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After 6 months of treatment, the density of hair on the scalp increased in all patients. The vellus hair was replaced by terminal hair. Hair regrowth was evaluated both from the clinical and trichoscopic point of view.
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Different drugs from various pharmacological classes were compared for their ability to protect against the nasal effects of acute allergen challenge in a guinea pig model. In the model, sneezing and nose rubbing were recorded after an initial allergen challenge in guinea pigs previously sensitized to egg albumin. Four days later the same guinea pigs were re-challenged a second time when anesthetised. In these anaesthetized animals, nasal airway pressure, pulmonary inflation pressure and cellular infiltration into nasal lavage fluid were measured. The drug tested were autacoid antagonists (mepyramine--3mg/kg, cetirizine--3mg/kg and montelukast--10mg/kg), L-NAME (10 or 20mg/kg), heparin (20mg/kg) and dexamethasone (20mg/kg) given either intraperitoneally or intravenously; all were given shortly before challenge. Sneezing induced by allergen challenge was statistically significantly reduced by mepyramine, cetirizine and dexamethasone whereas only cetirizine reduced nose rubbing. Changes in nasal airway pressure due to allergen exposure were reduced by cetirizine, montelukast, L-NAME, and heparin, but not by mepyramine, nor dexamethasone. In the presence of L-NAME, nasal airway pressure actually changed in the opposite direction. Cellular infiltration, as assessed by cytometry in nasal lavage fluid 60min after acute allergen challenge, was reduced by montelukast and heparin but not by antihistamines, L-NAME nor dexamethasone. This pattern of effects of the drugs, given by doses and routes previously described in the literature as being effective was not completely consistent with expected responses. The lack of effect of dexamethasone probably reflects the fact that it was given acutely whereas in the clinic chronic administration is used. The two antihistamines were not identical in their actions, presumably reflecting the fact that cetirizine has therapeutic actions not entirely confined to blockade of H1 receptors. Montelukast has not been reported to have major effects on sneezing and itching in the clinic but reduces nasal obstruction (lower nasal airway pressure or nasal patency). Montelukast's effects on cellular infiltration indicate the possible involvement of leukotrienes. Heparin has actions on inflammatory cell infiltration. This could explain its profile of reducing both cellular infiltration, and increased nasal airway pressure.
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To assess and compare the efficacy and safety of bilastine 20 mg vs. cetirizine 10 mg and placebo in relieving the symptoms of seasonal allergic rhinitis (SAR).
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A controlled-release formulation of an antihistamine, cetirizine, was synthesized using zinc-layered hydroxide as the host and cetirizine as the guest. The resulting well-ordered nanolayered structure, a cetirizine nanocomposite "CETN," had a basal spacing of 33.9 Å, averaged from six harmonics observed from X-ray diffraction. The guest, cetirizine, was arranged in a horizontal bilayer between the zinc-layered hydroxide (ZLH) inorganic interlayers. Fourier transform infrared spectroscopy studies indicated that the intercalation takes place without major change in the structure of the guest and that the thermal stability of the guest in the nanocomposites is markedly enhanced. The loading of the guest in the nanocomposites was estimated to be about 49.4% (w/w). The release study showed that about 96% of the guest could be released in 80 hours by phosphate buffer solution at pH 7.4 compared with about 97% in 73 hours at pH 4.8. It was found that release was governed by pseudo-second order kinetics. Release of histamine from rat basophilic leukemia cells was found to be more sensitive to the intercalated cetirizine in the CETN compared with its free counterpart, with inhibition of 56% and 29%, respectively, at 62.5 ng/mL. The cytotoxicity assay toward Chang liver cells line show the IC₅₀ for CETN and ZLH are 617 and 670 μg/mL, respectively.
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The antigen-induced expression of eotaxin by endothelial cells and the adherence and subsequent migration of eosinophils from the microvasculature to the tissues are rapid events partially under the control of histamine released from degranulating mast cells.
