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)

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

Therapy of the malabsorption syndrome centers on adequate diagnosis of the underlying pathology, with vigorous therapeutic efforts directed at correcting this and thereby preventing ongoing losses of nutrients. Dietary therapy includes a high-protein, high-calorie, low-fat diet often supplemented with MCTs in an effort to minimize steatorrhea. Water-soluble vitamin deficiency is rare, but supplementation with small daily doses is innocuous and probably should be prescribed. Significant fat-soluble vitamin deficiencies are seen more commonly and can be monitored by physical examination and the prothrombin time. Calcium, magnesium, and vitamin D deficiencies are more common than originally suspected. Adequate therapy requires monitoring of the serum calcium, magnesium, parathyroid hormone levels, and, optimally, 24-hour urinary collections for calcium. Supplementation of these mineral deficiencies requires ongoing close observation to prevent hypercalcemia. Iron deficiency can be easily diagnosed by available serum iron determination, and replacement with oral supplements is curative. Trace metal deficiencies occur, but our capabilities of detecting and treating them is still in its infancy. Figure 3 outlines our approach to the evaluation and treatment of the patients suspected of having the malabsorption syndrome.
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PMID:Nutritional aspects of malabsorption syndromes. 641 33

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

To define the mechanism for the hypercalciuria in spontaneously hypertensive rats (SHR), Ca clearance was evaluated in fasted 23-wk-old SHR and normotensive Wistar Kyoto (WKy) controls. There was no exaggerated calciuria before or after parathyroidectomy. Ca balance was therefore measured in the nonfasted animals, which revealed hyperabsorption in SHR of both sexes with increments 10-fold that of Ca excretion, supporting the primacy of intestinal hyperabsorption. In situ duodenal Ca uptake was also increased in the SHR. Parathyroidectomy did not affect the hyperabsorption. Hypercalcemia (total and ionized) and hypercalciuria in SHR associated with reduced adenosine 3',5'-cyclic monophosphate excretion, were abolished by fasting. Correction of hypertension for 6 mo failed to abolish the hypercalciuria. Bone Ca deposits were increased in 1-yr-old SHR. Ten-week-old SHR, in contrast, displayed mild malabsorption. Our data do not support the "renal leak" hypothesis. Instead, the adult SHR is characterized by increased Ca retention due to primary hyperabsorption, absorptive hypercalciuria, and increased bone Ca deposition. These phenomena are independent of sex, parathyroid hormone, and treatment of the established hypertension.
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PMID:Evidence for an intestinal mechanism in hypercalciuria of spontaneously hypertensive rats. 649 32

Hypocalcemia occurs in patients with psoriasis vulgaris, pustular psoriasis of von Zumbusch, and impetigo herpetiformis. In most cases hypocalcemia is caused by accompanying hypoalbuminemia, yet reductions in ionized serum calcium concentrations due to hypoparathyroidism or malabsorption have been reported. We report the case of a patient with surgical hypoparathyroidism in whom hypocalcemia precipitated typical pustular psoriasis of von Zumbusch. The psoriasis rapidly cleared on two occasions when the patient's serum calcium was corrected by therapy with oral calcium and vitamin D or its analogues, and reappeared when treatment was discontinued. The patient's psoriasis cleared on a third occasion when her serum calcium level returned to normal with a calcium infusion. Hypocalcemia can precipitate pustular psoriasis of von Zumbusch in susceptible persons. These psoriatic flares are due not to abnormal circulating levels of parathyroid hormone or vitamin D metabolites but to hypocalcemia.
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PMID:Hypocalcemia-induced pustular psoriasis of von Zumbusch. New experience with an old syndrome. 654 44

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

A 68 year old man with prostatic carcinoma and extensive painful osteoblastic metastases was discovered to have hypocalcemia (serum calcium 7.1 mg/dl) without evidence of hypoalbuminemia, renal failure or malabsorption. Baseline studies revealed hypocalciuria (24 hour urine calcium less than 5 mg/day), normal serum phosphate (3.4 mg/dl), low tubular reabsorption of phosphate (68 percent), undetectable serum calcitonin, normal serum 25-hydroxyvitamin D, slightly elevated serum parathyroid hormone level and increased urinary cyclic AMP (8.87 mumol/g creatinine). These studies were compatible with secondary hyperparathyroidism. The intravenous administration of parathyroid extract produced no further change in urinary phosphate but a 25-fold increase in nephrogenous cyclic AMP. Three days administration of intramuscular parathyroid extract slowly and temporarily restored serum calcium to normal levels while increasing urinary cyclic AMP and phosphate. Chemotherapy with cyclophosphamide and 5-fluorouracil rendered the patient free of pain while reducing serum acid and alkaline phosphatase levels and restoring serum total and ionized calcium and urinary cyclic AMP excretion to normal.
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PMID:Hypocalcemia with osteoblastic metastases in patient with prostate carcinoma. A cause of secondary hyperparathyroidism. 724 80

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

Inflammatory bowel disease (Crohn's disease and ulcerative colitis) is associated with decreased bone mineral density and increased risk of osteoporosis. However, the pathogenesis of this bone loss is not yet fully understood. In the present study we measured lumbar bone mineral density (by dual photon absorptiometry), serum levels of parathyroid hormone (PTH) and vitamin D metabolites, and serum markers of bone turnover (alkaline phosphatase and osteocalcin) in 15 patients with Crohn's disease and in 4 patients with ulcerative colitis. The median duration of the disease was 4 years and the median lifetime steroid dose was 10g of prednisone. We compared our results to a control group of 19 normal persons, who were matched for age and sex to the patients. We found that lumbar bone density was reduced by 11% in patients compared with control persons (Z-score -0.6 +/- 0.6 versus -0.1 +/- 0.8; p < 0.05). In patients, the serum levels of PTH, 25-hydroxyvitamin D3, and calcitriol (1,25(OH)2D3) were significantly reduced compared with control persons. Serum alkaline phosphatase activity (AP) was significantly higher in the patients and was inversely related to lumbar bone density. Osteocalcin values were not different between patients and control persons. There was also no difference in serum levels of calcium between the two groups, whereas phosphorus levels were higher in patients. We conclude that malabsorption of calcium was not a primary cause of bone loss in our patients, because we did not find secondary hyperparathyroidism. Accordingly, we did not find a severe vitamin D deficiency, since 25-hydroxyvitamin D3 levels were within the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bone mineral density and calcium regulating hormones in patients with inflammatory bowel disease (Crohn's disease and ulcerative colitis). 800 8

Hypomagnesemic hypocalcemia in chronic renal disease is a rare finding. Controversy remains regarding the role of decreased magnesium in producing impaired parathyroid hormone (PTH) secretion versus target organ unresponsiveness to PTH. We describe six patients with severe chronic renal disease in whom hypocalcemia and hypomagnesemia were detected. Five patients had chronic interstitial nephropathy; all of them showed renal magnesium wasting. One patient had chronic glomerulonephritis and a malabsorption syndrome and showed a low rate of urinary excretion of magnesium. The administration of magnesium increased calcium levels in all patients. We have found elevated PTH levels in absolute terms, which, however, were inappropriate to correct hypocalcemia; the PTH levels increased in three patients and not in the other three after magnesium replacement. We conclude that in patients with tubulointerstitial nephropathies, chronic renal losses of magnesium can produce hypomagnesemic hypocalcemia.
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PMID:Hypomagnesemic hypocalcemia in chronic renal failure. 843 Jun 77


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