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Biomedical subjects

P Marie

Publications and source records attributed to P Marie.

52 records · Page 3Linked to original sources
PubMed1978

Vitamin D metabolites and bone mineralization in man.

A comparison was made of the biochemical and osseous effects of 25-hydroxyvitamin D3 [25(OH)D3], 1 alpha-25-hydroxyvitamin D3 [1 alpha, 25(OH)2D3], and 24,25-dihydroxyvitamin D3 [24,25(OH)2D3] in adult vitamin D-deficient man. Administration of 50 micrograms/d of 25(OH)D3 for 8 weeks led to a return of the mineralization front to normal associated with a return of TmPO4/GFR to normal, an increase in serum phosphate and calcium concentrations, a fall in serum IPTH, and a rise in serum alkaline phosphatase activity. Giving 2.5 micrograms/d of 1 alpha,25(OH)2D3 did not produce these effects. Administration of 1 alpha, 25 (OH)2D3 caused an increase in intestinal calcium absorption, and a rise in serum calcium associated with a fall in serum immunoreactive parathormone (IPTH) concentrations but no sustained rise in either alkaline phosphatase, serum phosphate concentration, nor in TmPO4/GFR. Its administration caused an increase in the extent of the osteoclastic bone resorption surface but the extent of the mineralization front remained subnormal. Administration of 20 micrograms/d of 24,25(OH)2D3 caused a fall in urinary calcium excretion and in serum IPTH, and a rise in serum alkaline phosphatase, but no change in TmPO4/GFR or serum phosphate, and only a slight increase in the extent of the mineralization front. Combined treatment with 1 alpha, 25(OH)2D3 and 24,25(OH)2D3 led to a return of the mineralization front of normal even though both TmPO4/GFR and serum phosphate concentration remained low. It is concluded that 1alpha,25(OH)2D3 is not the sole biologically active metabolite of vitamin D in man. It is apparent that either 25(OH)D3 or some as yet unidentified metabolite of 25(OH)D3 stimulates the renal tubular reabsorption of calcium and phosphate, and that the subsequent rise in serum phosphate concentrations along with the direct actions of 1 alpha-25(OH)2D3, 24,25(OH)2D3, and possibly 25(OH)D3 on bone cells all participate in the restoration of normal bone formation and bone mineralization in vitamin D-deficient man.

Alkaline Phosphatase↗
PubMed1978

Anemia and secondary hyperparathyroidism.

Anemia has been recognized recently as a possible complication of primary hyperparathyroidism. If the hyperparathyroid state can induce anemia in patients with normal kidney function, the extremely high levels of circulating parathyroid hormone usually observed in hyperparathyroidism secondary to chronic renal failure may have an unfavorable influence on the anemia of uremic patients. We investigated the influence of subtotal parathyroidectomy on the severity of the anemia of 18 uremic subjects undergoing long-term hemodialysis therapy. Subtotal parathyroidectomy resulted in a significant increase of mean hematocrit value. RBC count, and hemoglobin level. Serial bone biopsies suggested a relationship between the amount of marrow fibrosis and the improvement of anemia after surgery, but the precise mechanism of this phenomenon is still unknown.

Adult↗
PubMed1977

Effects of high dialysate calcium concentration on bone remodelling, serum biochemistry, and parathyroid hormone in patients with renal osteodystrophy.

The influence of a dialysate calcium concentration of 8.0 mg/100 ml (treatment period 2) vs. 7.0 mg/100 ml (treatment period 1) on plasma calcium, phosphorus, serum immunoreactive parathyroid hormone (iPTH), bone histology, intestinal calcium absorption, and calcium transfer across the dialysis membrane was investigated in six patients with renal osteodystrophy undergoing intermittent hemodialysis. During the periods 1 and 2, the plasma calcium changes before and after dialysis were not significantly different. A significant increase in mean postdialysis plasma calcium level was observed during both periods when compared to mean predialysis level. A significant, inverse relation was found between predialysis plasma calcium and the increase in plasma calcium during hemodialysis runs. Calcium transfer across the dialysis membrane and fractional intestinal absorption of calcium in the postdialysis state were determined in four out of the six patients. During period 2, calcium transfer was higher in all four patients but intestinal calcium absorption was moderately higher only in one and strikingly lower in the remaining three patients when compared to period 1. Although brought up to 8.0 mg/100 ml, this higher dialysate calcium significantly decreased the level of serum iPTH only in one out of the six patients; in this patient, osteoclast count, active resorption surface, and periosteocytic osteolysis decreased. In a second patient, although the level of serum iPTH seemed to decrease markedly osteoclastic and osteocytic resorption did not change. In the remaining four patients, the level of serum iPTH was unchanged and bone resorption parameters were found unchanged or aggravated. It is concluded that providing additional calcium (using a dialysate calcium concentration of 8.0 mg/100 ml), the goal of which was to decrease secondary hyperparathyroidism, proved to be successful only in one patient and failed to do so in the five others. Secondary hyperparathyroidism was even found aggravated in three of them. Thus, the use of a dialysate calcium concentration of 8.0 mg/100 ml did not result in any advantage over that of 7.0 mg/100 ml in five out of six patients studied.

