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

Osteodystrophy frequently accompanies severe childhood hepatobiliary disease. Proposed causes include malabsorption of vitamin D and calcium, and diminished 25-hydroxylation of vitamin D. Two children, ages 23 and 35 months, with radiographic and biochemical evidence of rickets with extrahepatic biliary atresia, were treated with 1,25-dihydroxyvitamin D3. The minimal effective therapeutic dose and efficacy of 1,25-(OH)2D3 in the treatment of rickets associated with severe childhood hepatic disease were determined. Oral 1,25-(OH)2D3 was ineffective at doses of 0.10 microgram/kg/day. Parenteral doses of 0.20 microgram/kg/day effectively produced radiographic, bone mineral (photon absorptiometric), and biochemical evidence of healing. The need for four times the physiologic dose of 1,25-(OH)2D3 by the parenteral route suggested enhanced catabolism of, or end-organ resistance to, 1,25-(OH)2D3 in our patients with severe cholestatic liver disease treated with phenobarbital.
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PMID:1,25-Dihydroxyvitamin D3 in childhood hepatic osteodystrophy. 44 53

Experimentally diabetic rats have low serum 1,25-dihydroxyvitamin D, intestinal malabsorption of calcium, secondary hyperparathyroidism, and bone loss. To examine the hypothesis that abnormalities similar to those in the diabetic rat might explain human diabetic osteopenia, we studied calcium metabolism in 40 healthy control and 82 diabetic patients aged 18--75 yr [47 untreated: fasting plasma glucose (mean +/- SE), 267 +/- 8 mg/dl; 19 treated but hyperglycemic: glucose 305 +/- 24 mg/dl; 16 treated and in better control: glucose, 146 +/- 8 mg/dl]. Serum total calcium, ionic calcium, immunoreactive parathyroid hormone (Arnaud method, GP-1M and CH-12M antisera), 25-hydroxyvitamin D (Haddad method), and 1,25-dihydroxyvitamin D (Lambert method) concentrations were normal in all 3 groups of diabetics and were not significantly different from values in the control group. We determined absorption of calcium from the intestine by a double isotope method (100 mg Ca carrier; normal range, 40--80%) in 11 control and 13 untreated, uncontrolled diabetics (mean plasma glucose, 285 +/- 17 mg/dl). Absorption of calcium in controls was 60 +/- 3% and in diabetics was 56 +/- 3% (not significantly different). We have found no derangement of calcium metabolism in adults with insulin-requiring juvenile- and adult-onset diabetes regardless of treatment status. The experimental diabetic rat model does not appear to be useful for determining the pathogenesis of adult human diabetic osteopenia.
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PMID:Calcium homeostasis in diabetes mellitus. 46 80

The case history of a hypoparathyroid female with short bowel syndrome and long-standing therapy-resistant symptomatic hypocalcemia is reported. During treatment with massive doses of the potent vitamin D analog, 1 alpha-hydroxyvitamin D3(1 alpha(OH)D3), normocalcemia was re-established and clinical symptoms of hypocalcemia were relieved. Furthermore, significant improvement of t of intestinal calcium absorption and bone mineral content was observed after three months of treatment with 1 alpha(OH)D3. The data suggest that 1 alpha(OH)D3 may be of therapeutical value in patients with hypoparathyroidism and intestinal malabsorption.
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PMID:1 alpha-hydroxyvitamin D3 treatment of therapy-resistant symptomatic hypocalcemia in a hypoparathyroid patient with intestinal malabsorption. 47 89

To investigate the possibility of measuring urinary oxalate output instead of faecal fat excretion as an outpatient screening test for steatorrhoea, we determined 24 hour urinary oxalate and five day faecal fat excretion before and during an oral load of sodium oxalate 600 mg daily (oxalate 4.44 mmol), in 32 patients with suspected malabsorption on a diet containing oxalate 30 mg (0.33 mmol), fat 50 g (180 mmol), and calcium 1 g (25 mmol). Nineteen patients proved to have steatorrhoea (mean faecal fat 62 mmol/24 h, range 19--186 mmol) of varying aetiologies. On the diet alone, urinary oxalate was raised in only nine of these patients (mean 0.25 mmol/24 h, range 0.08--0.59 mmol) (normal less than 0.20). By contrast, when the diet was supplemented with oral sodium oxalate, all 19 patients with steatorrhoea had hyperoxaluria (mean 0.91 mmol/24 h, range 0.46--1.44 mmol) (normal less than 0.44). There was a significant positive linear relationship between urinary oxalate and faecal fat when the 32 patients were on the high oxalate intake (r = 0.73, P less than 0.001), but not when they were on the low oxalate intake. Mean percentage absorption of orally administered oxalate was 5.8 +/- 0.99% (+/- 1 SD) in normal subjects and 14.7 +/- 6.0% (P less than 0.002) in patients with steatorrhoea. Measurement of urinary oxalate output during oral sodium oxalate loading appears to be a reliable and convenient screening test for steatorrhoea.
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PMID:Oxalate loading test: a screening test for steatorrhoea. 52 84

