Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum vitamin B12 concentrations were measured in 60 patients undergoing repetitive hemodialysis and in undialyzed patients with chronic renal failure. Dialysis patients had significantly lower serum vitamin B12 levels than the nondialyzed group 321 +/- SEM 38 pg/ml versus 793 +/- 100), and 19 of 60 dialysis patients had vitamin B12 Concentrations less than 200 pg/ml. Folic acid concentration was 5 times greater in dialysis than in nondialysis patients, presumably because the latter received daily supplementation with folic acid. Serum vitamin B12 concentrations fell progressively during the patient's course of dialysis. Neither inadequate dietary intake nor vitamin B12 malabsorption accounted for the differences in the serum vitamin B12 concentrations seen in the two groups. Serum vitamin B12 levels and nerve conduction velocities in 51 dialyzed patients showed a significant correlation. Six dialyzed patients with low serum vitamin B12 levels and slow nerve conduction velocities showed improvement in nerve conduction (+ 14.6 +/- 3.3 m/sec) following the parenteral use of pharmacological doses of vitamin B12. The cause of the low serum vitamin B12 concentration is not clear, nevertheless, alterations in serum vitamin B12 seen in some dialysis patients may be a factor in the persistence of abnormal nerve conduction and may be reversed with large doses of parenteral vitamin B12.
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PMID:Vitamin B12 levels and nerve conduction velocities in patients undergoing maintenance hemodialysis. 18 Jul 88

Calcium and phosphate absorptions were studied by radiotracer techniques in 30 patients after successful cadaveric renal transplantation, and results were compared with those in a group of normal subjects and in groups of patients with chronic renal failure (CRF). Both calcium and phosphate absorptions were impared in patients with CRF, including those receiving haemodialysis. Abnormalities of calcium absorption, however, seemed to occur earlier in the course of advanced renal failure than abnormalities in phosphate absorption. Calcium absorption improved dramatically after successful renal transplantation, while phosphate absorption remained the same. A dissociation between calcium and phosphate absorptions is not often seen clinically, and the mechanisms for it are unknown. Phosphate malabsorption may be a further contributing factor in the development of persistent hypophosphataemia after transplantation.
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PMID:Dissociation of absorptions of calcium and phosphate after successful cadaveric renal transplantation. 37 43

Chronic renal failure is accompanied by secondary hyperparathyroidism. Inhibition of parathyroid hormone secretion has been reported to be induced by hypomagnesemia in conditions other than chronic renal failure, since severe hypomagnesemia is rare in chronic renal failure. In the case reported here, the patient had chronic renal failure and malabsorption-induced hypomagnesemia; she exhibited hypoparathyroidism while hypomagnesemic, and hyperparathyroidism after magnesium was replaced. Hypomagnesemia induced parathyroid hormone suppression in this patient with chronic renal failure, despite the presence of chronic hyperfunctioning parathyroid cells.
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PMID:Hypomagnesemia. Suppression of secondary hyperparathyroidism in chronic renal failure. 76 31

Intestinal absorption of calcium was evaluated in 6 uraemic patients and in 7 control subjects by a two isotope technique exploring absorption in the four hours following ingestion of the dose. In the first two hours, calcium absorption in the patients was markedly lower than normal and was corrected by 6-10 day administration of dihydrotachysterol, 0.66 mg per day. The administration of 0.33 mg per day proved less effective. The data indicate the existence of impaired intestinal calcium absorption in chronic renal failure and reversal of the defect after DHT administration. The method of investigation appears to be a valid procedure for the study of calcium malabsorption of CRF and in the evaluation of the effect of vitamin D metabolities and analogs.
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PMID:Defective calcium absorption in the proximal small intestine in chronic renal failure: effect of dihydrotachysterol. 94 Jan 79

Synthetic 1alpha-hydroxycholecalciferol (1alpha-OH-D3) was given intravenously in a dose of 2.5-10 mug per day to three patients with chronic renal failure. As little as 10 mug of 1alpha-OH-D3 daily for a week improved intestinal calcium absorption to a normal level, raised serum calcium, and reduced serum alkaline phosphatase. Severe rickets which had not responded to large amounts (greater than 200 mg in total) of vitamin D2 was markedly cured with 2.5 mug of 1alpha-OH-D3 given daily for 3 weeks. These clinical data hold promise that is certainly useful in the improvement of intestinal malabsorption of calcium and bone diseases in renal failure.
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PMID:Curative effects of 1alpha-hydroxycholecalciferol on calcium metabolism and bone disease in patients with chronic renal failure. 121 80