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Symptom scores and drug consumption were significantly lower (P < 0.05) in the cetrizine-treated group versus the placebo group. The greatest reductions were in cetirizine itself, inhaled corticosteroids, beta2-agonists, and antibiotics. No side effects were reported in either group.
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Thirty patients with refractory CIU were enrolled in the trial. After informed consent was obtained, patients were randomly assigned to 2 groups. The patients in group A received 10 mg/d montelukast and a nonsedating H(1) antihistamine (cetirizine) when needed for 6 weeks. After a 2-week washout period, they received placebo for 6 weeks and the same H(1) antihistamine as needed. Group B received the treatment vice versa. Improvement was monitored by using the self-estimated urticaria activity score, which is the sum of the wheal number score and the itch severity score, and the antihistamine counts used in each study period.
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Eighteen individuals completed a randomized, double-masked study. Participants were evaluated in a CAE (a chamber that regulates humidity, temperature, airflow, and visual tasking) at baseline and after taking 10 mg of either loratadine or cetirizine hydrochloride daily for 4 days. Keratitis, conjunctival staining, and tear film break-up time (TFBUT) were examined before and after a 45-minute CAE exposure. Participant-reported ocular discomfort was recorded every 5 minutes during CAE challenge.
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Levocetirizine has high bioavailability, high affinity for and occupancy of the H1 receptor, rapid onset of action, limited distribution and minimal hepatic metabolism. Clinical trials indicate that it is safe and effective for the treatment of allergic rhinitis and chronic idiopathic urticaria in adults and children with a minimal number of untoward effects. It is also becoming clearer that, in addition to its being a potent antihistamine, levocetirizine has several anti-inflammatory effects that are observed at clinically relevant concentrations that may enhance its therapeutic benefit. Furthermore, there appears to be a growing trend for the use of levocetirizine as long-term therapy in addition to it being used as a treatment for the immediate short-term manifestations of allergic disease.
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24 patients with CU underwent autologous plasma skin test (APST) as well as SPT with histamine 10 mg/ml while taking antihistamines. In 6 cases the same tests had been carried out also before the start of antihistamine treatment. Plasma levels of D-dimer, prothrombin F 1+2 fragment, and vascular endothelial growth factor (VEGF) were measured in 21 patients.
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To assess the efficacy and safety of oral cyclosporin A (CsA) in CIU.
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These findings suggest that one anti-allergic mechanism of cetirizine may inhibit mediator release which is, at least partially, mediated by a decrease in the transient Ca2+ influx in mast cells.
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The primary objective of the present study was to compare the absorption and disposition of levocetirizine, the eutomer of cetirizine, when administered alone (10 mg) or in presence of the distomer. An additional objective was also to investigate the configurational stability of levocetirizine in vivo in humans. The study was performed in a randomized, two-way cross-over, single-dose design with a wash-out phase of 7 days between the two periods. A total of 12 healthy male and 12 healthy female volunteers were included in the study. Bioequivalence can be concluded from the analysis of the pharmacokinetic parameters of levocetirizine when administered alone or as the racemate cetirizine. No chiral inversion occurs in humans when levocetirizine is administered, i.e. there is no formation of the distomer. When comparing the pharmacokinetic characteristics of levocetirizine and the distomer, the apparent volume of distribution of the eutomer is significantly smaller than that of the distomer (0.41 and 0.60 L/kg, respectively). For an H1-antagonist a small distribution volume can be considered as a positive aspect, both in terms of efficacy and safety. Moreover the non-renal clearance of levocetirizine is also significantly lower than that of the distomer (9.70 and 28.70 mL/min, respectively), which constitutes an additional positive aspect particularly as far as metabolism-based drug interactions are concerned. The information collected in the present study on the pharmacokinetics of levocetirizine and the distomer provide additional reasons for eliminating the distomer and developing levocetirizine as an improvement on cetirizine.
The investigation was carried out in six healthy volunteers, and the effects of the drug (5, 10, and 15 mg) were studied on sleep latency, subjective sleepiness, digit symbol substitution, tracking and vigilance from 0.5 h to 7.5 h after ingestion. The study was placebo-controlled and double-blind with a six-way cross-over design. Promethazine (10 mg) was used as an active control to establish the sensitivity of the experimental procedures.
