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Biomedical subjects

A Fournier

Publications and source records attributed to A Fournier.

At least 145 records · Page 8Linked to original sources
PubMed1998

Adherence of Streptococcus mutans to orthodontic brackets.

The affinity of Streptococcus mutans to orthodontic brackets made from metal, plastic, and ceramic was tested. Twelve saliva-coated brackets and 12 noncoated brackets of each type were immersed in a S. mutans solution labeled with [3H] thymidine. Each sample was then immersed in distilled water at 20 degrees C for 24, 48, and 72 hours to measure the adherence of S. mutans to these samples. During the first 24 hours, the adherence of S. mutans decreased with and without saliva coating. Between 24 and 72 hours, the adherence of S. mutans to the saliva-coated brackets remained unchanged; the adherence to uncoated brackets showed a decrease. Saliva coating caused a decreased affinity of S. mutans for all products tested. The initial affinity of S. mutans to metal brackets was statistically significantly lower than that to plastic and porcelain brackets with and without saliva coating.

Adult↗
PubMed1998

Effects of the two somatostatin variants somatostatin-14 and [Pro2, Met13]somatostatin-14 on receptor binding, adenylyl cyclase activity and growth hormone release from the frog pituitary.

Two isoforms of somatostatin from frog brain have been recently characterized, namely somatostatin-14 (SS1) and [Pro2, Met13]somatostatin-14 (SS2). The genes encoding for the precursors of these two somatostatin variants are expressed in hypothalamic nuclei involved in the control of the frog pituitary. The aim of the present study was to investigate the effect of SS1 and SS2 on adenohypophysial cells. Autoradiographic studies using [125I-Tyr, D-Trp8] SS1 as a radioligand revealed that somatostatin binding sites are evenly distributed in the frog pars distalis. The SS2 variant was significantly (P < 0.01) more potent than SS1 in competing with the radioligand (IC50= 1.2 +/- 0.2 and 5.6 +/- 0.6 nM, respectively). Both SS1 and SS2 induced a modest but significant reduction in cAMP formation in dispersed distal lobe cells but did not affect spontaneous growth hormone (GH) release. Synthetic human GRF (hGRF) induced a significant increase in cAMP accumulation and GH release in this system. Both SS1 and SS2 inhibited the stimulatory effects of hGRF on cAMP formation and GH secretion. These data show that the SS1 and SS2 variants can regulate adenohypophysial functions. The fact that GH cells are exclusively located in the dorsal area of the frog adenohypophysis, while somatostatin receptors are present throughout the pars distalis, indicates that the two somatostatin isoforms may control the secretion of pituitary hormones additional to GH in amphibians.

Adenylyl Cyclases↗
PubMed1998

Renal osteodystrophy in dialysis patients: diagnosis and treatment.

This article reviews the clinical, biological, radiological, and pathological procedures and their respective indications for the practical diagnosis of the following various histological patterns of renal osteodystrophy: osteitis fibrosa due to parathyroid hormone (PTH) hypersecretion: osteomalacia or rickets due to native vitamin D deficiency and/or aluminum overload; and adynamic bone disease (ABD) due to aluminum overload and/or PTH secretion oversuppression. Our advice regarding bone biopsy is to restrict it to patients with symptoms and hypercalcemia, especially those who have been previously exposed to aluminum. In other cases, we propose relying merely on the determination of the plasma concentrations of calcium, protide, phosphate, bicarbonate, intact PTH, aluminum, 25(OH)D3, and alkaline phosphatase (total and bony if hepatic disease is associated) to choose the appropriate treatment. Because of the danger of the desferrioxamine treatment necessary to chelate and remove aluminum, the suspicion of aluminic bone disease (osteomalacia or ABD) will always be confirmed by a bone biopsy. In the case of nonaluminic osteomalacia, correction of the vitamin D deficiency by native vitamin D or 25(OH)D3, and of the calcium deficiency and acidosis by alkaline salts of calcium and if necessary sodium bicarbonate are sufficient to cure the disease. In the case of nonaluminic ABD, the stimulation of PTH secretion by the discontinuation of 1alpha hydroxylated vitamin D and the induction of a negative calcium balance during dialysis by decreasing the calcium concentration in the dialysate will allow an increase of the CaCO3 dose to correct for hyperphosphatemia without inducing hypercalcemia. For hyperparathyroidism, i.e., plasma intact PTH levels greater than two- or four-fold the upper limit of normal levels (according to the absence or presence of previous aluminum exposure), the treatment will consist in increasing the CaCO3 dose to correct for hyperphosphatemia together with a decrease of the calcium concentration in the dialysate if the dose of CaCO3 is so high that it induces hypercalcemia. When the hyperphosphatemia has been corrected and there is still a low or normal corrected plasma calcium level, 1alpha(OH)D3 in an oral bolus 2 or 3 times a week should be given at the minimal dose of 1 microg. When the PTH level stays above 400 pg while hypercalcemia occurs and hyperphosphatemia persists, surgical subtotal parathyroidectomy is recommended or the injection of calcitriol into the big nodular hyperplastic parathyroid glands under sonography control in high surgical risk patients. Special recommendations are given for children.

