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Thirty-eight nonasthmatic patients, mean age (SEM) 30 years (1.4), with symptomatic SAR were evaluated in a placebo-controlled, single-blind, double-dummy, three way parallel group study. Patients received oral cetirizine 10 mg once daily and were randomized to receive, in addition, either: (i) intranasal mometasone furoate 200 microgram (n = 14); (ii) oral montelukast 10 mg (n = 11); or (iii) placebo (n = 13). All treatments were given once daily for 4 weeks and were preceded by a 1 week placebo period. Domiciliary diary cards were used to record morning (am) and evening (pm) domiciliary nasal PIFR and symptom (nasal, eye, throat) scores and impact on daily activity. A total daily symptom score was then calculated from the sum of these separate symptom scores.
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Hydroxyzine is the first generation H1 receptor antagonist drug that is now marketed as a racemic mixture. The paper describes a validated enantioselective liquid chromatography method for the resolution of hydroxyzine enantiomers and cyclizine (internal standard) from 200 µL of rabbit plasma by liquid-liquid extraction technique using n-hexane and isopropanol. Hydroxyzine enantiomers were resolved at 10.2 and 11.1 min with good baseline resolution (Rs = 1.9) on a Lux amylose-2 chiral column (250 mm × 4.0 mm, 5 microns) at ambient room temperature. The mobile phase consisted of n-hexane-ethanol-diethylamine (90:10:0.1 v/v/v) pumped at 0.9 mL/min. The eluted enantiomers were detected at 254 nm. The linear calibration curve was constructed in the range 20-1000 ng/mL for both the (S)- and (R)-enantiomers. The intra- and inter-day precision were 0.16-2.6% and 0.2-1.92% for (S)-hydroxyzine and (R)-hydroxyzine, respectively. The method was successfully applied to determine the kinetic parameters of (S)- and (R)-hydroxyzine enantiomers in rabbits. The results illustrate that the disposition of hydroxyzine enantiomers is not stereoselective in rabbits.
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Cetirizine, a peripheral H1 antagonist, was administered to patients with delayed pressure urticaria in a double-blind, placebo-controlled, crossover study. Efficacy in reducing pressure-induced wheals and flares was evaluated. Histologic changes were also assessed with the skin window technique in weight-induced wheals. Results showed a statistically significant reduction in weight-induced wheal area (p less than 0.01) after cetirizine therapy; this improvement was accompanied by a concomitant reduction in eosinophil recruitment as demonstrated by the skin window technique (p = 0.0029). Subsequently, 14 patients with delayed pressure urticaria underwent biopsy before and after 3 weeks of cetirizine therapy to evaluate the drug's histologic effects. A blinded observer performed the histologic studies. Weight-induced lesions showed a mixed inflammatory infiltrate, primarily polymorphonuclear (neutrophils and eosinophils), whereas the unchallenged skin sites were normal. Cell counts from pressure-induced lesions showed a significant reduction in eosinophils after cetirizine treatment.
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There is no consensus on the question of pain induced by injections of botulinum toxin in children. The objective of this study is the evaluation of our practice as well as the resources, which are employed to relieve children, in order to improve a better management of pain.
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H1-antihistamines are widely used to relieve symptoms of allergic disorders. A few skins reactions to H1-antihistamines have been described in the literature. We report the first case of cutaneous drug eruption as fixed drug eruption with 2 antihistamines of the same chemical family: cetirizine and hydroxyzine.
The search for evidence based information and its evaluation for planning the care of a woman with pruritus without visible signs on her skin is exemplified and described in this article. Literature was sought with the key words "itch", "pruritus", and "elderly" in medline, Cinahl and the Cochrane library. Retrieved studies were appraised by the criteria for valid information of evidence based nursing. Most pruritus studies were about pruritus with skin rash or about pruritus connected to liver or renal failure. Randomised controlled trials about the treatment of pruritus were characterised by small sample sizes or were done with only men or women. The little knowledge found in these studies did not help resolve the complex individual situation of the patient. Treatment suggestions from the studies: to assess the causes and exacerbating factors of pruritus; to wash the skin with water only, e.g. without soap; to emulsify the skin with Vaseline or oil at least once daily; to prevent too much heat by covering the patient just enough for him or her to feel no cold; prescribing Atarax, a histamin inhibitor of the first generation at night time; to try the antidepressant drug Doxepin; and emulsification with alcohol, menthol and cool water. There is no evidence to predict results of any one of these suggested interventions. Further research regarding the pathophysiology and the effectiveness of interventions against pruritus is needed.
