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Biomedical subjects

A Fournier

Publications and source records attributed to A Fournier.

At least 109 records · Page 6Linked to original sources
PubMed1999

Endothelin-1 enhances neutrophil adhesion to human coronary artery endothelial cells: role of ET(A) receptors and platelet-activating factor.

1. The potent coronary vasoconstrictor, endothelin-1 (ET-1) may also regulate neutrophil traffic into tissues. The aim of the present study was to characterize the endothelin receptors responsible and to investigate the underlying mechanisms. 2. ET-1 (1 nM - 1 microM) markedly enhanced attachment of human neutrophils to lipopolysaccharide-, and to a lesser extent, to ET-1-activated human coronary artery endothelial cells (HCAEC). This can partially be blocked by monoclonal antibodies against E-selectin, L-selectin or CD18, whereas combination of the three antibodies inhibited adhesion by approximately 83%. Increases in neutrophil adhesion evoked by ET-1 were also blocked by the platelet-activating factor (PAF) antagonists, BN 52021 (50 microM) and WEB 2086 (10 microM). 3. ET-1 downregulated the expression of L-selectin and upregulated expression of CD11b/CD18 and CD45 on the neutrophil surface and induced gelatinase release with EC50 values of approximately 2 nM. These actions of ET-1 were almost completely prevented by the ET(A) receptor antagonist FR 139317 (1 microM) and the ET(A)/ET(B) receptor antagonist bosentan (10 microM), whereas the ET(B) receptor antagonist BQ 788 (1 microM) had no effect. ET-1 slightly increased the expression of E-selectin and ICAM-1 on HCAEC, that was prevented by BQ 788, but not by FR 139317. 4. Receptor binding studies indicated the presence of ET(B) receptors (KD: 40 pM) on phosphoramidon-treated HCAEC and the predominant expression of ET(A) receptors (KD: 38 pM) on neutrophils. 5. These results indicate that promotion by ET-1 of neutrophil adhesion to HCAEC is predominantly mediated through activation of ET(A) receptors on neutrophils and subsequent generation of PAF.

Adult↗
PubMed1999

Is low plasma 25-(OH)vitamin D a major risk factor for hyperparathyroidism and Looser's zones independent of calcitriol?

BACKGROUND: Recent reports suggest that calcitriol might not be the sole active metabolite of vitamin D and that plasma concentrations of 25-(OH)vitamin D (25OHD) are often abnormally low in hemodialysis patients. We have therefore evaluated plasma 25OHD as a risk factor for parathyroid hormone (PTH) hypersecretion and radiological bone disease. We carried out a cross-sectional study during the month of September in an Algerian dialysis center of 113 patients who were not taking supplements of alphacalcidol or calcitriol. METHODS: Plasma 25OHD, calcitriol, PTH, calcium, phosphate, bicarbonate, and aluminum were measured, and x-rays of the hands and pelvis were obtained for evaluation of subperiosteal resorption and Looser's zones. RESULTS: The median plasma 25OHD was 47.5 nmol/liter (range 2.5 to 170.0). Univariate analysis showed that plasma PTH was correlated positively with months on maintenance dialysis and negatively with plasma 25OHD, calcitriol, calcium, bicarbonate and aluminum, but not with that of phosphate. plasma 25OHD was positively correlated with calcium and calcitriol. Using multiple regression analysis, only plasma 25OHD (negative) and the duration on maintenance dialysis (positive) were independently linked to plasma PTH. The prevalence of isolated subperiosteal resorption (ISR) was 34%, and that of the combination of resorption with Looser's zones (CRLZ) was 9%; thus, only 57% of the patients had a normal x-ray appearance. These groups were comparable with regards to age, gender, and duration on dialysis. When the biochemical measurements of the patients with CRLZ were compared with those from patients without radiological lesions, plasma 25OHD was the only parameter to show a statistically significant difference, being significantly lower in the CRLZ group (26 +/- 18 vs. 57 nmol/liter, ANOVA, P < 0.004). Plasma 25OHD was also significantly lower in the ISR group (44, P < 0.05) than in the normal x-ray group, and plasma Ca (P < 0.003) and bicarbonate (P < 0.02) were lower. Logistical analysis showed that the presence of resorption was independently linked only with plasma PTH. Looser's zones and subperiosteal resorption were not seen in patients with plasma 25OHD of more than 40 (Looser's zones) and more than 100 nmol/liter (subperiosteal resorption). The optimal range for intact PTH in hemodialysis patients with mild aluminum overload is 10 to 25 pmol/liter. We found that plasma PTH was inappropriately high only when plasma 25OHD was less than 100 nmol/liter. With a plasma 25OHD of between 100 and 170 nmol/liter, hypercalcemia was present with a plasma PTH of less than 10 pmol/liter in only one case. CONCLUSIONS: This cross sectional study shows that low plasma 25OHD is a major risk factor for hyperparathyroidism and Looser's zones. In dialysis patients, we suggest that the plasma levels of 25OHD are maintained around the upper limit of the reference range of sunny countries.

