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Claritin

Generic Claritin is an effective medication which helps to fight with the symptoms of allergies. It is used in treatment of watery eyes, sneezing, skin hives, runny nose and pruritus in people with chronic skin reactions. Generic Claritin acts by lowering the natural chemical histamine in the body.

Other names for this medication:

Similar Products:
Alavert

 

Also known as:  Loratadine.

Description

Generic Claritin is a perfect remedy, which helps to fight against the symptoms of allergies. Its target is to treat watery eyes, sneezing, skin hives, runny nose and pruritus in people with chronic skin reactions.

Generic Claritin acts by lowering the natural chemical histamine in the body. It is antihistamine.

Claritin is also known as Loratadine, Claritine, Clarityn, Clarityne, Fristamin, Lorfast, Lomilan, Symphoral, Roletra, Rinolan, AllergyX, Alavert, Tidilor.

Generic name of Generic Claritin is Loratadine.

Brand names of Generic Claritine are Alavert, Claritin, Claritin Hives Relief, Claritin Reditab, Clear-Atadine, Clear-Atadine Children's, Dimetapp ND, Loratadine Reditab, Tavist ND, Wal-itin.

Dosage

Take Generic Claritin tablets and liquid form orally with or without food. Do not crush or chew it.

Take Generic Claritin once a day at the same time.

If you want to achieve most effective results do not stop taking Generic Claritin suddenly.

Overdose

If you overdose Generic Claritin and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Claritin overdosage: feeling drowsy, abnormal heartbeats, migraine.

Storage

Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Claritin are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Generic Claritin if you are allergic to Generic Claritin components.

Try to be careful with Generic Claritin if you're pregnant or you plan to have a baby, or you are a nursing mother. Generic Claritin can harm your baby.

Generic Claritin is not used by children younger than 6 years old.

It can be dangerous to use Generic Claritin if you suffer from or have a history of liver or kidney disease.

Do not stop taking Generic Claritin suddenly.

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Asthma and seasonal allergic rhinitis (SAR) are recognized as manifestations of a single airway disease. Desloratadine has demonstrated efficacy in treating SAR symptoms, including nasal obstruction.

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For the evaluation of the action of histamine and LTD(4) on arteries and veins, porcine nasal mucosa was isolated and cut into slices (100-300 microm thick). Real-time images of the nasal arteries and veins were recorded and vessel activities estimated by changes in cross-sectional area before and after the tested drugs. For the in vivo studies, the effect of loratadine and montelukast given alone and in combination was examined on upper airway inflammation in ovalbumin-sensitized and -challenged Brown Norway rats.

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We have investigated the cardiac effects of the H1-receptor antagonists terfenadine, astemizole, loratadine and cetirizine, used in recommended doses, concomitantly or not with the antibiotic erythromycin.

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The anti-anaphylactic/anti-histamine activity of mizolastine (CAS 108612-45-9, SL 85.0324), a novel histamine H1 receptor antagonist devoid of sedative properties, has been evaluated in the rat, mouse and guinea pig. Mizolastine inhibited the passive cutaneous anaphylactic reduction caused by ovalbumin challenge in the rat (ED50 = 0.7 mg/kg i.v., 1.6 mg/kg p.o.) and effectively protected rats from the lethal shock induced by compound 48/80 (ED50 = 0.07 mg/kg p.o.). Mizolastine protected actively sensitized guinea pigs from anaphylactic mortality, bronchospasm and respiratory difficulties (increase in pulmonary resistance) preceding this event and from morphological modifications at doses from 0.05 mg/kg i.v. The pharmacological activity of mizolastine is linked to a selective blockade of histamine H1 receptors as indicated by the ability of this compound to antagonize rat paw edema induced by the subplantar injection of histamine (ED50 = 0.5 mg/kg p.o.) but not that induced by the injection of serotonin or bradykinin. Mizolastine also antagonized the increase in cutaneous capillary permeability caused by the intradermal injection of histamine (-80% at 0.3 mg/kg p.o.) and compound 48/80 (ED50 = 1.1 mg/kg p.o.) but not that induced by serotonin in the rat. In the guinea pig, mizolastine antagonized i.v. histamine-induced bronchoconstriction (ED50 = 0.03 mg/kg p.o.) and histamine-induced vascular permeability and edema in trachea and bronchi (ED50 < or = 0.05 mg/kg i.v.). Moreover, at higher doses, mizolastine antagonized the bronchospasm caused by systemic injection of platelet-activating factor (PAF) and leukotriene D4 (LTD4) (ED50's = 0.30 and 3.0 mg/kg p.o., respectively). However, mizolastine only weakly antagonized bronchospasm induced by aerosolized PAF (-67% at 50 mg/kg p.o.), failed to antagonize (up to 3 mg/kg i.v.) PAF-induced microvascular permeability of the tracheal mucosa in the guinea pig and was a weak inhibitor of PAF-induced platelet aggregation in the rabbit (IC50 = 74 mumol/l). In addition to antagonizing histamine H1 receptors, mizolastine also inhibits the release of histamine during allergic reactions in tissues. Thus, mizolastine antagonizes the antigen-induced in vivo release of histamine from mast cells in bronchoalveolar lavages of actively sensitized guinea pigs (minimal effective dose 0.3 mg/kg p.o.) and the release of histamine from mast cells in the peritoneal fluid of passively sensitized rats (ED50 = 0.9 mg/kg i.v.). In these various models, mizolastine was more potent than loratadine and terfenadine but less potent than ketotifen. The apparent half-life for the pharmacological actions of mizolastine ranged from 6 to 8 h.(ABSTRACT TRUNCATED AT 400 WORDS)

