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 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

Metabolic bone disease is common in patients with cholestatic liver disease. The importance of vitamin D status and calcium malabsorption in the pathogenesis of bone disease in these patients remains undefined. We have measured intestinal calcium absorption in relation to vitamin D status in 14 patients with chronic cholestatic liver disease including 11 with primary biliary cirrhosis. Fractional calcium absorption was determined from radioactive counts in the right forearm after separate oral and intravenous doses of 47CaCl2 in the fasting state. Eight of 14 patients (57%) had a decreased calcium absorption compared to controls. A significant correlation was observed between serum 25-hydroxyvitamin D levels and fractional calcium absorption (r = 0.623, p less than 0.02). Treatment with oral 25-hydroxyvitamin D3 in three patients with low serum 25-hydroxyvitamin D levels resulted in correction of serum 25-hydroxyvitamin D levels and improvement in fractional calcium absorption. No correlation was found between serum 1,25-dihydroxyvitamin D levels and fractional calcium absorption (r = 0.221). Calcium malabsorption was common in this series of patients, and serum 25-hydroxyvitamin D levels were useful in predicting fractional calcium absorption. Treatment with oral 25-hydroxyvitamin D3 was accompanied by improved calcium absorption.
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PMID:Intestinal calcium absorption and vitamin D status in chronic cholestatic liver disease. 670

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 38-year-old woman, who 5 years earlier had undergone a jejunoileal bypass for gross obesity, fractured the distal forearm by a minor trauma. Circulating 25-hydroxycholecalciferol was undetectable without vitamin D3 supplement but increased to the lower normal range on a daily dose of 1200 units of vitamin D3. Serum 1,25-dihydroxycholecalciferol was, however, in the upper normal range, both without and with vitamin D supplement. After intestinal reanastomosis the fracture healed and the biochemical changes normalized. Malabsorption due to reduced amount of functioning intestine may cause severe metabolic bone disease, which may not always be reverted by a high-calcium diet and vitamin D supplementation.
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PMID:Delayed fracture healing following jejunoileal bypass surgery for obesity. 680 54

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

Bone disease and low serum levels of 25-hydroxyvitamin D are prevalent in cholestatic syndromes such as primary biliary cirrhosis and biliary atresia. Defective hydroxylation, along with malabsorption of vitamin D, could be a factor in 25-hydroxyvitamin D depletion. To assess hepatic hydroxylation during experimental cholestasis, we studied vitamin D 25-hydroxylase activity in liver homogenates of rats after 7, 14, and 21 days of bile duct ligation. We have also studied the effects of bile acids on this enzyme in vitro. Hepatic 25-hydroxylation was depressed after 7 days ligation in only 1 of 4 animals, but by 14 days, all animals showed a marked reduction with a mean decrease of 64% in specific activity. Total liver enzyme activity was reduced by 43% at 14 days. In the ligated animals, liver histology showed progressive bile stasis, focal necrosis, bile ductular proliferation, periductular and periportal inflammation, and fibrosis. Addition of bile acids to the in vitro assay in concentrations approximating those found in cholestasis produced marked inhibition of vitamin D 25-hydroxylase activity.
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PMID:Hepatic vitamin D 25-hydroxylase: inhibition by bile duct ligation or bile salts. 697 44

Twenty-nine patients with chronic liver disease, nine of whom had symptoms suggesting bone disease, were studied by bone histology. Nine had osteomalacia; six associated with cholestatic liver disease and three with primarily hepatocellular disease. Two of these had clinical and biochemical features of cholestasis for at least a year and the other had alcoholic cirrhosis associated with severe malnutrition. Excluding the latter patient, histological osteomalacia was significantly associated with presence and duration of cholestasis. Plasma 25-hydroxyvitamin D was low and fasting urine hydroxyproline/creatinine ratio was high in all patients with osteomalacia but were abnormal also in some patients who did not have histological osteomalacia. Serum calcium, phosphate, alkaline phosphatase, vitamin D-binding protein and radiology were unhelpful in many patients with osteomalacia. Vitamin D-deficiency correlated significantly with deficiency of other fat-soluble vitamins and those patients with rachitic levels of plasma 25-hydroxyvitamin D showed no seasonal variation, suggesting a combination of malabsorption of vitamin D and reduced sunlight exposure. We suggest that patients with chronic liver disease with cholestasis for at least a year are at risk from osteomalacia and that those likely to have this complication may be identified by plasma 25-hydroxyvitamin D and/or fasting urine hydroxyproline/creatinine ratio measurements. The diagnosis can only be made with certainty by bone biopsy.
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PMID:Osteomalacia, vitamin D deficiency and cholestasis in chronic liver disease. 698 Nov 20

Assays of serum immunoreactive parathyroid hormone are clinically useful in the differential diagnosis of hypercalcaemic states and in the assessment of the severity of parathyroid bone disease in uraemic patients. Serum immunoreactive calcitonin measurements are essential in the investigation of individuals who might be suffering from medullary carcinoma and may be used in the detection of metastases. Serum 25-hydroxyvitamin D assays should be performed in patients receiving pharmacological doses of vitamin D to monitor patient compliance and to prevent the occurrence of vitamin D intoxication. Low values in patients with renal failure and in patients with malabsorption are highly suggestive of the presence of osteomalacia. The measurement of serum levels of dihydroxylated vitamin D metabolites is currently of doubtful relevance though such measurements may become useful in monitoring patients receiving these compounds therapeutically.
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PMID:The measurement of calcium-regulating hormones in clinical medicine. 720 1

Assays of serum immunoreactive parathyroid hormone are clinically useful in the differential diagnosis of hypercalcaemic states and in the assessment of the severity of parathyroid bone disease in uraemic patients. Serum immunoreactive calcitonin measurements are essential in the investigation of individuals who might be suffering from medullary carcinoma, and such measurements may be used in the detection of metastases. Serum 25-hydroxyvitamin D assays are useful in patients receiving pharmacological doses of vitamin D, to monitor patient compliance and to prevent the occurrence of vitamin D intoxication. Low values in patients with renal failure and in patients with malabsorption and highly suggestive of the presence of osteomalacia. The measurement of serum levels of dihydroxylated vitamin D metabolites is currently of doubtful clinical relevance, though such measurements may become useful in monitoring patients receiving these compounds therapeutically.
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PMID:Testing for disorders of calcium metabolism. 746 49

Privational vitamin D deficiency is assumed to be uncommon in the developed countries because of the routine fortification of foods with vitamin D. Malabsorption of vitamin D and calcium (especially in an environment of reduced sun exposure) therefore accounts for the majority of cases of metabolic bone disease seen in patients with various gastrointestinal disorders in the United States. Yet recognition of this often asymptomatic bone disease is unsatisfactory and frequently delayed for months or even years. This results in severe irreversible bone loss, putting patients at increased fracture risk for the remainders of their lives. As evident from the small number of published reports, it is obvious that little attention is given to understanding the pathogenesis and prevention of bone disease in patients with various gastrointestinal disorders. This review will summarize recent advances in the pathogenesis, prevention, and treatment of metabolic bone disease in patients with these disorders. We propose methods for identifying bone loss in such patients so that appropriate preventive measures can be instituted to avoid significant morbidity.
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PMID:Metabolic bone disease in gastrointestinal, hepatobiliary, and pancreatic disorders and total parenteral nutrition. 761 19


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