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Biomedical subjects

F Melsen

Publications and source records attributed to F Melsen.

At least 37 records · Page 2Linked to original sources
PubMed1978

Effect of antithyroid treatment on calcium-phosphorus metabolism in hyperthyroidism. I: Chemical quantities in serum and urine.

The effect of antithyroid treatment on the disturbed calcium-phosphorus metabolism in hyperthyroidism was studied in 16 patients. Elevated serum concentrations and urinary excretions of calcium and phosphorus were almost normalized 4 weeks after the start of medical treatment. Serum immunoreactive parathyroid hormone was decreased in the hyperthyroid state and became normal after medical treatment. Serum alkaline phosphatase levels were elevated throughout the study with an increase to a maximum peak after 8 weeks of antithyroid treatment. Urinary hydroxyproline excretion was initially markedly increased and fell rapidly during therapy. The observed changes suggest decreased bone resorption and increased bone formation with deposition of bone mineral after antithyroid treatment. Alterations in the serum albumin concentration during the investigation period influenced the total serum calcium concentration. Using albumin adjusted serum calcium values no hypocalcaemia was found during medical treatment or after a subsequent subtotal thyroidectomy.

Adult↗
PubMed1978

Effect of antithyroid treatment on calcium-phosphorus metabolism in hyperthyroidism. II: Bone histomorphometry.

Histomorphometric analysis of iliac crest biopsies was performed after tetracycline double-labelling in 22 hyperthyroid patients before and after medical antithyroid treatment for an average period of 4 months. The initially increased cortical porosity was normalized during treatment whereas the amount of trabecular bone was unchanged. The osteoclastic resorption in cortical bone decreased but was still elevated. The osteocytic osteolysis remained slightly increased. In trabecular bone, however, the bone turn-over decreased to a subnormal level following treatment and the surfaces were inactive in bone resorption and bone formation. An increase was observed in the amount, extent and width of osteoid seams due to an increase in the lifespan of bone forming sites and a prolongation of the maturity period of osteoid. The observed increased deposition of cortical bone after antithyroid treatment may explain the positive calcium balance in this period.

Adult↗
PubMed1978

Bone phosphorus/hydroxyproline ratio and bone histomorphometry in normals.

Bone phosphorus/hydroxyproline ratio (P/Hypro) was compared to bone histomorphometry in thirty-four normal individuals. Bone P/Hypro ratio correlated significantly to both the relative mineralized bone volume (r = 0.38, P less than 0.05), the relative osteoid volume (r = -0.38, P less than 0.05) and the percentage of osteoid covered surfaces in trabecular bone (r = -0.38, P less than 0.05).

Adolescent↗
PubMed1977

Bone disease, hypophosphatemia and hyperparathyroidism after renal transplantation.

UNLABELLED: Long-term survivors after renal transplantation (RT) show: 1) decreased s-phosphorus 2) increased s-PTH 3) no correlation between s-PTH and s-phosphorus 4) increased amount of non-mineralized bone (osteomalacia), inversely correlated to s-phosphorus 5) decreased amount of trabecular bone (osteopenia) in RT patients with aseptic necorsis of bone. CONCLUSION: aseptic necrosis of bone after RT is mainly due to osteoid-induced osteopenia, perhaps aggravated by hypophosphatemic osteomalacia.

Adolescent↗
PubMed1977

Morphometric and dynamic studies of bone changes in hyperthyroidism.

Bone biopsies were performed after tetracycline double-labelling by transfixing the right iliac crest in forty hyperthyroid patients. The bone changes in cortical and trabecular bone were determined by simple measurement and point counting on decalcified and undecalcified stained sections. A slight decrease in the amount of cancellous bone was found. The mean cortical width was normal. The amount of osteoid and the length of the osteoid seams were increased, whereas the mean width of osteoid seams was decreased. The cortical osteoclastic activity and porosity were markedly increased. The trabecular osteoclasic activity was moderately increased and the mean size of periosteocytic lacunae was slightly increased. The calcification rate in cancellous bone was increased as were the active calcification surfaces (tetracycline-labelled). The osteoclastic activity in cortical bone was positively correlated to the free thyroxine index and to the urinary calcium and phosphorus excretion. The findings indicate that the bone changes in hyperthyroidism are specific and that thyroid hormone(s) stimulates both bone formation and resorption followed by increased porosity in cortical bone and by mobilization of bone mineral.