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The efficacy of loratadine as prophylactic therapy for seasonal allergic rhinitis was evaluated in a randomized, double-blind, parallel group, placebo-controlled study. One hundred eighteen subjects received either loratadine, 10 mg once daily, or placebo for 6 weeks. Treatment was begun prior to the onset of grass pollen seasonal symptoms of allergic rhinitis. Total symptom-free days occurred more frequently in subjects receiving loratadine. More loratadine than placebo subjects (65% versus 49%) had no symptoms or mild rhinitis at the end of the study. In contrast, the differences between loratadine and placebo in symptom scores did not achieve significance. The incidence of sedation and anticholinergic effects were comparable between the groups. Prophylactic loratadine therapy was effective in suppressing symptoms of seasonal allergic rhinitis and providing patients with symptom-free days throughout the pollen season.

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Respondents were interviewed while they were at their residences.

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Mean patient characteristics and symptom scores at baseline were similar for the three treatment groups. The primary end-point, daytime nasal symptoms score (mean of nasal congestion, rhinorrhea, nasal pruritus, and sneezing scores; 0-3 scale), improved from baseline during treatment by (least squares mean, 95% confidence interval) - 0.37 (- 0.43, - 0.31), - 0.47 (- 0.52, - 0.43), and - 0.24 (- 0.29, - 0.18) in the montelukast, loratadine, and placebo groups, respectively (P < or = 0.001 comparing each active treatment with placebo). Mean changes from baseline in all other diary-based scores, including night-time and eye symptom scores, were significantly greater for each active treatment than for placebo. The rhinoconjunctivitis quality of life overall score improved significantly with montelukast and with loratadine as compared with placebo. Montelukast and loratadine showed a safety profile comparable to that of placebo.

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Forty-six grass pollen allergic SAR patients received desloratadine or placebo for 7 days, followed by a 10-day washout, and then crossed over to the other treatment for 7 days. A 6-h allergen exposure was performed at the end of each treatment period.

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In the 30 days after the first antihistamine prescription, the rate of all injuries was 308 per 1,000 person-years in the diphenhydramine cohort versus 137 per 1,000 person-years in the loratadine cohort. The rate ratio estimate adjusted for age and gender using Poisson regression was 2.27 (95% confidence limits [CL] 1.93, 2.66). In the corresponding 30 days of the preceding year, the injury rates in the diphenhydramine and loratadine cohorts were 128 and 125 per 1,000 person-years, and the adjusted rate ratio was 1.02 (CL 0.83, 1.26). Thus, the cohorts appeared to have similar preprescription injury rates. The differences between the cohorts declined with time from prescription: For all injuries, the estimated percentage decline in the rate ratio was 4.1% per day (CL 3.3, 4.9), and the estimated time from the initial prescription until the diphenhydramine cohort returned to baseline risk was 32.3 days (CL 26.9, 37.6).

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The use of loratadine was compared to dexchlorpheniramine in the treatment of children affected by perennial allergic rhinitis in order to assess its clinical efficacy and tolerability. Children were randomly assigned to two groups: 15 were treated with loratadine and 16 with dexchlorpheniramine. Loratadine was administered in a single daily dose of 5 mg (2.5 mg for children under 20 kg) and dexchlorpheniramine at a dose of 1 mg every 8 hours (0.5 mg for the youngest children). Clinical symptoms were recorded before and during the study using a score of 0.3 (from absent to severe). Symptoms were markedly reduced by both drugs. Eye burning was reduced more by loratadine (p less than 0.05) than the control drug. Rhinoscopic investigations revealed that both groups reacted favourably to the drugs used. Overall clinical assessment showed similar and revealed the good efficacy of both drugs. Tolerability was satisfactory and there were no signs of drowsiness. Hematological and hematochemical parameters showed no clinically significant changes and body weight remained constant. On the basis of these results, loratadine is preferable to dexchlorpheniramine thanks to its once-a-day dosing.

