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)

We developed a test procedure for the clinical evaluation of the absorption of vitamin D. Serum vitamin D concentrations were evaluated in seven patients with intestinal fat malabsorption syndromes and in seven healthy, normal subjects, after being given a single oral dose of 50,000 IU (1.25 mg) vitamin D2. In the normal subjects, serum vitamin D concentrations rose from a baseline of less than 5 ng/ml to a peak of over 50 ng/ml by 12 h, gradually falling to baseline levels by 3 days. In five of the seven patients with intestinal fat malabsorption, oral administration of 50,000 IU vitamin D2 did not raise serum vitamin D concentrations above 10 ng/ml. Two patients with severe inflammatory bowel disease had a normal absorption pattern, however. These findings suggest that an oral vitamin D absorption test may be of value for determination of patients at risk for development of vitamin D deficiency. They also raise questions about the efficacy of oral vitamin D preparations in patients with intestinal fat malabsorption.
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PMID:Vitamin D absorption in healthy subjects and in patients with intestinal malabsorption syndromes. 405 Jul 23

Severe osteomalacia of uncertain etiology was observed in a 44-year-old woman. There was no evidence of chronic renal insufficiency, malabsorption, or of the renal tubular defects classically associated with osteomalacia. However, the dietary history suggested vitamin D deficiency and most of the biochemical findings were compatible with this condition. The unusual feature of the case was a decrease in plasma bicarbonate levels which appeared to be due to a lowered renal tubular threshold for bicarbonate reabsorption. There was no renal tubular defect with respect to hydrogen ion excretion.Rapid symptomatic and radiologic improvement occurred when the dietary intake of vitamin D was increased to approximately 200 I.U. per day and the acidosis was simultaneously corrected with sodium bicarbonate. Although no firm conclusions could be drawn about the relative importance of vitamin D deficiency or chronic acidosis in the production of the osteomalacia, the possibility that the chronic acidosis may have been a major contributing factor is discussed.
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PMID:Osteomalacia associated with renal bicarbonate loss. 594 Jun 37

Vitamin D deficiency is in most cases subclinical and can only be detected by blood vitamin assays or biochemical changes in phosphorus and calcium metabolism. Clinical and radiological osteomalacia is much less common. It is due to prolonged and profound hypovitaminaemia, which in turn depends upon a variety of factors, the main one being defective photosynthesis. Low vitamin D dietary intake apparently does not result in osteomalacia unless it is accompanied by insufficient exposure to sun. Malabsorption of cholecalciferol results from steatorrhoea of various origina. Disorders in hepatic 25-hydroxylation are due to drug enzymatic induction and seem to be unrelated to the state of the renal function. Disorders in renal 1,25-hydroxylation may be consecutive to reduced renal tissue, impaired stimulation, or inhibiton or even congenital lack of 1-alpha hydroxylase.
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PMID:[Osteomalacia due to vitamin D deficiency. Part One: mechanisms (author's transl)]. 625 Jan 30

Elucidation of the vitamin D endocrine system and the availability of potent metabolites have led to new approaches to vitamin D therapy. The traditional management of exogenous (sunlight) or endogenous (malabsorption) vitamin D deficiency without evidence of disordered vitamin D metabolism has not changed, since it consists of treatment with vitamin D itself--a therapy which preserves the normal intrinsic mechanisms for regulating the rate of production of 1,25-dihydroxycholecalciferol. 1,25-DHCC and the analogue compound 1 alpha-CC should be reserved for treatment of hypocalcemia consequent on chronic renal failure or hypoparathyroidism, where 1-hydroxylation is lacking or impaired. Hypophosphatemic rickets has been treated with 1-hydroxylated compounds, with promising results; this use of the latter metabolites warrants further investigation. The use of vitamin D metabolites and of pharmacological doses of vitamin D itself must be regarded as substitution of a hormone or hormone precursors. Therefore, careful monitoring of serum and urine calcium is required in every patient receiving these compounds, in order to avoid excessive dosage. Special attention must be paid to patients with sarcoidosis since they often develop hypercalcemia after vitamin D or UV-light exposure, as a result of an intrinsic regulation defect in 1,25-DHCC synthesis.
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PMID:[Therapy with vitamin D and D-metabolites]. 626 26

