PubMed Health⌕ Search

Biomedical subjects

E Albengres

Publications and source records attributed to E Albengres.

At least 55 records · Page 3Linked to original sources
PubMed1987

Critical risk/benefit analysis of pefloxacine use in children under 15 years--the problem of arthralgias.

Pefloxacine belongs to a group of new quinolone antibiotics with more general indications than the urinary quinolones marketed about twenty years ago. The contraindication of the quinolones in children under 15 years of age limits their usage exclusively to adults. In this paper, the adverse arthralgic effects of these quinolones, which have largely motivated the contraindication, have been analyzed from an experimental, clinical and pathophysiological point of view. It is concluded that the pediatric benefits associated with the marked antibacterial activity of pefloxacine, particularly in pseudomonas and enterobacteriae infections, should be balanced against the risks associated with arthralgia whenever the condition of the patient is grave and decisions vital to a favorable prognosis for the sick child are necessary.

Acidosis↗
PubMed1986

Role of alpha-1 acid glycoprotein, albumin, and nonesterified fatty acids in serum binding of apazone and warfarin.

Altered concentrations of serum proteins and nonesterified fatty acids (NEFAs) often accompany malignant diseases. Free fractions (fu) of apazone and warfarin were measured by equilibrium dialysis in serum samples obtained from 31 patients with cancer and 18 control subjects. Mean fu values of both drugs were significantly higher in the patient group. Multivariate analysis showed albumin, NEFA, and AAG for apazone and albumin, NEFA, and age for warfarin accounted for 60% and 63%, respectively, of interpatient variation in bound/free drug concentration ratios in the group of patients with cancer. The interactions of apazone and warfarin with AAG were further characterized; the more avid site had association constants of 4.5 X 10(5) and 2.3 X 10(5) L/mol, respectively. Finally, it is strongly suggested that when hypoalbuminemia is present and a drug binds to AAG with an affinity constant comparable to or higher than that to albumin, then fu will become dependent on the concentration of AAG.

Adult↗
PubMed1986

[Rational posology and drug dosage].

Serum level monitoring of drugs allows an optimal drug therapy, because it can take into account individual pharmacokinetic (and metabolic) variations. Some special conditions in drugs and in patients are highly suggestive of drug monitoring. These include mainly physiological but also pharmacological situations and apply to drugs with low therapeutic indices. However, for some drugs, highly bound to proteins or to blood cells, another more specific measurements will take in the future the place of serum level monitoring.

Aged↗
PubMed1986

[Plasma binding of drugs in chronic renal failure].

As in many pathological states, changes in the plasma protein binding of drugs are observed in uremia. Renal failure reduces the fraction of many acidic drugs bound to serum albumin. This decreased binding is due to many factors: variations of protein concentrations, structural changes of proteins, competitive displacers in plasma of chronic uremic patients. When the margin between pharmacological and toxic doses is narrow, drug monitoring by measurement of plasma free drug concentrations seems necessary to adjust the dosage regimen in uremic patients.

Binding, Competitive↗
PubMed1985

Interactions between smectite, a mucus stabilizer, and acidic and basic drugs. In vitro and in vivo studies.

The interaction of phenylbutazone and diazepam with smectite were studied in in-vivo and in-vitro. The kinetics of both drugs were investigated in healthy subjects after oral administration as monotherapy or in association with smectite. Smectite did not substantially alter the kinetics of phenylbutazone, whereas the peak plasma concentration of diazepam was reduced to 91%, and the time of peak concentration was prolonged by 153% of the control values. The in-vitro investigations were conducted at pH 5.5 and 8 and showed that there was no interaction between phenylbutazone and smectite, but that it adsorbed diazepam. The findings suggest that smectite delays the absorption of basic drugs and does not alter the absorption kinetics of acidic drugs.

Absorption↗
PubMed1985

Lymphocyte transformation test in drug-induced toxic epidermal necrolysis.

Lymphocyte transformation tests (LTT) to drugs remain widely used in drug reactions, despite controversies about their real usefulness. We tested the lymphocytes of 12 patients recovering from a drug-induced Toxic epidermal necrolysis (TEN). There was no difference between the amounts of thymidine incorporated when patients' lymphocytes were cultivated with culprit or innocent drugs. In both situations the lymphocytes from patients reacted like the lymphocytes from controls cultivated with the same panel of drugs. These negative results do not exclude that a hypersensitivity reaction may play a role in the physiopathology of TEN. Anyhow, they clearly indicate that testing lymphocyte transformation to drugs has no practical value in the diagnosis of TEN.