The influence of malabsorption of lactose, as a result of primary lactase deficiency, on the absorption of the nutrients in milk was tested in four healthy controls and four subjects with lactase deficiency. An ileal perfusion technique was used to quantify arrival in the ileum of nutrients and a nonabsorbable marker (polyethylene glycol, PEG 4000) ingested as a test meal of milk. The meal was 250 ml of whole milk or milk in which the lactose had been hydrolyzed to glucose and galactose. In the fasting state, ileal flow of volume, protein, carbohydrate, and electrolytes was small and not different in controls and lactase-deficient subjects. Ileal flow increased in all subjects after the test meal of milk; more fluid and nutrient was recovered from the ileum in lactase-deficient subjects after whole milk than in control subjects or in lactase deficiency after hydrolyzed milk. Two deficient subjects showed marked malabsorption of lactose (35 and 50%); two did not. Protein, calcium, magnesium, and phosphorus were also recovered from the ileum in greater quantities in lactase deficients after whole milk. However, apart from decreased absorption of lactose, the nutritional consequences of malabsorption in association with primary lactase deficiency in adults are probably minimal.
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PMID:Absorption of nutrients in lactase deficiency. 58 2

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

Balance studies were performed in thirty-three post-menopausal women (all but five having vertebral crush fractures or femoral neck fractures) in the basal state and on treatment with 1alpha-hydroxyvitamin D3 and/or oestrogenic hormones. The results suggest that the effectiveness of oestrogen therapy is limited by calcium malabsorption and the effectiveness of 1alpha-hydroxyvitamin D3 is limited by oestrogen deficiency. The best results were obtained with combined therapy to remedy what appears to be two distinct deficiencies. To minimize the risks of hypercalcaemia and the possible risks of hormone therapy, we suggest that the treatment of choice in post-menopausal osteoporosis may be 1alpha-hydroxyvitamin D3 1microgram daily and ethinyloestrodiol 25 microgram daily for 3 weeks in every 4. Patients on a low dietary intake of calcium should probably be given calcium supplements. With this regimen, it should not be necessary to screen patients initially for calcium malabsorption or oestrogen deficiency because the majority of patients present with a combination of the two factors.
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PMID:The effect of 1alpha-hydroxyvitamin D3 with and without oestrogens on calcium balance in post-menopausal women. 60 14

This work was designed to investigate the site of oxalate hyperabsorption in malabsorption syndromes. 1) Urinary oxalate excretion was measured in 27 patients with ileal resection (IR) and steatorrhea. Mean urinary oxalate excretion was high in 13 patients with IR and intact colon and in 9 subjects with IR and right hemicolectomy (90.2 +/- 11.9 and 108 +/- 18.6 mg per 24 hours; mean +/- S.E.M.), whereas it was normal in 5 patients with IR and ileostomy (21.9 +/- 4.4 mg per 24 hours). Steatorrhea was similar in the three groups. 2) On one patient of the last group in whom the colon had not been removed initially but excluded closure of the ileostomy resulted in the development of frank hyperoxaluria. 3) Intracolonic perfusion of calcium (1.93 g per day) abolished or greatly reduced the hyperoxaluria in 3 patients. These results indicate that the colon is the major site of oxalate hyperabsorption, and the right colon is not necessary for the development of hyperoxaluria in malabsorption syndromes.
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PMID:Evidence for excessive absorption of oxalate by the colon in enteric hyperoxaluria. 63 58

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

143 patients (70 patients with Crohn's disease, 11 with ulcerative colitis, 40 with an intestinal by-pass operation, 9 with non-tropical sprue, 10 with short bowel syndrome, and 3 with other gastrointestinal disease) were studied during a metabolic regime including a fixed oral supply of 70 g fat, 800 mg calcium, and 200 mg oxalate. Faecal fat, 47Ca-absorption, 14C-oxalate absorption, and renal oxalate excretion were measured, and in the majority of patients a 14C-glyco-cholic acid breath test was also performed. 14Ca-absorption was practically identical (r = 0.92), whether determined by whole-body counting or from the accumulation of absorbed 47Ca in the skeleton of the underarm. 14C-oxalate absorption and renal oxalate excretion agreed well (r = 0.85). Steatorrhoea correlated weakly with renal oxalate excretion (r = 0.63, p less than 0.001), whereas no correlation was present between faecal fat and calcium absorption or between oxalate and calcium absorption under the constant conditions prevailing during the study. It is recommended that a "trifixed" regime with absorption studies of fat, calcium, and oxalate be undertaken previous to therapy that aims at a reduction of steatorrhoea or hyperoxaluria or an improvement of calcium absorption in chronic malabsorption syndromes, not least because therapy of these categories of patients most often continues for years.
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PMID:Standardized ("trifixed") diet in the study of chronic malabsorption syndromes. 67 51


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