Accordingly, we studied relationships between the ability to eliminate S. aureus during an anti-inflammatory treatment and selected clinical and immunological features.
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Forty-eight patients, ASA II-III, underwent surgical carotid endarterectomy. The anesthetic protocol began with preoxygenation for 2 min; induction with remifentanil 0.75-1 microgram kg-1 for 2 min., followed by perfusion of 1 microgram/kg-1.min-1 of remifentanil and propofol 1 microgram/kg-1; and orotracheal intubation by local anesthesia of the glottis with 5% lidocaine spray. Ventilation was with FiO2 100%, FR 12 min. and VT 8 ml. kg-1. For maintenance the dose of remifentanil was regulated to obtain a coordinated motor response (maximum 1.5 microgram/kg-1.min-1, minimum 0.35 microgram/kg-1. min-1). For all patients we monitored hemodynamics continuously and non-invasively, including aortic output by the transesophageal Doppler echocardiography.
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Recent reports have indicated cetirizine, a potent H(1)-receptor antagonist, to possess a number of anti-inflammatory effects, e.g. inhibition of mast cell degranulation and inhibition of leucocyte migration and activation.
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Twenty-two patients with seasonal allergic rhinitis were enrolled in a placebo controlled crossover study comparing 2 weeks therapy of either (a) 200 microg intranasal mometasone furoate (MF) once daily or (b) 10 mg oral montelukast plus 10 mg oral cetirizine once daily (MON/CZ), with a 7-10 day placebo period prior to each treatment period. Domiciliary measures of symptoms and nasal flow were recorded daily. Measurements of posterior rhinomanometry, acoustic rhinometry and nasal nitric oxide were made after all treatment and placebo periods.
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The objective of this study was to define the nature, magnitude, and mechanisms of histamine-induced leukocyte-endothelial cell interactions in postcapillary venules of the rat mesentery using intravital microscopic techniques. Superfusion of the mesentery with histamine (10(-7)-10(-5) M) resulted in a dose-related increase in the number of rolling leukocytes, a reduction in rolling velocity, and an increased clearance of FITC-labeled rat albumin from blood to superfusate. The histamine-induced recruitment of rolling leukocytes and increased albumin clearance were prevented by histamine H1 (hydroxyzine, diphenhydramine) but not H2 (cimetidine) receptor antagonists. Because histamine induces expression of the adhesion molecule P-selectin in cultured endothelial cells, a monoclonal antibody directed against rat P-selectin and soluble sialyl-LewisX oligosaccharide (the carbohydrate ligand to P-selectin) were also tested as inhibitors. Both were effective in preventing the histamine-induced recruitment of rolling leukocytes, but neither agent attenuated the increased albumin clearance. These observations suggest that (a) histamine recruits rolling leukocytes and increases albumin leakage in postcapillary venules via H1 receptor activation, (b) histamine-induced recruitment of rolling leukocytes is mediated in part by P-selectin expressed on the endothelial cell surface, and (c) the histamine-induced vascular albumin leakage is unrelated to leukocyte-endothelial cell adhesion. Our results are consistent with the view that histamine may act as a mediator of acute inflammatory reactions.
Desloratadine and levocetirizine treatment induced significant symptom relief and significant reduction of IL-4. Both antihistamines significantly affected all parameters in comparison with placebo.
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A series of N1-(substituted)aryl-5,7-dimethyl-2-(substituted)pyrido(2,3-d)pyrimidin-4(3H)-one was designed on the basis of the triangular pharmacophoric requirement of histamine H1-receptor antagonists. The designed series was synthesized by cyclo-condensation of monoaryl thiourea with ethyl cyanoacetate in the presence of dry HCl gas to give N1-(substituted aryl)-2-mercaptopyrimidine-4(3H)-one, which on cyclo-condensation with acetylacetone gave the pyridopyrimidinone. Further methylation of the mercapto group at C-2 with methyl iodide followed by nucleophilic displacement of the methylmercapto group by various amines gave the targeted compounds. All the synthesized compounds were screened for histamine H1-receptor antagonistic activity by the in vitro method of inhibition of the isotonic contraction induced by histamine on isolated guinea pig ileum using cetirizine as a standard drug. All the compounds exhibited potent histamine H1-receptor antagonistic activity with pA2 values from 7.30- 9.75 (cetirizine, pA2 value 9.40). The potent compounds were screened for their in vivo antihistaminic activity by protection of animal from asphyxic shock. The sedative potential of potent compounds was checked on albino mice by photoactometer and they had comparative sedative potential to the standard drug cetirizine. None of the compound exhibited anticholinergic activity in the in vitro rat ileum model.
