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Biomedical subjects

E Billaud

Publications and source records attributed to E Billaud.

At least 37 records · Page 2Linked to original sources
PubMed1997

Does long-term angiotensin converting enzyme inhibition affect the concentration of tissue-type plasminogen activator-plasminogen activator inhibitor-1 in the blood of patients with a previous myocardial infarction.

BACKGROUND: Large-scale studies have indicated that treatment with angiotensin converting enzyme (ACE) inhibitors reduces the incidence of myocardial infarction and unstable angina pectoris among patients with recent myocardial infarction and moderate left ventricular dysfunction. An improved endogenous fibrinolysis might be responsible for this effect. OBJECTIVES: To investigate the effect of trandolapril on the endogenous tissue-type plasminogen activator (t-PA) in patients with a recent myocardial infarction and moderate left ventricular dysfunction. METHODS: Fifty-six patients with acute myocardial infarction and a wall motion index < or = 1.2 were allocated randomly either to administration of trandolapril or to placebo. When possible, the study drug dose was increased gradually to 4 mg trandolapril or a corresponding amount of placebo during the first month after randomization. Blood samples for determination of the variables of the fibrinolytic system, ACE activity and ACE genotype were collected prior to randomization and during out-patient visits in months 1, 3, 6, 9 and 12. After the subject had fasted overnight, blood samples were collected in the morning (0800-1000 h) after the subject had rested supine for at least 15 min, from a venous cannula inserted into the forearm. The effect of trandolapril on the fibrinolytic variables was evaluated by calculating the area under the curve (AUC1-12) from month 1 to month 12. RESULTS: The trandolapril group and the placebo group were similar with respect to baseline clinical characteristics, baseline fibrinolytic variables and baseline plasma ACE activity. The trandolapril group did not differ significantly from the placebo group with respect to AUC1-12 t-PA antigen [11.67 (3.95-26.45) versus 10.34 ng/ml (3.71-19.62), P = 0.19] and AUC1-12 plasminogen activator inhibitor type-1 (PAI-1) antigen [27.57 (8.38-89.49) versus 24.40 ng/ml (7.94-90.62), P = 0.92]. A significant and clear trend in variation with time of t-PA antigen was observed for the trandolapril group, but not for the placebo group. The fibrinolytic variables were similar at baseline for the different ACE genotype insertion (I) and deletion (D) groups (II, ID and DD). Trandolapril treatment was associated with a significant (P < 0.04) increase in the AUC1-12 of t-PA antigen in the ID group compared with that of the placebo-treated ID group, whereas PAI-1 antigen concentration did not differ between the groups. Trandolapril treatment was not associated with any significant change in the fibrinolytic variables for the other genotype groups. CONCLUSIONS: Chronic ACE-inhibitor treatment with trandolapril was not associated with any significant difference in the blood concentrations of t-PA and PAI-1 compared with placebo. The suggested specific interaction between ACE inhibition and the increase in t-PA in patients with ACE genotype ID will require further confirmation.

Aged↗
PubMed1996

The urinary metanephrine-to-creatinine ratio for the diagnosis of pheochromocytoma.

OBJECTIVE: To compare the operating characteristics of two tests for diagnosing pheochromocytoma: 1) measurement of the ratio between urinary metanephrine and creatinine levels and 2) measurement of urinary metanephrine levels alone. A second objective was to ascertain the reasons for false-positive test results. DESIGN: Cross-sectional study. SETTING: Hypertension referral center. PATIENTS: 1013 patients referred for hypertension and tested for pheochromocytoma. MEASUREMENTS: 24-hour urinary levels of metanephrine (measured using liquid chromatography) and creatinine. The presence of pheochromocytoma was confirmed at surgery. In patients with positive test results, the absence of pheochromocytoma was documented by negative results of retests and imaging procedures. RESULTS: Of 58 patients with increased metanephrine levels or increased metanephrine-to-creatinine ratios, 20 had pheochromocytoma and 38 did not. Of the 38 patients without pheochromocytoma, 15 had high metanephrine levels but normal metanephrine-to-creatinine ratios. The respective operating characteristics of measurement of urinary metanephrine levels and measurement of the metanephrine-to-creatinine ratio were as follows: sensitivity, 95% and 100%; specificity, 98% and 98%; positive predictive value, 46% and 47%; and negative predictive value, 100% and 100%. In 13 of the 23 patients who had a high metanephrine-to-creatinine ratio, various acute events may have caused hypersecretion of catecholamines. CONCLUSIONS: Measurement of the metanephrine-to-creatinine ratio is a sensitive and specific test for pheochromocytoma. However, acute events may increase urinary metanephrine excretion to the level that occurs with tumors.

