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)

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

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

Twenty-five consecutive in-patients who had suffered from rheumatoid arthritis for at least five years were investigated radiologically, histologically and biochemically for evidence of metabolic bone disease. Dietary intake of vitamin D was universally well below recommended levels. Serum 25-hydroxycholecalciferol (25-OHD) concentrations did not correlate with dietary intake of vitamin D but correlated significantly with a sunlight exposure score (p less than 0.01). Despite seven patients having 25-OHD levels below the normal reference range, no cases of osteomalacia were found. Pathological fractures, often initially unrecognized, had occurred in the lower limb bones of seven patients in the previous five years. Those with fractures of the leg bones had evidence of more pronounced osteoporosis of the axial skeleton radiologically and histologically and five of the seven had been taking oral corticosteroids. There was close agreement between qualitative histological assessment of osteoporosis and radiographic evidence of vertebral collapse and those with the severest osteoporosis had lower serum levels of 25-OHD than the rest (p less than 0.02). Ten subjects had reduced xylose absorption tests, although frank malabsorption was not found, and in five patients studied the jejunal mucosa was normal.
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PMID:Metabolic bone disease among in-patients with rheumatoid arthritis. 648 30

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

In the present case a primary hyperparathyroidism was aggravated by postgastrectomy bone disease and led to a spontaneous fracture of the left femur and to a pseudofracture of the right femur. Renal symptoms like concrements or nephrocalcinosis were based on the intestinal conditioned malabsorption of vitamin-D and calcium not evident. Radiologically there was a mixed pattern of ostitis fibrosa cystica generalisata von Recklinghausen and osteomalacia respectively osteoporosis based on postgastrectomy bone disease. Treatment was fully effective consisting of exstirpation of the adenoma and substitution of calcium and vitamin-D and ingestion of digestive enzymes and many little meals corresponding to the prescriptions of nutrition for partially gastrectomised patients.
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PMID:[Left spontaneous femoral fracture in primary hyperparathyroidism and postgastrectomy bone disease following a Billroth II stomach resection]. 662 60

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

A patient presented with cutaneous mastocytosis, bone pains, biologic disorders typical of osteomalacia, and intestinal malabsorption. Bone biopsy with histomorphometric analysis and measure of calcification rate on undecalcified bone, confirmed the diagnosis of bone mastocytosis and osteomalacia. There are only 2 other reports of osteomalacia caused by malabsorption. The latter is possibly bound to a mast-cell infiltrate of the intestinal mucosa. Sometimes only villosity atrophy or oedema of the mucosa are observed.
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PMID:[Bone mastocytosis and osteomalacia. Apropos of a case with histodynamic analysis on non-decalcified bone]. 683 12

We describe a simplified assay for 24,25-and 1.25-dihydroxyvitamin D in human serum. It involves two preparative steps, and normal chick intestine is used in preparing cytosol-binding protein. Our results for 24,25-dihydroxyvitamin D include a reference interval of 2.9--16 nmol/L (1.2--6.7 microgram/L), a mean of 6.7 nmol/L (2.8 microgram/L), an intra-assay CV of 11%, and an interassay CV of 22%. For 1,25-dihydroxyvitamin D, these data were 29--168 pmol/L (12--70 ng/L), 86 pmol/L (36 ng/L), 12%, and 22%, respectively. In hypoparathyroid patients with vitamin D intoxication, mean concentrations of 25-hydroxyvitamin D and 24,25-dihydroxyvitamin D in serum were significantly above normal; the 1,25-dihydroxyvitamin D concentrations were significantly below normal. Patients with malabsorption and/or post-gastrectomy states had significantly subnormal values for both 25-hydroxyvitamin D and 24,25-dihydroxyvitamin D in serum, and there was a significantly negative correlation between each of these biochemical values and the severity of osteomalacia. We also discuss cost effectiveness of assaying vitamin D metabolites in human serum.
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PMID:A simplified assay for dihydroxylated vitamin D metabolites in human serum: application to hyper- and hypovitaminosis D. 689 91

Plasma 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] and 25-hydroxyvitamin D (25OHD) concentrations were measured in twenty patients with metabolic bone disease due either to privational causes (10 patients) or malabsorption (10 patients). Abnormally low plasma 1,25(OH)2D3 levels were found in eleven patients, six with privational and five with malabsorption bone disease. Normal plasma 1,25(OH)2D3 concentrations were found in the remaining nine patients; of these, five were either receiving anticonvulsant therapy or had been hospitalised prior to investigation. In the absence of either of these factors, normal plasma 1,25(OH)2D3 levels were only found in patients with malabsorption-associated bone disease. Plasma 25OHD levels were below normal in eleven patients; six had malabsorption and five had privational bone disease. In the fifteen patients not receiving anticonvulsants there were significant inverse correlations between plasma 1,25(OH)2D3 levels and the osteoid volume, surface and seam thickness index. This study indicates that plasma 1,25(OH)2D3 concentrations are low in privational osteomalacia in the absence of anticonvulsant therapy or hospitalisation, although normal levels may occur in malabsorption metabolic bone disease uncomplicated by these factors. The plasma 1,25(OH)2D3 concentration appears to be inversely related to the histological severity of bone disease in patients not receiving anticonvulsant therapy.
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PMID:Privational and malabsorption metabolic bone disease: plasma vitamin D metabolite concentrations and their relationship to quantitative bone histology. 689 97


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