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Three groups of infected and ovalbumin (OVA)-sensitized mice were studied: (1) infected and allergic mice treated with desloratadine, (2) infected and allergic mice treated with placebo, and (3) infected mice. A fourth group of uninfected, non-sensitized mice served as a control for the cellular changes. BALB/c mice were sensitized by two intraperitoneal injections of OVA given 8 days apart. One day after the second injection, the mice were nasally exposed daily to 6% OVA (the groups treated with desloratadine or placebo) or phosphate-buffered saline (PBS) (the infection-only group) for 5 days. After the second OVA exposure, the mice were intranasally inoculated with Streptococcus pneumoniae. Desloratadine or placebo was given daily throughout the OVA exposure period. Nasal allergic symptoms were observed by counting of nasal rubbing and sneezing for 10 min after OVA or PBS nasal challenge. On day 5 post-infection, nasal lavage culture was done, and the inflammatory cells in the sinuses were evaluated by flow cytometry.

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To identify experience with and attitudes towards paediatric off-label prescribing in primary care.

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Ingesting 10 mg of loratadine daily does not have sedative effects or impair cognitive-motor performance. Higher doses have demonstrated impairment. Aviation concerns that have not been addressed include centrifuge studies and color vision studies. It would be reasonable to employ loratadine in the high performance aerospace environment if these latter tests prove to be negative.

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Desloratadine at standard and high doses significantly improved objective signs of ACU provoked by cold exposure. Desloratadine at 4 times the standard dose significantly reduced ACU lesion severity versus 5 mg of desloratadine without an increase in AEs. This study supports current guidelines that increased desloratadine dosing might benefit patients with urticaria who do not respond to standard doses.

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Few randomized studies have compared the H1-receptor antagonists loratadine and ebastine in seasonal allergic rhinitis (SAR) patients. The objective of this study was to compare the efficacy and safety of ebastine 20 mg (E20), ebastine 10 mg (E10), loratadine 10 mg (L10), and placebo (P), once daily, in controlling symptoms of SAR over a 4-week period. This was a double-blind, placebo-controlled, randomized, parallel-group study. Efficacy was assessed in 749 patients (12 to 70 years old) by SAR symptom scores (nasal discharge, congestion, itching, sneezing, and total eye symptoms) entered on diary cards every morning and every evening over the previous 12 hours (reflective score) and at the time of recording (snapshot score). The E20 group showed greater reductions from baseline compared with the L10 group in 2 daily reflective composite scores (nasal index [with or without congestion]) and in all 4 daily snapshot composite scores. E10 and L10 groups showed no significant differences in either the daily reflective or snapshot scores overall although E10 showed a greater improvement of nasal discharge snapshot score than L10. The efficacy of E20 at controlling the symptoms of SAR was well sustained during the fourth week of treatment, with significant differences over placebo in 22/36 total rhinitis symptom scores, followed by E10 (6/36), whereas L10 showed no differences (0/36). Patient and physician global evaluations at the final visit were not statistically significant for any treatment group compared with placebo. There was no significant difference among all groups in the number of patients who reported adverse events. In conclusion, ebastine 20 mg given once daily for 4 weeks in the treatment of SAR showed larger mean reductions from baseline in most rhinitis symptoms scores than loratadine 10 mg. Sustained efficacy was most frequently observed with ebastine 20 mg over placebo, whereas loratadine 10 mg did not provide a statistically significant improvement in any individual or composite symptom score at the end of the fourth week. Both ebastine 20 and 10 mg were well tolerated and proved safe in the treatment of SAR.

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Cardiovascular safety of loratadine, a second generation H1-antagonist, is confirmed in long-term treatment of persistent allergic rhinitis at a recommended dose.

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Desloratadine and loratadine (0.1-10 micromol/L) inhibited rhinovirus-induced ICAM-1 upregulation in both primary bronchial or transformed (A549) respiratory epithelial cells. In A549 cells the 2 compounds showed a dose-dependent inhibition with similar efficacy (inhibitory concentration of 50%, 1 micromol/L). Desloratadine and loratadine also inhibited ICAM-1 mRNA induction caused by rhinovirus infection in a dose-dependent manner, and they completely inhibited rhinovirus-induced ICAM-1 promoter activation. Desloratadine also inhibited rhinovirus-induced nuclear factor kappa B activation. Desloratadine and loratadine had no direct effect on rhinovirus infectivity and replication in cultured epithelial cells.

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The possibility that non-sedating antihistamines could elicit sedation in mice due to drug-induced inhibition of brain PgP was evaluated by measuring the ability of desloratadine alone or in combination with verapamil to cause ataxia in mice. Also, the concentrations of desloratadine in plasma and in brain homogenates were measured by liquid chromatography-mass spectrometry. Relative to methylcellulose (control) treatment, verapamil plus desloratadine decreased rotarod performance of mice. Plasma concentrations of desloratadine appeared comparable in the mice treated with either desloratadine or verapamil plus desloratadine, however the rate of decline of desloratadine from brain tissue was slower in mice treated with verapamil plus desloratadine compared to mice treated with desloratadine only. These data suggest that inhibition of brain PgP can convert desloratadine to a sedating antihistamine in mice.