Adolescent↗
PubMed1995

Short-term effects of octreotide on blood pressure and plasma catecholamines and neuropeptide Y levels in patients with phaeochromocytoma: a placebo-controlled trial.

OBJECTIVE: The observation that phaeochromocytoma possess specific somatostatin binding sites led us to test the hypothesis that octreotide may have antisecretory potential in patients with phaeochromocytoma. We therefore compared the effects of octreotide and placebo on blood pressure and plasma catecholamines and neuropeptide Y. PATIENTS: Ten consecutive patients referred to a tertiary care centre for the diagnosis and treatment of a phaeochromocytoma. DESIGN AND MEASUREMENTS: We performed a crossover comparison of either three 100 micrograms subcutaneous injections of octreotide over one day or 3 injections of octreotide vehicle over another. Blood pressure was measured over 24 hours on each test day using an automatic ambulatory recorder. Blood samples were collected before (at 0800 and 0900 h) and after (at 1000, 1100, 1200, 1300 and 1500 h) placebo or octreotide injection. Plasma catecholamines were assayed by high-performance liquid chromatography and neuropeptide Y was determined using a two-site amplified enzyme immunoassay. All patients then underwent surgery and tumoral somatostatin binding site density was determined by quantitative autoradiography. RESULTS: Compared to placebo, octreotide did not alter mean 24-hour ambulatory blood pressure or plasma neuropeptide Y, or plasma or urinary catecholamine, levels. Although a moderate reduction in plasma noradrenaline was found in the two patients with the highest tumoral somatostatin binding site densities, overall octreotide-induced variations in plasma noradrenaline did not correlate with somatostatin binding site density. Blood glucose increased from 5.4 +/- 0.3 on placebo to 7.8 +/- 0.5 mmol/l on octreotide (P < 0.01). CONCLUSION: In the present controlled conditions, short-term administration of octreotide had no antisecretory effect in patients with phaeochromocytoma.

Adrenal Gland Neoplasms↗
PubMed1995

Epidemiology of adult Still's disease: estimate of the incidence by a retrospective study in west France.

OBJECTIVES: To estimate the incidence of adult Still's disease (ASD) and to specify, if possible, associated factors. METHODS: A retrospective study of the populations of the Brittany and Loire regions in west France was made from 1 January 1982 to 31 December 1991. All internal medicine and rheumatology practitioners of these regions were consulted. RESULTS: Sixty-two (62) cases were reported (93% response). The disease incidence calculated over five years was 0.16 per 100,000 inhabitants in the study population. There was no sex bias (sex ratio 1.06 in ASD v 1.05 in the overall population. The mean age of the study population was 36 years, with two peaks of distribution at 15-25 and 36-45 years. A history of allergy was present in 23% of patients (n = 14). In two patients, it was possible to correlate an environmental allergen to exacerbation of ASD. CONCLUSION: The yearly incidence of ASD was estimated to be 0.16 per 100,000 inhabitants. However, it was not possible to incriminate any infectious, toxic, or genetic factors in exacerbation of the disease.

Adolescent↗
PubMed1994

Administration of an anti-interleukin-6 monoclonal antibody to patients with acquired immunodeficiency syndrome and lymphoma: effect on lymphoma growth and on B clinical symptoms.

Increased interleukin-6 (IL-6) production and expression by malignant cells of the IL-6 receptor has been evidenced in a subgroup of non-Hodgkin's lymphomas, suggesting that this cytokine plays a role in lymphoma growth and in B clinical symptoms. In this study, the effect of the administration of an anti-IL-6 monoclonal antibody (MoAb) was analyzed in 11 patients seropositive for human immunodeficiency virus-1 and suffering from an immunoblastic or a polymorphic large-cell lymphoma. The antibody (BE-8, 10 to 40 mg/day) was administered for 21 days. Neutralization of in vivo IL-6 effect was assessed by monitoring C-reactive protein levels in the serum. In 5 patients, the lymphoma progressed during treatment. Among them were the 2 patients in whom endogenous IL-6 effect was not neutralized. Five patients experienced a stabilization, and 1 a partial remission. This effect on lymphoma growth lasted for 8 to 28 weeks. The anti-IL-6 MoAb had a clear effect on lymphoma-associated fever and cachexia. The mean body weight increase was 1.4 +/- 0.5 kg between day 1 and day 21, and reached 12 kg in 120 days in 1 patient who received three courses of treatment. Side effects were a consistent but moderate thrombocytopenia, and an occasional and moderate decrease of neutrophil counts. Immunization against the MoAb was observed in only 2 patients. These results indicate that in some cases of lymphomas growth of malignant cells may be partially IL-6-dependent and that neutralizing endogenous effect of IL-6 completely abrogates B clinical symptoms.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Plasma angiotensin-converting enzyme activity and carotid wall thickening.