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The mean UAS decreased to 0.10 in the levocetirizine group and to 0.38 in the rupatadine group. Patients in the levocetirizine group showed a more significant (P < 0.001) improvement, although symptoms improved in both groups. Significant reductions in mean DLQI scores were observed in both groups, but the decrease was statistically significant in the levocetirizine group (P < 0.05). Somnolence was the most common side effect in both groups. Patients in the levocetirizine group showed more psychomotor impairment based on the CFFT test. Findings on the VAS showed sedative effects in both groups (P < 0.05).
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A 32-week randomized, double-blind, placebo-controlled, crossover study was performed in 2 arms: 20 patients received montelukast 10 mg/d and/or desloratadine 5 mg/d or placebo; 20 patients received montelukast 10 mg/d and/or levocetirizine 5 mg/d or placebo. The treatment periods were separated by 2-week washout periods. Quality of life was assessed on the day before starting treatment and on the last day of each treatment period using the Rhinoconjunctivitis Quality of Life Questionnaire. Sleep problems were also assessed.
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Allergic rhinitis affects 20 million of people in United States and a higher figure all around the world.
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This first study with levocetirizine in children aged 12-24 months shows the adequate pharmacokinetic/pharmacodynamic profile and the good safety profile of 0.125 mg/kg levocetirizine given twice a day, which can be proposed for further studies in this age group.
Weal formation in human skin may be induced by histamine, histamine releasers and other inflammatory mediators. Weals occur spontaneously in chronic urticaria, and in response to frictional pressure in dermographic urticaria. We present an improved method for the analysis of wealing in human skin by the use of non-linear regression. The method has the advantage of speed, and by the use of non-linear regression permits the full characterization of the response curves. The time course of histamine-induced wealing is a double exponential function corresponding to the separate components of weal appearance and disappearance. Dermographic wealing corresponds to an increasing exponential function with increasing pressure. The method of computerized non-linear regression is a considerable advance on previous methods for the analysis of urticarial wealing, the effect of vasoactive agents, and their therapeutic action.
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The administration of histamine with iontophoresis is an alternative method to skin prick tests or intradermal injections. Skin reactions obtained with this method can be recorded with laser Doppler flowmetry (LDF) and previous studies with this method have shown histamine-induced laser Doppler changes in the wheal area.
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Formalin injected in the knee joint of rats produces concentration-dependent nociception, edema, and plasma leakage (PL). Herein, we investigated the effect of histamine H1 receptor (H1R) antagonists in this model. Articular nociception was inferred from the paw elevation time (PET; seconds) during 1-minute periods of stimulated walking, determined every 5 minutes, throughout a 60-minute experimental session. Edema was evaluated by the increase in articular diameter (AD; mm), and PL was measured by the amount of Evans blue dye in the synovial fluid (PL; μg/mL). Loratadine and cetirizine, given systemically, both increased the PET. None of the treatments changed the AD and PL. Loratadine given locally with formalin increased the PET but was without effect when given in the contralateral knee. Systemic loratadine was also without effect when formalin was coinjected with sodium cromoglycate. Histamine and the selective H1R agonist 2-pyridylethylamine decreased the PET and potentiated morphine spinal analgesia, but did not affect the AD and PL. Cetirizine prevented the antinociceptive effect of the H1R agonist. The N-methyl-D-aspartate/histamine-site agonist tele-methylhistamine coinjected with formalin only increased PET. Serotonin alone had no effect on the PET and increased the AD, and the highest dose increased the PL. When coinjected with formalin, serotonin only caused hypernociception, and the highest dose also increased AD. NAN 190, cyproheptadine, and ondansetron (respectively, 5-HT1, 5-HT2, and 5-HT3 receptor antagonists) decreased the PET without changing the AD or PL. Collectively, these results suggest that in rats, the H1R plays an antinociceptive role within the knee joint, while serotonin receptors play a pronociceptive role.