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Clinical, prospective, open, non comparative trial.
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Combination of duloxetine with hydroxyzine is not beneficial in anxiolytic treatment than the respective monotherapies. There is a need to study the pharmacokinetic drug-drug interactions to understand the present study outcomes.
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In the present study, the effect of the blockade of membrane calcium channels activated by intracellular Ca(2+) store depletion on basal and depolarization-induced [3H]norepinephrine ([3H]NE) release from SH-SY5Y human neuroblastoma cells was examined. The second-generation H(1) receptor blockers astemizole, terfenadine, and loratadine, as well as the first-generation compound hydroxyzine, inhibited [3H]NE release induced by high extracellular K(+) concentration ([K(+)](e)) depolarization in a concentration-dependent manner (the IC(50)s were 2.3, 1.7, 4.8, and 9.4 microM, respectively). In contrast, the more hydrophilic second-generation H(1) receptor blocker cetirizine was completely ineffective (0.1-30 microM). The inhibition of high [K(+)](e)-induced [3H]NE release by H(1) receptor blockers seems to be related to their ability to inhibit Ca(2+) channels activated by Ca(i)(2+) store depletion (SOCs). In fact, astemizole, terfenadine, loratadine, and hydroxyzine, but not cetirizine, displayed a dose-dependent inhibitory action on the increase in intracellular Ca(2+) concentrations ([Ca(2+)](i)) obtained with extracellular Ca(2+) reintroduction after Ca(i)(2+) store depletion with thapsigargin (1 microM), an inhibitor of the sarcoplasmic-endoplasmic reticulum calcium ATPase (SERCA) pump. The rank order of potency for SOC inhibition by these compounds closely correlated with their inhibitory properties on depolarization-induced [3H]NE release from SH-SY5Y human neuroblastoma cells. Nimodipine (1 microM) plus omega-conotoxin (100 nM) did not interfere with the present model for SOC activation. In addition, the inhibition of depolarization-induced [3H]NE release does not seem to be attributable to the blockade of the K(+) currents carried by the K(+) channels encoded by the human Ether-a-Gogo Related Gene (I(HERG)) by these antihistamines. In fact, whole-cell voltage-clamp experiments revealed that the IC(50) for astemizole-induced hERG blockade is about 300-fold lower than that for the inhibition of high K(+)-induced [3H]NE release. Furthermore, current-clamp experiments in SH-SY5Y cells showed that concentrations of astemizole (3 microM) which were effective in preventing depolarization-induced [3H]NE release were unable to interfere with the cell membrane potential under depolarizing conditions (100 mM [K(+)](e)), suggesting that hERG K(+) channels do not contribute to membrane potential control during exposure to elevated [K(+)](e). Collectively, the results of the present study suggest that, in SH-SY5Y human neuroblastoma cells, the inhibition of SOCs by some second-generation antihistamines can prevent depolarization-induced neurotransmitter release.
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This diagnostic approach allowed us to identify a large group (47 patients) with UV. Most did not present the clinical (prolonged duration of weals and bruising) and laboratory features that have previously been described as characteristic of UV. Cinnarizine was found to be a valuable treatment option.
Bilastine reduced patients' mean reflective and instantaneous TSS from baseline to a significantly greater degree than placebo (P < 0.001); from day 2 onwards of treatment. The DLQI, general discomfort, and sleep disruption were also improved significantly in bilastine-treated patients as compared with placebo-treated patients (P < 0.001 for all parameters). Comparison with levocetirizine indicated both treatments to be equally efficacious as well as equally safe and well tolerated as compared with placebo.
