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A Bourdeau

Publications and source records attributed to A Bourdeau.

At least 55 records · Page 3Linked to original sources

[Circulating metabolites of vitamin D in 14 children with hypercalcemia].

Circulating vitamin D metabolite concentrations, i.e. 25-(OH)D, 24,25-(OH)2D, 1,25-(OH)2D have been assayed in 14 hypercalcemic children. Results are as follows: a) Children with vitamin D intoxication (n = 2) had elevated serum 25-(OH)D and 24,25-(OH)2D concentrations but their 1,25-(OH)2D concentrations were similar to those found in normocalcemic children (10-110 pg/ml); b) Children with familial idiopathic hypercalcemia and hypocalciuria (n = 5), children with hypercalcemia and either Bartter's syndrome (n = 1), hemangiomatosis (n = 1), osteopetrosis after medullary graft (n = 1), also had 1,25-(OH)2D concentrations in the normal range; c) In contrast, 1,25-(OH)2D were elevated (160-470 pg/ml) in the four children with severe idiopathic hypercalcemia and elfin facies.

24,25-Dihydroxyvitamin D 3↗

Does vitamin K excess induce ectopic calcifications in hemodialysis patients?

Vitamin K promotes the formation of gamma-carboxylated glutamic acid (Gla) residues within different protein classes such as vitamin K-dependent clotting factors, bone Gla-protein (BGP or osteocalcin), and atherocalcin. Gla-containing proteins have a high affinity for the Ca2+ ion. In addition to bone and atheromatous plaques they are also regularly found in ectopic calcifications, but not in uncalcified soft tissue. In the present study we investigate the possibility that vitamin K and BGP, in addition to previously recognized factors, may play a role in soft tissue calcification of chronic hemodialysis patients. Patients without radiovisible ectopic calcifications (group A) are compared to patients with such Ca deposits (group B). Both patient groups have comparable values of predialysis plasma Ca, P, alkaline phosphatases, parathyroid hormone (PTH) and 25 hydroxyvitamin D. The CaxP product is slightly higher in group B than in group A patients. Plasma vitamin K1 levels of group B patients are increased to more than twice the values observed in group A patients. Plasma BGP, even though not significantly different, shows a trend towards decreased levels in group B patients. A positive correlation exists between plasma vitamin K1 and BGP for patient group A alone, but not for group B alone. A correlation is also observed between plasma PTH and BGP (all patients) and between serum alkaline phosphatases and plasma BGP (all patients). Taken together, these results favor the hypothesis that in addition to an increased CaxP product a vitamin K excess may induce soft tissue calcification in hemodialysis patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Primary hyperparathyroidism. Lack of effect of cimetidine on plasma levels of parathyroid hormone and calcium].

Because of the contradictory results formerly published as regards the effect of cimetidine in primary hyperparathyroidism, we have studied the effect of cimetidine at the daily dose of 1200 mg in 14 cases of primary hyperparathyroidism. The diagnosis was ascertained in all cases by the coexistence of an otherwise unexplained hypercalcemia and of a concomitantly elevated plasma concentration of immunoreactive parathyroid hormone (PiPTH) measured by 2 different antibodies and confirmed in 10 cases by surgical neck exploration. In 5 cases with severe hypercalcemia (greater than 12.0 mg/l) cimetidine was discontinued after 5 days because of its lack of effect on both plasma concentrations of calcium and PiPTH, and the patients were successfully operated. In 8 cases with milder hypercalcemia, cimetidine was given for 1.5-6 months. There was no significant change in both plasma concentrations of calcium (PCa) and PiPTH but a regression analysis showed that PCa was negatively correlated to time with a correlation coefficient which would have become significant if the follow-up had been 9 months. In the last patient severe hypercalcemia was controlled by simultaneous administration of phosphate, indomethacin and cimetidine without concomitant decrease of PiPTH; and 6 weeks after cimetidine discontinuation no significant increase of PCa and PiPTH occurred. These data show that cimetidine has no clinically therapeutic value in primary hyperparathyroidism.

Adolescent↗

Total parathyroidectomy and delayed parathyroid autotransplantation using a simplified cryopreservation technique: human and animal studies.

