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)

In recent years it has become possible by means of a radioimmunoassay to measure Digoxin concentration in the serum of digitalized patients. With this method it could be shown that the resorption of Digoxin is decreased by partial resection of the samll intestines, by malabsorption syndromes, after ingestion of Neomycin, Colestyramine and antacids. In renal insufficiency, however, the elimination half-life period of Digoxin is increased conspiciously (from about 35 hours up to about 120 hours). This results in a raised serum concentration of cardiac glycosides unless the dosage is decreased considerably. The incidence of Digitalis intoxication in Digitalis treated patients has been reported to rank as high as 20%. There is, however, no strict correlation between the serum glycoside level and the clinical symptoms, because the glykoside concentration in the serum does not represent the pharmacologically active concentration at the receptor. Experimental investigations of cardiac glycoside binding to the receptor for cardiac glycosides in human heart cell membranes revealed, that receptor bound Digoxin for instance is diminished in serious renal insufficiency and it depends on the serum concentration of potassium, calcium and magnesium. In hypoxia, after myocardial infarction and in myxedema the sensitivity for cardiac glycosides is increased. The opposite is true in hyperthyreoidism, fever and in children. All of these factors have to be kept in mind and paid attention to in the clinical evaluation of the measured Digoxin concentration in the serum.
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PMID:[Significance of serum digoxin concentration and its influencing factors]. 6 Nov 53

Patients undergoing radical surgical treatment of head and neck neoplasms often are seen with a history of cirrhotic liver disease, electrolyte abnormalities, and other stigma of chronic disease. Despite skillful thyroid surgical technique performed as an isolated procedure or in combination with other procedures such as laryngectomy, hypocalcemia can occur. Common causes of lowered serum calcium levels secondary to removal of parathyroid glands, blood transfusions, hypoalbuminemia, gastrointestinal malabsorption, and renal insufficiency are well known. Less well known is the recently elucidated role of dependence of calcium metabolism on magnesium. Recently, it has been well documented that alcoholism directly lowers serum magnesium levels in both human and animal models without prior liver disease or malabsorption. The fact that three mechanisms are needed to explain calcium homeostasis implies that the magnesium-calcium interdependence is not clearly understood.
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PMID:Thyroid surgery: surgical and metabolic causes of hypocalcemia. 64 19

Magnesium deficiency can occur in congestive heart failure, after diuresis with furoxemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delerium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with hypoparathyroidism, primary aldosteronism, juxta-glomerular hyperplasia and pancreatitis. Two cases of serious ventricular arrhythmias associated with magnesium depletion are described. Clinical manifestations are vague but center around neurologic symptoms such as weakness, tremors, stupor, coma, nausea, vomiting and anorexia. Serious cardiac arrhythmias also occur with magnesium depletion. Magnesium appears to be very useful in hypomagnesemic or digitalis-toxic tachyarrhythmias. Magnesium may also be valuable in normomagnesemic tachyarrhythmias. Ten to fifteen milliliters of a 20 percent magnesium sulfate solution, given intravenously over 1 minute, followed by a slow 4 to 6 hour infusion of 500 ml of 2 per cent magnesium sulfate in 5 per cent dextrose in water is recommended. Recurrence of arrhythmias is common and a second infusion of magnesium sulfate may be necessary. Hypermagnesemia occurs frequently in renal insufficiency, and magnesium therapy may then be contraindicated. Serum levels above 5.5 meq/liter should be avoided. Loss of deep tendon reflexes and a decrease in respiratory rate can be used as guides to magnesium therapy. A plea is made for frequent analysis of serum magnesium so that more knowledge can be gained regarding this important biologic element in cardiovascular disorders.
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PMID:Magnesium deficiency and cardiac disorders. 80 29