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Concomitant administration of an H1-receptor antagonist with an H2-receptor antagonist may enhance the wheal and flare suppression produced by the H1-antagonist. This synergism may be due, at least in part, to a pharmacokinetic effect.
Scores on SF-36 questionnaire and clinical global impression scale.
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A liposome formulation of cetirizine-dinitrate (2.44 mg per nasal cavity) was delivered via a nasal spray device as 2 consecutive actuations per nasal cavity in a placebo-controlled design. The nasal mucosal surface was challenged and lavaged with a histamine solution (100 microg/mL) 5, 15, 25, and 55 minutes after each treatment. In addition, the mucosa was lavaged with saline before each treatment. The lavage fluid levels of alpha2-macroglobulin were measured as an index of mucosal exudation (luminal entry) of plasma.
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In a double-blind study performed in 81 healthy volunteers, 10 mg cetirizine and 60 mg terfenadine given orally in a single administration significantly inhibited skin reactivity to histamine. Astemizole (10 mg) was completely ineffective. The inhibitory effect of cetirizine was potent and regular whereas 6/28 (21%) volunteers did not respond to terfenadine. The difference observed between cetirizine and terfenadine might be due to differences in the metabolism of the two drugs after administration: terfenadine is rapidly and extensively metabolized whereas cetirizine is directly active without the need for biotransformation and, indeed is poorly metabolized.
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As mite allergy is characterized by a continuous allergen exposure, persistent inflammation is always detectable even during symptomless periods. It has been reported that mite allergic patients present a nonspecific hyperreactivity to different stimuli, including hyperosmolar solution. Since it has been reported previously that cetirizine is able to reduce minimal persistent inflammation due to mite allergy, the aim of the study was to investigate the effect of cetirizine on nonspecific conjunctival hyperreactivity. Twenty children with mite allergy were studied; two hyperosmolar conjunctival challenges were performed before and after cetirizine or placebo treatment, lasting one week. Patients treated with cetirizine showed a significant reduction in nonspecific conjunctival hyperreactivity compared to the placebo group (p < 0.05). In conclusion, cetirizine was able to reduce nonspecific hyperreactivity related to allergic inflammation.
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Desloratadine, acting through the histamine H1 receptor, inhibited basal NF-kappaB activity and can thus be classified as an inverse agonist. Inhibition of basal and histamine-stimulated NF-kappaB activity may help to explain previously reported inhibitory effects of desloratadine on allergic inflammatory mediators.
Protease-activated receptor-2 (PAR2) has been shown to play a key role in the pathophysiology of itch. However, the precise mechanism of PAR2-mediated itch remains largely unknown. In the present study, we investigated the effects of several agents on the scratching behavior induced by PAR2-activating peptide (SLIGRL-NH2). Pretreatment of experimental animals with tacrolimus or the 5-lipoxygenase inhibitor zileuton significantly reduced SLIGRL-NH2-induced scratching behavior, whereas histamine H(1) receptor antagonist cetirizine or the cyclooxygenase inhibitor indomethacin had little effect. Furthermore, intradermal injection of SLIGRL-NH2 increased cutaneous levels of LTB(4) and PGE(2). In vitro, SLIGRL-NH2 treatment enhanced LTB(4) and PGE(2) release from primary keratinocytes in a concentration-dependent manner. Preincubation of keratinocytes with zileuton resulted in a significant decrease of LTB(4) release and treatment of indomethacin led to a significant decrease of PGE(2) in response to SLIGRL-NH2 stimulation. In addition, SLIGRL-NH2-induced secretion of LTB(4) and PGE(2) was significantly inhibited by tacrolimus, whereas cetirizine had no effect. These results indicate that SLIGRL-NH2 stimulates LTB(4) and PGE(2) release from mouse keratinocytes and that enhancement of LTB(4) and PGE(2) secretion contributes to SLIGRL-NH2-induced scratching behavior in ICR mice.