Adult↗
PubMed1998

Role of calcium carbonate administration timing in relation to food intake on its efficiency in controlling hyperphosphatemia in patients on maintenance dialysis.

A study has claimed that at an equal elemental calcium dose, CaCO3 was not less but equally as efficient in controlling predialysis hyperphosphatemia as calcium acetate, provided both calcium salts were ingested 5 min before meals instead of during meals because the higher acidity of the fasting gastric juice would allow for better dissociation of CaCO3. However, this study did not directly demonstrate that the efficiency of CaCO3 in controlling hyperphosphatemia was actually greater when it was administered before a meal than during a meal. To examine this point, we performed a 3 month randomized crossover trial in 12 reliable and stable patients maintained on chronic hemodialysis. Their plasma concentrations of calcium, protein, phosphate, bicarbonate, urea, and creatinine were measured before the first dialysis of each week and the amount of intact parathyroid hormone (PTH) at the beginning and at the end of each of the 3 months. Comparison of the plasma concentrations measured during the 2 modes of administration showed no significant differences in creatinine, urea, bicarbonate, or intact PTH. The mean (+/-SD) plasma concentration of PO4 was not significantly lower (1.88+/-0.50 vs. 1.74+/-0.41 mM) whereas the corrected level of plasma Ca was significantly lower (2.30+/-0.17 vs. 2.38+/-0.16 mM; p < 0.04) when CaCO3 was given before meals than during meals. In conclusion, the administration of CaCO3 before a meal does not increase its efficiency in controlling hyperphosphatemia because the level of plasma PO4 was actually slightly higher with this timing of administration whereas the comparison of the creatinine and urea levels suggested a stability of phosphate intake and the comparison of the PTH and bicarbonate levels suggested the stability of osteolysis and of the transcellular membrane shift of phosphate. Also, administration of CaCO3 before a meal is associated with significantly lower plasma corrected calcium, suggesting less absorption of calcium, which may be an advantage but only in hypercalcemic patients. There is no reason other than the prevention of its hypercalcemic effect to recommend the administration of CaCO3 just before meals rather than during meals.

Absorption↗
PubMed1998

Inhibition of gastric secretion by omeprazole and efficiency of calcium carbonate on the control of hyperphosphatemia in patients on chronic hemodialysis.

Contradictions exist in the literature regarding the effect of gastric secretion inhibition on phosphate absorption. In healthy controls, omeprazole would decrease the hyperphosphatemia or the hyperphosphaturia induced by an acute phosphate load, suggesting an inhibition of phosphate absorption. In chronic hemodialysis patients, gastric hypersecretion is associated with hyperphosphatemia, but inhibition of gastric hypersecretion by ranitidine in those receiving calcium carbonate (CaCO3) as a phosphate binder would paradoxically exacerbate their hyperphosphatemia. Because of these conflicting observations, we performed an open crossover study on 16 chronic stable hemodialyzed patients with a daily mean intake of 9.4+/-4 g of CaCO3, and we compared the plasmatic predialysis levels of phosphate, calcium, protides, bicarbonates, intact parathyroid hormone (PTH), urea, and creatininemia during 2 successive periods of 2 months, the first one without omeprazole and the second one with 20 mg omeprazole intake in the morning. Phosphatemia increased with omeprazole but not significantly from 1.80+/-0.38 to 1.89+/-0.42 mM whereas corrected calcemia decreased significantly (p = 0.04) from 2.41+/-0.18 to 2.36+/-0.16 mM as did bicarbonatemia from 26.7+/-3.5 to 25.7+/-3.1 mM (p < 0.05). No change in creatininemia or in blood urea was observed, suggesting the stable efficiency of dialysis as well as the stable intakes of protein and therefore of phosphate during the two study periods. In conclusion, inhibition of gastric secretion by omeprazole increases the plasmatic phosphate predialytic level but in a nonsignificant way. This increase may be explained by a slight but significant concomitant decrease of calcemia and bicarbonatemia. These results do not support the phosphate binding efficiency of CaCO3 being decreased by the inhibition of gastric acid secretion.