Following earlier studies using a simplified cryopreservation method in rats, we report the successful use of this technique in a hemodialysis patient who had previously undergone total parathyroidectomy. In additional studies, parathyroid glands from rats were conserved by this rapid freezing procedure after total parathyroidectomy. Six weeks after parathyroid autotransplantation the animals were submitted to a low-calcium diet and their parathyroid gland function compared to that of rats that had previously undergone sham operation, immediate autotransplantation, or delayed autotransplantation using the classical cryopreservation method. With both cryopreservation techniques, plasma calcium, phosphorus, and 1,25 (OH)2 vitamin D concentrations after low-calcium diet were similar although results were less satisfactory than with immediate autotransplantation or after sham operation. We suggest that this simplified cryopreservation technique, developed in rats, yields functioning parathyroid gland tissue and can be successfully used in the human.

Adult↗

Bone ultrastructure and x-ray microanalysis of aluminum-intoxicated hemodialyzed patients.

In hemodialyzed patients aluminum (Al) intoxication may induce osteomalacic lesions which are mainly observed when plasma immunoreactive parathyroid hormone (iPTH) concentrations are low, and osteitis fibrosa absent. In this study, the bone tissue of eight hemodialyzed patients with elevated plasma and bone Al concentrations was examined by histomorphometry, electron microscopy, and x-ray microanalysis. Five patients (group 1) had osteomalacia and minimal osteitis fibrosa, three patients (group 2) had severe osteitis fibrosa. In group 1, Al was concentrated at the mineralizing front, in hexagonal structures measuring 200 to 1,000 A which also contained phosphorus, but not calcium. Hydroxyapatite needles had a normal aspect. Osteoblasts appeared inactive. In group 2, Al was also present at the mineralizing layer of osteoid, but, in these cases, in small clusters next to abnormal calcium deposits. Osteoblasts appeared very active. Their mitochondria contained calcium and phosphorus granules, or amorphous material, measuring 1,500 to 2,000 A, emitting x-rays characteristic for Al and phosphorus. These results suggest that secondary hyperparathyroidism, by stimulating the cellular activity, may increase the uptake and release of Al by the osteoblasts. The presence of Al within the mitochondria of these cells may be one of the factors inducing the mineralization defect.

Adult↗

[Hyperparathyroidism secondary to renal insufficiency: anatomo-clinical relations and the potential role of an aluminum overload].

Severe secondary hyperparathyroidism is still observed at present in 5-10% of haemodialysis patients. It requires surgical correction. Fifty-eight haemodialysis patients had neck surgery and their 222 parathyroid glands analysed. The individual gland weight was comprised between 22 and 3880 mg (mean +/- SEM, 689 +/- 62 mg). Mean total parathyroid gland weight per patient was comprised between 2 and 3 g. Schematically, 4 types of gland architecture could be distinguished: diffuse hyperplasia alone; diffuse hyperplasia associated with incipient nodule formation; hyperplasia with pronounced nodule formation; and nodule formations alone. Total gland weight was significantly higher for the latter two histological forms than for the former suggesting transformation with time of pure hyperplasia to nodular hyperplasia. Patients with chronic pyelonephritis had a mean gland weight higher than that of patients with chronic glomerulonephritis (3308 +/- 498 mg versus 1824 +/- 358 mg, p less than 0.01). No relation was found between total gland weight and plasma calcium, phosphate or alkaline phosphatases. However, a weak relation existed between total gland weight and plasma immunoreactive parathyroid hormone. In addition, a negative relation was observed between highest prior plasma aluminium and gland weight when considering only patients with a gland weight less than 2000 mg. Parathyroid gland aluminium content was significantly higher in haemodialysis patients than in nonuraemic patients with primary hyperparathyroidism. A direct relation was found between parathyroid gland and bone aluminium. In conclusion, in haemodialysis patients with evolving hyperparathyroidism initially diffuse gland hyperplasia appears to be associated progressively with nodule formation. Circulating immunoreactive parathyroid hormone is positively related to total gland weight.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Changes in 25-hydroxyvitamin D3 alpha- and 24-hydroxylase activities of kidney cells isolated from rats with either unilateral kidney damage or acute renal insufficiency.