Adult↗
PubMed1999

Renal and hypertensive complications of extracorporeal shock wave lithotripsy: who is at risk?

Extracorporeal shock wave lithotripsy (ESWL) is now used in the treatment of about 90% of renal and ureteral stones. Because of the non-punctual delivery of energy to the stone, a small volume of renal parenchyma is injured giving place to a fibrous scar which can be shown by highly resolutive imaging techniques like magnetic nuclear resonance. Isotopic clearances point to a reduction of 15% in the renal plasma flow on the side of the lithotripsy, but this alteration appears to be transient in nature. In a few cases an abrupt onset of transient hypertension has been reported in clear relation to a compressive perirenal hematoma. The responsibility of ESWL in the late occurrence of permanent hypertension is, however, still uncertain, probably because of the difficulty in showing that this occurrence is not only related to the older age of the patient. The American Food and Drug Administration-sponsored multicentric study begun in 1992 should solve this issue in the future. Recent articles suggest that altered renal function prior to ESWL would predict the late occurrence of hypertension and worsening of renal failure. Furthermore, age and the resistance index of arcuate or interlobar renal arteries (measured by Doppler) could help to screen patients at risk of developing hypertension. In practice in patients over 60 years of age and/or with a plasma creatinine of >to 300 micromol/l, ESWL should be performed with caution, and renal function and blood pressure should be carefully monitored.

Animals↗
PubMed1999

Bronchoprotector properties of calcitonin gene-related peptide in guinea pig and human airways. Effect of pulmonary inflammation.

Calcitonin gene-related peptide (CGRP), a neuropeptide released from sensory nerves during axonal reflexes, has strong bronchoprotector properties in rat isolated airways. In this study, we examined this ability of CGRP to prevent agonist-induced contraction in guinea pig and human airways and determined whether inflammatory reaction affects its function. CGRP administered intravenously (0.38 to 114 microgram/kg) in anesthesized guinea pig had no effect per se on airway resistance but caused a dose-related inhibition of substance P (SP; 13.5 microgram/kg)-induced bronchoconstriction (60% at 114 microgram/kg). Similarly, CGRP (10(-)9 to 10(-)6 M) prevented in a concentration-dependent manner the contraction elicited by SP (5 x 10(-)8 M) in guinea pig isolated main bronchi and parenchymal strips, the inhibition caused by CGRP being more pronounced in distal than in proximal airways (47 and 20%, respectively, at 10(-)6 M). The breaking effect of CGRP on SP-induced constriction was however significantly reduced (p < 0.05) in guinea pig actively sensitized to ovalbumin (OA) and the loss in its potency was of similar magnitude (> 40%) whether it was administered in vivo or in vitro. A same phenomenon was observed in human isolated peripheral bronchi. CGRP (10(-)6 M) reduced by more than 75% the extent of the contraction evoked by 10(-)6 M of carbamylcholine and its protector effect was totally abolished in bronchi showing clear morphological manifestation of inflammatory reaction. It is concluded that CGRP acts as a potent bronchoprotector agent on both guinea pig and human airways but its ability to limit the extent of airway responsiveness is strongly impaired in inflammatory conditions.

