Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C1864663 (HCC)
 2,985 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The long-term effects of the vitamin D metabolite, 25-hydroxycholecalciferol (25-HCC), were evaluated in 2 children with hypophosphatemic vitamin D-resistant rickets. Serial total balance studies demonstrated an apparent lack of correlation between the effects of the vitamin on intestinal absorption of calcium and phosphorus and both the onset of healing in 1 of the 2 patients treated with 5,000 to 7,500 u of the metabolite and the absence of demonstrable radiologic improvement in another patient in whom the final dosage was 20,000 u. per day. At first, the metabolite induced a positive calcium balance in both patients resulting largely from a reduction in intestinal calcium excretion. Despite a continued positive calcium balance, 1 of the 2 patients did not demonstrate further healing, while in the other patient healing was noted even when total calcium balance was negative. Serum phosphate levels did not return to normal in either patient, nor was phosphate excretion altered by 25-HCC. Serum alkaline phosphatase remained elevated in both. Serum immunoassayable parathyroid hormone levels were consistently normal to high-normal in the 2 patients throughout more than 24 months of observation. No instances of hypercalcemia and only occasional hypercalciuric episodes were noted.
 ...
PMID:Long-term therapy of viramin D-resistant richets with 25-hydroxycholecalciferol. 16 13

Quantitative morphometric analyses of iliac crest biopsies from 20 epileptic patients receiving chronic anticonvulsant therapy have been performed before and after 4-8 months of vitamin D2 treatment with 9 000 U per day. Biochemical quantities, including serum 25-hydroxycholecalciferol (25-HCC) and serum parathyroid hormone (iPTH), were measured. The anticonvulsant osteomalacia found in the initial bone biopsies was characterized by an increased amount of ummineralized bone, an increased bone resorption and, contrary to vitamin D deficiency, an increased bone mineralization and bone formation. Bone resorption and bone formation were probably equally increased since the amount of cancellous bone was normal. Except for a slight increase in osteoidcovered surfaces and osteoclastic resorption surfaces, the bone changes were normalized after vitamin D2 treatment, leading to a mean serum level of 25-HCC 2.4 times above normal. Serum iPTH was normal before and unchanged during D2 therapy. The urinary calcium excretion remained decreased. The investigation characterizes anticonvulsant osteomalacia as a specific bone disease different from that of vitamin D deects of vitamin D metabolites on receptor cells.
 ...
PMID:Effect of long-term vitamin D2 treatment on bone morphometry and biochemical values in anticonvulsant osteomalacia. 30 May 47

Serum 25-hydroxycholecalciferol (25-HCC) and serum parathyroid hormone (iPTH) were measured in 59 randomly selected adult epileptic outpatients receiving chronic anticonvulsant therapy. Quantitative morphometric analysis of iliac crest biopsies was performed. A mild degree of osteomalacia was found which was inversely correlated to dietary vitamin D intake. Serum 25-HCC was reduced in the epileptic patients compared to a control group, although dietary intake of vitamin D was higher than the mean daily intake in the Danish population. Serum 25-HCC was positively correlated to dietary vitamin D intake, but not correlated to the severity of bone changes, indicating that other factors than circulating 25-HCC are responsible for the development of anticonvulsant osteomalacia. Serum 25-HCG was inversely correlated to serum iPTH in patients with a low dietary calcium intake. The mean value of serum iPTH was not increased, and there was no correlation between serum iPTH and bone morphometry.
 ...
PMID:The interrelationships between serum 25-hydroxycholecalciferol, serum parathyroid hormone and bone changes in anticonvulsant osteomalacia. 57 30

In 10 patients undergoing hemofiltration treatment acute changes of parameters in the calcium-phosphate metaboism were investigated. Balance studies were also performed in all patients. Control studies were conducted after a 3-month interval in 7 patients. Whereas ionized calcium and 25-HCC remained constant, there was a significant decrease in phosphate, magnesium, fluoride and parathyroid hormone. Corresponding to these results, negative balances could be seen during the course of a hemofiltration treatment: for phosphate a mean value of -593 mg, for magnesium -8.4 mEq and for fluoride -458 microgram. When a calcium content of 3.75 mEq/l was used in the substitution solution, an only slightly positive calcium balance of +1.51 mEq/l (mean value) was found. A significant correlation between calcium and fluid balance was demonstrated by means of 197 filtration treatments of one patient: the calcium balance became negative whenever the fluid loss was greater than 3.86 liters. After a 3-month period no significant changes in the above parameters were found, which indicates, that disturbances in the calcium-phosphate-parathyroid hormone metabolism do not only lie in a reduced renal elimination. Even though our results do not indicate that hemofiltration treatment induces or increases the chances of renal osteodystrophy, the calcium concentration of the substitution solution should be increased to 4.0 mEq/l, in order to guarentee a positive calcium balance even by forced filtration.
 ...
PMID:[Calcium and phosphate metabolism in hemofiltration (author's transl)]. 71 37