Adolescent↗
PubMed1985

Present and future trends in drug monitoring.

The concept of drug monitoring is generally accepted for toxic drugs and for some particular pathological states. However its basis and its limits are still controversial. This paper outlines under which circumstances drug monitoring is of absolute necessity. This paper also deals with pharmacokinetics, i.e. the measurement of drug concentration as a tool in drug monitoring. Finally it tries to forecast future developments in this field using the analysis of receptors, found in blood cells, as probes of tissue receptors.

Forecasting↗
PubMed1985

[Lyell's syndrome and ectodermosis pluriorificialis during treatment with oxicams: 11 cases].

Piroxicam (Feldene) and isoxicam (Vectren) form a part of a new family of non-steroid anti-inflammatory drugs (NSAID) highly used in France: the oxicams. The cutaneous accidents of all kinds are frequent, estimated from 1 to 3 p. 100 of the patients with piroxicam (16, 20). In addition to the maculo-papular eruptions, there has been reported: lichenoid eruption (21), erythroderma (7), purpuric vasculitis (1, 10, 21), pemphigus (12, 14), bullous dermatosis difficult to classify (15), erythema multiforme and Stevens-Johnson's syndrome (3, 6, 7, 9, 13, 21, 23) and at last many photosensitization accidents (3, 8, 11, 19, 20, 21). We report 11 observations of Lyell's syndrome (8 cases) or Stevens-Johnson's syndrome (3 cases) occurred during treatments by isoxicam or piroxicam. Eight women and 3 men aged from 35 to 80 years begin a Lyell's syndrome or a Stevens-Johnson's syndrome after 9 to 45 days (at an average of 16 days) of a treatment by isoxicam (6 cases) or piroxicam (5 cases). Five patients attacked by a Lyell's syndrome are intubated and ventilated and 2 patients die of a septic shock at the ninth and the thirteenth day of evolution: the duration of hospitalization is from 11 days to 3 and a half months for the Lyell's syndromes survivors and from 7 to 19 days in the cases of Stevens-Johnson's syndrome: 7 surviving patients have ocular sequelae with in 2 cases a complete or partial blindness. A slight hepatic cytolysis is observed 5 times and a neutropenia mainly as a lymphopenia 4 times. In 2 observations, the CMV serology is positive.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Multiple binding of bepridil in human blood.

Using radiolabelled bepridil, equilibrium dialysis experiments and direct ligand-binding studies were conducted to characterize the binding of bepridil to some human serum proteins, and to blood cells and platelets, respectively. Bepridil was bound to serum albumin with K = 26 +/- 1.6 X 10(3) mol-1 X 1, n = 1.07 +/- 0.04; to alpha 1-acid glycoprotein with K = 442 +/- 68 X 10(3) mol-1 X 1, n = 0.90 +/- 0.04; and with a lesser extent to lipoproteins and gamma-globulins. Bepridil, propranolol, quinidine and erythromycin were found to share the same site on alpha 1-acid glycoprotein. The binding of bepridil to both RBC and WBC was nonspecific with the following parameters: NK = 10.55 +/- 0.10 per 5 X 10(6) RBC/mm3 and NK = 0.34 +/- 0.01 per 10(3) WBC/mm3, whereas the binding to platelets was saturable with N = 10.97 +/- 1.06 mumol/l per 108 +/- 10(3) platelets/mm3 and K = 40 +/- 8 X 10(3) mol-1 X 1. The binding parameters were used to simulate the distribution of bepridil between serum proteins, blood cells and platelets over the therapeutic range and showed that serum albumin, alpha 1-acid glycoprotein and RBC were the major binding components.

Bepridil↗
PubMed1984

In vitro studies on the distribution of probucol among human plasma lipoproteins.