Bilastine had a rapid onset of action, within 1 h, and a long duration of action, greater than 26 h. Cetirizine was similar. Fexofenadine was similar on day 1 but less effective on day 2, indicating a shorter duration of action. Bilastine, like cetirizine and fexofenadine, was safe and well tolerated in this study.
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Recent pathophysiologic research demonstrated the crucial role played by adhesion molecules in recruiting and activating inflammatory cells during allergic reaction.
Observations of torsades de pointes during therapy with terfenadine and astemizole has raised concern about the cardiac safety of non-sedating H1-antagonist agents. We compared cetirizine, another compound of that class, to D-sotalol and to astemizole in a model of acquired long QT syndrome. Open-chest surgery was performed in adult beagle dogs anaesthetized with halothane and thiopental. Bradycardia was produced with beta-adrenergic blockade and sinus node crush. Four left ventricular intramyocardial unipolar monophasic action potentials (MAP) were recorded during atrial pacing at basic cycle lengths (BCL) 400-1500 msec, before and during three successive 1-h drug infusions (0.14, 0.45 and 1.4 mg/kg/h for astemizole and cetirizine and 1.1, 2.2 and 4.5 mg/kg/h for D-sotalol). Dose- and bradycardia-dependent prolongations of MAP duration (MAPD) were produced by D-sotalol (P < 0.001) and astemizole (P < 0.001) but not by cetirizine. At BCL 1500 ms, the three infusions of astemizole prolonged endocardial MAPD from 323 +/- 8 msec (mean +/- SE) at baseline to 343 +/- 10, 379 +/- 13 and 468 +/- 26 msec, respectively (n = 9). Sotalol prolonged that MAPD from 339 +/- 6 msec to 377 +/- 7, 444 +/- 15 and 485 +/- 24 msec (n = 7). In contrast, cetirizine did not prolong MAPD: 341 +/- 8 msec at baseline Vs 330 +/- 8, 324 +/- 9 and 323 +/- 11 msec (n = 9). Drug-induced increase in transmural dispersion reached +79 +/- 19 msec after astemizole, +59 +/- 21 msec after D-sotalol and only +7 +/- 11 msec after cetirizine. Runs of ventricular tachycardias and torsades de pointes occurred during dose three of astemizole (5/9 dogs) and D-sotalol (4/7 dogs) but never during cetirizine. In the present model, astemizole and D-sotalol but not cetirizine prolonged MAPD and transmural dispersions of repolarization and produced torsades de pointes. These results suggest that the halothane-anaesthetized bradycardic dog could be a valuable model to discriminate drugs for their class III effects and proarrhythmic potencies.
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The pharmacokinetics and pharmacodynamics of medications may differ between children and adults, necessitating different dose regimens for different age groups. Levocetirizine, the active enantiomer of cetirizine, is used in the treatment of allergic rhinitis and chronic urticaria in Europe. Its pharmacokinetics and pharmacodynamics have not yet been studied prospectively in school-age children.
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Of the 311 patients randomized to treatment, 283 completed the study. Cetirizine produced a marked improvement in symptoms scores compared with placebo after 1 week of therapy (P = .001). By the end of week 1, total symptom complex scores were improved by 37% with cetirizine compared with 29% for terfenadine, and 23% for placebo. An overall treatment effect was evident at week 1 (P = .0019), with marked differences between cetirizine and both placebo (P = .0004) and terfenadine (P = .0464) but not between terfenadine and placebo (P = .1215). A more marked treatment effect was evident during the first week of the study; this appeared to be related to spontaneous resolution of symptoms, since mean pollen counts derived for each patient declined significantly each week of the study. Therapy was generally well tolerated. Headache was the most common side effect in each group. Four patients on cetirizine, one on terfenadine, and two on placebo withdrew because of side effects. Somnolence was reported in 12 patients on cetirizine (P < .05), 2 on terfenadine, and 3 on placebo.
