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)

The surface pH of human proximal jejunum was measured in biopsy samples and found to be more acid than the phosphate buffer in which they were incubated. The in vitro jejunal surface pH was 5.93 +/- 0.05 in control subjects and 6.19 +/- 0.09 in treated coeliac patients. A group of untreated coeliac patients with a surface pH of 6.56 +/- 0.14 had a significantly less acid surface pH compared to controls, as did a group of Crohn's patients with a surface pH of 6.21 +/- 0.04. These two groups with a significantly raised surface pH were subdivisible into 'high' and 'low'groups. Surface pH was found to remain low in the treated coeliac and control groups but became more acid over the incubation period reaching almost normal values in the Crohn's group and the untreated coelic initial surface pH. The raised surface pH in untreated coeliac disease and Crohn's disease would alter the amount of a weak acid available for non-ionic diffusion. Therefore the present results may help to explain the folate malabsorption known to occur in untreated coeliac disease and the frequently seen low serum folate levels in Crohn's disease.
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PMID:Acid microclimate in coeliac and Crohn's disease: a model for folate malabsorption. 2 71

Four patients who had been on regular haemodialysis for periods of 3 1/2 to 7 years became hypophosphataemic with plasma-phosphate concentrations of 2.5 mg/dl or less before dialysis. None of them had been taking oral phosphate-binders for 2 years or more. Histologically all the patients had an excess of osteoid on bone biopsy. Intestinal absorption of phosphate and calcium was impaired, despite normal or high serum-25-hydroxycholecaliferol concentrations. Treatment with oral dihydrotachysterol resulted in corrections of the phosphate malabsorption and increases in plasma-phosphate concentration. The initial low plasma-phosphate values in these patients before dialysis probably reflected a state of phosphate depletion caused by the combination of malabsorption, loss during dialysis, and a low dietary intake.
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PMID:Persistent hypophosphataemia and osteomalacia in dialysis patients not on oral phosphate-binders: Response to dihydrotachysterol therapy. 7 42

To determine the functional capabilities of the parathyroid glands, 17 EDTA infusions were given to 11 children (ages 1 month to 12 years) and to two mothers of four of the children. Serum ionized Ca fell from 4.1 mg/dl to 3.4 mg/dl. Excessive parathyroid hormone responses were elicited during seven of nine EDTA infusions in five children and in one adult with hypophosphatemic rickets, during the active phase of rickets. In four of five subjects with problems related to hypercalcemia, borderline low or undetectable PTH responses were elicited. Three relatively normal PTH responses were obtained, two in an infant after phosphate-induced hypocalcemic tetany was corrected, and one in a child with a malabsorption syndrome. The renal tubular reabsorption of phosphate was inversely related and the urinary cyclic AMP excretion was positively related to the PTH response. Thus EDTA infusions in infants and children might be useful in the identification of hyper-, normo-, or hypoparathyroid states and would be of value in defining the functional condition of the parathyroid glands in children with deranged Ca or P metabolism.
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PMID:Parathyroid function tests with EDTA infusions in infancy and childhood. 17 44

To determine whether the phosphaturic response to circulating parathyroid hormone (PTH) is exaggerated in patients with familial x-linked hypophosphatemic vitamin D-resistant rickets (FHR), we examined the phosphaturic response to parathyroid extract (PTE) (administered intravenously in the posthypercalcemic state) in two unrelated adult hemizygotes with FHR. In these two patients whose plasma concentration of PTH was normal (determined by radioimmunoassay). neither vitamin D nor phosphate therapy had been given during the past 10 yr. Two normal men and a hypophosphatemic man with intestinal malabsorption, hypocalcemia, and osteomalacia served as control subjects. In all subjects, calcium gluconate was adminstered intravenously from 6 p.m. to 12 midnight at a rate that maintained the concentration of serum calcium at 13-15 mg/100 ml during the administration of calcium. When normocalcemia had recurred the next morning, and the plasma PTH concentration and urinary excretion of cyclic 3', 5'-AMP were reduced. PTE was administered intravenously at successively increasing rates of 0.1, 0.4, and 0.8 U/kg per h, each rate lasting 90 min. Minutes after the initiation of PTE in the affected hemizygotes, fractional excretion of filtered phosphate increased from negligible values to values strikingly greater than those of similarly studied control subjects and plateaued at strikingly greater values throughout further administration of PTE. This phenomenon of exaggerated phosphaturia could not be attributed to volume expansion, decreases in serum concentration of calcium during the study, differences in percent of administered calcium retained, or hemodynamic changes. Only the phosphaturic response to PTE appeared to be exaggerated. At any cumulative dose of PTE, urinary excretion of cyclic 3', 5'-AMP in the hemizogytes was indistinguishable from that of control subjects. The findings in this study suggest that in patients with FHR, circulating PTH is required for the genetically transmitted abnormality to be physiologically expressed as a reduction in net renal reabsorption of phosphate, and that this physiological expression of the genetic abnormality is expressed fully at normal or nearly normal circulating levels of PTH.
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PMID:Exaggerated phosphaturic response to circulating parathyroid hormone in patients with familial X-linked hypophosphatemic rickets. 18 58

