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Biomedical subjects

M Rostin

Publications and source records attributed to M Rostin.

At least 19 recordsLinked to original sources
PubMed1994

Local steroid therapy and bacterial skin flora in atopic dermatitis.

A double-blind, randomized trial was conducted to determine the influence of topical steroid therapy on atopic skin flora. The bacteriological and clinical effects of desonide (Locapred), compared with those of its excipient, were studied in 40 children. Clinical scoring and bacteriological sampling were performed before the start of the trial and after 7 days of once-daily topical treatment. Before treatment, no differences in clinical score or Staphylococcus aureus colonization were noted between the two groups. After treatment, the clinical score improved (P < 0.001) in the desonide group, and S. aureus density decreased dramatically (P < 0.001). In the excipient group, no significant differences in clinical score or S. aureus density were noted. A comparison of the two groups demonstrated statistically significant differences with regard to clinical score (P < 0.001) and S. aureus density (P < 0.05). These results show the efficacy of topical corticosteroid treatment alone on S. aureus colonization in atopic skin, and confirm the critical role of inflammation in bacterial colonization.

Adolescent↗
PubMed1994

[Topical tretinoin in the treatment of lichen planus and leukoplakia of the oral mucosa. A biochemical evaluation of the keratinization].

In earlier work, we demonstrated that 0.1 p. 100 topical tretinoin is clinically effective and well tolerated compared with placebo for the treatment of oral leukoplakia and oral keratosic or erythematous lichen planus. Here we aimed to complete this clinical protocol with histological and biochemical analyses comparing the biopsy specimens collected at inclusion and those collected after 4 months of treatment. Histological results were based on changes in keratinization observed between onset of treatment and 4 months treatment. Biochemical studies included the use of antibodies (anti-cytokeratins 10-11, anti-filaggrine) for the immunohistochemical evaluation of keratinization and 2-dimensional gel electrophoresis for measuring cytokeratins. In patients with lichen planus, histological changes during treatment showed that, in the 10 patients in the tretinoin group, keratinization disappeared in 6 and decreased significantly in 3. Immunohistochemistry revealed that cytokeratins 10-11 and filaggrin disappeared in 57 p. 100 of the patients treated with tretinoin versus 25 p. 100 in the patients given placebo. Bidimensional gel electrophoresis showed that cytokeratins 1, 2, 10 and 11 disappeared only in the tretinoin group (60 p. 100 of the cases). In patients with leukoplakia, histological changes during treatment showed that, in the tretinoin group, keratinization disappeared in 5 cases and decreased in 5 others. Immunohistochemistry revealed that cytokeratins 10-11 disappeared in 30 p. 100 of the patients treated with tretinoin versus 25 p. 100 in the placebo group. Bidimensional electrophoresis demonstrated that cytokeratins 1, 2, 10 and 11 disappeared in 43 p. 100 of the patients treated with tretinoin.

Administration, Topical↗
PubMed1994

[Topical tretinoin in the treatment of lichen planus and leukoplakia of the mouth mucosa. A clinical evaluation].

A randomized study was conducted to evaluate the effect of tretinoin and patient tolerance to treatment with topical applications in series of 20 cases of smoking-related or traumatic oral keratoses leukoplakia and of 20 cases of lichen planus. In each group, patients applied the topical ointment containing tretinoin (10 patients) or placebo (10 patients) twice daily. Clinical outcome was evaluated on the basis of the surface area of the lesion, measured monthly during treatment, as compared with the area observed at treatment onset. After 4 months treatment, there was a significant decrease in the surface area of the lesion in the patients with lichen planus (p < 0.02): 94 p. 100 in the tretinoin group versus 21.4 p. 100 in the placebo group. In patients with leukoplakias, there was also a very significant reduction in the surface area of the lesion after 4 months of treatment (p < 0.001): 80 p. 100 in the tretinoin group and 16 p. 100 in the placebo group. Tolerance to treatment was generally good despite a few complaints of quite temporary burning sensation at application rapidly resolutive.

Administration, Topical↗
PubMed1990

Pharmacokinetics of prednisolone in children with the nephrotic syndrome.

The aim of this study was to establish whether the criteria for the clinical effectiveness of steroids are correlated with the pharmacokinetics of prednisolone in children treated with prednisone during an attack of idiopathic nephrotic syndrome (INS). Thirteen patients with nephrosis were included. Prednisolone, prednisone and cortisol levels were measured using a specific high-performance liquid chromatography assay after an oral dose of 1 mg/kg body weight of prednisone taken at the onset of the disease. All the pharmacokinetic parameters, including the conversion of prednisone to prednisolone were similar to the data already published in children with INS. No correlation was found between the values of pharmacokinetic parameters and criteria of clinical effectiveness. Hypo-albuminaemia was significantly correlated with the area under the plasma-concentration curve but not with the elimination half-life of prednisolone. Moreover, the prednisolone elimination half-life correlated with the urinary excretion of 17-hydroxycorticosteroids achieved in the first 6 h. The present study suggests that routine measurements of prednisolone kinetics do not help when assessing the treatment of children with INS.