25-Hydroxyvitamin D3 1 alpha- and 24-hydroxylase, NADPH-cytochrome c reductase, heme oxygenase, and ATPase activities were studied in viable kidney cells isolated from rats submitted to unilateral kidney damage (cortical electrocoagulation) and during the development of acute renal failure subsequent to excision of the contralateral undamaged kidney. Measurements of blood pH, plasma total and ionized calcium, phosphorus, creatinine, kidney histology, and phosphorus nuclear magnetic resonance spectroscopy determinations of phosphorus-containing compounds in kidney tissue were also performed. Seventy-two hours after unilateral kidney damage, no significant changes were observed in blood pH or in the plasma parameters studied. During this period, a significant increase in the activity of the 25-hydroxyvitamin D3 hydroxylases could be demonstrated in the cells of the contralateral undamaged kidney. A similar pattern of compensatory rise in the activity of the other enzymes studied was not detected. However, in the damaged kidney viable cells, the hydroxylase activities remained unchanged relative to those in sham-operated controls, despite a 5-fold increase in the inorganic phosphate content and a marked decrease in the organophosphorus and ATP content of this tissue. During the development of acute renal failure, a significant decrease in the activity of the hydroxylases occurred only when the rise in plasma creatinine concentration suggested severe renal insufficiency.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗

Rickets and alopecia with resistance to 1,25-dihydroxyvitamin D: two different clinical courses with two different cellular defects.

UNLABELLED: Two unrelated patients, aged 22 months and 31 months, with alopecia and rickets resistant to 1,25-dihydroxyvitamin D (1,25-(OH)2D] (vitamin D-dependency type II) presented with similar biochemical and radiologic features. They were treated with large doses of vitamin D3 derivatives [25-hydroxyvitamin D3 (25-(OH)D3), 1,25-(OH)2D3, and 1 alpha-hydroxyvitamin D3] for 28 months and 6 yr, respectively. In both patients, serum 1,25-(OH)2D levels remained high (approximately 10- to 100-fold normal) during the different therapeutic regimens. Circulating 1,25-(OH)2D and 24,25-dihydroxyvitamin D levels at various stages of the disease suggested in these children disturbances in the regulation of 25-hydroxyvitamin D (25(OH)D) 1 alpha- and 24-hydroxylase systems. In one child, all therapeutic trials were unsuccessful. Studies of her cultured skin fibroblasts showed low capacity (10% normal) for saturable (presumably receptor mediated) nuclear uptake of tritiated 1,25-(OH)2D3; the uptake process of nucleus associated 1,25-(OH)2D3 was normal in apparent affinity for 1,25-(OH)2D3 and in sedimentation velocity of nucleus-associated hormone. In the second child, correction of biochemical abnormalities, healing of rickets, and catch-up growth were obtained during similar therapeutic trials up to the age of 6 yr when a relapse occurred. This relapse has persisted for 2 yr in spite of similar or higher circulating concentrations of 25-(OH)D and 1,25-(OH)2D than those obtained previously when she was responsive to therapy. In her cultured skin fibroblasts, saturable high affinity nuclear uptake of 1,25(OH)2D was unmeasurable. IN CONCLUSION: 1) distinct patterns of clinical response can occur in patients with the syndrome of vitamin D-dependency type II, and can be associated with differing abnormalities in interaction of 1,25-(OH)2D3 with cultured skin fibroblasts; 2) aggravation of the resistance to 1,25-(OH)2D3 may occur during long term therapy in some patients.

24,25-Dihydroxyvitamin D 3↗

Secondary hyperparathyroidism in chronic haemodialysis patients: a clinico-pathological study.

Fifty-eight patients on intermittent haemodialysis underwent parathyroidectomy because of severe secondary hyperparathyroidism. Mean individual parathyroid gland weight was 689 +/- 62 (SEM) mg. Mean total gland weight per patient was between two and three grams. Increasing nodule formation within hyperplastic glands appeared to develop with increasing time of duration of hyperparathyroidism. Patients with chronic pyelonephritis had a higher gland weight than those with chronic glomerulonephritis. A direct relationship was found between gland weight and circulating immunoreactive parathyroid hormone, but an inverse relationship between gland weight and plasma aluminium concentration. The higher the parathyroid gland aluminium, the higher was the bone aluminium concentration.

Adolescent↗

Effects of weight and glucose ingestion on urinary calcium and phosphate excretion: implications for calcium urolithiasis.