Five patients with primary biliary cirrhosis and vitamin D deficiency (serum 25-hydroxyvitamin D less than 6 ng/ml) are presented. All patients had low serum 24,25-dihydroxyvitamin D3 concentrations. Three patients had histological osteomalacia, negative calcium balance, and subnormal serum 1,25-dihydroxyvitamin D3. Malabsorption of a standard dose of [3H]vitamin D3 was found in three of four patients with steatorrhea, enabling the effective dose of vitamin D3 given to be calculated. Oral vitamin D3 400-4000 IU/day (effectively 400-1860 IU/day) resulted in a return to normal of the serum vitamin D metabolites, correction of the impaired intestinal calcium absorption and healing of the osteomalacia. Increases in serum calcium, phosphate, and the renal tubular reabsorption of phosphate occurred with a concomitant decrease in serum parathyroid hormone. It is suggested that osteomalacia in primary biliary cirrhosis is the end result of vitamin D deficiency; the hepatic and renal hydroxylations of vitamin D are normal and target tissues are responsive to endogenously produced metabolites of vitamin D.
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PMID:Vitamin D deficiency, osteomalacia, and primary biliary cirrhosis. Response to orally administered vitamin D3. 629 63

Calcium malabsorption is common in the elderly and may contribute to the development of age-related bone loss. To investigate its cause, we have measured radio-calcium absorption, plasma 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D and parathyroid hormone in forty-eight elderly women with a normal plasma creatinine. Calcium malabsorption was associated with low 25-hydroxyvitamin D concentrations and was corrected by increasing these into the normal range by treatment with oral 25-hydroxyvitamin D3. Treatment also increased 1,25-dihydroxyvitamin D, and decreased parathyroid hormone concentrations. Before treatment, plasma parathyroid hormone was related to plasma creatinine but not to 25-hydroxyvitamin D, and the change in absorption on treatment correlated inversely with plasma creatinine. 51Cr EDTA clearance was measured in sixteen elderly women and confirmed that renal impairment was common even with a plasma creatinine in the normal range. Our results suggest that calcium malabsorption in the elderly is predominantly due to vitamin D deficiency; renal impairment is also common and contributes to the malabsorption by increasing the requirements for vitamin D.
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PMID:Calcium malabsorption in the elderly: the effect of treatment with oral 25-hydroxyvitamin D3. 641 53

A survey of vitamin D status in 152 patients with chronic gastrointestinal conditions and 104 patients with chronic liver diseases is presented. Mild deficiency was common and severe deficiency, as judged by plasma 25-OHD levels less than 8 nmol/l, was encountered in every disease category tested. In the gastrointestinal disease patients, deficiency was significantly more common in patients following gastroenterostomy than other gastric surgery, in patients with active Crohn's disease than in those with inactive disease and in patients with chronic pancreatitis or pancreatic carcinoma with cholestatic features than in those without cholestatic features. Deficiency was as common in patients with Crohn's disease who had not been treated surgically as in those who had. There was no significant correlation between plasma 25-OHD levels and any laboratory index of malabsorption or malnutrition except for serum albumin in the gastric surgery patients, haemoglobin and ESR in the Crohn's disease patients and albumin and vitamin E in the group of patients with gastrointestinal disorders taken as a whole. In the chronic liver disease patients, those with late primary biliary cirrhosis had lower plasma 25-OHD levels than those with histological Stage I and II disease who all had normal levels, and those with pruritus and jaundice were more commonly severely deficient. Whatever the underlying disease process, patients with other coincidental medical conditions were much more likely to be deficient as were patients with cholestasis. Evidence of secondary hyperparathyroidism and osteomalacia on bone histology indicated the clinical relevance of the vitamin D deficiency. This study showed no relationship between abnormal plasma vitamin D binding protein levels and vitamin deficiency.
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PMID:A survey of vitamin D deficiency in gastrointestinal and liver disorders. 654