17-Hydroxycorticosteroids↗
PubMed1990

Pharmacodynamics of CY 216 in healthy volunteers: inter-individual variations.

The pharmacodynamic parameters of a low molecular weight heparin (LMWH, CY 216) and their inter-individual variations were investigated. In a cross over study 100 anti-factor Xa IC U/kg were injected, one week apart, to 12 healthy volunteers by intravenous (IV) or subcutaneous (SC) route. The pharmacological effects were followed by performing activated partial thromboplastin time (APTT), thrombin clotting time (TCT) and a chromogenic anti-factor Xa assay. The main pharmacodynamic parameters were calculated from the anti-factor Xa activity disappearance curves. Five to ten min after IV injection, the APTT ranged between 56 and 98 sec (baseline 40 sec), the TCT between 28 and 99 sec (baseline 19 sec) and the anti-factor Xa activity between 1.58 and 2.28 IC U/ml. The anti-factor Xa activity half-life ranged between 1.5 and 2.9 h. After SC injection, there were no detectable APTT and TCT prolongations; the maximum anti-factor Xa activity ranged between 0.36 and 0.88 IC U/ml and the half life between 1.5 and 6.4 h. These results indicate that, as for standard heparin, there are large inter-individual variations in the anticoagulant responses to a given dose of CY 216 an observation which may have clinical implications.

Adult↗
PubMed1989

Pharmacodynamics and pharmacokinetics of dermatan sulfate in humans.

Dermatan sulfate (DS), a catalyst of the thrombin-heparin cofactor II interaction, has antithrombotic activity and is devoid of significant hemorrhagic risk in several animal models. We investigated the pharmacodynamic and pharmacokinetic properties of DS in humans. DS was injected in single bolus intravenous injections of four increasing doses (0.5, 1, 1.5, 2 mg/kg) to six healthy volunteers. The resulting anticoagulant activities were assessed by the activated partial thromboplastin time (APTT) and the thrombin clotting time (TCT). There were dose-dependent prolongations of the APTT and TCT, and the anticoagulant activities disappeared in less than three hours. The pharmacokinetic parameters were calculated from the plasma concentrations of DS measured with a new chromogenic assay. The volume of distribution was approximately 1.8 times greater than the theoretical plasma volume and was independent of dose. In contrast, the clearance decreased with dose and the terminal half-life ranged from 0.45 +/- 0.08 hours at 0.5 mg/kg to 0.72 +/- 0.11 hours (mean +/- SD) at 2 mg/kg. The bioavailabilities of subcutaneous (SC) and intramuscular (IM) administration relative to those of intravenous administration were determined in 12 other volunteers. The respective bioavailabilities were 24.7% +/- 12.9% and 12.4% +/- 9.2% for SC and IM administration. There was no detectable change in the APTT and the TCT when the volunteers were injected with 1.5 mg/kg SC or IM. In addition, the pharmacokinetic parameters derived from plasma concentrations of DS showed considerable interindividual variations by the two later routes of administration. Peak concentrations were noted 2.7 +/- 1.3 hours after SC injection and 4.3 +/- 4.9 hours after IM injection. The average peak concentrations were 0.7 +/- 0.3 and 0.4 +/- 0.2 mg/L after SC and IM injections, respectively. The half-lives of DS were 7.9 +/- 6.5 hours (SC) and 6.3 +/- 7.4 hours (IM). No adverse reaction to DS was recorded during this study.

Adult↗
PubMed1987

Effect of clonidine on adrenal medulla catecholamine levels in rats.

The effects of clonidine on adrenal medulla catecholamines levels were studied in normotensive rats. Intraperitoneal injections (50,100 micrograms/kg) of clonidine caused a dose-dependent decrease in adrenaline content of the gland. This effect was suppressed by denervation of the adrenal medulla, i.e. unilateral section of splanchnic fibers performed 5 days before. These results demonstrate that clonidine decreases the catecholamine content of the adrenal medulla only through a central action. They suggest that the adrenal medulla is involved in the hypotensive effect of clonidine.

Adrenal Medulla↗
PubMed1987

Effect of size and dosage strength on the bioavailability of two diltiazem formulations during repeated administrations in humans.