Absorption↗
PubMed1998

Heparin-induced hyperkalemia in chronic hemodialysis patients: comparison of low molecular weight and unfractionated heparin.

Aldosterone suppression and subsequent hyperkalemia are well described reversible side effects of prolonged treatment with heparin. This study was designed to examine whether the discontinuous use of heparin three times a week to prevent thrombosis formation during hemodialysis sessions could also induce hypoaldosteronism and might contribute to increased predialysis kalemia in hemodialysis patients. Two different heparinization regimens were prospectively compared in a crossover study of 11 chronic hemodialysis patients. During 2 consecutive weeks, the patients were dialyzed each week with either their usual doses of unfractionated heparin (UH) (6,160 IU +/- 1,350 IU) or low molecular weight heparin (LMWH) (15 anti-Xa activity [aXa] U/kg + 5 aXa U/kg/h). In all but 2 patients, the predialysis level of plasma K+ was higher with UH than with LMWH, and the mean value was higher (5.66+/-0.83 versus 5.15+/-0.68 mM, p = 0.01) while no differences in the predialysis plasma concentrations of creatinine, phosphate, urea, and bicarbonate were observed, excluding the potential role of differences in diet and dialysis efficacy in explaining the higher plasma K+ concentration with UH. The mean plasma aldosterone to plasma renin activity (pRA) ratio was higher with LMWH than with UH (149.54+/-123.1 versus 111.91+/-86.22 pg/ng/ h, p < 0.05). Individual plasma aldosterone values were found to be correlated to pRAs both during the UH period and the LMWH period, and the slope of the positive linear relation between plasma aldosterone and pRA was lower during the UH treatment period (63 versus 105 pg/ng/h). Finally, a negative linear correlation was found between the differences in individual predialysis plasma K+ observed during the 2 protocols and the differences in the corresponding plasma aldosterone levels, suggesting a link between the higher kalemia and the lower aldosterone responsiveness to angiotensin with unfractionated heparin. Although it cannot be concluded whether or not LMWH inhibits aldosterone synthesis, should LMWH decrease aldosterone production, this side effect is 33% less marked than that of UH so that the predialysis plasma K+ levels are 10% lower. This property makes LMWH use preferable to that of UH in patients with elevated predialysis kalemia.

Adult↗
PubMed1998

Influence of the postoperative period and surgical procedure on ambulatory blood pressure-determination of hypertension load after successful surgical repair of coarctation of the aorta.

AIMS: This study quantified hypertension load using 24-h ambulatory blood pressure monitoring after successful repair of coarctation of the aorta less than (1) or more than 10 years previously (2) and examined the influence of the surgical procedure (anastomosis or subclavian flap). METHODS AND RESULTS: Ambulatory blood pressure recordings were obtained using an Accutracker II monitor every 30 min during the day and hourly, at night. Day and night systolic and diastolic values were higher in coarctation of the aorta than in controls: (day: systolic blood pressure/diastolic blood pressure: 133/71 +/- 6/4 vs 115/66 +/- 3/2 night: systolic blood pressure/diastolic blood pressure: 117/61 +/- 4/4 vs 107/57 +/- 3/2 mmHg, P < 0.01) and at all times, were higher in coarctation of the aorta (2) than in coarctation of the aorta (1). Clinical daytime systolic hypertension was observed in 20% of recordings from coarctation of the aorta (1) and 49% from coarctation of the aorta (2) while diastolic hypertension was not observed. However, systolic blood pressure and diastolic blood pressure responses to daily activities were significantly higher in coarctation of the aorta than in controls and this was more marked in coarctation of the aorta (2) than in coarctation of the aorta (1). Type of surgery did not affect either hypertension prevalence or blood pressure reactivity. CONCLUSIONS: These observations indicate exaggerated systolic blood pressure and diastolic blood pressure reactivity after repair of coarctation of the aorta, the prevalence of systolic hypertension doubling 10 years after surgery.

