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Biomedical subjects

P Bataille

Publications and source records attributed to P Bataille.

At least 19 recordsLinked to original sources
PubMed1995

[Bone involvement in idiopathic calcium lithiasis].

Bone involvement in idiopathic calcium nephrolithiasis is characterized by the following abnormalities: a) the bone density is decreased, the severity of bone loss being dependent upon the existence of hypercalciuria and upon the pathophysiology of this latter: it is inconsistent in the absence of hypercalciuria or when hypercalciuria is of the absorptive type I or II, whereas it is almost constant in fasting hypercalciuria without secondary hyperparathyroidism and constant and severe in the rare true renal hypercalciuria. b) The bone histology (which has been evaluated only in idiopathic hypercalciuric patients) mainly shows a defect in bone formation at the exception of the rare renal hypercalciuria. Osteoclastic hyperresorption is only seen in this latter type of hypercalciuria whereas in the other types of hypercalciuria only an increase of the total or inactive resorption surface is observed. This phenomenon is possibly explained only by a delayed refilling of the resorption lacunae secondary to the decreased bone formation. The osteoid thickness is either normal or decreased despite decrease in mineralization apposition rate which seems therefore to be secondary to the decreased bone formation. c) Symptomatic bone disease in hypercalciuric stone formers is exceptional and always related to a severe long term calcium restriction. d) The biochemical markers of bone resorption tend to be increased in idiopathic hypercalciuria. Hydroxyprolinuria is more often elevated than pyridinolinuria. However pyridinolinuria is negatively correlated to bone density. The contrast between the increase of these bone resorption markers and the usual normality of plasma PTH and of the osteoclastic resorptive surfaces, suggest the role of meat induced acid load which may favor inactive resorption by dissolution of bone buffers. A disturbed profile synthesis of cytokines which induce differentiation and proliferation of the osteoclasts and which modulate the osteoblastic proliferation and function (IL-1, IL-6, TNF-alpha, GM-CSF...) may play a role in the bone loss of calcium stone formers but further studies are necessary to precise its transient or permanent involvement in their bone disease. e) The decrease of bone formation may be explained by the suppressed PTH secretion which may be explained by hypercalcitriolemia. This excess of calcitriol synthesis may be secondary either to monocyte increased synthesis of IL-1 which stimulates the renal 1 alpha-hydroxylase by the mean of an increased PGE2 synthesis or to the relative hypophosphatemia of the calcium stone formers comparatively to healthy controls. Hypercalcitriolemia may originate from the activated monocyte itself. The decrease in bone formation may also be secondary to the action of monokines on the osteoblast differentiation and/or function.

Animals↗
PubMed1994

[Late renal and hypertensive complications of extracorporeal lithotripsy. Myth or reality?].

Extracorporeal shock wave lithotripsy (ESWL) has produced dramatic advances in the surgical management of urinary calculi. However this new procedure could induce deleterious effects as loss of renal function and hypertension. Animal studies show that ESWL induces focal areas of necrosis and subsequent fibrosis in renal tissue. In humans, imaging technics demonstrate renal alterations in 80% of the patients. Acute renal hemodynamic and functional changes is frequent but transient in most of the cases. Some studies have shown a tendancy to an increase in blood pressure related to a decrease in renal plasma flow in one study. However most of these results are based on retrospective surveys of blood pressure and renal function. Therefore prospective clinical trials are needed to investigate the important questions of ESWL-induced hypertension and decrease renal function.

Animals↗
PubMed1992

[Vertebral density of hypercalciuric lithiasis. Its relation to calcium-protein intake and vitamin D metabolism].

Forty-two patients with calcium calculi were selected based on calciuria > 0.1 mmol/kg/d on an uncontrolled diet. To measure excretion of sodium, calcium, phosphates and hydroxyproline, a 24-hr urine sample was collected on the 4th day of a milk product-free diet, a fasting urine specimen was collected on the morning of the 5th day and another sample was taken 4 hr after the oral administration of calcium. On the 5th day, plasma levels of calcium, phosphates, intact parathyroid hormone (PTH), calcidiol and calcitriol were determined on an empty stomach and after administration of a calcium load. The results, compared to those of healthy subjects evaluated under the same conditions, enabled classification of the stone-formers as having dietary hypercalciuria (n = 18), when calciuria returned to normal on a low calcium diet, and idiopathic hypercalciuria (n = 24), when the urinary calcium level remained high. Patients with idiopathic hypercalciuria were then classified, according to Pak's criteria, as having absorptive hypercalciuria (n = 8), when the fasting calciuric levels was normal, renal hypercalciuria (n = 1), when fasting hypercalciuria with elevated circulating PTH was controlled by a calcium load, or undetermined hypercalciuria (n = 15) for those individuals with fasting hypercalciuria and normal plasma PTH levels. In addition, vertebral density was measured tomodensitometrically and expressed as a percentage of the normal as a function of sex and age based on a regression line calculated with the results of 239 normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Bone Density↗
PubMed1991

[Bone density in idiopathic hypercalciuria in men. Study by dual photon absorptiometry, X-ray computed tomography and histomorphometry].