Adolescent↗
PubMed1999

Androgens down-regulate bcl-2 protooncogene expression in ZR-75-1 human breast cancer cells.

Although a large proportion of primary human breast cancers express the androgen receptor, and treatment with androgens exerts beneficial effects in women with breast cancer, the role and especially the mechanism of action of androgens in breast cancer development and growth are not well understood. The potential effect of androgens on bcl-2 protooncogene expression was investigated in a human breast cancer cell line whose proliferation is known to be inhibited by androgens. The estrogen-responsive ZR-75-1 cells were grown in the presence or absence of 5alpha-dihydrotestosterone (DHT), alone or in combination with 17beta-estradiol. DHT caused a marked down-regulation of Bcl-2 protein and messenger RNA levels in both the presence and absence of 17beta-estradiol. The inhibitory effect of DHT was completely prevented by coincubation with the pure antiandrogen hydroxyflutamide. The present data indicate that androgens can down-regulate bcl-2 protooncogene levels via an androgen receptor-mediated mechanism, thus providing a novel mechanism for their known inhibitory effect on breast cancer cell growth.

Androgen Antagonists↗
PubMed1999

A cloned frog vasoactive intestinal polypeptide/pituitary adenylate cyclase-activating polypeptide receptor exhibits pharmacological and tissue distribution characteristics of both VPAC1 and VPAC2 receptors in mammals.

Three receptor subtypes for the neuropeptides vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) have been identified in mammals: the PAC1 receptor (PAC1-R) which is selectively activated by PACAP, and two VPAC receptors (VPAC1-R and VPAC2-R), which are equally stimulated by PACAP and VIP. The structures of PACAP and VIP have been well conserved during evolution, but little is known about VIP/PACAP receptors in nonmammalian species. An amphibian VIP/PACAP receptor complementary DNA (cDNA) has been cloned and characterized from a frog (Rana ridibunda) pituitary cDNA library. The predicted protein contains seven putative transmembrane domains and exhibits the highest sequence identity (65%) with the human VPAC1-R. The cloned cDNA was transiently expressed in LLC-PK1 cells, and its pharmacological profile was determined in comparison with the human VPAC1-R. Both PACAP and VIP stimulated cAMP accumulation through the cloned receptor with an EC50 of about 30 nM. In contrast, secretin, at concentrations that stimulate the human VPAC1-R, had no effect on cAMP production. RT-PCR analysis revealed the widespread distribution of this frog VIP/PACAP receptor in peripheral tissues. In situ hybridization histochemistry using a complementary RNA probe showed that the receptor gene is highly expressed in several hypothalamic and thalamic nuclei and to a lesser extent in the pallium and striatum. In the pituitary, the highest messenger RNA levels were detected in the distal lobe. Taken together, these data show that the cloned frog receptor shares several common features with both the VPAC1-R and VPAC2-R of mammals; the frog receptor exhibits the highest sequence identity with mammalian VPAC1-R, but the lack of effect of secretin and the brain distribution of the receptor are reminiscent of the characteristics of the mammalian VPAC2-R. The sequence of the frog receptor should thus prove useful to decipher the structure-activity relationships of the VIP/PACAP receptor family.

Adenylyl Cyclases↗
PubMed1999

[Factors in the progression of renal insufficiency during the 2 years preceding the use of dialysis].