BACKGROUND: Mechanisms underlying the previously reported association between a deletion polymorphism in the gene encoding for angiotensin-converting enzyme (ACE) and the risk of myocardial infarction in low-risk subjects are unclear. The purpose of this case-control study was to examine the relation of plasma ACE activity to intimal-medial thickness of the carotid wall measured ultrasonographically in an apparently healthy population. METHODS AND RESULTS: We determined plasma ACE activity in 80 pairs of subjects without any history of ischemic heart disease or any treatment of hypertension and diabetes. Cases and control subjects were defined on the basis of intimal-medial thickness measured in the common carotid arteries by B-mode ultrasound and were matched for sex, sonographer, and the presence of atheromatous plaques. Subjects were selected from a sample of 434 men and 602 women between 60 and 69 years old participating in an ongoing study on vascular aging (EVA). Subjects with intimal-medial thickening (cases) showed a slight but not significant increase in plasma ACE activity in comparison with control subjects (P < .16). However, after exclusion of subjects receiving lipid-lowering drugs, the mean plasma ACE activity became significantly higher in cases than in control subjects (29.9 +/- 7.7 U/L versus 27.5 +/- 8.0 U/L; n = 54 pairs, P < .03). The mean case-control difference in plasma ACE activity was further increased when analysis was restricted to pairs without carotid atheromatous plaques (n = 42 pairs). After adjustment for body mass index, smoking, and systolic blood pressure, the odds ratio for having carotid wall thickening based on 1 SD difference in log ACE was 2.29 (95% confidence interval, 1.16 to 4.52; P < .02). CONCLUSIONS: The results of the study suggest that chronic exposure to high levels of plasma ACE could be involved in structural changes of the arterial wall.

Aged↗
PubMed1994

Carotid artery distensibility and distending pressure in hypertensive humans.

Whether the decrease in large-artery distensibility observed in hypertensive patients is due primarily to an increase in distending pressure or to hypertension-induced changes in structural properties has been much debated. We determined noninvasively the diameter-pressure curve of the common carotid artery over the systolic-diastolic range by continuously recording both the pulsatile changes in internal diameter (high-resolution echo-tracking system) and, simultaneously on the contralateral artery, the pressure waveform (high-fidelity applanation tonometry). We then derived the distensibility/pressure curve and compared arterial distensibility in 14 normotensive subjects and 15 age- and sex-matched hypertensive subjects at their respective mean arterial pressures (MAP) and at a common distending pressure: 100 mm Hg. Distensibility decreased as blood pressure increased, and distensibility at MAP was significantly lower in hypertensive than in normotensive subjects (7.8 +/- 0.7 versus 11.7 +/- 1.7 kPa-1.10(-3), mean +/- SEM; P < .05). In hypertensive subjects, the distensibility-pressure curve was shifted toward higher levels of blood pressure, and a large part of the curve overlapped that of normotensive subjects. No significant downward shift of the distensibility-pressure curve was observed in hypertensive subjects, and distensibility at 100 mm Hg was not significantly different from that of normotensive subjects (10.0 +/- 1.0 versus 9.0 +/- 1.1 kPa-1.10(-3)). Distensibility at 100 mm Hg decreased with aging (P < .05) and was not reduced in hypertensive subjects compared with normotensive subjects after adjustment for age.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

[Hemodynamic effects of chronic treatment by cilazapril in normotensive patients with obliterative arterial diseases of the lower limbs].