Adolescent↗
PubMed1998

Pathophysiology and treatment of idiopathic hypercalciuria.

Nearly 50 years after its initial description by Dr. F. Albright, the term idiopathic hypercalciuria (IH) is still in use. The exact mechanism of hypercalciuria is still unknown despite extensive pathophysiologic investigations; recent advances represent the focus of this review. A precise definition of true IH is proposed, taking into account the various nutritional conditions influencing calcium excretion. The potential pathogenic mechanisms are discussed, and the limits of the classical Pak's pathophysiological classification are recalled. The evidence supporting the role of an increased intestinal calcium absorption, a defect in renal tubular calcium reabsorption, or an increased bone loss as a primary mechanism in IH are successively examined. Since overall available human data indicates that all three mechanisms may be found in IH, the hypothesis that a broader disorder encompassing all these various abnormalities may be involved in IH is discussed. Three global hypotheses to account for IH physiopathology are examined: a diffuse defect in fatty acid content of cell membranes, an increased expression of the vitamin D receptor of the 25(OH) vitamin D 1 alpha-hydroxylase, or of the calcium sensor receptor and a monocyte disease. Finally, the available clinical data justifying the therapeutic approaches are reviewed, and guidelines for dietary recommendations regarding calcium and also animal protein, sodium chloride, alcohol, carbohydrate, phosphate, and potassium intakes are proposed, and drug therapy indications are discussed.

Bone Diseases, Metabolic↗
PubMed1998

Ventriculo-atrial time interval measured on M mode echocardiography: a determining element in diagnosis, treatment, and prognosis of fetal supraventricular tachycardia.

OBJECTIVE: To determine whether M mode echocardiography can differentiate fetal supraventricular tachycardia according to the ventriculo-atrial (VA) time interval, and if the resulting division into short and long VA intervals holds any relation with clinical presentation, management, and fetal outcome. DESIGN: Retrospective case series. SUBJECTS: 23 fetuses with supraventricular tachycardia. MAIN OUTCOME MEASURES: A systematic review of the M mode echocardiograms (for VA and atrioventricular (AV) interval measurements), clinical profile, and final outcome. RESULTS: 19 fetuses (82.6%) had supraventricular tachycardia of the short VA type (mean (SD) VA/AV ratio 0.34 (0.16); heart rate 231 (29) beats/min). Tachycardia was sustained in six and intermittent in 13. Hydrops was present in three (15.7%). Digoxin, the first drug given in 14, failed to control tachycardia in five. Three of these then received sotalol and converted to sinus rhythm. All fetuses of this group survived. Postnatally, supraventricular tachycardia recurred in three, two having Wolff-Parkinson-White syndrome. Four fetuses (17.4%) had long VA tachycardia (VA/AV ratio 3.89 (0.82); heart rate 226 (10) beats/min). Initial treatment with digoxin was ineffective in all, but sotalol was effective in two. Heart failure caused fetal death in one and premature delivery in one. All three surviving fetuses had recurrences of supraventricular tachycardia after birth: two had the permanent form of junctional reciprocating tachycardia and one had atrial ectopic tachycardia. CONCLUSIONS: Careful measurement of ventriculo-atrial intervals on fetal M mode echocardiography can be used to distinguish short from long VA supraventricular tachycardia and may be helpful in optimising management. Digoxin, when indicated, may remain the drug of choice in the short VA type but appears ineffective in the long VA type.

Anti-Arrhythmia Agents↗
PubMed1998

Distribution, characterization, and growth hormone-releasing activity of pituitary adenylate cyclase-activating polypeptide in the European eel, Anguilla anguilla.