Lumbar bone mineral density (BMD) of the L3 vertebra was evaluated by double photon absorptiometry or tomodensitometry (TDM) in 55 hypercalciuric individuals in two separate studies. In the first, in a department of nephrology, 29 lithiasis patients were studied by TDM of L3. By this technique, trabecular density was 75 +/- 23% of normal. It was lower in the 17 patients in whom hypercalciuria persisted after calcium restriction (66 +/- 15% of normal and below the "fracture threshold" in 9 cases) than in the 12 patients in whom it disappeared after the prescription of such a diet (88 +/- 26%, below the "fracture threshold" in 3 cases), this difference being significant (p less than 0.01). In another 26 patients, seen in a department of rheumatology, three of whom had osteoporosis with vertebral fracture, density was measured in 21 cases by double photon absorptiometry (mean Z score -1.9 +/- 1.0) and in 5 cases by TDM (mean BMD of L3 69 +/- 21% of normal). Mean iliac trabecular volume, measured in 8 cases only, was 70 +/- 25% of normal and was below the "fracture threshold" in 3 cases. Comparison of the two study groups was not possible because of differences in recruitment and methods of investigation. These two studies nevertheless show the existence of significant vertebral bone rarefaction during hypercalciuria in the young man. Confirmed and quantified in patients in whom the metabolic disturbance was discovered as a result of radiological abnormalities, this quantitative abnormality was also seen in patients in whom hypercalciurie was found because of renal lithiasis.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorptiometry, Photon↗
PubMed1991

[Physiopathology, exploration and treatment of calcium lithiasis].

The main risk factors for calcium urolithiasis that are clinically detectable are low diuresis, hypercalciuria, hyperruricuria, alkaline urinary pH, hyperoxaluria, hypomagnesuria, hypocitraturia. They should be evaluated, all the more precisely that the disease is active, under both the urological and metabolic points of view, using 24 hour urine collection made at home on a free diet with a dietary record. In the majority of the cases the calcic urolithiasis is idiopathic, i.e. not related to a cause of secondary hypercalciuria like primary hyperparathyroidism, or to a hyperroxaluria either primary or of digestive or toxic origin. Its treatment if mainly dietary with high fluid intake (diuresis greater than 2 1/24 h), normoclacic diet (800-1000h mh/24 h) with meat but not dairy product restriction, oxalate salts, carbohydrate and alcohol restriction. These dietary recommendations should be controlled by measuring the above cited parameters in the 24 hour urine samples and by measuring urea excretion which should not exceed 0.33 g/kg of body weight. When diet fails, drugs may be added mainly allopurinol, thiazides and potassium citrate.

Calcium↗
PubMed1991

Diet, vitamin D and vertebral mineral density in hypercalciuric calcium stone formers.

To elucidate the pathophysiology of dietary calcium independent hypercalciuria, 42 calcium stone formers (Ca SF) were selected because they had on free diet a calciuria greater than 0.1 mmol/kg/day. For four days they were put on a diet restricted in calcium (Ca RD) by exclusion of the dairy products. They collected 24 hour urines on free diet and on day 4 of Ca RD as well as the two-hour fasting urines on the morning of the day 5 and the four-hour urines passed after an oral calcium load of 1 g, for measurement of creatinine, Ca, PO4, urea and total hydroxyprolinuria (THP). On day 5 fasting plasma concentrations of Ca, PO4, intact PTH, Gla protein, calcidiol and calcitriol were measured. The patients were firstly classified into dietary hypercalciuria (DH, 18 patients) and dietary calcium-independent hypercalciuria (IH, 24 patients) on the basis of the disappearance or not of hypercalciuria on Ca RD. Then the patients with IH were subclassified into absorptive hypercalciuria (AH) because of normal fasting calciuria (8 patients) and into fasting hypercalciuria (16 patients). Fasting hypercalciuric patients were subsequently divided according to the PTH levels into renal hypercalciuria (RH, 1 patient) with elevated fasting PTH becoming normal after the Ca load and undetermined hypercalciuria (UH, 15 patients) with normal PTH levels. Furthermore, their vertebral mineral density (VMD) was measured by quantitative computerized tomography which was normal in DH (91 +/- 6% of the normal mean for age and sex) but was decreased in IH to 69 +/- 4%. No difference in VMD was observed between AH and UH. Urinary excretions of urea, phosphate and THP was higher in IH than in DH and comparable in AH and UH. Sodium excretion Ca RD was the same in all groups and subgroups as well as the plasma parameters. Plasma calcitriol was increased in IH and DH comparatively to normal in spite of normal plasma calcidiol. Calciuria increase after oral calcium load, an index of Ca absorption, was higher in IH than in controls and comparable in IH and DH as well as in the three subgroups of IH. From these data and correlation studies in IH it is concluded: (1.) VMD is decreased in Ca stone formers with IH but not in those with DH, making the distinction of these two groups of hypercalciuria patients clinically relevant.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1990

