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Biomedical subjects

A Roux

Publications and source records attributed to A Roux.

At least 73 records · Page 4Linked to original sources
PubMed1982

Comparison of 125I-fibrinogen kinetics and fibrinopeptide A in patients with disseminated neoplasias.

To provide more information on the pathways of fibrinogen catabolism in generalized cancer, the effect of heparin on fibrinopeptide A (fpA) and on 125I-fibrinogen kinetics was studied in 15 patients with disseminated neoplasia. Three patients had evidence of venous thrombosis and in 2 additional patients a low fibrinogen level together with increased amounts of FDP/fdp and a positive ethanol test indicated disseminated intravascular coagulation (DIC). The plasma levels of fpA were grossly elevated (4.6--20, mean 11.4 ng/ml, normal values 1.01 +/- 0.45 ng/ml) in patients with thrombosis or DIC, and normal to grossly elevated (0.4--10.4, mean 6.1 ng/ml) in the other patients. Intravenous heparin bolus lowered the fpA level in 11/11 patients, and continuous heparin treatment led to an impressive suppression or complete normalization of the plasma fpA in 5/6 patients. This finding is thought to reflect heparin suppression of thrombin activity on fibrinogen. In some cases, the fpA fall after heparin bolus was slow and/or incomplete, suggesting fpA generation at sites not easily accessible to heparin or insufficient heparin dosage. The 125I-fibrinogen kinetics were characterized by a significantly shorter half-life (t1/2: 2.5 days), increased catabolic rate constant (j: 0.44 days-1), and increased absolute turnover (68.9 mg fibrinogen/kg/day) as compared to 4 normal subjects (t1/2: 4.2 days; j: 0.26 days-1; turnover 21.7 mg fibrinogen/kg/day). As estimated from the fpA generation rates, intravascular thrombin action on fibrinogen contributed only in minor part to increase the turnover of 125I-fibrinogen. In particular, the turnover was greatly accelerated in heparin-treated patients despite impressive suppression or normalization of the fpA levels in 5/6 cases.

Adult↗
PubMed1981

Pharmacokinetics and bioavailability of diacetolol, the main metabolite of acebutolol.

The pharmacokinetics and bioavailability of diacetolol, the principal metabolite of acebutolol, were studied in 6 healthy subjects. Plasma concentrations were determined following a single intravenous injection of diacetolol 100 mg and three oral doses of diacetolol 100, 400 and 800 mg, in random order. The average oral bioavailability of diacetolol was F: 0.302 +/- 0.052 (100 mg), 0.363 +/- 0.052 (400 mg) and 0.426 +/- 0.068 (800 mg); the differences are not significant. The mean plasma half-life of the terminal phase, 7.94 +/- 0.26 h after intravenous administration, was significantly higher than after oral administration 12.27 +/- 1.00 h (100 mg), 12.82 +/- 1.59 h (400 mg) and 13.05 +/- 13.05 +/- 1.22 h (800 mg) (p less than 0.02 to 0.05); the mean urine half-lives of the terminal phase were not significantly different. Renal clearance of diacetolol 10.2 +/- 0.81 . h-1 represented about wo-thirds of total body clearance 15.9 +/- 1.21 . h-1. The results suggest either a first-pass effect or incomplete absorption of diacetolol after oral administration.

Acebutolol↗
PubMed1980

[Treatment of severe febrile neutropenia (author's transl)].

Random allocation of 22 patients with benign and malignant diseases with neutrophil counts of up to 1 X 10(9)/l blood and probably infection-caused fever of more than 38 degrees C to intravenous treatment with one of the following antibiotic combinations was performed: carbenicillin (6 g/m(2) . 6 h) plus sisomicin (45 g/m2 . 6 h) or mezlocillin (3 g/m2 . 6 h) plus sisomicin (45 g/m2 . 6 h). Both combinations were tolerated equally well. Patients became afebrile in 16 out of 23 treatment periods. Seven out of 11 patients responded to carbenicillin - sisomicin, and 9 out of 12 to mezlocillin - sisomicin. Mezlocillin thus leads to equal success of treatment in febrile neutropenia as the double dose of carbenicillin when both antibiotics are combined with the same aminoglycoside.

Agranulocytosis↗
PubMed1980

Effects of selective and nonselective beta adrenergic agents on renin secretion in isolated perfused rat kidney.

The effects of selective and nonselective beta adrenergic drugs on the renin secretion rate (RSR) in isolated perfused rat kidneys were studied. Both isoproterenol (Ipr) (nonselective agonist) and salbutamol (Salb) (beta-2 selective agonist) stimulated RSR in a dose-dependent manner. The lowest doses able to induce a significant RSR increase were 5 nM for Ipr and 50 nM for Salb. A 5-fold increase in RSR was induced by 500 nM Ipr and a 3.2-fold increase by 5 microM Salb. Renin stimulation by both agonists was suppressed by propranolol (nonselective) and by acebutolol and its derivative M&B 16,942 (beta-1 selective antagonists). Thus, renin release was stimulated or inhibited effectively by all the drugs tested, regardless of the beta selectivity of agonists and antagonists. There were no consistent relationships observed between changes in renal hemodynamics and in RSR, suggesting that the used drugs affected renin release from in vitro-perfused rat kidney through their direct effects on juxtaglomerular cells. These results indicate that renal beta adrenoreceptors involved in renin release do not fall into two distinct beta subtypes.