The authors describe a rare case of amyloidosis in a female patient suffering from periodic disease (PD) for 18 years without any clinico-laboratory signs of renal impairment but with marked clinical, (malabsorption, cachexia), endoscopic, x-ray and other manifestations of gastrointestinal amyloidosis. This case is of interest since patients suffering from amyloidosis due to PB develop malabsorption very rarely, namely in 2-3% of cases. As a rule, it develops in patients with pronounced chronic renal failure on hemodialysis or with a history of kidney transplantation. In this particular case, the patient demonstrated selective marked damage to the gastrointestinal tract, with the kidneys remaining practically intact. A possibility of the indicated variety of amyloidosis should be considered in specification of the genesis of persistent diarrhea in PB patients.
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PMID:[Selective involvement of the gastrointestinal tract in amyloidosis in a female patient with periodic disease and intact kidneys]. 179

Individuals with chronic renal failure (CRF) may have a variety of gastrointestinal (GI) problems, including dyspepsia, acid peptic disease, and bacterial overgrowth. We investigated gastrointestinal function in 11 uremic patients, seven of whom were on dialysis three times a week and four who were not on dialysis. Ten normal subjects were studied as controls. The nutritional status of the patients did not differ from that of the control subjects. Seven patients demonstrated abnormal GI endoscopic findings, although none was severe; they also had prolonged oral-cecal transit times but had no evidence of bacterial overgrowth, and all had normal numbers of lymphocyte subpopulations within the intestinal mucosa. The patients had significantly reduced activities of mucosal sucrase and maltase but not of lactase. In spite of the reductions in these enzymatic activities, carbohydrate malabsorption was not evident in the CRF group, probably because of the vast reserve of the small intestine. No differences were noted between the groups in the activities of several intestinal peptidases. From these data, we concluded that GI function is essentially normal in patients with CRF and postulate that this normality, which is in contrast to previous findings, is related to recent advances in the clinical management of uremic patients.
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PMID:Gastrointestinal function, morphology, and immune status in uremia. 213 74

Selenium (Se) is a metalloid with chemical properties closed to those of sulfur, but they can not substitute for one another in vivo. Se body content reflected soil Se content (13 to 20 mg in North Americans, 3 to 6 in New Zealand residents). The daily intake recommended is 50 to 200 micrograms. In the diet Se occurs in mineral or organic forms, the bioavailability of these latter is better. Se as selenocysteine is incorporated in specific proteins such as glutathione peroxidase (GSH-Px). Se is metabolized in H2Se by reductive pathways. H2Se is methylated and methylated compounds are excreted in the urines. The Se urinary excretion represents the principal known process of Se regulation. Se bound to GSH-Px participates to free radical destruction and cellular membrane protection. Its role is complementary of vitamin E effect. Se also seems indispensable to appropriate immune response. It can chelate various metals allowing their detoxication. Se metabolism can be studied by Se assay in serum, whole blood, urine (reference values must be performed for each studied population) and by GSH-Px activity determination in erythrocytes or platelets. Vitamin E assay completes estimation of the antioxidative status of organism. Few Se intoxications have been recognized but Se deficiencies often happen. They can lead to a cardiomyopathy (Keshan disease), increase the risk of cardiovascular diseases or cancer. Se deficiencies are found in chronic renal failure, malnutrition malabsorption, long term parenteral nutrition. At the present time it is not known how Se deficiency interfers with chronic infections which often go with these diseases. A better knowledge of Se requirements and Se role could allow an appropriate supplementation in various diseases.
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PMID:[Selenium: physiologic role and value in human pathology]. 305 85

We studied plasma vitamin E levels in children/adolescents 3-19 years of age (10.9 +/- 4.5; mean +/- 1 SD) with chronic renal failure treated conservatively, on hemodialysis, on continuous ambulatory peritoneal dialysis and after renal transplantation. In all 4 groups of patients vitamin E levels (0.66-0.90 mg/dl) were within the normal range (0.76 +/- 0.19 mg/dl). The lowest levels of vitamin E (0.59 +/- 0.1 mg/dl) were found in nonuremic patients with a good functioning renal transplant. These data do not support the notion that uremia is accompanied by vitamin E malabsorption.
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PMID:Plasma vitamin E levels in uremic children and adolescents. 307 4

Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.
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PMID:Magnesium metabolism in health and disease. 328 51


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