OBJECTIVE: To determine whether long-term treatment with cilazapril (CIL) may improve pulse pressure (PP), arterial compliance and ankle-arm systolic index (AAI) in patients with lower-extremity arterial disease (LEAD). Indeed, in both systolic hypertension and LEAD, the increase in pulse pressure has been attributed to a reduced compliance. DESIGN AND METHODS: Thirteen patients (age: 65 +/- 5 yrs; AAI: 0.78 +/- 0.15; m +/- SD) were included in a double-blind randomized parallel study to compare the effects of a 6 month treatment with CIL (10 mg per day; n = 6) to those of placebo (PL; n = 7) Blood pressure, AAI and arterial compliance were determined at baseline (MO) and after 3 (M3) and 6 months (M6). Common carotid (CC) and common femoral (CF) artery compliances were noninvasively determined from pulsatile changes in arterial diameter (Wall Track System, Hoeks et al., 1990) and pressure (PP). RESULTS: Both groups were comparable at MO. Compared to PL, CIL significantly reduced PP (-22 +/- 4 vs -2 +/- 9 mmHg) and MAP (-16 +/- 11 vs -4 +/- 7 mmHg) and improved CC (+54 +/- 34 vs +5 +/- 21 mm2.mmHg-1.10(-3)) at M6. Weaker effects were observed at M3. No significant changes in AAI and CF compliance were observed. CONCLUSIONS: A direct effect of CIL on the large artery wall was suggested by 1) a greater reduction in PP than in MAP and 2) a disproportionately greater improvement in CC compliance compared with the reduction in distending pressure (MAP). These results indicate that long-term treatment with CIL may improve large artery function in patients with LEAD.

Adult↗
PubMed1993

Effects of clonidine on plasma catecholamines and neuropeptide Y in hypertensive patients at rest and during stress.

Neuropeptide Y (NPY), a potent vasoconstrictor agent reported to be released, in addition to norepinephrine (NE), by sympathetic nerve endings during stress, may contribute to the pressor response to various stimuli. The objectives of this study were to determine (a) whether plasma NPY concentrations are altered during different types of stress (cold pressor test, mental stress, and active orthostatism) and (b) whether clonidine, via its central sympatholytic effect, affects the stress-induced blood pressure, NPY, and/or catecholamine changes. Eighteen untreated patients with mild essential or borderline hypertension participated in an acute randomized, double-blind, parallel study. The blood pressure and heart rate were recorded during three control periods, each followed by either a cold pressor test (CPT), a mental stress test (MS: mental arithmetic), or active orthostatism (AO), performed in a random order. Venous blood samples for catecholamines and NPY determination were taken at the end of each control and test period. This entire procedure was repeated after oral clonidine (150 micrograms) or placebo. Before treatment, a CPT, MS, or AO increased the blood pressure to the same extent. The stress-induced increase in plasma NE was greater during AO (+99 +/- 23%) than during CPT (+35 +/- 8%) and MS (+55 +/- 12%). The stress-induced increase in plasma epinephrine was only significant during MS (+142 +/- 69%). A small but significant increase in NPY (p < 0.05) was observed during AO only (+10 +/- 7%). Compared to placebo, clonidine significantly decreased the basal blood pressure and the pressor response to CPT, but did not change the pressor response to MS and AO.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

[Do converting enzyme inhibitors differ from each other in the treatment of hypertension?].

Novel angiotensin converting enzyme inhibitors (ACE inhibitors) have recently been commercialized and the question arises whether differences in pharmacodynamic and pharmacokinetic properties should lead to specific therapeutic choices. To our knowledge there is no data which allows the physician to conclude to any different antihypertensive efficacy when ACE inhibitors are used at adequate dosage. Their pharmacokinetic characteristics may differ at every level: absorption, distribution, metabolism and excretion. Differences in chemical structure may also influence their diffusion in various tissues, therefrom the amplitude and duration of inhibition of angiotensin II at these sites. The duration of maximum blockade of ACE and the amplitude of residual blockade may theoretically influence the duration of the hypotensive effect and the number of daily dosages. Once-daily administered long acting ACE inhibitors keep their antihypertensive action through the whole 24-hour period, during chronic treatment. The theoretical advantage of such a property is an improved control of 24-hour blood pressure. However, no study, to our knowledge, concluded to any difference between long acting ACE inhibitors as far as this parameter was concerned. In addition, except captopril which has been reported to induce major untoward effects at the time high dosages were introduced, ACE inhibitors do not seem to bear different undesirable effects.

Angiotensin-Converting Enzyme Inhibitors↗