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The basophil activation test (BAT) is a widely validated and reliable tool especially for the diagnosis of hymenoptera venom allergy. Nevertheless, several pitfalls have to be considered and outcomes may differ because of diverse in-house protocols and commercially available kits. We aimed to identify the factors that may influence results of the CD63-based BAT.

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The interaction of mizolastine (CAS 108612-45-9, SL 85.0324) with histamine H1 receptors has been evaluated in the rodent. Mizolastine inhibited with high affinity (IC50 = 47 nmol/l) the binding of [3H]pyrilamine to histamine H1 receptors in guinea pig cerebellar membranes and sections. The order of potency of mizolastine and various H1 antagonists in this binding assay was the following: cyproheptadine > pyrilamine > mequitazine > mizolastine > astemizole > terfenadine > cetirizine > loratadine. Mizolastine also potently antagonized the contractile effects of histamine in the guinea pig ileum (pA2 = 8.5) and histamine-induced stimulation of phosphoinositide turnover in rat cortical slices (IC50 = 0.35 mumol/l). In contrast, this compound displayed very low affinity for serotonergic, noradrenergic and muscarinic cholinergic receptors as evidenced in both binding assays and functional tests. In guinea pig cerebellar membranes, [3H]mizolastine labelled in a saturable and reversible manner a single population of binding sites with Kd and Bmax values of 1.1 nmol/l and 635 fmol/mg protein, respectively. [3H]Mizolastine binding in guinea pig cerebellar membranes was inhibited by histamine (IC50 = 30 mumol/l) and by drugs that possess affinity for the H1 receptor such as pyrilamine (IC50 = 1 nmol/1), DL-chlorphenyramine (IC50 = 6.4 nmol/l) terfenadine (IC50 = 6 nmol/l) and loratadine (IC50 = 50 nmol/l). At concentrations lower than 10 mumol/l, the H2 receptor ligands dimaprit and cimetidine and the H3 receptor ligands burimamide and 4-methyl-histamine failed to displace [3H]mizolastine binding.(ABSTRACT TRUNCATED AT 250 WORDS)

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Mizolastine is a nonsedating H1 histamine receptor antagonist with additional antiallergic properties currently marketed in Europe for the treatment of seasonal and perennial allergic rhinitis (PAR) and urticaria.

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To compare the efficacy and safety of epinastine 10 mg plus pseudoephedrine 120 mg vs loratadine 5 mg plus pseudoephedrine 120 mg, twice a day, in the treatment of perennial allergic rhinitis.

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Ebastine is a long-acting nonsedating second generation histamine H1 receptor antagonist which binds preferentially to peripheral H1 receptors in vivo. It has shown antihistamine and antiallergic activity in healthy volunteers and patients with allergies, and protected against histamine-induced bronchoconstriction in patients with asthma. Significant symptom improvement is observed in patients with seasonal or perennial allergic rhinitis or chronic idiopathic urticaria following administration of ebastine 10 mg/day, or 20 mg/day in severe rhinitis. In clinical trials, the efficacy of ebastine 10 or 20 mg/day was generally similar to standard dosages of terfenadine, cetirizine, astemizole and loratadine in patients with seasonal allergic rhinitis, astemizole, terfenadine and ketotifen in patients with chronic idiopathic urticaria, and ketotifen, terfenadine, chlorpheniramine and mequitazine in patients with perennial allergic rhinitis. The most frequent adverse events reported during ebastine therapy are drowsiness, headache and dry mouth, the incidence being similar to that reported in placebo recipients. Serious adverse cardiac events, observed on rare occasions with some other histamine H1 receptor antagonists, have not been reported with ebastine, and there has been no evidence of QTc interval prolongation related to ebastine therapy. Thus, once-daily ebastine offers an effective and well-tolerated alternative to other second generation antihistamines in current use for the first-line treatment of seasonal and perennial allergic rhinitis and chronic idiopathic urticaria.

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Desloratadine and budesonide caused a significant increase in NPIF compared with baseline on the evening of the first dose (P < .01). Budesonide, however, led to a significantly greater increase in NPIF than did desloratadine when the change from baseline was compared for the entire treatment period (median, 475 vs 150 L/min; P = .01). Both treatments resulted in clinically significant reductions of the individual domains and overall scores on the Rhinoconjunctivitis Quality of Life Questionnaire (P < .01). There was a significant reduction in total symptom scores (P < or = .01) compared with baseline during all treatment days in both treatment groups, with no statistically significant differences between treatments (median, -60.0 vs -59.5; P = .67).

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The conversion of loratadine from prescription (Rx)-only to over-the-counter (OTC) status on November 27, 2002, brought about the question of how OTC products may influence utilization of both OTC and Rx-only low-sedating antihistamines (LSAs) simultaneously. North Carolina (NC) Medicaid initially did not cover loratadine OTC but subsequently changed the policy 1 year after OTC conversion, on November 23, 2003. The objective of this study was to determine patterns of LSA utilization in relation to changes in OTC availability and Medicaid coverage policy and to assess the rate of product switching associated with these policies.