The state of vitamin D nutrition depends on synthesis in the skin under the influence of sunlight as well as on dietary intake. In European countries that do not fortify milk with vitamin D, reduced sun exposure is the major factor leading to a fall in body stores of vitamin D with age and to a high frequency of hypovitaminosis D in the elderly sick. In the US, because vitamin D is added to milk and the use of vitamin D supplements is more common, the dietary intake of vitamin D is relatively more important than in Europe, and the total vitamin D intake and body stores of vitamin D are generally higher. Nevertheless, body stores of vitamin D probably fall with age in the US as they do in Europe, and it is likely that some sick elderly persons in the US, especially among those confined to institutions, become vitamin D deficient. For several reasons, the vitamin D requirement increases with age, and a total supply of 15 to 20 micrograms/day (600 to 800 IU) from all sources is recommended. Special attention should be paid to persons most likely to need supplementation, such as the housebound, persons with malabsorption, and persons with interruption of the enterohepatic circulation. Osteomalacia, the bone disease produced by severe vitamin D deficiency, is less common in the US than in Europe, but subclinical vitamin D deficiency may contribute to the pathogenesis of hip fractures, both through increased liability to fall and through PTH-mediated bone loss. The extent to which vitamin D deficiency contributes to hip fractures in the US is unknown, and is an important area for future research. Excess intake of vitamin D or of its metabolites may result in hypercalcemia and extra-osseous calcification, particularly in arterial walls and in the kidney, leading to chronic renal failure. The dose of vitamin D that causes significant hypercalcemia is highly variable between individuals but is rarely less than 1000 micrograms/day. Smaller doses can cause hypercalciuria and nephrolithiasis and possibly impaired renal function. Vitamin D administration may raise plasma cholesterol but there is no convincing evidence that the risk of myocardial infarction is increased. The recommended total supply for the elderly of 20 micrograms/day is most unlikely to be harmful, except in patients with sarcoidosis or renal calculi.
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PMID:Vitamin D and bone health in the elderly. 676 68

Four infants with less than 35 cm of jejunum and ileum remaining following neonatal operations and after being weaned from long-term total parenteral nutrition onto an "elemental" formula, developed the syndrome of vitamin D deficiency rickets at 9-15 mo of age. The diagnosis of rickets was confirmed by biochemical and radiographic findings. Serum 25 hydroxy vitamin D (25 OHD) values were significantly lower than normal and oral 25 OHD absorption studies indicated severe vitamin D malabsorption. This report emphasizes the importance of prospective assessment of all neonates having distal ileal resection to detect the early stages of vitamin D deficiency rickets.
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PMID:Vitamin D deficiency rickets as a late complication of the short gut syndrome during infancy. 697 20

Faecal tritium excretion after intravenous 3H-25-hydroxyvitamin D3 administration was measured in three control subjects and in six patients with small intestine resection or bypass. The mean daily faecal tritium excretion over four to six days ranged from 0.8-1.6% of the injected dose in the controls (mean 1.2) and 0.9-6.8% in the patients (mean 3.7). There was a significant positive correlation between stool volume and the mean daily faecal tritium excretion. No correlation was found between the faecal tritium excretion and the plasma 25-hydroxyvitamin D concentration. Between 2.5 and 19.0% of faecal radioactivity eluted as 3H-25-hydroxyvitamin D3 on silicic acid chromatography. We conclude that faecal loss of endogenous 25-hydroxyvitamin D may be increased after small intestinal resection or bypass. Although the amount lost by this route is relatively small, it may contribute to the development of vitamin D deficiency in patients with malabsorption when endogenous vitamin D3 synthesis is also reduced.
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PMID:Faecal tritium excretion after intravenous administration of 3H-25-hydroxyvitamin D3 in control subjects and in patients with malabsorption. 707 8


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