Production of poly-(beta-hydroxybutyric-co-beta-hydroxyvaleric) acids.

Alcaligenes latus, Alcaligenes eutrophus, Bacillus cereus, Pseudomonas pseudoflava, Pseudomonas cepacia, and Micrococcus halodenitrificans were found to accumulate poly-(beta-hydroxybutyric-co-beta-hydroxyvaleric) acid [P(HB-co-HV)] copolymer when supplied with glucose (or sucrose in the case of A. latus) and propionic acid under nitrogen-limited conditions. A fed-batch culture of A. eutrophus produced 24 g of poly-beta-hydroxybutyric acid (PHB) liter-1 under ammonium limitation conditions. When the glucose feed was replaced with glucose and propionic acid during the polymer accumulation phase, 17 g of P(HB-co-HV) liter-1 was produced. The P(HB-co-HV) contained 5.0 mol% beta-hydroxyvaleric acid (HV). Varying the carbon-to-nitrogen ratio at a dilution rate of 0.15 h-1 in a chemostat culture of A. eutrophus resulted in a maximum value of 33% (wt/wt) PHB in the biomass. In comparison, A. latus accumulated about 40% (wt/wt) PHB in chemostat culture under nitrogen-limited conditions at the same dilution rate. When propionic acid was added to the first stage of a two-stage chemostat, A. latus produced 43% (wt/wt) P(HB-co-HV) containing 18.5 mol% HV. In the second stage, the P(HB-co-HV) increased to 58% (wt/wt) with an HV content of 11 mol% without further addition of carbon substrate. The HV composition in P(HB-co-HV) was controlled by regulating the concentration of propionic acid in the feed. Poly-beta-hydroxyalkanoates containing a higher percentage of HV were produced when pentanoic acid replaced propionic acid.

Alcaligenes↗
PubMed1990

[Physiopathology of idiopathic calcium lithiasis].

In this review article the various steps and local mechanisms of stone formations are summarized. Then the pathophysiology of the various risk factors namely urinary excretion of calcium, oxalate, uric acid, urine volume, urine pH and urinary inhibitors of stone formation is extensively discussed.

Calcium↗
PubMed1990

[Epidemiology of primary glomerulonephritis in Picardie].

Between 1 January 1976 and 31 December 1986, primary glomerulonephritis was histologically diagnosed in 319 patients, living in a region of 675,000 inhabitants at the time of renal biopsy. The prevalence of primary glomerulopathy was 0.4/1000 inhabitants. The annual incidence was determined during two 5 year periods: period A (1976-1980) and period B (1981-1985): they were, respectively, 3.4 and 4.5 for 100,000 inhabitants. Berger's focal glomerulonephritis was the most common (30 p. 100) and its incidence was increasing. In contrast, membranoproliferative and acute glomerulonephritides were sharply decreased (almost disappeared), while membranous glomerulonephropathies and glomerulopathies with minimal glomerular lesions or proliferative forms with crescents increased. All primary glomerulonephritides were more prevalent in men and their frequencies increased with age. Our findings lead to the following conclusions: a) the low prevalence and incidence of primary glomerulopathies (3 times less than in other published studies) probably reflect the under medicalization of our region and the attractiveness of neighbouring metropolis, rather than a real decrease in the disease; b) the quasi- disappearance of acute and membranoproliferative glomerulonephropathies and the high incidence of IgA glomerulonephropathies suggest that their pathogenetic associations with infections sensitive to antibiotics are different; c) the increased frequency of membranous glomerulonephropathy and the glomerulopathy with minimal glomerular lesions in aged subjects is most likely due to their polymedication.

Adult↗
PubMed1985

Comparison of 1 alpha-OH-vitamin D3 and high doses of calcium carbonate for the control of hyperparathyroidism and hyperaluminemia in patients on maintenance dialysis.