Vitamin D has been proposed as a risk factor of ischaemic heart disease. In 12 patients with acute myocardial infarction the major circulating vitamin D metabolite, 25-hydroxy-cholecalciferol (25-HCC), did not show any fluctuations during the first 4 days after onset of symptoms. The serum 25-HCC level was then measured in 128 patients consecutively admitted because of chest pain, 53 of whom had myocardial infarction and 75 had angina pectoris. The values found did not differ from those measured in 409 normal persons. The seasonal variations of serum 25-HCC were less pronounced in heart patients than in normals, probably due to less sun exposure in the summer months. The levels of serum 25-HCC did not correlate with the concentrations of serum cholesterol, glycerides, calcium or magnesium. Low serum calcium and magnesium were observed in all patients. Serum calcium was further reduced in the course of acute myocardial infarctions while serum parathyroid hormone rose significantly. We conclude that patients with ischaemic heart disease are not ingesting or producing in their skin elevated amount of vitamin D.
 ...
PMID:Vitamin D and ischaemic heart disease. 74 75

The blood levels of 25-hydroxyvitamin D (25-HCC) in 26 patients with nephrotic syndrome (proteinuria of 6.5 g/24 h +/- 0.8 SEM) ranged between 1 and 18.6 ng/ml (8.6 +/- 1.0 SEM). This value was significantly lower (P less than 0.01) than that in normal subjects (21.8 +/- 2.3 ng/ml) and patients with chronic renal failure (24.8 +/- 2.3 ng/ml). There was inverse correlation (P less than 0.01) between levels of 25-HCC and magnitude of proteinuria and a direct relation (P less than 0.01) with serum albumin. Reduction in proteinuria was rapidly followed by a rise in blood 25-HCC toward normal. Ionized calcium levels were low in 16 of 26 nephrotic patients irrespective of degree of renal failure. In four of seven nephrotic patients with normal renal function, ionized calcium levels were low and showed an inverse relation with levels of parathyroid hormone. These data show that patients with nephrotic syndrome have low blood levels of 25-HCC probably due to its loss in urine. This derangement is probably responsible for the disorders of calcium metabolism in nephrosis.
 ...
PMID:Blood levels of 25-hydroxyvitamin D in nephrotic syndrome. Studies in 26 patients. 93 Dec 2

The effect on phosphate excretion of graded doses of parathyroid hormone (PTH) and the biologically active vitamin D3 metabolite, 25-hydroxycholecalciferol (25-HCC), administered singly and in combination, were studied in the nonexpanded, vitamin D-depleted thyroparathyroidectomized rat. Infusion of 1 unit of 25-HCC per hour for 6 hours induced an antiphosphaturia only when administered with 0.2 units of PTH per hour, while neither agent alone changed phosphate excretion. A dose of 2.0 units of PTH per hour did not cause phosphaturia unless given with 1 unit of 25-HCC per hour. In pharmacologic dosage (5 units per hour), PTH produced phosphaturia in the absence of the metabolite.
 ...
PMID:Parathyroid hormone and 25-hydroxy vitamin D3: synergistic and antagonistic effects on renal phosphate transport. 116 16

As there is little evidence of the efficacy of 25-hydroxyvitamin D3 (25-HCC) in reducing the risk of new fractures in osteoporotic women, we performed an open, prospective study with a follow-up of 1 yr in 58 females over 65 yr of age with osteoporosis and proximal femoral fractures. The patient group received 1 g calcium per day and 10 640 IU 25-HCC per week, while the control group received 1 g calcium daily. Biochemical markers of bone remodelling, serum calcium and parathyroid hormone were determined. Bone mineral density was assessed in the lumbar spine and in the proximal femur by two methods. After 1 yr of treatment, 25-HCC corrected secondary hyperparathyroidism, increased urine calcium excretion, and increased bone mass in the femoral neck, but had no effect upon the appearance of new fractures.
 ...
PMID:The effect of 25-dihydroxyvitamin D on the bone mineral metabolism of elderly women with hip fracture. 1108 7