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Cynomolgus monkeys are used widely in preclinical studies as non-human primate species. The amino acid sequence of cynomolgus monkey cytochrome P450 (P450 or CYP) 2C19 is reportedly highly correlated to that of human CYP2C19 (92%) and CYP2C9 (93%). In the present study, 89 commercially available compounds were screened to find potential substrates for cynomolgus monkey CYP2C19. Of 89 drugs, 34 were metabolically depleted by cynomolgus monkey CYP2C19 with relatively high rates. Among them, 30 compounds have been reported as substrates or inhibitors of, either or both, human CYP2C19 and CYP2C9. Several compounds, including loratadine, showed high selectivity to cynomolgus monkey CYP2C19, and all of these have been reported as human CYP2C19 and/or CYP2C9 substrates. In addition, cynomolgus monkey CYP2C19 formed the same loratadine metabolite as human CYP2C19, descarboethoxyloratadine. These results suggest that cynomolgus monkey CYP2C19 is generally similar to human CYP2C19 and CYP2C9 in its substrate recognition functionality.

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Pharmacists can play an important role in the management of allergic rhinitis and CIU by considering the relative advantages of newer-generation agents when reviewing treatment options.

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The present study aims to investigate the effects of prednisolone on the pharmacokinetics of orally and intravenously administered loratadine in rats. A single dose of loratadine was administered orally (4 mg/kg) and intravenously (1 mg/kg) in the presence or absence of prednisolone (0.2 or 0.8 mg/kg). Compared to the oral control group, prednisolone (0.2 mg/kg, p < 0.05; 0.8 mg/kg, p < 0.01) significantly increased the area under the plasma concentrationtime curve of orally administered loratadine by 54.0-96.4%. After oral administration, the peak plasma concentration of loratadine was significantly (0.2 mg/kg, p < 0.05; 0.8 mg/kg, p < 0.01) increased by 20.9-65.3% in the presence of prednisolone. Consequently, the relative bioavailability of loratadine was increased by 1.54- to 1.96-fold. Compared to the intravenous control group, the presence of prednisolone significantly (0.8 mg/kg, p < 0.05) increased the area under the plasma concentration-time curve of loratadine. Prednisolone enhanced the oral bioavailability of loratadine in this study. The enhanced bioavailability of loratadine may be due to inhibition both cytochrome P450 3A4-mediated metabolism and the efflux pump P-glycoprotein (P-gp) in the intestine and/or liver by the presence of prednisolone.

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Few randomized studies have compared the efficacy of ebastine and loratadine in the symptomatic treatment of seasonal allergic rhinitis (SAR).

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claritin 80 tablets 2016-07-20

This was a randomized, double-masked, placebo- and active-controlled, single-center clinical trial. At visit l, the dose of allergen necessary to elicit a qualifying allergic reaction was determined for subjects meeting the entry criteria. At visit 2, the allergen dose determined at visit 1 was confirmed, and all subjects who had a qualifying ocular and nasal allergic reaction were randomized to 1 of 3 treatment groups: ketotifen ophthalmic solution and placebo tablet, desloratadine tablet and placebo eyedrop, or ketotifen and desloratadine. Subjects were instructed to instill 1 drop into each eye twice daily and take 1 tablet with water once daily at the same time as the morning eyedrop for approximately 4 weeks. At visit 3, subjects brought in their medication and were given 1 drop of the eyedrop bilaterally and 1 tablet with water. Bilateral CAC was performed 2 hours after administration of medication. Using standardized scales, subjects rated ocular itching at 3, 5, and 7 minutes after CAC; ocular tearing and eyelid swelling at 10, 15, and buy claritin 20 minutes after CAC; and nasal signs and symptoms (sneezing, rhinorrhea and postnasal drip, pruritus, and nasal congestion) at 10, 20, 30, 40, and 50 minutes after CAC. The investigator graded ocular redness and chemosis at 10, 15, and 20 minutes after CAC. At all visits, subjects were offered an anti-allergy eyedrop to relieve any immediate ocular discomfort caused by CAC.

claritin mg dosage 2016-12-17

A novel stability-indicating gradient reverse phase ultra-performance liquid chromatographic (RP-UPLC) method was developed for the determination of purity of desloratadine in presence of its impurities and forced degradation products. The method was developed using Waters Aquity BEH C18 column with mobile phase containing a gradient mixture of solvents A and B. The eluted compounds were monitored at 280nm. The run time was 8min within which desloratadine and its five impurities were well separated. Desloratadine was subjected to the stress conditions of oxidative, acid, base, hydrolytic, thermal and photolytic degradation. Desloratadine was found to degrade significantly in oxidative and thermal stress conditions and stable in acid, base, hydrolytic buy claritin and photolytic degradation conditions. The degradation products were well resolved from main peak and its impurities, thus proved the stability-indicating power of the method. The developed method was validated as per ICH guidelines with respect to specificity, linearity, limit of detection, limit of quantification, accuracy, precision and robustness. This method was also suitable for the assay determination of desloratadine in pharmaceutical dosage forms.