UNLABELLED: The respective contribution of sex, type of nephropathy, degree of proteinuria, blood pressure, protein and sodium daily intake, lipid profile, protidemia, hemoglobinemia, acidosis and CaPO4 product on the rate of renal failure progression is debated. The link between these parameters and the decrease of creatinine clearance, delta Ccr (according to Cockroft) was assessed in uni and multivariate analysis in a population of 49 patients (26 men, 23 women; age 60 +/- 15 years, weight 73 +/- 15 kg) selected out of 173 presently treated hemodialysis patients on the basis of availability of a quarterly follow-up for two years before starting dialysis. The patients were advised a moderate protein and salt restriction which could be retrospectively assessed (on urinary excretion of urea and sodium) at respectively 0.82 g/kg/day and 6.5 g/day. The two years delta Ccr was 14 +/- 14 ml/min. It was not different in men and women (specially when expressed in % of initial value). This decrease in Ccr was neither significantly different in glomerular disease (17 +/- 8, n = 14), diabetic nephropathy (12 +/- 6, n = 7), nephroangiosclerosis (15 +/- 8, n = 5), interstitial nephritis (12 +/- 10, n = 14), and PKD (11 +/- 12, n = 9). Patients with antihypertensive drugs (n = 42) had a faster progression than those without drugs (n = 7): delta Ccr = 15 +/- 14 vs 7 +/- 7 ml/min (p < 0.05) in spite of comparable blood pressure but with higher proteinuria. Linear regression of delta Ccr with the initial and two year averaged values of the quantitative parameters showed a significant positive link for both values with cholesterol, hemoglobin and proteinuria and a negative one with protidemia. A positive link was observed with the initial value of bicarbonate and the two year mean of diastolic and mean blood pressures. No link at all was observed with urea and Na excretion, CaPO4 product and triglycerides. Multiple regression disclosed a significant link only for protidemia (negative with both initial and two years averaged value), diastolic BP (only for the two year averaged value and hemoglobinemia (for the initial value). When the patients were classified according to a threshold value of their protidemia, DBP, hemoglobinemia, and cholesterolemia those with the combination of two risk factors of progression (pro-tidemia < 66 g/l, DBP > or = 90 mmHg, hemoglobinemia > 11 g/dl, proteinuria > 3g/d, CT > 5 mmol/l) had a significantly greater decrease of Ccr than those with the three other combinations at the exception of the association of low protidemia with DBP. CONCLUSION: 1. diastolic hypertension and low protidemia are the two most important factors predicting progression of renal failure; 2. a predictive synergy was furthermore pointed out between on one hand low protidemia and diastolic hypertension and on the other hand proteinuria and cholesterol; 3. on the contrary, anemia attenuates progression linked to low protidemia, diastolic hypertension, proteinuria and high cholesterol.

Acidosis↗
PubMed1999

[Fenofibrate increases blood creatinine, but does not change the glomerular filtration rate in patients with mild renal insufficiency].

Fenofibrate is a potent hypolipemic agent, widely used in patients with mild to severe renal failure in whom hyperlipoproteinemia is frequent. A moderate reversible increase in creatinine plasma levels has been reported with fenofibrate therapy; however, it is not known whether this increased creatininemia reflects a fenofibrate induced alteration of renal function or if fenofibrate interferes with creatinine tubular handling. We prospectively examined the effect of 2 weeks fenofibrate treatment (200 mg daily) on renal function in thirteen hyperlipidemic patients with normal renal function or mild to moderate renal failure (Creat Cl: 110 to 30 ml/min). This study confirms that fenofibrate therapy significantly increases creatininemia in patients with mild to moderate renal failure (147 +/- 12 versus 170 +/- 15 mmol/l; p = 0.014), but does not alter renal hemodynamic nor glomerular filtration rate as assessed by the stability of PAH (304 +/- 56 versus 311 +/- 49 ml/min; p = NS) and inulin clearances (51.7 +/- 6 versus 52.3 +/- 7 ml/min; p = NS). The increase in creatininemia is neither due to an inhibition of creatinine tubular excretion, since no change in creatinine clearance was observed (69 +/- 8 versus 68 +/- 8 ml/min; p = NS), but appears to be associated to a parallel increase in creatinine daily urinary excretion (13.7 +/- 5 versus 15.4 +/- 4 mmol; p = 0.03). In conclusion, fenofibrate therapy in renal patients does not worsen renal function, nor diminish the reliability of creatinine clearance for its follow-up in spite of a significant rise in creatininemia. The mechanism of the fenofibrate-induced increase in urinary creatinine excretion remains to be determined.

