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Biomedical subjects

J Gueris

Publications and source records attributed to J Gueris.

At least 55 records · Page 3Linked to original sources
PubMed1981

Bone histomorphometry in hemodialysed patients.

We performed bone histomorphometry in thirty hemodialysed patients. Ten patients had a double iliac bone biopsy to estimate bone histomorphometry reproductibility. There was no difference between the mean results for each of the 10 patients at each site. However, there was an intra-individual variation which was small for the parameters of formation and particularly osteoid thickness and mineralizing rate and greater for resorption parameters. Mineralization rate appeared the most reliable and discriminant parameter. These 30 patients were separated in two groups according to their mineralizing rate (MR); patients with an MR greater than 0.3 mu/day were in group I and had severe hyperparathyroidism without major impairment of bone mineralization and high formation rate. They also had high serum alkaline phosphatases and high serum parathyroid levels measured with a COOH terminal antibody (iPTH). Patients with a low MR less than 0.3 mu/day (group II) had a severe mineralization defect with low formation rate, normal alkaline phosphatase and significantly lower levels of iPTH than in group I. This last type of histological bone lesion could not be due to aluminum intoxication since the level of serum aluminum was the same in the two groups. The mineralizing defect appeared to be inversely correlated with the percent of osteoid surfaces covered by osteoblast and with the iPTH level. These data suggest that during the course of renal osteodystrophy PTH stimulates not only bone resorption but also bone mineralization by increasing osteoblastic number.

Adolescent↗
PubMed1980

Effects of somatostatin on intestinal calcium absorption in man with primary hyperparathyroidism.

Eight patients suffering from primary hyperparathyroidism were studied in basal conditions, i.e. during a saline infusion and under somatostatin administration (a 250 micrograms bolus injection followed by continuous infusion of 500 micrograms per hour over 240 min). The calcium metabolism was estimated from (i) concentrations of plasma calcium, phosphorus, 25-hydroxyvitamin D (25-OH-D), iPTH and (ii) intestinal calcium absorption determined by a double radiotracer technique using oral 47Ca and IV 45Ca. The results show that somatostatin produced no significant change in calcium, phosphorus, 25-OH-D or iPTH levels. On the contrary, the fractional absorption of calcium (FA Ca), expressed as a percentage of the total oral dose and measured at 30 minute intervals over 240 min, was significantly depressed with somatostatin during the first 2 hours. Beyond the second hour FA Ca remained slightly depressed with somatostatin, but was not significantly different from the basal conditions. From the present results, we conclude that somatostatin slows down calcium absorption, while the total amount of calcium absorbed at the completion of the absorption process is not significantly diminished. Furthermore, as 25-OH-D and iPTH remained unchanged, somatostatin seems to have no effect on the hormonal control of calcium absorption. Therefore, we suggest that somatostatin has only a mechanical effect on calcium absorption, slowing down the intestinal transit.

Calcifediol↗
PubMed1979

[Idiopathic hypercalciuria: effects of acute phosphorus deficiency (author's transl)].

Eleven patients with kidney stone disease and idiopathic hypercalciuria (urinary calcium above 4 mg/kg/j), without phosphorus renal leak and 6 control subjects have been put for 3 days on a diet containing 1 g calcium and 1 phosphorus daily (period A), and then for 4 days on a diet containing 1 g calcium, 450 mg phosphorus and 3 g aluminium hydroxyde daily (period B). During period A, no significant difference in blood calcium, phosphorus and magnesium, not in phosphaturia, rate of phosphorus reabsorption (RPR) and ratio maximum RPR/creatinine clearance was found between the two groups. After 2 days on a low phosphate diet (period B) the blood phosphorus decreased significantly in the hypercalciuric patients but not in the control subjects, thus revealing among the forme a latent abnormality in the retention of phosphates. This abnormality could play an important role in the pathogenesis of hypercalciuria.

Adult↗
PubMed1978

[Immobilisation hypercalcaemia. 1 case (author's transl)].

A 21-year-old man suffered severe (up to 15.5 mg%) and prolonged (7 months) hypercalcaemia as a result of immobilisation following severe trauma. During the period of hypercalcaemia, plasma parathormone and calcitonin levels were undetectable. A study using radioactive calcium revealed a very marked increase in bone resorption, a moderate increase in accretion and virtually no intestinal absorption. Iliac biopsy revealed dense calcification front and there was no osteoid substance. This hypercalcaemia appeared to be due to increased bone resorption, while the synthesis of osteoid substance seemed to be insufficient to permit an equivalent increase in calcium accretion.