Previous studies from this laboratory demonstrated that secondary hyperparathyroidism in dogs with chronic renal disease may occur, at least in part, as a consequence of the need for progressive adaptation in renal phosphorus (P) excretion that occurs as glomerular filtration rate falls. However, the studies were of relatively short duration. Moreover, no information emerged regarding a potential role of calcium malabsorption in the pathogenesis of secondary hyperparathyroidism. The short duration of the protocol did not lend itself to the study of the effect of P control or the administration of vitamin D in the pathogenesis of renal osteodystrophy. In the present studies, 14 dogs with experimental chronic renal disease were studied serially for a period of 2 yr. Each animal was studied first with two normal kidneys on an intake of P of 1,200 mg/day. Then, renal insufficiency was produced by 5/6 nephrectomy. The dogs then were divided into three groups. In group I, 1,200 mg/day P intake was administered for the full 2 yr. In group II, P intake was reduced from the initial 1,200 mg/day, in proportion to the measured fall in glomerular filtration rate, in an effort to obviate the renal adaptation in P excretion. In group III, "proportional reduction" of P intake also was employed; but in addition, 20 mug of 25(OH)D(3) were administered orally three times a week. In group I, parathyroid hormone (PTH) levels rose throughout the 2-yr period reaching a final concentration of 557+/-70 U (normal 10-60). In group II, values for PTH remained normal throughout the 1st yr, increased modestly between the 12th and the 18th mo, but then did not rise after the 18th mo. In group III, no elevation of PTH levels was observed at any time; however, these animals were hypercalcemic. Histomorphologic analyses of the ribs of these dogs were performed serially throughout the 2-yr period. A linear relationship was obtained between the osteoclastic resorption surface and the concentration of circulating immunoreactive PTH. The osteoid volume was greater in group I animals when compared to those in group II. None of the morphologic abnormalities associated with renal osteodystrophy were observed in the animals in the third group.
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PMID:Phosphate control and 25-hydroxycholecalciferol administration in preventing experimental renal osteodystrophy in the dog. 87 95

Primary hypoparathyroidism caused by lymphocytic parathyroiditis was diagnosed in a cat. Other causes of hypocalcemia (ethylene glycol toxicosis, phosphate enema administration, pancreatitis, renal insufficiency, and malabsorption) were ruled out on the basis of history, clinicopathologic data, and lack of supportive clinical signs, which in this cat included inappetence and tetanic muscle spasms. The diagnosis was confirmed by histologic examination of a surgically excised thyroparathyroid lobe that comprised lack of recognizable parathyroid tissue and a lymphocytic plasmacytic infiltrate adjacent to the cranial pole. A treatment regimen similar to that for iatrogenic postthyroidectomy hypoparathyroidism was successful in controlling clinical signs of the disease.
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PMID:Primary hypoparathyroidism in a cat. 233 77

The level of serum 25-hydroxyvitamin D (25-OH-D3) was determined in 94 cases of healthy volunteers and 98 patients with various diseases. The mean level of the controls was 16.2 +/- 4.6 ng/ml (x /- S). The patients were divided into 5 groups, 1) Osteomalacia and rickets 42 cases, showing typical changes of bone in X-ray films. In 12 of them the disease was caused by vitamin D deficiency. The mean value of 25-OH-D3 was 3.3 +/- 2.0 ng/ml, being much lower than that of controls (P less than 0.001). In 14 cases of hypophosphatemia, 8 cases of renal tubular acidosis and 8 cases of renal insufficiency all complicated with osteomalacia the mean value of 25-OH-D3 was 17.9 +/- 11.4, 18.2 +/- 9.6 and 19.2 +/- 5.6 ng/ml (P greater than 0.05) respectively. 2) Intestinal malabsorption 18 cases. The mean level of 25-OH-D3 was 4.5 +/- 3.2 ng/ml (P less than 0.001). Some of them had hypocalcemia and/or secondary hyperparathyroidism. 2 showed osteoporosis and 1 osteomalacia. 3) Chronic liver disease 24 cases, the mean value of 25-OH-D3 was 6.2 +/- 5.6 ng/ml, being much lower than that of the controls (P less than 0.001). 4) 10 cases after taking anti-epileptic drugs had a mean level of 25-OH-C3 6.9 +/- 5.8 ng/ml (P less than 0.001). 1 had X-ray evidence of osteomalacia. 5) 4 cases of overdosage of vitamin D had a mean value of 110.3 +/- 22.5 ng/ml, being much higher than that of the controls (P less than 0.001). Competitive protein binding assay for measuring 25-OH-D3 is a simple and economic method. It is sensitive and specific as it provides distinct discrimination between healthy controls and patients with vitamin D deficiency or overdosage.
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PMID:[Clinical significance of competitive protein binding assay of 25-hydroxyvitamin D concentration]. 273 43