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Eighty participants, comprising doctors, nurses, pharmacists, technicians and lay people, completed a battery of laboratory tests assessing visual perception, auditory perception and short-term memory of look-alike and sound-alike drug name pairs (eg, hydroxyzine/hydralazine).
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Anxiolytic effect of agents and of pre-operative visit. Time interval between premedication and induction of anaesthesia. Blood pressure, heart rate, respiratory rate, other signs of autonomic hyperactivity (restlessness, tremors, sweating).
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Chronic idiopathic urticaria, daily hives that last >6 weeks, can be resistant to antihistamines, even when higher than conventional doses are used. Other pharmacologic agents have been associated with inconsistent benefit.
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The term "chronic idiopathic urticaria" denotes a spectrum of conditions with different poorly understood pathogenetic mechanisms in which the release of histamine plays a role. Nonsedating second-generation H1 antihistamines are postulated to be the first line of treatment of chronic idiopathic urticaria by national and international guidelines, but as control is not always achievable with the usually recommended doses, first-generation sedating antihistamines like hydroxyzine and diphenhydramine at high daily doses (200 mg) have been proposed as an alternative before resorting to treatment with systemic corticosteroids and other potentially hazardous agents. Our long time experience and recent research give us grounds to believe that increasing the doses of nonsedating H1 antihistamines up to fourfold improves significantly the chances of successful treatment. Our data suggest that the urticaria-associated discomfort is relieved by higher than conventional doses of levocetirizine and desloratadine in about 75% of the patients and that sedation/somnolence does not seem to be a major deterrent. The dose increase also improves the urticaria-specific quality of life. Contrary to the belief that individual patients may benefit from one antihistamine or another, we demonstrate that the drug with better ability to suppress the histamine skin effects in experiments in healthy volunteers (levocetirizine) is also superior in improving the different aspects of control of chronic urticaria (subjective and objective symptoms, quality of life) and that increasing its dose of up to fourfold may even paradoxically reduce the sense of sedation/somnolence in parallel with the relief of urticaria discomfort.
This is an update of the original Cochrane review published in 2013 (Issue 6). Pruritus occurs in patients with disparate underlying diseases and is caused by different pathologic mechanisms. In palliative care patients, pruritus is not the most prevalent but is one of the most puzzling symptoms. It can cause considerable discomfort and affects patients' quality of life.
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The effect of 2-[2-[4-(diphenylmethyl)-1-piperadinyl]ethoxy] benzoic acid maleate (ZCR-2060) on passive systemic anaphylaxis (PSA) and antigen-induced immediate- and late-phase increase in airway resistance (Rrs) in either passively or actively sensitized guinea pigs were investigated. ZCR-2060 inhibited PSA in guinea pigs. ID50 values of ZCR-2060, ketotifen, terfenadine and cetirizine on PSA were 0.03, 0.02, 0.8 and 0.3 mg/kg, respectively, when administered orally 1 h before the antigen challenge. The protective effect of ZCR-2060 was observed until 12 h before the antigen challenge. Aeroantigen-induce immediate increase in Rrs in passively sensitized guinea pigs with and without metyrapone treatment was inhibited by ZCR-2060, ketotifen, terfenadine and cetirizine. In contrast, prednisolone did not affect the aeroantigen-induced immediate increase in Rrs in animals not treated with metyrapone, but significantly inhibited the metyrapone-induced enhanced immediate response. In actively sensitized animals, the immediate- and late-phase increases in Rrs were observed within 30 min and between 3 and 8 h after the aeroantigen challenge. Pretreatment with metyrapone accelerated both antigen-induced responses. ZCR-2060 (1 mg/kg) significantly inhibited both responses. Ketotifen (1 mg/kg), terfenadine (10 mg/kg) and prednisolone (10 mg/kg) significantly the inhibited the late-phase response, but did not affect the immediate-phase response. In contrast, Cetirizine (10 mg/kg) did not affect either response. The effect of ZCR-2060 on late-phase response was stronger than that of ketotifen, terfenadine and cetirizine, and was almost the same as that of prednisolone. These results suggest that ZCR-2060 has a potent protective effect on immediate- and late-phase increases in Rrs.