Adult↗
PubMed1977

Phosphate control and 25-hydroxycholecalciferol administration in preventing experimental renal osteodystrophy in the dog.

Previous studies from this laboratory demonstrated that secondary hyperparathyroidism in dogs with chronic renal disease may occur, at least in part, as a consequence of the need for progressive adaptation in renal phosphorus (P) excretion that occurs as glomerular filtration rate falls. However, the studies were of relatively short duration. Moreover, no information emerged regarding a potential role of calcium malabsorption in the pathogenesis of secondary hyperparathyroidism. The short duration of the protocol did not lend itself to the study of the effect of P control or the administration of vitamin D in the pathogenesis of renal osteodystrophy. In the present studies, 14 dogs with experimental chronic renal disease were studied serially for a period of 2 yr. Each animal was studied first with two normal kidneys on an intake of P of 1,200 mg/day. Then, renal insufficiency was produced by 5/6 nephrectomy. The dogs then were divided into three groups. In group I, 1,200 mg/day P intake was administered for the full 2 yr. In group II, P intake was reduced from the initial 1,200 mg/day, in proportion to the measured fall in glomerular filtration rate, in an effort to obviate the renal adaptation in P excretion. In group III, "proportional reduction" of P intake also was employed; but in addition, 20 mug of 25(OH)D(3) were administered orally three times a week. In group I, parathyroid hormone (PTH) levels rose throughout the 2-yr period reaching a final concentration of 557+/-70 U (normal 10-60). In group II, values for PTH remained normal throughout the 1st yr, increased modestly between the 12th and the 18th mo, but then did not rise after the 18th mo. In group III, no elevation of PTH levels was observed at any time; however, these animals were hypercalcemic. Histomorphologic analyses of the ribs of these dogs were performed serially throughout the 2-yr period. A linear relationship was obtained between the osteoclastic resorption surface and the concentration of circulating immunoreactive PTH. The osteoid volume was greater in group I animals when compared to those in group II. None of the morphologic abnormalities associated with renal osteodystrophy were observed in the animals in the third group.

Animals↗
PubMed1976

1 alpha hydroxycholecalciferol and 25 hydroxycholecalciferol in renal bone disease.

Four microgrammes of 1-alpha-hydroxycholecalciferol (1-alpha-OH D3) or 200 mug of 25-hydroxycholecalciferol (25-OH D3) were given orally every other day respectively to 10 uraemic patients (8 on chronic haemodialysis) for 1-12 weeks and to 3 patients on chronic haemodialysis for 4-8 weeks. A transilial bone biopsy and serial evaluation of serum immunoreactive PTH (iPTH) calcium phosphate and alkaline phosphatase were performed before and at the end of therapy. Both 1-alpha-OH D3 and 25-OH D3 (the latter at a 50 times higher dose) were able to depress hyperparathyroidism in two-thirds of the cases and to consistently improve the mineralisation defect. In no case did iPTH or the bone histomorphometric parameters return to normal, so that long term evaluation of these two drugs is warranted.

Absorption↗
PubMedDate not supplied

[Rapid centrifugation for routine coagulation testing].

Routine coagulation assays are performed with platelet-poor plasma obtained after centrifugation of whole citrated blood. Usually clinical laboratories centrifuge blood from 2,000 to 2,500 g for 15-30 minutes. Thirty two blood samples routinely submitted to coagulation tests, were assayed for the prothrombin time, activated partial thromboplastin time, and fibrinogen level, in order to compare results obtained using 2 types of centrifugation : centrifugation at 2,500 g for 15 minutes and rapid centrifugation on StatSpin Express 2 at 4,440 g for 2 minutes. A good correlation was observed for the prothrombin time, activated partial thromboplastin time, and fibrinogen levels being respectively 1,009, 0,908 and 1. We concluded that rapid centrifugation at 4,440 g for 2 minutes does not modify results and contributes, by decreasing duration of the pre-analytical variable to reduce the completion time of these tests.

Blood Coagulation Tests↗
PubMedDate not supplied

[Long-term effects of a combination of 25-hydroxycholecalciferol and 1-alpha-hydroxycholecalciferol on osteodystrophy in chronic hemodialysis patients].

vitamin compounds to the basic dialytic treatment of renal osteodystrophy is of contestable interest. Because 1) optimum conditions of dialysis without D vitamin addition prevent efficiently the progress of severe gyperparathyroidism and osteomalacia 2) the D vitamin compunds could render the phosphatemia control more difficult thus contributing to aggravate the histologic lesions of hyperparathyroidism.

Adult↗