In angina pectoris, diltiazem is usually prescribed as two 60 mg tablets in the morning and two 60 mg tablets in the evening. In the course of the pharmaceutical development of this drug, it was therefore planned to study an experimental formulation containing 120 mg of diltiazem. On the basis of dissolution tests in vitro, a bioavailability study was initiated to compare the 120 mg experimental formulation to the standard 60 mg tablet. The study was conducted in 12 healthy volunteers who received the 2 treatments (one 120 mg tablet bid for 7 days versus two 60 mg standard tablets bid for 7 days) according to a cross-over design. Blood and urine samples were analysed by HPLC method with a UV spectrophotometric detection (sensitivity: 5 ng/ml). Analysis of variance did not show any significant difference between the two formulations for the following parameters: maximum plasma levels observed at steady-state, area under the curves and unchanged urinary diltiazem. From these results the extent of absorption of the 120 mg experimental formulation can be considered as bioequivalent to the administration of 2 tablets of the 60 mg commercially available diltiazem formulation. The time to peak, however, was delayed in 75% of the subjects with the 120 mg diltiazem tablet, showing that the surface area of the pharmaceutical preparation is of primary importance for drug dissolution and rate of absorption.

Angina Pectoris↗
PubMed1987

A study of the action of clonidine on secretion from the adrenal medulla in dogs.

The effects of clonidine on adrenal catecholamine (adrenaline and noradrenaline) secretion were investigated in chloralose-anaesthetized dogs. Intravenous administration of clonidine (10 and 20 micrograms kg-1) induced a decrease in both adrenal catecholamine secretion rates and cardiovascular parameters (blood pressure and heart rate). In contrast, a dose of 5 micrograms kg-1 was ineffective. Intracisternal clonidine (in a lower dose of 3 micrograms kg-1) also decreased adrenaline and noradrenaline release from the adrenal gland. Clonidine failed to modify adrenal catecholamine release evoked by electrical stimulation of the splanchnic nerve. These results demonstrate that clonidine decreases adrenaline release from the adrenal gland through a central and not a peripheral mechanism in dogs. This action might contribute to its antihypertensive effects.

Adrenal Medulla↗
PubMed1987

Experimental and clinical approaches to treatment of hypertension by dopamine receptor agonists.

The action of several dopamine agonists on blood pressure was investigated. In dogs, apomorphine induced a decrease in blood pressure and an increase in heart rate. These effects were suppressed by intravenous haloperidol or phentolamine. Intravenous but not intracisternal domperidone suppressed the hypotensive responses elicited by intravenous or intracisternal apomorphine. Furthermore, the hypotensive effect of bromocriptine or apomorphine was abolished in adrenal demedullated dogs. Apomorphine and bromocriptine decreased adrenal catecholamine levels. In men, the acute hypotensive property of apomorphine (but not the long term effect of bromocriptine) was suppressed by pretreatment with domperidone. In hypertensive Parkinsonians, bromocriptine reduced blood pressure, induced an increase in inulin clearance, a decrease in plasma creatinine concentration and in renal vascular resistances. These results suggest that dopamine agonists (like apomorphine or bromocriptine) reduce blood pressure through both a decrease in sympathetic tone and an improvement in renal function. However, the mechanism of the acute and long term hypotensive effects could be different only involving peripheral mechanisms after acute administration and both peripheral and central structure under chronic treatment. In addition, preliminary results suggesting the potential interest of dopamine antagonists in the management of orthostatic hypotension are discussed.

Dopamine↗
PubMed1987

Involvement of cholinergic mechanisms in the central cardiovascular actions of nicardipine in dogs.

The involvement of cholinergic mechanisms in the central cardiovascular effects of a dihydropyridine, nicardipine, was investigated in pentobarbital-anaesthetized normotensive dogs. Nicardipine (1 microgram/kg) injected intracisternally (i.c.) induced a rise in both blood pressure and heart rate. This induced hypertension was suppressed by pretreatment with intravenous (i.v.) atropine or i.c. methylatropine but not i.v. methylatropine. I.c. methylatropine reduced nicardipine-induced tachycardia. These results demonstrate the involvement of cholinergic pathways in the central cardiovascular effects of i.c. nicardipine in dogs and suggest a functional interaction between dihydropyridine binding sites and cardiovascular cholinergic mechanisms in the brain.

Animals↗
PubMed1986

Long term therapy by captopril in children with renal hypertension.

We report on 29 treatment courses in 25 children aged 1.5-18 years who received captopril because of severe renal hypertension. The mean initial dosage was 1.3 (0.5 to 3) mg/kg/day and the mean sustaining dose 2.2 mg/kg/day. The treatment was followed for 2-40 (mean 15) months. We observed a lowering of both systolic and diastolic blood pressure (BP) from 26% at the 2nd day to 65% at the 6th month. The isolated use of captopril was ineffective in 13% of cases, but blood pressure dropped in all of them after addition of beta blocking agents. No clear-cut relation was found between response of blood pressure and etiology, degree of HT or plasma renin activity (PRA). No side effects occurred during treatment except for one case of reversible acute renal failure in a transplanted patient with renal artery stenosis.

Acute Kidney Injury↗