Renal handling of phosphate and calcium was studied in 17 hypercalciuric stone-formers, 6 normocalciuric stone-formers and 10 normal subjects before (fasting state) and 45 and 75 min after the ingestion of 100 g glucose. The ratio of fasting urinary calcium to creatinine (UCa/creat) was higher in hypercalciuric than in normocalciuric stone-formers or controls. A positive correlation was found between weight index and fasting UCa/creat for all subjects studied (r = 0.36; P less than 0.05). A negative correlation was apparent between the weight index and the fasting renal threshold phosphate concentration (TmP/GFR) (r = 0.40; P less than 0.02), the latter parameter being slightly but insignificantly lower in hypercalciuric stone-formers than in controls. After glucose ingestion. UCa/creat rose significantly in all groups. The maximal rise in UCa/creat was also positively correlated with the weight index for all patients ( r = 0.42; P less than 0.02), and 75 min after glucose ingestion, TmP/GFR decreased in all groups, dropping to a significantly lower level in the hypercalciuric patients than in the controls. No correlation was apparent between the weight index and the magnitude of the reduction in TmP/GFR. Plasma 1, 25-dihydroxyvitamin D3 and immunoreactive parathyroid hormone were measured before glucose ingestion and were not correlated either with each other or with plasma phosphorus, TmP/GFR, or UCa/creat before or after glucose ingestion. These results imply that weight is a determining factor in the renal handling of calcium and phosphorus. Such findings might be of importance to the clinical investigation and management of calcium stone-formers.

Adult↗

[Vitamin D metabolites in a new case of drug-induced hypercalcemia (author's transl)].

The authors report on a new case of severe hypercalcaemia induced by prolonged oral treatment with high doses of vitamin D2. (6 mg/day for 9 months). Blood calcium level did not return to normal until 6 months after the drug was discontinued. The plasma concentration of 25 (OH) D was more than three times the normal value and remained very high throughout the observation period. The plasma concentration of 24, 25 (OH)2 D was slightly raised during treatment but became normal after 15 days, while that of 1,25 (OH)2 D, the active form of vitamin D, remained normal throughout, suggesting that the pathogenesis of vitamin D-induced hypercalcaemia is probably complex.

25-Hydroxyvitamin D 2↗

Aluminum localization in bone from hemodialyzed patients: relationship to matrix mineralization.

It has been suggested that in uremic bone, aluminum interferes with normal mineralization. Aluminum content and aluminum localization were studied in iliac crest biopsies of two groups of patients on regular hemodialysis; one group had histologic osteomalacia, and little or no bone resorption (group 1); the other, osteitis fibrosa and no mineralization defect (group 2). Group 1 patients had significantly higher plasma aluminum concentrations than those of group 2. No difference was found in bone aluminum content, which was above normal in both groups. In the bone samples of the osteomalacic subjects, aluminum was mainly localized at the limit between osteoid and calcified tissue, the site where the bone mineral is normally first deposited. Osteomalacia could not be related to hypocalcemia or to phosphate depletion. Active vitamin D derivatives (25-hydroxycholecalciferol and 1alpha-hydroxycholecalciferol) failed to prevent or to improve the bone disease. In the bone samples of group 2 subjects, aluminum could not be localized by the methods used, except in the two cases with greatly elevated bone aluminum, where it was mainly localized on cement lines. In group 2 subjects, immunoreactive parathyroid hormone plasma concentration, osteoclast surface, and marrow fibrosis were significantly higher than they were in group 1 subjects. It is concluded that in bone from uremic patients on regular dialysis, aluminum can induce a particular form of osteomalacia, resistant to the vitamin D active derivatives. The bone disease is only observed in the absence of severe secondary hyperparathyroidism. This suggests that parathyroid hormone may be involved in the development of the aluminum-induced mineralization defect.

Adult↗

Changes in plasma 1,25 and 24,25-dihydroxyvitamin D after renal transplantation in children.

The purpose of this investigation is to analyze changes in plasma 1,25-(OH)2D and 24,25-(OH)2D after successful renal transplantation in 20 children and young adults. Studies were performed on 8 subjects between the 1st and 10th month and on 12 others between the 20th and 30th to 36th month. Samples were assayed for plasma and urinary calcium, inorganic phosphate, creatinine, plasma bicarbonate, immunoreactive parathyroid hormone, 25-(OH)D, 24,25-(OH)2D, and 1,25-(OH)2D concentrations. Results showed the following: (1) All subjects had normal or high plasma levels of dihydroxyvitamin D metabolites. (2) In subjects with normal GFR's there was a significant inverse correlation between plasma 1,25-(OH)2D concentrations and tubular reabsorption of phosphorus. (3) These correlations were not found in subjects with subnormal creatinine clearances (50 to 100 ml/min/1.73 m2) even though plasma 1,25-(OH)2D concentrations in these subjects were similar to those with normal creatinine clearances. (4) In subjects with subnormal creatinine clearances, an increase in plasma 1,25-(OH)2D concentrations to very high levels was observed during the first months following renal transplantation.

