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Desloratadine appears to be a "me-too" agent, with no major differences compared with other second-generation antihistamines.
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The mean blocking duration on cutaneous reactivity for loratadine was 6.9 days and for terfenadine, 7.2 days. The mean duration of the blocking effect on PC20 histamine was 8.5 days for loratadine and 7.2 days for terfenadine. These figures were significantly longer than for the placebo.
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Forty patients with perennial allergic rhinitis were enrolled in the study. There were 25 males and 15 females, aged 50 to 88 years (mean, 64.4-years-old). 17 cases (42.5%) had a history of cardiovascular diseases and/or presented abnormal ECG parameters, but had no prolonged QT-interval. The subjects received loratadine 10 mg once-daily for 30 days. A series of baseline ECG recordings was obtained before treatment. ECG effects of the treatments were then compared with the baseline ECGs.
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24 healthy volunteers (12 men, 12 women; age 19 to 50 years).
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Forty two healthy subjects (aged 22+/-18 years) were randomized into seven groups which received orally: cetirizine 10 mg, loratadine 10 mg, desloratadine 5 mg, levocetirizine 5 mg, fexofenadne 120 mg and 180 mg, or placebo respectively. The skin microcirculation reaction after 10 mg/ml histamine administration was estimated visually on the forearm (diameter of wheal and flare) and by Laser Doppler flowmetry before and after study drug or placebo administration prior and, 2, 4, 6, 8, 10, 12, 18, 24 h and one time daily every next 9 days.
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As-needed intranasal corticosteroids reduce allergic inflammation and are more effective than as-needed H(1) receptor antagonists in the treatment of seasonal allergic rhinitis.
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We carried out a cohort study with a nested case-control analysis using the UK-based General Practice Research database (GPRD). The study cohort included persons aged less than 80 years old who received their first prescription for any of the five study drugs between January 1, 1992 and September 30, 1996. We estimated relative risks and 95% confidence intervals of idiopathic ventricular arrhythmias with current use of antihistamines as compared with non use.
After an initial challenge with methacholine chloride, subjects received treatment with placebo, loratadine (10 mg by mouth daily), or terfenadine (60 mg by mouth twice daily) for 1 week, followed by a nasal allergen challenge with lavages; 24 hours later, while the subjects were still receiving medication, the quantity of cells in the nasal lavage was determined, and another challenge with methacholine was done. Mediator levels were quantified in the nasal lavages after the allergen c hallenge, and the weight of the methacholine-induced nasal secretions was measured.
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Montelukast alone, levocetirizine alone, desloratadine alone, and the montelukast/antihistamine combinations significantly improved nasal symptoms during the first 24 hours. Improvement gradually increased during the 6 weeks of treatment, especially in patients receiving montelukast alone or in combination therapy with the antihistamine in both arms. Improvement at 42 days of treatment was significantly greater than that achieved on the 1st day of therapy in patients treated with the combination of montelukast and levocetirizine.
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It was the aim of this study to characterize the effects of histamine receptor blockade in severe bacterial infections in more detail.
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To establish a sensitive and specific liquid chromatography-mass spectrometry (time-of-flight) [LC-MS (TOF)] method for the determination of donepezil in human plasma after an oral administration of 5 mg donepezil hydrochloride tablet.
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The early response to inhaled allergen was unchanged after desloratadine therapy and partially inhibited with montelukast therapy. The combination of desloratadine and montelukast provided superior efficacy to either blocker administered alone. Investigations into the possible mechanisms of the enhanced inhibition are necessary.
Azelastine is a potent H(1)-antihistamine, which is available as a topical nasal spray and indicated for both seasonal allergic and non-allergic vasomotor rhinitis. In addition to its antihistaminic effects, it has also been shown to have a number of other potentially important attributes, including effects on cytokines, adhesion molecules and inflammatory cells. Azelastine nasal spray has been shown to benefit patients who have not responded adequately to loratadine and fexofenadine, and is significantly more efficacious than cetirizine and levocabastine in patients with seasonal allergic rhinitis. Given its unique pharmacologic properties and clinical profile, azelastine maintains an important role in the treatment of chronic rhinitis.
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If monotherapy with an intranasal corticosteroid can alleviate both nasal and ocular symptoms of allergic rhinitis, treatment may be simplified and costs may be reduced.
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A total of 720 injections were given (309 injections in 21 patients receiving loratadine and 411 injections in 24 patients receiving placebo). The median numbers of injections to reach maintenance dose were 15 (range, 14 to 18) in the loratadine group and 16 (range, 14 to 23) in the placebo group (p = 0.037). The numbers of patients with systemic reactions were seven (33%) and 19 (79%) in the loratadine and placebo groups, respectively (p = 0.002). Twenty-five reductions caused by systemic reactions were observed in the placebo group in contrast to nine in the loratadine group (p = 0.047). No life-threatening systemic reactions were observed in either group. Systemic reactions were, however, more severe in the placebo group, mainly because of a significantly higher incidence of urticaria (10 vs 1, p = 0.022).
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A new classification of persistent allergic rhinitis (PER) has been developed by the ARIA working group. Although the burden of AR is significant, treatment itself is also costly. It is unclear if treatment based on the new definition of PER is cost-effective.
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Compared to placebo, montelukast/desloratadine conferred improvements (P < 0.05) in adenosine monophosphate (AMP) threshold concentration and mannitol threshold dose: a 3.2-fold (95% CI 2.2-4.6) and 2.4-fold (95% CI 1.7-3.3) difference, respectively, while compared to montelukast this amounted to a 2.0-fold (95% CI 1.2-3.4) and 1.5-fold (95% CI 1.1-2.4) improvement, respectively. Montelukast was not significantly different from placebo. Both montelukast/desloratadine and montelukast compared to placebo, shortened recovery following both challenges (P < 0.05): a 27-min (95% CI 17-37) and 29-min (95% CI 20-36) reduction, respectively, for AMP, and a 27-min (95% CI 17-37) and 26-min (95% CI 17-35) reduction, respectively for mannitol.