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Some recent clinical studies carried out with the potent H1-antihistamine cetirizine (CTZ) suggest that this drug could be useful for the treatment of mild to moderate asthma and even for the prevention of the disease. Besides a potent antagonism of H1-receptors at bronchial level, this drug was also shown to exert a large series of anti-inflammatory effects in in vitro, ex vivo and in vivo pharmacological models and also in clinical situations in atopic subjects. All the data collected up to now suggest the possible existence in the molecule of a central key mechanism of action on resident cells especially involved in cell trafficking and bronchial inflammation, i.e a down-regulating effect on the nuclear factorKappaB (NFkappaB). This hypothesis was tested on human endothelial cells and a human epithelial pulmonary cell line using different experimental methods. The results showed that CTZ down-regulates the TNF-alpha-induced hyperactivation of NFKappaB in these two different resident cells at physiological concentrations.
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We examined the relative clinical efficacy of three commonly used antianxiety medications and a placebo as adjuncts to analgesic treatment of chronic cancer and arthritic pain. Nine patients with chronic pain, including six with malignancy and three with rheumatic diseases, were each exposed to three treatment phases with antianxiety drugs (hydroxyzine, prochlorperazine, and chlordiazepoxide) and one placebo phase in a double-blind, counter-balanced design. Each phase lasted 2 weeks, with analgesic medication given throughout. Pre- and post-phase measures of anxiety, depression, and hostility were taken, together with daily reports by the patients on pain, mood, and medication intake. None of the antianxiety drugs were significantly more effective than the placebo in reducing pain levels, daily medication usage or hostility. Chlordiazepoxide significantly reduced anxiety and depression compared with the placebo, but also produced the most side effects (e.g., drowsiness). The preliminary findings failed to support the efficacy of the three antianxiety medications as analgesic adjuncts.
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Cetirizine 10 mg, ebastine 10 mg, epinastine 20 mg, fexofenadine 60 mg, terfenadine 60 mg, loratadine 10 mg, or placebo was given to 14 healthy male volunteers in a double-blind, crossover randomized manner. Inhibition of the wheal and flare response to epicutaneous histamine phosphate (100 mg/ml) challenge was measured at 0, 0.5, 1, 2, 4, 6, 8, 10, 12, and 24 h after doses.
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A case of Giardia lamblia infestation with concomitent urticaria is presented. No mechanisms of association are suggested. With treatment of the Giardia, the urticaria cleared. The urticaria could also be suprressed with Atarax.
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Selection of appropriate treatment for generalized anxiety disorder (GAD) is influenced by several considerations, including psychiatric comorbidity. Emerging data suggest that GAD has a chronic course and a high comorbidity with depression. Successful treatment can be facilitated by first establishing treatment goals, which include managing acute anxiety and following through to remission. Prevention of GAD recurrence should be the ultimate objective. Many treatments exist to aid in the realization of treatment goals, including benzodiazepines, hydroxyzine, buspirone, selective serotonin reuptake inhibitors (SSRIs), and serotonin-norepinephrine reuptake inhibitors (SNRIs). Some SSRIs and an SNRI have been demonstrated effective in both acute and long-term trials, establishing them as first-line therapies. Benzodiazepines are helpful because of their rapid onset of action and efficacy in somatic and autonomic symptoms of GAD. Other medications in the pipeline include gamma-aminobutyric acid (GABA) modulators, which may have lower abuse potential than currently available agents that act at the GABA receptor; corticotropin-releasing hormone (CRH) antagonists; and pregabalin. The recent realization of the chronic nature of GAD and the recognition of its frequent comorbidity with depression, coupled with data from randomized clinical trials of newer generation agents, should help physicians better diagnose GAD and achieve the goal of bringing patients to full remission.
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High performance liquid chromatography (HPLC) was hyphenated with a previously reported carbamazepine-specific enzyme-linked immunosorbent assay (ELISA) as a screening approach to water analysis in order to identify possible interferences from transformation products. Treated wastewater was analysed and three substances were recognized by the antibody besides carbamazepine: the metabolites 10,11-dihydro-10,11-epoxycarbamazepine and 2-hydroxycarbamazepine plus the structurally not obviously related antihistamine cetirizine. The molar cross-reactivity against cetirizine was found to be pH-dependent and assessed to be 400% at pH 4.5 and 22% at pH 10.5. Performing the ELISA at pH 10.5 greatly improved the accuracy when carbamazepine was determined in surface and wastewater samples.