Acebutolol↗
PubMed1979

[Fibrinogen metabolism and plasma fibrinopeptide A in disseminated neoplasms].

FPA immunoreactivity was elevated in 14 out of 15 patients with disseminated neoplasia. Two of the patients showed signs of DIC, two had clinically evident thrombosis and one a positive 125I-fibrinogen uptake test suggesting thrombosis. Infusion of heparin produced a prompt fall in FPA levels. FPA immunoreactivity correlated well with the turnover of intravasal 125I-fibrinogen. The results confirm that the RIA of FPA provides a specific and quantitative index of the conversion of fibrinogen into fibrin and indirectly of the thrombin action in vivo.

Disseminated Intravascular Coagulation↗
PubMed1979

[Bartter's syndrome: the long term effects of indomethacin on growth (author's transl)].

Six children with Bartter's syndrome aged 6 years 4 months to 13 years 11 months were treated with indomethacin (1.7 to 4.3 mg/kg/day) during 7 to 27 months. A catch up growth was first observed, then growth curve was parallel to the normal. A catch up weight was also observed. The osseous maturation was the faster it was more delayed. These changes were observed despite a partial correction of potassium and plasma renine activity.

Adolescent↗
PubMed1979

[Therapy results in hairy cell leukemia].

20 patients with hairy cell leukemia were treated between 1966 and 1978. All modalities of treatment for lymphoproliferative disorders have been used in at least some patients. Besides prednisone, vincristine, cyclophosphamide and their combinations as well as irradiation of enlarged spleens, cell depletion was achieved by splenectomy and leukapheresis. Cytostatics had no beneficial effect. Cytostatic therapy exposed some patients to the hazards of severe infections. On the contrary splenectomy lead to the improvement of some blood parameters. Leukapheresis seemed to work nearly identically. The survival of the splenectomized patients was longer than of controls. Because of the variability of the duration of the disease no definite statement could be made concerning the survival of both groups. 12 patients died during the observation period. Splenectomy was followed by one death, 11 patients died of septicemia.

Adult↗
PubMed1979

[Average steady-state plasma levels with slow release quinidine preparations].

Arabogalactane sulphate of quinidine (AGSQ) is a slow release preparation of quinidine. The aim of this study was to compare the plasma levels of quinidine obtained by different preparations of AGSQ (AGSQ I, II and III) and to determine which was best suited to therapeutics. The "in vitro" study showed different amounts of quinidine liberated in 6 hours, 34% with AGSQ I, 58% with AGSQ II and 100% with AGSQ III. The plasma quinidine levels were studied after administration of a dose corresponding to 330 mg quinidine base, morning and evening for 7 consecutive days to 27 hospitalised patients; 7 received AGSQ I, 11 received AGSQ II 5, received AGSQ III and 4 quinidine sulphate. The delay in reaching a steady state was 24 hours for the quinidine sulphate 36 hours for AGSQ I, 48 hours for AGSQ II and 60 hours for AGSQ III. The average plasma level on the 7th day (Cee) was 2.74 +/- 0.71 microgram/ml, 2.62 +/- 0.74 microgram/ml and 3.29 +/- 0.72 microgram/ml respectively. The plasma quinidine levels were maintained between toxic and therapeutic levels (3,5 and 1,7 microgram/ml) only with AGSQ II by suppressing the peak observed 1 hour administration of quinidine sulphate. An excellent correlation (r = 0,984) was observed between the plasma quinidine 6 hours after ingestion and the Cee. A blood test during the steady state, 6 hours after ingestion of the drug, is useful in adjusting the dosage. These results suggest that AGSQ II is the preparation best suited for therapeutic usage although it does not give the best relative bioavailability of the drug.

Delayed-Action Preparations↗
PubMed1978

[Spectrofluorimetric estimation in biological fluids of a new beta-blockader: atenolol. Application to its pharmacokinetic study (author's transl)].

The authors describe a simple method of fluorimetric estimation of atenolol, applicable to blood and urine, sufficiently sensitive to permit a pharmacokinetic study. After administration of a dose of 200 mg by the oral route to hypertensive subjects, one may observe a maximal plasma concentration 3 hours after the dose average value 3.91 +/- 0.71 mumol/l (1.04 +/- 0.19 mg/l). The apparent half life of elimination of phase beta is 14.1 +/- 4.9 h, values comparable with those calculated from urinary data 14.6 +/- 2.0 h. The renal clearance was 140 +/- 32 ml/min; 54 +/- 14% of the administered dose are excreted in the urine. After administration by the venous route, urinary excretion represents 96% of the dose administered.

Adult↗
PubMed1975

[Study of acebutolol dialysis and pharmacokinetic data in patients with renal insufficiency undergoing hemodialysis].

The dialysance of acebutolol, in vitro, has been found to be equal to 87 ml/mn for a blood flow of 200 ml/mn through an artificial kidney; at the same flow rate, that of urea is 136 ml/mn. In subjects with normal renal function, half-life of acebutolol in plasma, after oral administration, is 4.4 +/- 0.6 h; in haemodialysed patients with renal failure, it is very increased; during haemodialysis, it is near normal (mean: 5.9 h in 4 subjects). Authors discuss the meaning of acebutolol dialysance, in vivo, considering a possible protein binding of this drug.

Acebutolol↗