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There is no control group for comparisons between the study's online responses and those that would have resulted from another survey methodology. Further, response biases do exist across countries based on cultural norms.
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To compare the efficacy of nasal budesonide plus oral zafirlukast against nasal budesonide plus oral loratadine/pseudoephedrine combination in the control of symptoms of rhinitis and asthma.
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With Ze 339, the patient's time to recovery (5.4 ± 1.6 hours) from nasal obstruction after allergen challenge (time for return to 90% of baseline value ± SEM) was significantly shorter than with placebo (9.1 ± 2.3 hours, P = .035) and desloratadine (10.7 ± 2.5 hours, P = .022). Likewise, Ze 339's standardized symptom assessment for nasal obstruction (3.2 ± 1.3 hours) showed significantly faster relief (time for return to baseline value ± SEM compared with placebo, 8.3 ± 2.4 hours; P = .027) and desloratadine (4.5 ± 1.2 hours, P = .030). One interesting finding was that Ze 339 significantly reduced IL-8 and leukotriene B(4) levels in nasal secretions before challenge.
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A total of 62 healthy Jordanian male volunteers were included in this study. A single 5 mg desloratadine oral tablet was given and blood samples were taken to determine the desloratadine and 3-hydroxydesloratadine (3-OH-desloratadine) concentrations using a specific liquid chromatography-mass spectrometric method (LC/MS/MS). The determination of pharmacokinetic parameters of all the individuals was determined by using Kinetica® program version 4.1. Poor metabolizers or slow metabolizers of desloratadine were determined as individuals having a 3-OH-desloratadine to desloratadine exposure ratio lower than 10% or a desloratadine half-life ≥ 50 h.
Patients with CSU showed varied responses of positive ASST and varied sensitivity to HDM, Patients with positive ASST and/or positive SPT had more disease activity compared with patients with negative ASST and/or negative SPT. Further classification can be made based on the result of SPT and ASST.
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Previous studies have shown that diphenhydramine and desloratadine effectively relieve symptoms of seasonal allergic rhinitis (SAR).
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These findings suggest that a neural reflex or systemic allergic inflammation is responsible for the sinus inflammatory response and that this inflammatory response might play a role in the development of rhinosinusitis in allergic subjects.
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Mean values of eotaxin concentrations in serum during Evaluations 0-3 did not significantly differ in the healthy subjects and the patients with IgE-mediated rhinoconjunctivitis (P > 0.05). Moreover, no statistically significant differences in the serum eotaxin levels between the visits were observed in the patients who received immunotherapy (P > 0.05); however, immediately after immunotherapy (Evaluation 1) the mean serum level of eotaxin was lowest and closest to the serum eotaxin concentration in the control group at the same visit. No significant correlation between the mean value of the serum eotaxin level in the height of pollen season (r = -0.12, P > 0.05) or mean changes of the eotaxin levels between Evaluations 2 and 1 (r = -0.03, P > 0.05), on the one hand, and the cumulative score of symptoms and drug, on the other, were found.
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A previous study showed the inhibitory effects of loratadine on histamine-induced wheal, flare and itch in human skin to be very variable between individuals. It was hypothesised that this variability may have been due to differences in the rates of metabolism of loratadine to its active form, desloratadine. This double blind, crossover study examined the effects of desloratadine in 12 healthy volunteers. Levocetirizine was used as a comparator.
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Sustained vigilance is required by pilots and crew during flight; therefore, the use of antihistamines with sedating properties is widely prohibited. The purpose of this study was to determine the effects of desloratadine, a long-acting, nonsedating antihistamine, on healthy volunteers placed under conditions of simulated cabin pressure.
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Patients with allergic rhinitis and exercise induced broncho-constriction must be treated with either a beta(2)-agonist or LRTA for relief or prophylaxis of their EIB.
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Antihistaminic drugs are widely prescribed across a multitude of medical specialties such as Allergy and Dermatology. The potentially serious sedative effect of these valuable agents has previously restricted their full use and the choice of drug has been dictated more by individual patient acceptability than by any laboratory demonstrations of comparative efficacy. Unsurprisingly therefore, there is a trend towards prescribing those newer preparations which leave the central nervous system unclouded. We have studied the most frequently prescribed non-sedating antihistamine preparations, terfenadine (Triludan, Triludan Forte), cetirizine (Zirtek) and loratadine (Clarityn) in pharmacodynamic and relative efficacy trials using a quantifiable and reproducible extension of the classic Lewis model. The results indicate that two preparations, terfenadine 120 mg (Triludan Forte) and cetirizine 10 mg (Zirtek) are superior to their immediate rivals in degree of efficacy and/or speed of action. These results should assist clinicians in the positioning of effective, rapidly acting antihistamines for the symptomatic treatment of immediate hypersensitivity reactions such as urticaria and rhinitis.
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A combined method was used for a comparative study of some H1 and H2 antagonists and methysergide. In male rats of the Wistar strain weighing 130 +/- 5 g, oedema was induced in the hind paw by the subplantar injection of zymosan, and simultaneously in the ear by the application of croton oil to the inner surface of the ear. Intraperitoneally orally administered H1 antagonists (dimethindene, clemastine, cyproheptadine, astemizole, cetirizine, loratadine and terfenadine) inhibited the oedema to a statistically significant extent, in a dose-dependent manner. Outstanding inhibition was observed after simultaneous administration of the antiserotonin methysergide with dimethindene, clemastine, loratadine or cetirizine.