24,25-Dihydroxyvitamin D 3↗

Suppressive effects of 24,25-dihydroxycholecalciferol on bone resorption induced by acute bilateral nephrectomy in rats.

The possible suppressive effects of 24,25-dihydroxycholecalciferol on secondary hyperparathyroidism and increased bone resorption were investigated in adult rats raised on a diet normal in calcium, phosphorus, and vitamin D, and subjected to acute bilateral nephrectomy. The animals had received subcutaneous radiocalcium 4 wk before the experiment. 5 h after nephrectomy an increase in serum total calcium, (45)Ca-specific activity, citrate, phosphorus, and magnesium concentrations were observed. Serum immunoreactive parathyroid hormone increased, while serum calcitonin decreased. The osteoclast count in the tibial metaphyses was augmented. The biochemical and histological changes observed were partly parathyroid hormone and calcitonin independent, as they also occurred in parathyroidectomized hypocalcemic rats. Pretreatment with 650 pmol of 24,25-dihydroxycholecalciferol 16 h before nephrectomy prevented bone calcium mobilization and diminished the rise in serum total calcium and citrate both in parathyroid-intact and in parathyroidectomized animals. In parathyroid-intact rats, serum immunoreactive parathyroid hormone and calcitonin remained normal in spite of the fall in serum-ionized calcium, and the number of osteoclasts did not increase. In parathyroidectomized rats, 24,25-dihydroxycholecalciferol did not prevent the postnephrectomy rise in the osteoclast count. This latter observation suggests that this metabolite exerts its effect on bone either by acting on cells other than osteoclasts, i.e., the osteocytes, or by inhibiting cell activity. At equimolar dosage 1,25-dihydroxycholecalciferol had a potent stimulatory effect on bone resorption. This effect of 1,25-dihydroxycholecalciferol was partly blocked by the simultaneous administration of 24,25-dihydroxycholecalciferol. The potential clinical significance of these observations remains to be determined.

24,25-Dihydroxyvitamin D 3↗

[Serum concentrations of vitamin D metabolites in idiopathic juvenile osteoporosis (author's transl)].

This report concerns a 13 year old girl with the clinical and radiological features of mild idiopathic juvenile osteoporosis. In this patient, no alteration was detected in serum calcium (total + ionized) and phosphorus concentration, serum alkaline phosphatase activity, nor in urinary calcium and phosphorus excretions. Plasma concentrations of cortisol were normal during daytime and sleep. Circulating immunoreactive parathyroid hormone was normal or low. The serum 25-(OH)D and 24,25-(OH)2D concentrations were below the normal range, and the 1,25-(OH)2D concentrations were above the normal range (720 pmol/l) at the beginning of the investigation. All vitamin D metabolites concentrations returned to normal values at the time of radiological recovery and after calcium and 25-(OH)D3 supplementation. A possible relationship between alterations of bone and of circulating vitamin D metabolites is discussed.

Adolescent↗

Plasma vitamin D metabolites in a patient with sporadic hypophosphataemic osteomalacia (adult-onset type).

Sporadic hypophosphataemic osteomalacia (adult-onset type) was demonstrated in a 40-year-old man on the basis of severe osteomalacia, hypophosphataemia, hyperphosphaturia and glycinuria. Plasma immunoreactive parathyroid hormone (iPTH) concentration was 9.3 ng prot./ml (normal range: 4-8 ng prot./ml). Plasma 25-hydroxy-vitamin D and 24,25-dihydroxy-vitamin D concentrations were 11 and 2.4 ng/ml respectively. Basal 1 alpha,25-dihydroxy-vitamin D concentrations were slightly elevated (116 and 96 pg/ml) and increased to 240 pg/ml after 3 days on a low-phosphorus diet. The patient was put on oral treatment with 25-hydroxycholecalciferol (100 microgram per day) and phosphorus (1500 mg per day). On the 4th month on treatment, a clinical improvement was apparent. Plasma 25(OH)D was 44 ng/ml, plasma 1,25(OH)2D was 256 pg/ml. However, plasma phosphorus remained low (0.77 mmol/l). On the 9th month of treatment a radiological improvement was evident despite a persistent hypophosphataemia (0.68 mmol/l). These facts suggest in our patient the existence of a vitamin D-independent renal phosphorus leak.

Adult↗