claritin syrup ingredients 2016-07-11

First- and second-generation antihistamines may significantly impair driving performance. In the context of driving safety but also taking into account the buy claritin cardiotoxic properties of some of the second-generation antihistamines, we advise treating patients with third-generation antihistamines such as fexofenadine and levocetirizine.

claritin dosage weight 2015-09-14

Since the demonstration of an inhibiting effect of cetirizine on an antigen induced eosinophils' migration in the skin of atopic subjects, a series of in vitro and in vivo studies were performed in order to clarify the mechanism of action of this new H1-blocker. The studies used buy claritin FMLP and PAF as agonists, and BN 52021, dexchlorpheniramine, terfenadine and loratadine as reference compounds. The results suggest that the inhibiting effect of cetirizine on the eosinophils' migration is independent of its specific H1 blocking activity.

claritin tabs 2016-12-26

Nasal histamine challenge led to a reproducible, dose-dependent increase in sneezing and nose rubs. The response to histamine exposure was blocked by desloratadine (P < or = .05). Allergic mice had a significant increase in responsiveness (P < or = .05) over baseline after exposure to antigen. Mice with buy claritin acute sinusitis had a sustained increase in responsiveness, although less severe than after allergy, compared with baseline values that lasted 12 days after infection (P < or = .05).

claritin dosage chart 2015-08-27

Loratadine inhibited in a concentration-dependent manner the hKv1.5 current, the apparent affinity being 1.2 +/- 0.2 microM. The blockade increased steeply between -30 and 0 mV which corresponded with the voltage range for channel opening, thus suggesting that the drug binds preferentially to the open state of the channel. The apparent association and dissociation rate constants were (3.6 +/- 0.5) x 10(6).M-1.s-1 and 3.7 +/- 1.6.s-1, respectively. Loratadine, 1 microM, increased the time constant of deactivation of tail currents elicited on return to -40 mV after 500 ms depolarizing pulses to +60 mV from 36.2 +/- 3.4 to 64.9 +/- 3.6 ms (n = 6, P < 0.01), thus inducing a 'crossover' phenomenon. Application of trains of pulses at 1 Hz lead to a progressive increase in the buy claritin blockade reaching a final value of 48.6 +/- 4.3%. Recovery from loratadine-induced block at -80 mV exhibited a time constant of 743.0 +/- 78.0 ms. Finally, the results of a mathematical stimulation of the effects of loratadine, based on an open-channel block model, reproduced fairly well the main effects of the drug.

claritin reviews 2017-07-06

Triamcinolone is a commonly used synthetic corticosteroid that has recently been tested in a large clinical trial for chronic obstructive pulmonary disease and shown to have some benefits. To our knowledge, there are no reviews of the pharmacotherapy buy claritin of triamcinolone. This review has a brief overview of the pharmacology of triamcinolone, followed by a discussion of the clinical trials with triamcinolone. Triamcinolone is used in the treatment of respiratory inflammation, rheumatoid arthritis and a variety of other inflammatory conditions.

claritin children dosage 2016-07-18

A sensitive, selective and simple high performance liquid chromatographyelectrospray ionization-mass spectrometry (HPLC-ESI-MS) was developed and validated for the quantification of ticlopidine hydrochloride (CAS 53885-35-1) in human plasma using loratadine (CAS 79794-75-5) as internal standard (IS). Following liquid-liquid extraction, the analyte and the IS were extracted from plasma samples by n-hexane:isopropanol (95:5, v/v), separated by HPLC on a commercially available column (150 mm x 2.0 mm ID, 5 microm) with a mobile phase of acetonitrile: 10 mmol/L ammonium acetate buffer solution (85:15, v/v) and analyzed on a quadrupole mass spectrometer with ESI interface operating in the positive-ion mode. The correlation coefficient of the calibration curve was linear (r2 > 0.99) over the concentration range of 1-1000 ng/mL for ticlopidine hydrochloride. The intra- and inter-batch precisions were less than 15% of the relative standard deviation and the accuracy ranged from 85 to 115% in terms of percent accuracy. The limit of buy claritin detection (LOD) of ticlopidine hydrochloride was 0.5 ng/mL. The extraction recovery of ticlopidine hydrochloride was more than 80%. The proposed method enables the unambiguous identification and quantification of ticlopidine hydrochloride for pharmacokinetic, bioavailability or bioequivalence studies.