The complementary DNA encoding pituitary adenylate cyclase-activating polypeptide (PACAP) has been cloned from two species of teleost fishes, the Sockeye salmon and the Thai catfish, and the amino acid sequence of PACAP has been determined in another teleost, the stargazer. However, to date, the detailed distribution of PACAP immunoreactivity has never been investigated in the fish brain. In the present study, we have determined the localization of PACAP-immunoreactive neurons in the central nervous system of a primitive teleost fish, the European eel Anguilla anguilla, using an antiserum raised against PACAP27. PACAP-positive perikarya were exclusively observed in the diencephalon, i.e. in the preoptic nucleus of the hypothalamus and in the dorsal and ventral nuclei of the thalamus. PACAP-immunoreactive fibers were detected in various areas of the brain, notably in the ventral telencephalon, the diencephalon, the mesencephalon, the cerebellar valvula, and the medulla oblongata. In addition, a dense accumulation of PACAP-containing nerve terminals was found in the pars distalis of the pituitary. The PACAP-like immunoreactivity contained in the eel brain was characterized by HPLC analysis combined with RIA quantification. The major form of PACAP-immunoreactive material coeluted with mammalian PACAP38. Molecular cloning of the PACAP precursor has previously shown that in fish, PACAP and GH-releasing hormone (GHRH) originate from the same precursor. We have thus investigated the effects of PACAP and GHRH on GH secretion from eel pituitary cells in primary culture. Dose-response experiments revealed that PACAP27 and PACAP38 possessed the same efficacy, but PACAP38 was 12 times more potent than PACAP27 in stimulating GH release (ED50 = 4.3 x 10(-10) and 3.5 x 10(-9) M, respectively). In contrast, GHRH, even at a high concentration (10(-6) M), had no effect on GH release. Taken together, these data indicate that in the eel, PACAP may play a significant role in the regulation of somatotrope cells: 1) PACAP-immunoreactive neurons are exclusively located in the diencephalon and send numerous projections in the pars distalis; and 2) PACAP, but not GHRH, dose dependently stimulates GH secretion from cultured eel pituitary cells.

Anguilla↗
PubMed1998

Localization, characterization, and second messenger coupling of pituitary adenylate cyclase-activating polypeptide receptors in the fetal human adrenal gland during the second trimester of gestation.

The distribution and pharmacological properties of pituitary adenylate cyclase-activating polypeptide (PACAP) receptors were studied in the fetal human adrenal gland during the second trimester of gestation. Autoradiographic studies, using [125I]PACAP27 as a radioligand, revealed that PACAP-binding sites are exclusively located on chromaffin cells of adrenals from fetuses 14-20 weeks old. Biochemical characterization of binding revealed the occurrence of a single class of PACAP-binding sites with a dissociation constant value of 0.32-0.74 nmol/L and a binding capacity of 0.30-0.81 pmol/mg wet tissue. PACAP27 and PACAP38 were equipotent in competing for [125I]PACAP27 binding (IC50 = 0.28-0.64 nmol/L and 0.15-0.81 nmol/L, respectively), and the Hill coefficients were close to 1. In contrast, vasoactive intestinal polypeptide was much less efficient in displacing the tracer (IC50 = 4-362 nmol/L), and the Hill coefficients were less than 0.6. PACAP38 induced a dose-dependent increase in cAMP production in fetal human adrenal cell suspension (ED50 = 0.07 +/- 0.02 nmol/L), as well as in cells maintained in culture for 5 days (5.4 +/- 1.8 nmol/L). In contrast, PACAP38 induced a modest increase in inositol phosphate formation. These data indicate that type I PACAP receptors are present in the early stages of the human medulla organization during the process of migration of chromaffin cells from the periphery to the central part of the gland. The present results suggest that PACAP could be involved in the regulation of the human adrenochromaffin cells during ontogenesis.

Adrenal Glands↗
PubMed1998

Renal ostodystrophy during the developing stage of maintenance dialysis in Transylvania. Early development of periarticular calcifications and beta 2 microglobulin amyloidosis in spite of a relatively good prevention of secondary hyperparathyroidism.