The effects of doxepin and hydroxyzine on the cognitive performance of 60 patients with anxiety were compared under different levels of experimentally induced motivation and experience of success or failure. Both drugs reduced the inhibiting effects of failure on concept learning. The combination of high motivation and failure interfered more with the performance of control patients than the drug groups. The cognitive facilitation effects of doxepin were most pronounced in the low motivation-failure condition, while hydroxyzine yielded superior performance in both success and failure conditions, regardless of motivation level.
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Systemic administration of the known H1-antagonists suppresses histamine sensitivity of both skin and nasal mucosa in the same degree. Drugs with more potent antihistaminic activity (fexofenadin and cetirisin) inhibited allergen-induced reactions more effectively. The order of the tested drugs by suppression of allergen-provoked skin and nasal reactions (by lowering antiallergic activity) is the following: fexofenadin and cetirisin > ebastin and loratadin > clemastin.
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The effects of a newly synthesized anti-allergic agent, HSR-609, on allergic airway hyperresponsiveness and airway inflammation have been studied in sensitized mice. The effects were compared with those of two histamine H(1) receptor antagonists, cetirizine and terfenadine, and prednisolone. Three inhalations of antigen caused an increase in leukocytes (including eosinophils) with increases in IL-5 in BALF and airway hyperresponsiveness to acetylcholine in BALB/c mice. All drugs were orally administered once a day for 10 days from the day before the first inhalation of antigen. HSR-609 (10 mg/kg) and prednisolone (5 mg/kg) significantly inhibited the antigen-induced airway hyperresponsiveness, whereas cetirizine (10 mg/kg) or terfenadine (100 mg/kg) did not affect this airway response. At the same time HSR-609 inhibited the antigen-induced eosinophilia and IL-5 production in BALF. Prednisolone also showed an inhibitory effect on the airway eosinophilia and IL-5 production but not cetirizine and terfenadine in the same experiments. In addition, HSR-609 (p.o.) dose-dependently suppressed the accumulation of eosinophils elicited by antigen-stimulated D10G4.1 cells, a murine Th2 clone, in peritoneal cavity lavage fluid in AKR/J mice. These results suggest that HSR-609 inhibits allergic airway hyperresponsiveness to acetylcholine probably because of the inhibition of Th2-dependent eosinophilia caused by IL-5. In addition, effects of HSR-609 were different from those of cetirizine and terfenadine concerning the inhibition of antigen-induced airway hyperresponsiveness in mice.
A 32-year-old woman, gravida 4, para 2, visited Teikyo University Hospital with complaints of abnormal uterine bleeding and lower abdominal pain. Urine hCG level was 1,024 x 10(3) IU/l. MRI examination showed a vascular, rich solid mass 10 cm in diameter at the posterior region of the uterus. Under the clinical diagnosis of choriocarcinoma, she underwent total hysterectomy with right salpingooophorectomy. The ovarian choriocarcinoma was confirmed by pathologic examination. Additional chemotherapy was planned using the combined regimen of etoposide, methotrexate, actinomycin D, cyclophosphamide and oncovin. After 2 min of etoposide administration (100 mg/m2), the patient complained of acute dyspnea, which was caused by bronchospasms and cutaneous flushing. Etoposide infusion was immediately stopped, and anti-anaphylaxic treatment was done by administering hydroxyzine hydrochloride. Five min after the episode had occurred, the patient recovered. This episode was thought to have been induced by etoposide, but etoposide was a key agent for choriocarcinoma. Thus, we devised a modified chemotherapy using etoposide as follows. The regimen was hydrocortisone 100 mg i.v. q6 h and promethazine hydrochloride 50 mg i.m. q6 h for 24 h before infusion of etoposide. The etoposide concentration was diluted to 50%, and the drug administration rate reduced by half. With the modified regimen, the patient showed no anaphylaxic symptoms. The few reports on anaphylaxic reactions to chemotherapeutic agents induced by side effects must be taken into account when we use these drugs.
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There are limited comparative studies on classic and new-generation antihistamines that affect sleep quality and mood. The purpose of this study was to determine and compare the effects of classic and new-generation antihistamines on sleep quality, daytime sleepiness, dream anxiety, and mood.
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Taken together, these findings suggest that CCR5 delta32 heterozygosity exerts a protective effect against perinatal transmission in children exposed to a low maternal viral burden of an R5-type isolate.