Adult↗
PubMed1978

[The estimation of parathormone in primary hyperparathyroidism (author's transl)].

In a recent series of 110 cases of primary hyperparathyroidism, estimations of plasma immuno-parathormone (PTH) were carried out in fifty two patients. This estimation proved reliable, making possible the confirmation of the diagnosis. In the absence of renal insufficiency, there was a highly positive relationship between PTH levels and plasma calcium. The relationship between PTH and the weight of the parathyroid tumour was less significant. For technical reasons, this long and difficult estimation cannot be used on a routine basis. However, it is most useful in cases in which other laboratory findings are not typical.

Adenoma↗
PubMed1978

The effect of 1alpha(OH)D3 and 1alpha,25(OH)2D3 on the bone in patients with renal osteodystrophy.

Six patients with chronic renal disease and variable degrees of renal osteodystrophy were treated for three weeks with either 1alpha,25-dihydroxyvitamin D3 (1alpha25(OH)D3) or 1alpha,hydroxyvitamin D3 (1alpha(OH)D3) and both the biochemical and osseous responses measured. The most consistent changes seen were an increase in serum calcium concentration to normal, a decrease in immunoreactive parathyroid hormone toward normal, an increase in the extent of the calcification front and a decrease in the extent of fibrous dysplasia in the marrow cavity. Two important parameters which did not change significantly were serum alkaline phosphatase activity and the osteoid volume. These data, in conjunction with that from previous studies, indicate that therapy with 1alpha,25(OH)2D3 or 1alpha(OH)D3 does not heal the osteomalacia of renal osteodystrophy, but that it does suppress the secondary hyperparathyroidism, and ameliorate the osteitis fibrosa seen in patients with chronic renal disease. They raise the likelihood that additional factors, such as metabolites of vitamin D other than 1alpha,25(OH)2D3, play a role in regulating bone formation and/or mineralization.

Aged↗
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

[Effects of the main derivatives of vitmain D in 3 siblings with "pseudo-deficiency" rickets].

Three siblings, respectively 20, 16 and 12 years old, presented with hypocalcemic vitamin D resistant rickets (Prader's type). Their clinical history included several periods of spontaneous cessation of therapy, with severe relapses. Since 1973, treatment was strictly observed, allowing to test the therapeutic effects of 25 OH D3, 1-25 (OH) 2 D3 and 1-alpha (OH) D3. The clinical effects are reported as well as biochemical data. Among them, an inactive form of hyperparathyroidism is emphasized, which may resemble some cases of pseudohypoparathyroidism. Simultaneous resistance to exogenous PTE was also demonstraded.

Adolescent↗
PubMed1978

[Current data on prolactin].

Prolactin has been lately singled-out among the pituitary hormones, and as such the object of considerable research in the past 15 years. The frequency of prolactin secreting adenomes is established now. The responsibility of iatrogenic factors (neuroleptics, oral contraceptives) in some hyperprolactinaemias is a known fact. The study of the inhibiting dopaminergic system was a landmark in the treatment of hyperprolactinaemia. During the recent Nice Congress, some issues remained unsettled on the physiological activities of prolactin. The matter is clearer when it comes to prolactin secretion. In equilibrium between inhibiting and stimulant factors, the secretion is controlled by the CNS, influenced by the hormonal environment, and its timing is the object of a retrocontrol. This is a very instructive pattern in endocrinology.

Animals↗
PubMed1977

[The relationship between parathormone and calcium blood levels in primary hyperparathyroidism. Diagnostic value (authors transl)].

The results of radio-immunoassay of parathormone in peripheral venous blood (using an anti-serum preferentially recognising fragments from the carboxyl-terminal pole) were compared with those of blood calcium measured on the same day in 33 cases of primary hyperparathyroidism. In the 28 patients with hypercalcaemia, PTH was invariably high (27 cases) or at the upper limit of normal (1 case). In the 5 patients with normal blood calcium levels, it was normal in 3 cases. It is thus important to take blood calcium levels into account in the interpretation of PTH estimation, that latter being more valid during a hypercalcaemic phase.

Calcium↗