BACKGROUND: Dialysis facilities have been introduced only recently in Transylvania with many limitations, in particular a standard high calcium dialysate, Al(OH)3 as phosphate binder and pharmacological doses of native vitamin D2, but neither CaCO3 nor 1 alpha hydroxylated vitamin D. Rheumatological complaints and metastatic calcifications were frequent, leading to suspect either overt hyperparathyroidism, adynamic bone disease or beta 2 microglobulin amyloidosis. AIMS OF THE STUDY: Evaluate the prevalence of radiological osteitis fibrosa, amyloid osteoarthropathy and periarticular calcification and their link with PTH secretion, phophocalcic disorders, acidosis, bone turn over, aluminum and beta 2 microglobulin accumulation in the dialysis population of Sibiu (Transylvania). METHODS: The clinical and radiological rheumatological data of the 49 uremic patients dialyzed in Sibiu since 1990 were reviewed as well as the monthly routine monitoring of their plasma phosphocalcic parameters. Furthermore in July 1994, 36 of them had an X rays of the hands for evaluation of subperiosteal resorption of the phalanges, periarticular calcifications and carpal cysts as well as a determination of plasma concentrations of intact PTH (normal range: 10-55; optimal range: 100-200 pg/ml), osteocalcin, bone alkaline phosphatase, aluminum and 25 OH vitamin D. RESULTS: The prevalence of subperiostal resorption of the phalanges was 8% and that of severe biological hyperparathyroidism (PTH > 400 pg/ml) 22%, whereas that of a relative hypoparathyroidism (PTH < 100 pg/ml) was 31%. Mean plasma concentrations of calcium was 2.07 +/- 0.15; of phosphate 2.50 +/- 0.35; of bicarbonate 15 +/- 2.0 mmol/l, of 25 OHD 30 +/- 20 ng/ml, of aluminum 1.1 +/- 0.5 mumol/l. Plasma PTH concentrations were negatively correlated to dialysis duration, and to plasma concentrations of aluminum, calcium and 25 OH vitamin D but not to those of phosphate and bicarbonate. Multivariate analysis showed however that only duration of dialysis and plasma aluminum concentration were independently and negatively correlated to plasma PTH concentrations. The prevalence of periarticular calcifications (26%) and of carpal cysts suggestive of beta 2 microglobulin amyloidosis (10%) were relatively high considering the young age of the population (42 years) and the short duration of dialysis (2.6 years). Patients with calcifications comparatively to those without calcifications were older, had longer duration on dialysis, higher prevalence of carpal cysts and higher plasma beta 2 microglobulin concentrations, lower plasma PTH (98 versus 313 pg/ml) and higher plasma aluminum concentration (1.3 versus 0.8 mumol/l). Patients with carpal cysts comparatively to those without cyst were older, had a longer duration on dialysis and a higher prevalence of periarticular calcifications. CONCLUSIONS: a) In spite of no use of 1 alpha hydroxylated vitamin D derivatives, and poor control of hyperphosphatemia and acidosis, hyperparathyroidism declined with duration of dialysis due to the use of a high dialysate calcium concentration, Al(OH)3 as sole phosphate binder and high supplement of native vitamin D. b) Considering the relative young age and short duration on dialysis, the prevalence of periarticular calcifications and carpal cysts were high. c) Calcifications were possibly favored by relative hypoparathyroidism and moderate aluminum overload. d) The association of periarticular calcifications and subchondrial cysts suggest a causal relationship.

Adult↗
PubMed1998

Comparison of Echinostoma caproni mother sporocyst development in vivo and in vitro using Biomphalaria glabrata snails and a B. glabrata embryonic cell line.

Biomphalaria glabrata embryonic (Bge) cells have previously been shown to permit a successful cocultivation of Schistosoma mansoni and Schistosoma japonicum from miracidia to mother sporocysts (MS) and then to the production of daughter sporocysts (DS). To investigate further the properties of the Bge culturing system we used Echinostoma caproni under identical in vitro conditions. In vitro-derived miracidia were used either for experimental infections of B. glabrata snails, or for in vitro cultivation with Bge cells. Histological analysis showed that the development of MS in B. glabrata was similar to the previously described development in Biomphalaria pfeifferi in terms of final site of infection, development dynamics, growth dynamics, reproduction intensity, and life spans. Only short delays in migration dynamics were observed in B. glabrata. When cultivated under in vitro conditions, E. caproni MS could live for up to 17 wk in the presence of Bge cells, as compared with 2 wk in cell-free Bge medium. The presence of Bge cells also permitted significant growth of MS and development through complete embryogenesis of the next intramolluscan stage (embryos of 100-110 cells). However, degeneration of MS consistently occurred before production of this second generation. During the entire cultivation period, no visible contact was observed between MS and Bge cells, suggesting that development of MS was only triggered by soluble factors released by Bge cells.