This investigation confirms that 1alpha-hydroxyvitamin D3 (1alpha-OHD3) is a potent drug for the treatment of patients with pseudo-deficiency rickets (Balsan et al., 1975a; Reade et al., 1975; Prader et al., 1976). 1alpha-OHD3 corrects their intestinal malabsorption of calcium and phosphorus, normalizes their serum calcium and phosphate concentrations and promotes healing of skeletal lesions. This study also shows differences in the needs for 1alpha-OHD3 of children with PDR. Three factors appear to be of importance: familial sensitivity, severity of chronic secondary hyperparathyroidism, and periods of increased growth velocity. Tolerance to long-term 1alpha-OHD3 therapy, at doses varying from 0.5 to 2 microgram/d is excellent. Surveillance of patients should include regular measurements of 24 h urinary excretion of calcium, since hypercalciuria is the first signal of overdosage.
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PMID:Long-term therapy with 1alpha-hydroxyvitamin D3 in children with 'pseudo-deficiency' rickets. 20 17

Ten patients with vitamin D resistant hypophosphataemic osteomalacia are described. They had hypophosphataemia with a decreased tubular reabsorption of phosphate, malabsorption of calcium and phosphorus, proximal myopathy and extensive osteomalacic changes on iliac crest bone biopsy. The plasma alkaline phosphatase and urine hydroxyproline, however, were raised in only some of the patients. Treatment with 1alpha-hydroxyvitamin D3 in high doses rapidly cured the myopathy, increased calcium and phosphorus absorption and retention and healed the osteomalacia. Phosphorus supplements were not required.
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PMID:Vitamin D resistant hypophosphataemic osteomalacia: treatment with 1alpha-hydroxyvitamin D3. 20 18

Five patients with nutritional osteomalacia or rickets and six children with rickets unresponsive to physiological doses of vitamin D were treated with 1alpha-hydroxyvitamin D3 (1alpha-OHD3). Patients with nutritional osteomalacia responded to 1--2 microgram/day of 1alpha-OHD3. The most striking findings were rises in plasma calcium and, in one case, a decrease in faecal calcium. In some cases there was a rise in plasma phosphorus, alkaline phosphatase remained unchanged. There was radiological healing. In three patients with cystinosis and one with hypophosphataemia and Barrter's syndrome 2 microgram of 1alpha-OHD3 produced healing of rickets. Plasma phosphate rose on treatment, possibly by a suppression of parathyroid activity. The response to such low doses of 1alpha-OHD3 suggests impaired 1alpha-hydroxylation of 25-hydroxyvitamin D in these patients. A patient with intestinal malabsorption was resistant to high doses of 1alpha-OHD3 by mouth but responded to parenteral administration. A boy with osteopetrosis and the biochemical changes of rickets was resistant to large doses of 1alpha-OHD3 presumably because of failure of osseous response.
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PMID:1alpha-hydroxyvitamin D3 in the treatment of nutritional and metabolic rickets and osteomalacia. 20 19

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

To investigate whether hepatobiliary rickets is caused by defective intestinal absorption of vitamin D or by impaired hepatic hydroxylation of the vitamin, we studied three children who developed severe rickets, hypocalcemia, and hypophosphatemia, two despite having received 400 to 800 IU vitamin D per day by mouth, and one despite prolonged treatment with 10,000 IU daily. On oral vitamin D therapy, plasma vitamin D and 25-hydroxyvitamin D levels were low. When two children were treated with weekly intravenous doses of 3,000 IU vitamin D to approximate the recommended prophylactic allowance, their plasma calcium and phosphate values improved promptly, the radiographic lesions healed, and the plasma concentrations of vitamin D and 25-hydroxyvitamin D became normal. Our studies indicate that the primary cause of hepatobiliary rickets is intestinal malabsorption of vitamin D, not impairment of the hepatic metabolism of the vitamin.
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PMID:Pathogenesis of rickets in chronic hepatobiliary disease in children. 44 26

Hypophosphatemia is common in hospitalized patients and occurs under a variety of circumstances other than parathyroid hormone excess. Charts of 100 inpatients with hypophosphatemia were reviewed and the patients divided into five groups on the basis of serum phosphate level: 18, 2.1 to 2.4 mg/dL; 49, 1.6 to 2.0 mg/dL; 20, 1.1 to 1.5 mg/dL; 12, 0.6 to 1.0 mg/dL; 1, 0.1 to 0.5 mg/dL. The effect of glucose ingestion on serum phosphate level was shown in one normal patient. Whenever carbohydrate was administered intravenously (45 cases), this was considered the primary cause of the hypophosphatemia. Other causes were as follows: diuretics, hyperalimentation, alcoholism, respiratory alkalosis, dialysis, insulin, corticosteroids, diabetic ketoacidosis, vomiting, phosphate-binding antacid, Gram-negative sepsis, primary hyperparathyroidism, saline, epinephrine, gastrointestinal malabsorption, and unknown. Hypophosphatemia in hospitalized patients may have multiple causes.
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PMID:Hypophosphatemia in hospitalized patients. 44 90


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