The efficacy of D-xylose testing in clinical situations has been reviewed in the light of recent kinetic studies. The standard 25-g D-xylose test in adults, based on analysis of 5-h urine collection and a 1-h serum sample, discriminates between normal subjects and patients with proximal small intestinal malabsorption with greater than 95% specificity and sensitivity. The 1-h serum level measured after administering this dose is also useful in evaluating malabsorption in patients with intermediate degrees of renal insufficiency and in the elderly. The 1-h serum test after administration of 5 g of D-xylose should be used in pediatrics and is greater than 91% sensitive and close to 100% specific. The [14C]D-xylose breath test with 1 g of D-xylose has been useful in identifying malabsorption caused by bacterial overgrowth in the small intestine.
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PMID:D-xylose testing: a review. 265 67

Clinical, pathologic, and biochemical data are reported in two male infants who had rapidly progressive renal failure, enlarged kidneys, hepatosplenomegaly, and fat malabsorption. One infant, studied prior to the onset of significant renal insufficiency, manifested renal Fanconi syndrome, hyperparathyroidism, and marked hypocalcemia. After a brief period of dialysis, both received renal transplants. Neither has clinical evidence of reoccurrence of the renal disorder in the transplant, but both still have hepatic abnormalities. Morphologic features present in both patients include a renal lesion characterized by tubulointerstitial injury with a tubulocystic component and hepatic abnormalities with bile duct proliferation, portal fibrosis, and inflammation. These cases do not readily conform to any single published diagnostic category, including nephronophthisis-congenital hepatic fibrosis or infantile polycystic kidney disease, and appear to be unique.
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PMID:Progressive tubulointerstitial renal disease in infancy with associated hepatic abnormalities. 352 22

A coagulopathy due to vitamin K deficiency was discovered in 42 hospitalized patients, most of whom had been misdiagnosed as having disseminated intravascular coagulation. Factors contributing to vitamin deficiency included inadequate diet, malabsorption, failure of physicians to prescribe vitamin K supplements, antibiotic therapy, renal insufficiency, hepatic dysfunction, recent major surgery, and possibly pregnancy. Sixteen patients (34%) bled sufficiently to need red blood cell transfusions and ten patients (24%) ultimately died. Of 18 patients who also had thrombocytopenia, three did have disseminated intravascular coagulation. The deficiency, a contributor to morbidity and mortality, can be prevented by prophylactic administration of vitamin K to severely ill patients who are eating inadequately and receiving antibiotics.
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PMID:Coagulopathy caused by vitamin K deficiency in critically ill, hospitalized patients. 365 2

The intestinal absorption of calcium is often depressed in patients with chronic renal insufficiency. Furthermore, the malabsorption of calcium and the osteodystrophy which occur in association with chronic renal disease are often "resistant" to vitamin D; the basis for this resistance remains uncertain however. Recent studies by others have emphasized the role of an abnormality in the metabolism of vitamin D in accounting for the alterations in the calcium absorption and the apparent vitamin D-resistance which accompany the uremic syndrome. The present studies with an experimentally uremic animal model demonstrate a defect in the active transport of calcium by duodenal gut sacs in vitro. This abnormality is not due to the semistarvation associated with renal insufficiency and cannot be corrected by the administration of physiologic amounts of vitamin D(3): it is reversed by massive doses of the vitamin. Neither the metabolism of vitamin D(3) nor the levels of calcium binding protein activity in the duodenal mucosa are affected by renal insufficiency under the conditions employed in the present studies. The results of the present studies strongly suggest that in addition to the recently proposed mechanism involving an interference with the metabolism of vitamin D renal insufficiency also affects the cellular mechanisms for calcium transport in a manner which, while opposite in direction to that of vitamin D, is independent of a direct interaction with the vitamin or its metabolites.
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PMID:Effect of renal insufficiency on the active transport of calcium by the small intestine. 542 27


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