claritin user reviews 2015-07-26

Rupatadine is a new oral antihistaminic agent used for the management of allergic inflammatory conditions, such as rhinitis and chronic urticaria. The aim of the present study was to develop a population pharmacokinetic/pharmacodynamic (PKPD) model for the description of the effect of rupatadine and one of its active metabolites, desloratadine, on the histamine-induced flare reaction and to predict the response to treatment after repeated administrations of rupatadine. Both rupatadine and desloratadine were characterized by two-compartmental kinetics. For both compounds, covariates sex and weight had a significant effect on several parameters. The pharmacodynamics were described by an indirect model for the inhibition of flare formation that accounted for the contribution of both rupatadine and desloratadine to the antihistaminic effect. The final PKPD model adequately described the original data. The simulated response buy claritin after repeated once-daily administrations of 10 mg rupatadine showed a significant and maintained antihistaminic effect over time, between two consecutive dosing intervals.

claritin mg 2016-07-19

The cured and markedly effective rate was 91.3% (73/80) in the acupuncture bloodletting group, which was similar to 81.3% (65/80) in the loratadine group (P > 0.05). The scores of symptom-sign in the two groups were buy claritin reduced after treatment (10.14 +/- 1.95 vs 2.12 +/- 40.32, 10.30 +/- 1.82 vs 3.21 +/- 0.28, both P < 0.01), but there was no statistically significant difference between two groups after treatment (P > 0.05). There was no obvious adverse effect in the acupuncture bloodletting group while 3 cases of mild somnolence were reported in the loratadine group.

claritin generic equivalent 2016-06-22

All active medications effectively suppressed the histamine-induced wheal and flare for 24 buy claritin hours compared with placebo. Fexofenadine 60 mg twice daily and fexofenadine 120 mg once daily had a faster onset of action than loratadine in this experimental model.

claritin pill 2015-02-16

Ebastine 10 mg FDT demonstrated significantly superior antihistamine activity compared with buy claritin desloratadine and placebo.

claritin off brand 2017-08-06

Olopatadine ophthalmic solution 0.1% (Patanol, Alcon Laboratories, Fort Woth, TX) is approved for the treatment of the signs and symptoms of allergic conjunctivitis. Loratadine 10 mg (Claritin buy claritin , Schering-Plough, Madison, NJ) is a nonsedating oral antihistamine approved for the treatment of the signs and symptoms of allergic rhinitis.

claritin 40 tablets 2016-03-17

Nonsedating H1-receptor antagonists appear to have wide and variable effects on the QT interval, mediated through modulation of cardiac K+ channels. By using the whole-cell patch-clamp technique, we examined the effects of terfenadine, loratadine, and descarboethoxyloratadine on a large family of K+ channels in ventricular myocytes and in Xenopus oocytes expressing the HERG delayed rectifier. The channels studied included the inward rectifier (I(Kl)) of rat and guinea pig, the transient outward K+ current (I(to)) of rat, the maintained K+ current (I(ped)) of rat, and the delayed rectifier K+ channels (I(Ks) and I(Kr)) of guinea pig myocytes. Loratadine and descarboethoxyloratadine, at therapeutic concentrations (30 to 100 nM), had no measurable effect on any one of the five types of K+ channels studied. At higher concentrations, 0.3 to 1.0 microM, only terfenadine had a significant suppressive effect on I(Kl) and delayed rectifier K+ channels, I(Kr) and I(Ks). At higher concentrations (1 to 2.5 microM), there were marked differences in the ability of the three drugs to suppress the five K+ channels. Generally, terfenadine was the most and loratadine, the least effective blocker of all K+ channels examined. The most susceptible K+ channels were the delayed rectifier channels (I(Ks) and I(Kr)) in guinea pig and I(ped) in rat myocytes. Comparative effects of loratadine and terfenadine examined on the I(Kr) channel (HERG) expressed in Xenopus oocytes suggest much higher affinity of this channel to terfenadine, such that 1 microM terfenadine completely suppressed the current, whereas buy claritin loratadine had little or no effect. The preferential suppressive effect of terfenadine on the expressed HERG channel was consistent with data obtained on I(Kr) in isolated guinea pig ventricular myocytes. The strong suppressive effect of terfenadine, noted particularly on the I(Kr) and to a lesser extent on I(to), I(Kl), and I(Ks), may be the cause of the reported incidence of QT prolongation and arrhythmogenesis. The absence of significant effect of loratadine and descarboethoxyloratadine, especially on I(Kr), I(to), I(ped), and I(Kl), even at 100 x highest plasma concentrations achieved, may explain the absence of significant reports of QT prolongation and arrhythmogenesis by the latter drugs.

claritin gel dosage 2017-05-16

To study Vasaka Syrup the roles of leukotriene and histamine in the pathogenesis of allergic rhinitis and to compare the efficacy between leukotriene receptor antagonist and antihistamine by mensurating specific IgE in serum and eosinophil in peripheral blood and nose secretion of patients with allergic rhinitis respectively.

claritin alcohol 2016-08-03

The primary parameter to assess dose proportionality and linearity was AUC Mysoline 10 Mg from time zero to final concentration time point (AUC(S)).