The abortifacient effect of an initial PGF2alpha impact was examined in 10 obstetrically normal first trimester pregnant patients. Sedated patients were given extraamniotically an average initial dose of 8.1 + or - 0.8 mg PGF2alpha during a 10 minute instillation. Side effects occurred occasionally but were minimal. Uterine contracture developed rapidly reaching an average pressure of 83.2 + or - 11.3mm Hg in about 20 minutes and then slightly declined in time. Superimposed on the contracture response were gradually increasing cyclic changes in intrauterine pressure which reached a magnitude of 129.8 + or - 12.2mm Hg by 10 hours after initial treatment. Initial therapy was augmented in some cases by an average of 4mg PGF2alpha; only 4 patients required oxytocin supportive therapy. The patients aborted in an average of 10.9 + or - 2.0 hours. 7 aborted completely, 2 left behind small placental residues, and 1 retained the placenta during a period of 11.5 hours. An (AbS) abortion score of 92 was obtained in the study which is the highest in 6 consecutive studies using various methods of PGF2alpha administration. Plasma estradiol-17beta and progesterone levels decreased continuously during the instillation abortion time in the complete aborters, while the incomplete aborters showed lesser changes. It is concluded that massive intrauterine PGF2alpha injection is a more efficacious and acceptable form of postconceptional therapy than protracted treatment. Such therapy appears to convert the refractory uterus into a spontaneously active and pharmacologiclly reactive organ by inducing vasoconstriction, myometrial stretch, and fetoplacental insufficiency.
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This is a cross-sectional study that included 451 nursing homes across France. Information about the medications received by the 30,702 residents (73.8% women) living in these nursing homes was extracted from the system that assists in the preparation of pill dispensers in pharmacies. The anonymized database included age, sex, and medications prescribed to residents, as well as nursing home characteristics (capacity, legal status). Factors associated with excessive polypharmacy (≥10 different drugs) and PIMs according to the Laroche list were studied using multilevel regression models.
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The bronchial resistances in 17 patients scheduled for ENT surgery were studied during general anaesthesia carried out with propofol and alfentanil. There were nine controls, all free from any allergic pathology. The other eight had bronchial hyperreactivity, with clinical asthma (one or two crises a month) treated with bronchodilators. Two had a complete Fernand-Widal syndrome, and the remaining six documented allergic asthma. All the patients were premedicated with hydroxyzine 2 mg.kg-1 orally on the eve of surgery, and two hours beforehand. Those patients who were on bronchodilators were given their drugs as usual with the premedication. Because bronchial resistances were measured with the patient breathing spontaneously (forced oscillation technique), induction was carried out in two steps, first with propofol 1.5 mg.kg-1, followed, two minutes later, by alfentanil 7 micrograms.kg-1. Once the bronchial resistances had been assessed the patient was given a further 2 mg.kg-1 dose of propofol, and alfentanil 40 micrograms.kg-1. The patient was then intubated, and anaesthesia maintained with propofol 9 mg.kg-1.h-1, and alfentanil 15 micrograms.kg-1 every fifteen minutes. In all, bronchial resistances were measured on the day before surgery, after premedication but before the patient had been given any anaesthetic drug, two minutes after the first injection of propofol, two minutes after the first injection of alfentanil, and after extubation. There were no significant differences between the two groups. Despite the small number of patients included in this study, it would seem that hydroxyzine, propofol and alfentanil may be used safely in patients with hyperreactive bronchi.