27 patients on hemodialysis (dialysate aluminium less than 0.7 mumol/l for 2 years, and 2 mumol/l before) whose plasma Ca and PO4 were adequately controlled for already 6 months by high doses of CaCO3 alone (mean +/- SD: 9 +/- 5 g/day), were randomly divided into 2 groups, a control group (c group) which was kept on the same treatment, and a group in which CaCO3 was reduced to 3 g/day but in which plasma Ca was kept normal due to 1 alpha-OH-vitamin D3 administration (1 microgram/day at the beginning, 0.3 microgram/day after 6 months; 1 alpha group) whereas plasma phosphate was kept below 6.0 mg/dl because of Al(OH)3 (2.7-5 g/day). Initially, the 2 groups were comparable as regards the plasma concentrations of total and ionized Ca, phosphate, alkaline phosphatases, medium and C-terminal parathyroid hormone (PTH) and aluminium, but the control group had lower plasma 25-OH-vitamin D (25-OHD.) After 6 months, the same difference in plasma 25-OHD was found with comparable plasma concentrations of total and ionized calcium as well as of medium and C-terminal PTH (beta error 1%). However, plasma concentration of phosphate and the plasma Ca phosphate product, as well as the plasma aluminium were higher in the 1 alpha group whereas their PCO3H- was lower. Although the alkaline phosphatase values were not significantly different between the 2 groups, they increased only in the control group because of 1 patient who developed a vitamin-D-deficient osteomalacia (plasma 25-OHD 3 ng/ml), which was subsequently cured by physiological doses of 25-OHD3. The incidence of transient hypercalcemia (15 vs. 21 episodes) and worsening of soft tissue calcifications (3 in each group) was the same in the 2 groups.

Adult↗
PubMed1985

Critical role of oxalate restriction in association with calcium restriction to decrease the probability of being a stone former: insufficient effect in idiopathic hypercalciuria.

The probability of being a stone former (PSF) was calculated in 3 groups of idiopathic calcium stone formers [with normocalciuria (NC), dietary hypercalciuria (DH) and idiopathic hypercalciuria (IH)] in 4 conditions: while on a free diet; on a calcium- and oxalate-restricted diet during 4 days; after an oxalate load, while on a 1.5-gram calcium diet, and after an oxalate load while on a calcium-restricted diet. Combined calcium and oxalate restriction significantly decreased PSF only in NC and DH whereas the decrease was not significant in IH because of a concomitant significant increase in oxalate excretion. Increase of PSF with the oxalate load was significantly greater during a calcium-restricted diet than during the 1.5-gram calcium diet in all groups of patients (4, 6 and 12 times greater in NC, DH and IH, respectively). These data show the critical role of oxalate restriction when calcium is restricted in order to decrease the PSF. This combined restriction is however not sufficient in idiopathic hypercalciuric patients to decrease their PSF.

Calcium↗
PubMed1985

[Medical treatment of idiopathic calcium lithiasis (I)].

Calcium stones is responsible for 80 per cent of the stones in the upper track. It is a frequent and particularly recurrent disease and for this reason it is important to prevent its recurrence by medical treatment, dissolution of calcium stones being impossible. In the first part of this review, we have presented the theoretical basis and the clinical studies concerning conservative therapy involving high fluid intake and dietary advice on calcium and oxalate intake. Then, for the various drugs proposed for recurrence prevention we have reviewed their mechanisms of action and the controlled clinical trials concerning these drugs. Finally, the practical therapeutical choices for the management of these patients are presented according to the results of the previous metabolic evaluation.

Calcium Oxalate↗
PubMed1985

Magnesium renal wasting in calcium stone formers with idiopathic hypercalciuria contrasting with lower magnesium:calcium urinary ratio.

Plasma magnesium (PMg) and urinary calcium (UCaV) and magnesium (UMgV) were measured after four days of calcium-restricted diet in 60 controls and 82 patients classified according to their calcium excretion in three groups: normo-calciuric (NCa), dietary hypercalciuria (DH) and idiopathic hypercalciuria (IH). When compared to controls, higher UMgV (4.26 +/- 0.28 mmol/d versus 3.4 +/- 0.16, p less than 0.01), lower PMg (0.79 +/- 0.01 mmol/d versus 0.84 +/- 0.01, p less than 0.05) and lower UMg/UCa ratio (0.6 +/- 0.04 versus 1.68 +/- 0.15, p less than 0.001) were observed only in IH. A significant correlation between UMgV and UCaV was found in controls, in NCa and in DH but not in IH. In conclusion, (1) the coexistence of a higher UMgV and of a lower PMg in IH suggests that there is a magnesium depletion in this group of patients; (2) since the lower UMg/UCa ratio may favour a higher propensity for calcium crystallisation and is seen only in IH, magnesium supplements may be specially indicated in this group.

Calcium↗