The role of human plasma lipoproteins as carriers in the blood transport of the cholesterol-lowering and water-insoluble drug, probucol, was investigated in in vitro studies. [14C]Probucol was incubated in whole human blood, a serum pool, individual diluted sera, and isolated protein and lipoprotein fractions. In whole blood, about 90% partitioned in plasma. Following ultracentrifugal fractionation of the serum, it was found that less than 5% distributed in the d greater than 1.20 protein fraction (albumin-rich fraction) and more than 95% in the lipoprotein fractions. The distribution of probucol in the lipoprotein fractions correlated with the lipoprotein total lipid volume under saturation conditions (incubation of isolated lipoprotein fractions) as well as nonsaturation conditions (fractionation of serum exposed to [14C]probucol). Incubation of the albumin-rich fraction and of apolipoproteins originating from the isolated lipoprotein fractions showed that they account for a negligible part in the interaction of probucol with blood components. The probucol uptake of individual sera was shown to be correlated to the lipid content of the serum. When probucol was incubated in erythrocyte suspensions containing variable amounts of lipoproteins, probucol partitioned less in erythrocytes as the lipoprotein concentration increased in the suspension.

Apolipoproteins↗
PubMed1983

Phenytoin in pregnancy: a review of the reported risks.

Over the last 12 years several studies have found that the frequency of certain anomalies in children born to mothers treated with antiepileptic drugs during pregnancy has almost doubled. In 1968 Meadow reported certain malformations that suggest a congenital syndrome involving craniofacial abnormalities and that add to the high level of suspicion pointing to phenytoin. Moreover, multi-drug antiepileptics including phenytoin have been reported to induce carcinogenic damage and coagulation defects. In such instances it is always very difficult to distinguish the individual toxic effects of each component. Nevertheless, the possible role of phenytoin in the development of these diseases must be investigated. In addition, the eventual role of the pathologic state itself, epilepsy, cannot be disregarded. Two main aspects must be considered: the disease and its severity which determines the necessity of high dosages of antiepileptic drugs. The administration of phenytoin to pregnant epileptic patients is clearly questionable. Thus the aim of this paper is to evaluate the risks of this drug and compare them with its expected therapeutic benefits.

Abnormalities, Drug-Induced↗
PubMed1982

Evidence for binding of certain acidic drugs to alpha 1-acid glycoprotein.

The binding of some acidic drugs to alpha 1-AGP was studied by equilibrium dialysis at 37 degrees, pH 7.4. Certain acidic drugs bound to alpha 1-AGP at one binding site with a high affinity. Though the alpha 1-AGP plasma concentration is far lower than the HSA concentration, the association constants of some acidic drugs with alpha 1-AGP are high enough to suggest that binding to alpha 1-AGP will contribute significantly to the total plasma binding of these drugs.

Humans↗
PubMed1982

Benoxaprofen: plasma binding and binding interactions with some drugs and endogenous compounds.

The binding of benoxaprofen to human serum albumin (HSA) was investigated by equilibrium dialysis at pH 7.4 and 37 degrees C. As most acidic drugs, almost completely ionized at plasma pH, benoxaprofen was avidly bound to HSA (7.5 x 10(-6) M) with the following parameters: n1 = 3.3 and K1 = 325 x 10(3) M-1; n2 = 16.2 and K2 = 2.1 x 10(3) M-1 At normal HSA plasma concentration in humans benoxaprofen was more than 99.5% bound, either when a pure HSA solution or when a pooled serum was used. Such results were obtained within a wide range of benoxaprofen concentrations and benoxaprofen binding did not significantly differ whatever its concentration might be. The influence of liver failure on benoxaprofen serum binding was investigated in five patients whose bilirubinaemia was from 15 to 28 x 10(-6) M, and the results were compared to those of five normal volunteers. There was no difference between the two groups: 99.30 +/- 0.30% versus 99.62 +/- 0.30%. However, in four other patients whose bilirubinaemia was greater than 130 x 10(-6) M, the binding of benoxaprofen decreased to 98.0 +/- 1.6% (p] less than 0.05). Addition of FFA (palmitic acid, 2000 . 10(-6) M) to H SA (580 x 10(-6) M) involved a slight decrease in HSA binding of benoxaprofen: 99.8 +/- 0.1 versus 99.66 +/- 0.03%. Serum binding of benoxaprofen was not affected by therapeutic levels of tolbutamide, was slightly decreased from 99.7 to 9.2% by furosemide, to 99.4% by CPIB, and to 99.4% by salicylic acid. At the reverse, therapeutic plasma levels of benoxaprofen did not displace warfarin and acenocoumarol, but they displaced CPIB from 90.1 to 86.1%, glibenclamide from 95.2 to 94.2% and phenylbutazone 99.6 to 93.0%.

Anti-Inflammatory Agents↗