Aged↗
PubMed1999

Synergism between neuropeptide Y and norepinephrine highlights sympathetic cotransmission: studies in rat arterial mesenteric bed with neuropeptide Y, analogs, and BIBP 3226.

Although abundant literature supports the notion that neuropeptide Y (NPY) synergizes in vivo and in vitro, the vasomotor activity elicited by norepinephrine (NE), the converse interaction (i.e., the adrenergic modulation of the NPY vasomotor response) has been less characterized. To assess whether NE synergizes the vasomotor effect of NPY, the rat arterial mesenteric bed was chosen as a model experimental system. Mesenteries were precontracted with NE and few minutes later were perfused with exogenous NPY. Under these conditions, NPY contracted the arterial mesenteric bed with an EC50 value of 0.72 +/- 0.06 nM. NPY was unable to contract this vascular territory without an agonist-induced precontraction. Other agonists, such as endothelin-1, a synthetic analog of prostaglandin F2alpha, or 5-hydroxytryptamine, also were effective primers because in their presence, NPY was a potent vasoconstrictor. In contrast, mesenteries precontracted with KCl failed to evidence the NPY-induced rise in perfusion pressure. Two structural analogs of NPY, PYY and [Leu31, Pro34]NPY, mimicked the activity of NPY. The NPY fragment 13-36 did not elicit such a response. All NPY analogs exhibited less efficacy and potency relative to NPY. The NPY- and related structural analog-induced vasoconstriction was competitively and reversibly antagonized by BIBP 3226; the pA2 of the NPY interaction was 7.0. The application of 0.1 to 1 microM BIBP 3226 or 0.1 to 10 nM prazosin at the peak of the NPY vasomotor response elicited a gradual blockade of the vasoconstriction. Although BIBP 3226 blocked the increase in perfusion pressure elicited by NPY, leaving unaffected the NE-induced tone, 10 nM prazosin blocked the full response, including the NE-induced component. Tissue preincubation with 200 nM nifedipine abolished the NPY-induced vasoconstriction; likewise, the acute application of 10 to 100 nM nifedipine blocked gradually the maximal NPY-induced contraction. Removal of the mesenteric endothelial layer increased the potency of NPY by 2-fold; it also slightly potentiated the antagonist activity of BIBP 3226. The synergism between NPY and NE backs the principle of sympathetic cotransmission.

Animals↗
PubMed1999

Risk factors of renal failure progression two years prior to dialysis.

AIM: The respective contribution of sex, type of nephropathy, degree of proteinuria, blood pressure, protein and sodium daily intakes, blood lipid profile, protidemia, hemoglobinemia, acidosis and CaPO4 product on the rate of renal failure progression is debated. PATIENTS AND METHODS: The link between these parameters and the decrease of creatinine clearance, deltaCcr (according to Cockroft) was assessed in uni- and multivariate analysis in a population of 49 patients (26 women; age 60+/-15 years, weight 79+/-15 kg) selected out of 173 presently treated hemodialysis patients on the basis of availability of a quarterly follow-up for 2 years before starting dialysis. The patients were advised a moderate protein and salt restriction which could be retrospectively assessed (on urinary excretion of urea and sodium) at, respectively, 0.82 g/kg/day and 6.5 g/day. RESULTS: The 2-year deltaCcr was 14+/-14 ml/min. It was not different in men and women. This decrease in Ccr was neither significantly different in gomerular disease (17+/-8, n = 14), diabetic nephropathy (12+/-6, n = 7), nephroangiosclerosis (15+/-8, n = 5), interstitial nephritis (12+/-10, n = 14), and PKD (11 +/-12, n = 9). Patients with antihypertensive drugs (n = 42) had a faster progression than those without drugs (n = 7): deltaCcr = 15+/-14 vs 7+/-7 ml/min (p < 0.05) in spite of comparable blood pressure but with higher proteinuria. Linear regression of deltaCcr with the initial and 2-year averaged values of the quantitative parameters showed a significant positive link for both values with cholesterol, hemoglobine and proteinuria and a negative one with protidemia. A positive link was observed with the initial value of bicarbonate and the 2-year mean of diastolic and mean blood pressures. No link at all was observed with urea and Na excretion, CaPO4 product and triglycerides. Multiple regression disclosed a significant link only for protidemia (negative with both initial and 2-year averaged value), diastolic BP (only for the 2-year averaged value and hemoglobinemia (for the initial value). When the patients were classified according to a threshold value of their protidemia, DBP, hemoglobinemia, and cholesterolemia those with the combination of 2 risk factors of progression (protidemia > or = 66 g/l, DBP > or = 90 mmHg, hemoglobinemia > 11 g/dl, proteinuria > or = 3 g/d, CT > 5 mmol/l) had a significantly greater decrease of Ccr than those with the 3 other combinations at the exception of the association of low protidemia with DBP. CONCLUSION: Diastolic hypertension and low protidemia are the 2 most important factors predicting progression of renal failure. A predictive synergy was furthermore pointed out between low protidemia or diastolic hypertension with proteinuria and cholesterol. On the contrary anemia attenuates progression linked to low protidemia, diastolic hypertension, proteinuria and high cholesterol.

