with ulcerative colitis were studied using the hepatic venous catheter technique. Systemic turnover and regional exchange of free fatty acid were evaluated using intravenous infusion of 14C-labelled oleic acid. All measurements were made in the postabsorptive, overnight fasted state. Arterial glucose concentrations were 10% lower in the patients but net splanchnic glucose output was similar in patients and controls. Glucose precursor uptake (lactate, pyruvate, and glycerol), however, was increased two to five fold in the patients. Arterial amino acid concentrations were generally reduced but net splanchnic amino acid uptake was the same in patients and controls. Arterial concentrations of free fatty acid and oleic acid as well as systemic and fractional turnover were similar in patients and controls. The patients' splanchnic uptake of oleic acid was increased more than three fold in comparison with controls. Splanchnic release of oleic acid was also augmented in the patients. Both arterial concentrations and splanchnic production of ketone bodies were raised in the patients. The proportion of splanchnic free fatty acid uptake which could be accounted for by ketone body production was significantly greater in the patients (37 +/- 4%) than the controls (20 +/- 5%, p less than 0.025). Estimated hepatic blood flow was 55% greater (p less than 0.01) in the patients as compared with the controls (1930 +/- 150 vs 1240 +/- 70 ml/min), while splanchnic oxygen uptake was similar in the two groups. From these findings it is concluded that patients with chronic inflammatory bowel disease show (1) markedly increased hepatic blood flow, reflecting an inflammatory hyperaemia in the splanchnic region, (2) a normal net splanchnic glucose output, (3) accelerated hepatic gluconeogenesis as well as ketogenesis, probably as a consequence of the altered hormonal milieau, and (4) low concentrations of most amino acids possibly because of protein malabsorption. These findings underscore the importance of adequate protein and carbohydrate administration to this patient group.
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PMID:Splanchnic exchange of glucose, amino acids and free fatty acids in patients with chronic inflammatory bowel disease. 664 79

Plasma vitamin E levels were found to be decreased (less than 0.5 mg) in thalassemia and in 17 out of 20 patients with Gaucher's disease, where the levels were two standard deviations below the normal mean value. In the latter, the decrease in vitamin E levels correlated with the severity of the clinical expression of the disease and correlated inversely with the degree of hepatosplenomegaly and serum tartrate-resistant acid phosphatase activity. In both diseases, there was no evidence for intestinal malabsorption of the lipid-soluble vitamin. In spite of the different etiology, pathophysiology, and clinical expression, severe vitamin E deficiency could result in both diseases by a common mechanism. In thalassemia, rapid consumption of vitamin E occurs while neutralizing oxidative damage in the pathological erythrocyte membranes and in other tissues. In Gaucher's disease, lysosomal accumulation of glucocerebroside may stimulate phagocytes into a maintained "respiratory burst" with excessive production of oxygen free radicals, resulting in increased utilization and eventual deficiency of vitamin E. Efficacy of antioxidant therapy was evaluated by administration of vitamin E with and without canthaxanthin, which has similar antioxidant properties to beta-carotene, to patients with beta-thalassemia. The results showed increased serum vitamin E levels and a decrease in the extent of erythrocyte lipid membrane peroxidation, while no significant changes occurred in hemoglobin levels and in transfusion requirements.
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PMID:Vitamin E deficiency due to increased consumption in beta-thalassemia and in Gaucher's disease. 675 58

A toxic effect of alcohol is the principal cause of the development of liver disease in alcoholism. Fatty infiltration of the liver is a consequence of ethanol metabolism due mainly to an increased synthesis and decreased degradation of fatty acids. Mechanisms that have been suggested for ethanol-induced hepatocellular necrosis include centrolobular hypoxia due to an increased oxygen requirement and intracellular accumulation of protein, fat, and water which results in increased cell size. Hepatocellular necrosis, however, may not be a necessary stage in the development of cirrhosis. Chronic ethanol administration increases hepatic collagen deposition, and acute and chronic ethanol administration inhibit liver cell regeneration. Increased humoral and cellular immunological activity to liver tissue and its components may contribute to the persistence of liver disease in the alcoholic. However, only a small proportion of alcoholics and baboons fed alcohol develop cirrhosis, suggesting that other factors, either genetic, environmental, or nutritional, play a role. Malnutrition is common in alcoholics. Liver disease is more common in some malnourished populations, and has been produced by nutrient deficiencies. Decreased dietary intake, as well as malabsorption and alterations in the metabolism of nutrients, are causes of nutrient deficiencies in alcoholism. Some of the effects of alcohol on the liver may be mediated by its actions on nutrient absorption and metabolism.
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PMID:Alcoholic liver disease: roles of alcohol and malnutrition. 700 89

The effect of proctocolectomy and small bowel resection on working capacity has not been assessed objectively in previous research. Twenty-nine patients with Crohn's disease were investigated with cycle ergometry and a questionnaire, following proctocolectomy with and without small bowel resection. Maximal exercise load is known to correspond well with working capacity, particularly when account is taken of body composition and metabolic variables. Maximal exercise load was reduced marginally (by 9 per cent) in patients without small bowel resection and by 22 per cent in patients with moderate small bowel resection (15-30 per cent resection). Patients with extensive bowel resection (more than 50 per cent) had a 40 per cent reduction in the maximal exercise load. This reduction in maximal exercise load was greater than predicted when accounting for reduction in muscle mass. All patients had a normal oxygen uptake including resting energy expenditure. Urinary sodium and magnesium excretion was low in the group with moderate bowel resection, whereas the extensively resected patients were malnourished and had a reduced body cell mass. The authors conclude that the significantly reduced working capacity was of multifactorial origin secondary to malabsorption. However, the patients seemed unaware of the degree of their diminished working capacity. This reduced capacity makes it unlikely that they would be able to perform any labour involving high energy consumption at the level of 500-700 W, and this inability was reflected by a high rate of unemployment among the patients.
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PMID:Exercise capacity in patients undergoing proctocolectomy and small bowel resection for Crohn's disease. 764 47

Cystic fibrosis often combines an infectious pathology with a syndrome of malabsorption, both potentially capable of favoring the deleterious effects of reactive oxygen species. This study was a simultaneous evaluation of the main antioxidant systems dependent on micronutrients and of lipid peroxidation products in 27 children with cystic fibrosis and 17 healthy children. Plasma of cystic fibrosis patients showed very low concentrations of beta-carotene (0.30 +/- 0.2 vs 1.63 +/- 0.5 mumol/g cholesterol, P < 0.0001) and a lower activity of selenium-dependent glutathione peroxidase (263.6 +/- 42 vs 296.9 +/- 57 U/L, P = 0.028). In parallel, the higher plasma concentrations of organic hydroperoxides (171.5 +/- 54.4 vs 122.6 +/- 23.3 mumol/L, P = 0.001) and of thiobarbituric acid reactants (2.9 +/- 0.6 vs 2.4 +/- 0.3 mumol/L, P = 0.004) reflected oxidative stress in this pathology. In addition, in these patients the major substrates of lipoperoxidation were significantly lower, whether they be linoleic acid (2.26 +/- 0.8 vs 3.60 +/- 0.9 mmol/L, P < 0.0001) or arachidonic acid (0.55 +/- 0.2 vs 0.74 +/- 0.2 mmol/L, P = 0.006). These results suggested that nutritional deficiencies resulting from malabsorption could considerably amplify disorders related to toxicity of reactive oxygen species. These nutritional deficits could also be aggravated by the destruction of antioxidant compounds by the inflammatory process.
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PMID:Altered antioxidant status and increased lipid peroxidation in children with cystic fibrosis. 860 62


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