Animals↗
PubMed1998

[Percutaneous recanalization of proximal venous thromboses in chronic hemodialysis patients].

Occlusion of the proximal vein in chronic hemodialysis patients results in vein hypertension and a "swollen arm". The usual treatment for this "swollen arm" consists in closing up the fistula and making another access on the contralateral member. But this is not always possible and, with some patients, recanalization is the only solution. We have performed 4 recanalizations successfully: 2 accesses remain permeable after 10 and 24 months, another patient needed to be fitted with two endoprosthesis just after recanalization and access, in his case, remained permeable until he died of intestinal ischemic syndrome six months later. The fourth patient presented a reocclusion two months later but could not be reoperated on because of bad general state of health. An attempt to perform recanalization on a fifth patient was a failure. Such results show that recanalization of a thrombosed proximal vein is worth attempting before closing access for good.

Adult↗
PubMed1998

The dependency of calcium set point on basal plasma calcium in dialysis patients: a better explanation for the discrepancies regarding its link with PTH secretion than methodological differences.

BACKGROUND: The increase of calcium (Ca) set point in uremic hyperparathyroid patients and its decrease with calcitriol therapy are controversial. Besides methodological differences regarding the experimental protocol for obtaining the sigmoidal curve, mainly differences in definitions of maximal PTH (peak or steady value) and of calcium set point itself have been proposed for the discrepant conclusions. However, two other explanations are possible: the various aluminum load of the patients and the dependency of Ca set point upon the basal plasma ionized calcium (PCa). PATIENTS AND METHODS: Therefore the Ca set point was measured in 2 groups of patients on maintenance dialysis never exposed to aluminum, one of 7 patients with normosecretion of PTH (NPT) and the other of 8 patients with hyperparathyroidism (HPT) before and after 3 intravenous administration of 4 microg of alfacalcidol in a week. The sigmoidal curve was established during a zero Ca dialysis, without Ca replacement for the first 90 minutes and with intravenous infusion of 41 mmoles of Ca during the 150 last minutes. The curvilinear decrease of PCa induced a peak of PTH followed by a decrease while PCa was still decreasing up to the 90th minute. Therefore PTHmax was taken both at the peak and at its lower value observed at the 90th minute (steady PTHmax). Experimental determinations of the Ca set point were made using both definitions of Brown and Felsenfeld and both PTHmax values. In basal conditions, while using any of the values given by the same calculation methodology, Ca set point was not different in NPT and HPT patients. After alfacalcidol, no change in plasma PTH nor in Ca set point was observed in HPT patients. In contrast, in NPT patients alfacalcidol induced a significant decrease of plasma PTH concentrations in association with an increase in basal PCa and in Ca set point, whatever the definitions of the latter and of PTHmax. Calcitriol induced changes in Ca set point and basal PCa were correlated. CONCLUSIONS: 1) In normocalcemic dialysis patients never exposed to aluminium hyperparathyroidism is not explained by an increased Ca set point 2) Calcitriol suppressive effect on PTH secretion is neither explained by a decrease in Ca set point. 3) Ca set point as measured in vivo does not reflect an intrinsic characteristic of the parathyroid glands since it varies with basal PCa. Better than methodological differences, this dependency may explain the discrepant conclusions between the various clinical investigations.

Aluminum↗
PubMed1998

[Can the results of large-scale clinical trials be applied to clinical practice?].

The management of a patient in cardiac failure should lead the physician to ask if the patient might benefit from treatment with an angiotensin converting inhibitor. Meta-analyses give a positive reply but often lack detail. Analysis of large scale therapeutic trials is the only way to determine whether the results are applicable in an individual case. This analysis starts with validation of the methodology (correct randomisation, respect of double blind protocol, identity of groups) and synthesis of results expressed, if possible, in absolute values. In a second stage, the criteria of inclusion, exclusion, and the comorbidity of enrolled patients, should be compared with those of the patient under consideration. In addition, the amplitude of the therapeutic benefit and the importance of undesired effects must be taken into account in the therapeutic decision. This approach allows a reasoned prescription based on documented facts.

Angiotensin-Converting Enzyme Inhibitors↗