Anemia↗
PubMed1999

[Role of the time of administration of calcium carbonate (before or during mealtime) in the control of hyperphosphatemia in patients on maintenance hemodialysis].

UNLABELLED: A study has claimed that at equal elemental calcium dose, CaCO3 was not less but equally efficient in controlling predialysis hyperphosphatemia as calcium acetate provided both calcium salts were given five minutes before the meals instead of during the meals because the higher acidity of a fasting gastric juice would allow a better dissociation of CaCO3. To examine the point that CaCO3 is more efficient if it is taken five minutes before compared to during the meal, we performed a two month randomised cross-over trial in twelve reliable and stable patients maintained on chronic hemodialysis while their treatment and diet remained constant. Comparison of the plasma concentrations measured during the two modes of administration showed no significant difference in creatinine, urea, bicarbonate, intact-PTH. Mean (+/- SD) plasma PO4 was significantly higher (1.93 +/- 0.50 versus 1.72 +/- 0.40 mmol/l; p = 0.02) whereas corrected plasma Ca was significantly lower (2.30 +/- 0.15 versus 2.38 +/- 0.17 mmol/l; p = 0.01) when CaCO3 was given before the meals than during the meals. CONCLUSIONS: a) administration of CaCO3 before the meal decreases its efficiency in controlling hyperphosphatemia since plasma PO4 was actually slightly higher with this timing of administration; b) administration of CaCO3 before the meal is associated with significantly lower plasma corrected calcium suggesting a smaller absorption of calcium which may be an advantage but only in hypercalcemic patients; c) there is no reason other than the prevention of its hypercalcemic effect to recommend the administration of CaCO3 just before the meals than during the meals.

Aged↗
PubMed1999

[Inhibition of gastric secretion by omeprazole and efficacy of calcium carbonate in the control of hyperphosphatemia in patients on maintenance hemodialysis].

UNLABELLED: Apparent contradictions exist in the literature regarding the effect of gastric secretion inhibition on phosphatemia. In healthy adults, omeprazole has been reported to prevent the increase of plasma phosphate or of phosphaturia observed after an acute phosphate load suggesting an inhibition of phosphate absorption. In patients on chronic hemodialysis their hyperphosphatemia is associated to gastric hypersecretion but the inhibition of this latter by ranitidine in patients taking CaCO3 has been reported to increase their plasma phosphate. Because of this contradiction, we have made an open cross-over study in 16 stable and compliant patients in chronic hemodialysis taking a mean daily dose of 9.4 +/- 4 g of CaCO3 and compared their predialysis plasma concentration of phosphate, calcium, protides, bicarbonates, intact PTH, urea and creatine for two successive periods of two months without or with 20 mg of omeprazole. Plasma phosphate did not increased significantly with omeprazole (from 1.80 +/- 0.38 to 1.89 +/- 0.42 mmol/l) whereas plasma corrected calcium significantly decreased from 2.41 +/- 0.18 to 2.36 +/- 0.16 mmol/l (p = 0.04) and plasma bicarbonate decreased significantly from 26.7 +/- 3.5 to 25.7 +/- 3.1 mmol/l (p < 0.05). No significant change was observed in plasma creatine and urea suggesting stability of dialysis efficiency and of protein and therefore phosphate intake. CONCLUSION: These data do not support that CaCO3 efficiency as phosphate binder is decreased with inhibition of the gastric secretion by omeprazole.