Adolescent↗
PubMed1977

Effect of long-term vitamin D2 treatment on bone morphometry and biochemical values in anticonvulsant osteomalacia.

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.

Adult↗
PubMed1977

Aseptic necrosis of bone following renal transplantation. Clinical and biochemical aspects and bone morphometry.

Aseptic necrosis of bone has developed 5--48 months (mean 23) after renal transplantation in 22 (11%) of 195 patients with graft function for more than 6 months. The bone lesions were mainly localized to weight-bearing cancellous bone areas, most often the femoral heads. The mean duration of hemodialysis was significantly longer in recipients with aspetic necrosis than in those without. The serum concentration of phosphate was reduced and the serum concentration of parathyroid hormone increased in both groups of recipients. Quantitative histological examination of iliac crest biopsies showed a pronounced reduction of spongy bone (osteopenia) in recipients with aseptic necrosis compared with both normals and recipients without aseptic necrosis. Both patient groups showed similar changes in bone remodelling, indicating decreased bone formation. These findings suggest that osteopenia is an important contributory factor in the development of aseptic necrosis of bone after transplantation. The osteopenia may be a consequence of both the uremic bone disease before transplantation and the immunosuppressive treatment after transplantation.

Adolescent↗
PubMed1977

Bone histomorphometry in patients with chronic renal failure: effect of 1alpha-hydroxyvitamin D3.

Morphometric and dynamic studies of iliac crest bone biopsies were carried out in twelve patients with chronic renal failure (six on chronic haemodialysis and six with renal insufficiency) before and after 6 months of 1alpha-hydroxyvitamin D3 treatment. Pre-treatment biopsies showed signs of osteomalacia and hyperparathyroidism. Biopsies taken during treatment showed changes towards normality, indicating a beneficial effect of 1alpha-hydroxyvitamin D3.

Adult↗
PubMed1977

Effect of 1alpha-hydroxyvitamin D3 on parathyroid function in patients with chronic renal failure.

The effect of 1alpha-hydroxyvitamin D3 (1alpha-OHD3) on parathyroid function was studied in sixteen patients (ten on haemodialysis, six with chronic renal insufficiency) during treatment for 6--8 months. During treatment, a decrease in serum parathyroid hormone (s-PTH) and an increase in serum calcium were seen. An inverse linear correlation was found between serum calcium and logarithmic values of s-PTH in fifteen of sixteen patients, but the slopes of the regression lines varied considerably. This indicates that the suppression of parathyroid function seen during treatment with 1alpha-OHD3 is mediated by a rise in the serum concentration of calcium. For normalization of s-PTH, the serum concentration of calcium had to be above normal range in several patients, indicating a defect in calcium-mediated regulation of the secretion of parathyroid hormone. This abnormality was seen especially in long-term haemodialysed patients.

Adolescent↗
PubMed1977

Treatment of senile osteoporosis with 1alpha-hydroxyvitamin D3.

About 30% of patients with clinical osteoporosis had histological signs of osteomalacia, in spite of normal serum 25-hydroxyvitamin D3 (25-OHD3). The excess osteoid disappeared during treatment with 1alpha-hydroxyvitamin D3 (1alpha-OHD3). These patients might have reduced ability to convert 25-OHD3 to 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3). The intestinal calcium absorption increased during treatment with 1alpha-OHD3, but this was accompanied by a rise in urinary calcium excretion. Photon absorptiometry of the forearm indicated increased bone mineral content during treatment with a daily dose of 2 microgram 1alpha-OHD3 and a supplement of 1 g of calcium. This therapeutic combination, however, caused frequent episodes of hypercalcaemia, so further studies are necessary to evaluate an appropriate dose of 1alpha-OHD3 with or without a calcium supplement.

Aged↗