claritin kids dosage 2017-05-28

This study, involving subjects with seasonal allergic rhinitis, examines the effects of loratadine treatment on allergen Levitra Ratings Reviews -induced nasal mucosal output of tryptase and alpha 2-macroglobulin. Effects on nasal symptoms and eosinophils are also examined.

claritin otc dose 2017-06-14

Two new spectrophotometric methods are described for the simultaneous analysis of pseudoephedrine sulfate-dexbrompheniramine maleate (DBP) and pseudoephedrine sulfate-loratadine combinations. In the first, derivative spectrophotometry, dA/dlambda values were read at zero-crossing points. In the second, ratio spectra derivative spectrophotometry, analytical signals were measured at the wavelengths corresponding to either maxima or minima for these drugs in the first derivative spectra of their ratio spectra. The procedures do not require any separation step. Mean recoveries were found to be >99% in the methods for these compounds in their synthetic mixtures. All the spectrophotometric methods proposed were compared with each other and HPLC Micronase Drug Information which was also developed by us and applied to the pharmaceutical preparations selected.

claritin ready tablets 2016-11-10

Buccoadhesive wafer dosage form containing Loratadine Cymbalta Liver Alcohol is formulated utilizing Formulation by Design (FbD) approach incorporating sodium alginate and lactose monohydrate as independent variable employing solvent casting method.

claritin coupon online 2015-10-04

CD203c-based BAT was determined in 82 healthy controls and in 79 allergic Betnovate Cream Order patients. The effects of interleukin (IL)-3 and degranulation enhancing substances were investigated and compared with CD63 upregulation. Furthermore, the influence of different storage conditions and incubation times was evaluated and the impact of antiallergic drugs on the test results was assessed.

claritin normal dosage 2015-09-21

Nighttime problems constitute a significant burden on the quality of life of patients with seasonal allergic rhinitis (SAR). The aim of this study was to evaluate the effectiveness of montelukast on nighttime AR symptoms.

claritin generic 2017-01-21

The combination of montelukast tablets and fluticasone propionate nasal spray improved symptom control and overall quality of life for moderate to severe allergic rhinitis patients.

claritin d generic 2015-03-16

The addition of topical Patanol to systemic Claritin therapy significantly reduced ocular itching associated with allergic conjunctivitis compared to treatment with Claritin alone. These findings prove the added benefit of local Patanol therapy in the treatment of ocular allergic symptoms in patients receiving systemic antihistamines for concomitant systemic allergies.

claritin drug interactions 2016-09-25

Epithelial cells obtained from nasal mucosa or polyps were stimulated with 10% fetal bovine serum in presence of mometasone (10(-11) M-10(-5) M) with/without desloratadine (10(-5) M). Cytokine and sICAM-1 concentrations in supernatants were measured by ELISA. Peripheral blood eosinophils were incubated during 4 days with epithelial cell secretions with (10(-11) M-10(-5) M) and/or desloratadine (10(-5) M) and survival assessed by Trypan blue. Results are expressed as percentage (mean ± SEM) compared to control.

claritin 30 tablets 2017-12-31

More than 89% of new LM starts had no history of an ICS in the claims database. Overall, 61% of all (new and existing) LM patients did not have a claim for an ICS in their drug claims profile during the study period. An estimated 25% of LM utilization was not for asthma. No differences in ER utilization were found between ICS users and LM users; however, the ER utilization rate (0.090 ER visits per patient per year) was lower with combination therapy compared with monotherapy with ICS (0.110 ER visits per patient per year, P = 0.001) or LM (0.119 emergency room visits per patient per year, P<0.001).

claritin gel caps 2017-09-27

Inter- and intra-individual variability of the loratadine (LOR) metabolism in Caucasian subjects was assessed during a bioequivalence study for two pharmaceutical formulations (solid oral dosage forms) containing 10 mg of the active substance. The analytical data were obtained by applying a reliable, low-cost and sensitive ion pair liquid chromatography/fluorescence (IPLC/FLD) method for determination of both loratadine and descarboethoxyloratadine (DCL) in human plasma samples. The sample preparation procedure is based on liquid-liquid extraction of the target analytes from alkalinized plasma using diethyl-ether. The separation of the analytes and 8-chloroazatadine as internal standard (IS) was achieved through an isocratic ion pair (IP) elution on a Purospher((R)) STAR RP-18 column. The mobile phase containing sodium dodecyl sulfate (SDS) as ion pairing agent was pumped at a flow rate of 1 mL/min. Fluorescence detection (FLD) was achieved at 280 nm (excitation) and 440 nm (emission) wavelengths. The increased sensitivity of the method is also based on a large sample injected volume (250 microL). Linear response was found over the 0.5-20 ng/mL concentration interval for both target compounds. Low limits of quantification (LLOQ) around 0.3 ng/mL were found for LOR and DCL. Method validation is presented.