Adult↗
PubMed1999

[Could angiotensin II type I receptor antagonists have a superior beneficial effect than that of angiotensin II converting enzyme inhibitors with respect to the risk of cerebrovascular accident?].

In contrast with the expected results, the Captopril Prevention Project study has found that the relative risk of stroke was greater by 25% in patients treated with ACEI than in patients receiving the conventional diuretics +/- betablockers regimen (Hanson et al. ISH Amsterdam, June 98). This difference persisted after adjustment for the initial differences of blood pressure levels between the groups after randomisation. This does not mean that ACEI would worsen the risk of stroke when compared to a placebo, since a potent protective effect of diuretics and betablockers on the relative risk of stroke has long been demonstrated. Nonetheless, these results suggest that for a similar blood pressure lowering effect, conventional therapy is more effective than ACEI to prevent stroke. This finding, in discrepancy with the current prevailing opinion that ACEI have emerged as the most effective preventive treatment to reduce cardiovascular morbidity, is regarded as surprising by the investigators. However, a number of animal experimental data may help to envisage the complete inhibition of angiotensin II formation as a two-edged sword, because of the multiplicity of its receptors mediating different, and even opposite effects. In a series of experimental studies in mammals, the group of Fernandez has provided a bundle of observations suggesting that angiotensin II contributes to early reperfusion following acute ischemia by enabling the recruitment of pre-existing collateral vascularisation, an effect mediated via the stimulation of non-AT1 receptors (possibly AT2). Indeed, the worsening of stroke in the gerbil after incomplete ligation of the carotid by pre-treatment with ACEI had been demonstrated by these authors (J Cerebral Blood Flow Metab, 1988; 24:937), and they further show that pre-administration of losartan significantly reduced the ischemic brain damage and the mortality induced by the abrupt ligation of one carotid, but that this preventive effect of losartan was abolished if enalapril was co-administrated (J Cardiovasc Pharmacol 1994; 24:937). The first available clinical data on stroke risk with ACEI reported in the CPP study, showing a less effective prevention of stroke with ACEI than diuretics supports the hypothesis that similar mechanism may also prevail in humans, and lead us to propose to discuss the rationale for a large multicentric trial aiming to compare the protective effect of ARAT1 and ACEI on the risk of recurrence of stroke.

Angiotensin Receptor Antagonists↗
PubMed1999

[Hemodialysis and strongyloidiasis: a presumed cause of eosinophilia able to mask the other].

The authors report a case of recurrent strongyloidiasis in a former French soldier of the Indochina colonial war (1946-54). Strongyloidiasis was associated with inaugural renal failure (acute steroid-resistant interstitial-type), requiring permanent hemodialysis. Despite antiparasitic treatment, relapse with digestive and pulmonary symptoms occurred 10 years later, following chronic eosinophilia. This observation emphasises that in dialysed subjects, eosinophilia should always stimulate a search for parasitic etiologies before incriminating dialysis-material allergy. Strongyloidiasis is a self-perpetuating helminthiasis whose distribution area is far greater than the intertropical zone. It can be completely asymptomatic, appear as late digestive complications and be responsible for bacteraemic peaks with septic visceral localizations. It causes a chronic oscillating eosinophilia. Diagnosis is usually performed by iterative stool examinations by Baermann technique in order to detect Strongyloides stercoralis rhabditoid larvae. In dialysed patients with unexplained eosinophilia awaiting renal transplant, the options of systematic thiabendazole (50 mg/kg) or ivermectine (0.2 mg/kg) single-dose to overcame the risk of disseminated strongyloidiasis induced by immunosuppressive post-transplantation therapy could be debated.

Aged↗